Critical

<div class="ec-hub-wrap"><div class="ec-hub-topbar"><div class="ec-hub-title">Welcome to Critical</div><div class="ec-theme-switch" id="ec-theme-switch"><button type="button" data-mode="light" aria-label="Light mode" aria-pressed="false"><svg viewBox="0 0 24 24" fill="none" stroke="currentColor" stroke-width="2" stroke-linecap="round"><circle cx="12" cy="12" r="4"></circle><path d="M12 2v2M12 20v2M4.9 4.9l1.4 1.4M17.7 17.7l1.4 1.4M2 12h2M20 12h2M4.9 19.1l1.4-1.4M17.7 6.3l1.4-1.4"></path></svg></button><button type="button" data-mode="sepia" aria-label="Sepia mode" aria-pressed="true"><svg viewBox="0 0 24 24" fill="none" stroke="currentColor" stroke-width="2" stroke-linecap="round" stroke-linejoin="round"><path d="M4 5.5C4 4.67 4.67 4 5.5 4H12v16H5.5A1.5 1.5 0 0 1 4 18.5z"></path><path d="M20 5.5C20 4.67 19.33 4 18.5 4H12v16h6.5a1.5 1.5 0 0 0 1.5-1.5z"></path></svg></button><button type="button" data-mode="dark" aria-label="Dark mode" aria-pressed="false"><svg viewBox="0 0 24 24" fill="none" stroke="currentColor" stroke-width="2" stroke-linecap="round" stroke-linejoin="round"><path d="M21 12.8A9 9 0 1 1 11.2 3a7 7 0 0 0 9.8 9.8z"></path></svg></button></div></div><div class="ec-hub-intro">A free, independent USMLE Step 2 CK–style practice tool, 299 cases, one best answer per item, immediate feedback, retries, and a sourced debrief for every choice. Built for medical students. Not affiliated with, endorsed by, or sponsored by USMLE, NBME, FSMB, or ECFMG.</div><div class="ec-start-btn">[[Start a case →->STEMI - Ix]]</div><div class="ec-note ec-note-short">Practice tool, not medical advice. No physician has formally reviewed the full bank yet. Spot an error? <a href="https://github.com/xairu23/Critical/issues" target="_blank" rel="noopener">Report it on GitHub</a>. Full disclaimer at the bottom.</div><div class="ec-hub-intro" style="font-size:.9rem;">299 questions. Jump to one by number, hit random, or scroll the full list.</div><input type="text" inputmode="numeric" class="ec-search" id="ec-case-search" placeholder="Jump to question number…" autocomplete="off"><div class="ec-search-preview" id="ec-search-preview"></div><div id="ec-continue-slot"></div><button type="button" class="ec-random-btn" id="ec-random-btn">Random question</button><div class="ec-history" id="ec-history"><div class="ec-history-head" id="ec-history-head"><div class="ec-history-title">Recent attempts</div><div class="ec-history-toggle" id="ec-history-toggle"></div></div><div class="ec-history-list" id="ec-history-list"></div></div><div class="ec-hub-links"><div class="ec-hub-item">[[Question 1->STEMI - Ix]]<span class="ec-status" data-case="STEMI. Ix"></span></div><div class="ec-hub-item">[[Question 2->STEMI prognosis - Dx]]<span class="ec-status" data-case="STEMI prognosis. Dx"></span></div><div class="ec-hub-item">[[Question 3->AF anticoagulation - Rx]]<span class="ec-status" data-case="AF anticoagulation. Rx"></span></div><div class="ec-hub-item">[[Question 4->SVT - Dx]]<span class="ec-status" data-case="SVT. Dx"></span></div><div class="ec-hub-item">[[Question 5->Unstable bradycardia - Rx]]<span class="ec-status" data-case="Unstable bradycardia. Rx"></span></div><div class="ec-hub-item">[[Question 6->Aortic stenosis - Rx]]<span class="ec-status" data-case="Aortic stenosis. Rx"></span></div><div class="ec-hub-item">[[Question 7->HCM - Rx]]<span class="ec-status" data-case="HCM. Rx"></span></div><div class="ec-hub-item">[[Question 8->Cardiac tamponade - Dx]]<span class="ec-status" data-case="Cardiac tamponade. Dx"></span></div><div class="ec-hub-item">[[Question 9->Cocaine chest pain - Opening]]<span class="ec-status" data-case="Cocaine chest pain. Opening"></span></div><div class="ec-hub-item">[[Question 10->Exercise stress test - Ix]]<span class="ec-status" data-case="Exercise stress test. Ix"></span></div><div class="ec-hub-item">[[Question 11->Aortic dissection - Dx]]<span class="ec-status" data-case="Aortic dissection. Dx"></span></div><div class="ec-hub-item">[[Question 12->Ruptured AAA - Ix]]<span class="ec-status" data-case="Ruptured AAA. Ix"></span></div><div class="ec-hub-item">[[Question 13->AAA screening - Opening]]<span class="ec-status" data-case="AAA screening. Opening"></span></div><div class="ec-hub-item">[[Question 14->Infective endocarditis - Rx]]<span class="ec-status" data-case="Infective endocarditis. Rx"></span></div><div class="ec-hub-item">[[Question 15->Viridans endocarditis - Micro]]<span class="ec-status" data-case="Viridans endocarditis. Micro"></span></div><div class="ec-hub-item">[[Question 16->Acute rheumatic fever - Dx]]<span class="ec-status" data-case="Acute rheumatic fever. Dx"></span></div><div class="ec-hub-item">[[Question 17->HFrEF pillars - Rx]]<span class="ec-status" data-case="HFrEF pillars. Rx"></span></div><div class="ec-hub-item">[[Question 18->HFrEF cardiac output - Prog]]<span class="ec-status" data-case="HFrEF cardiac output. Prog"></span></div><div class="ec-hub-item">[[Question 19->Post-MI remodeling - Mech]]<span class="ec-status" data-case="Post-MI remodeling. Mech"></span></div><div class="ec-hub-item">[[Question 20->Post-MI sudden death risk - Prog]]<span class="ec-status" data-case="Post-MI sudden death risk. Prog"></span></div><div class="ec-hub-item">[[Question 21->ACE inhibitor angioedema - Mech]]<span class="ec-status" data-case="ACE inhibitor angioedema. Mech"></span></div><div class="ec-hub-item">[[Question 22->Stroke risk in atrial fibrillation - Prog]]<span class="ec-status" data-case="Stroke risk in atrial fibrillation. Prog"></span></div><div class="ec-hub-item">[[Question 23->Hypertrophic cardiomyopathy risk - Prog]]<span class="ec-status" data-case="Hypertrophic cardiomyopathy risk. Prog"></span></div><div class="ec-hub-item">[[Question 24->Pulmonary embolism - Ix]]<span class="ec-status" data-case="Pulmonary embolism. Ix"></span></div><div class="ec-hub-item">[[Question 25->Unstable PE - Rx]]<span class="ec-status" data-case="Unstable PE. Rx"></span></div><div class="ec-hub-item">[[Question 26->CAP CURB-65 - Dx]]<span class="ec-status" data-case="CAP CURB-65. Dx"></span></div><div class="ec-hub-item">[[Question 27->Tension pneumothorax - Dx]]<span class="ec-status" data-case="Tension pneumothorax. Dx"></span></div><div class="ec-hub-item">[[Question 28->Tension PTX - Rx]]<span class="ec-status" data-case="Tension PTX. Rx"></span></div><div class="ec-hub-item">[[Question 29->Status asthmaticus - Opening]]<span class="ec-status" data-case="Status asthmaticus. Opening"></span></div><div class="ec-hub-item">[[Question 30->Asthma ICS - Rx]]<span class="ec-status" data-case="Asthma ICS. Rx"></span></div><div class="ec-hub-item">[[Question 31->Allergic asthma mechanism - Mech]]<span class="ec-status" data-case="Allergic asthma mechanism. Mech"></span></div><div class="ec-hub-item">[[Question 32->Methacholine challenge - Dx]]<span class="ec-status" data-case="Methacholine challenge. Dx"></span></div><div class="ec-hub-item">[[Question 33->Anaphylaxis - Ix]]<span class="ec-status" data-case="Anaphylaxis. Ix"></span></div><div class="ec-hub-item">[[Question 34->COPD ventilation - Rx]]<span class="ec-status" data-case="COPD ventilation. Rx"></span></div><div class="ec-hub-item">[[Question 35->DLCO in emphysema - Ix]]<span class="ec-status" data-case="DLCO in emphysema. Ix"></span></div><div class="ec-hub-item">[[Question 36->Sleep apnea - Ix]]<span class="ec-status" data-case="Sleep apnea. Ix"></span></div><div class="ec-hub-item">[[Question 37->IPF FVC decline - Prog]]<span class="ec-status" data-case="IPF FVC decline. Prog"></span></div><div class="ec-hub-item">[[Question 38->SSc-ILD mortality - Prog]]<span class="ec-status" data-case="SSc-ILD mortality. Prog"></span></div><div class="ec-hub-item">[[Question 39->Bronchiolitis - Dx]]<span class="ec-status" data-case="Bronchiolitis. Dx"></span></div><div class="ec-hub-item">[[Question 40->Epiglottitis - Dx]]<span class="ec-status" data-case="Epiglottitis. Dx"></span></div><div class="ec-hub-item">[[Question 41->Aspirin-exacerbated respiratory disease - Mech]]<span class="ec-status" data-case="Aspirin-exacerbated respiratory disease. Mech"></span></div><div class="ec-hub-item">[[Question 42->Incidental pulmonary nodule - Ix]]<span class="ec-status" data-case="Incidental pulmonary nodule. Ix"></span></div><div class="ec-hub-item">[[Question 43->Pulmonary embolism risk stratification - Prog]]<span class="ec-status" data-case="Pulmonary embolism risk stratification. Prog"></span></div><div class="ec-hub-item">[[Question 44->Acute GI bleed (Sequential - 3 Questions) - Ix]]<span class="ec-status" data-case="Acute GI bleed (Sequential, 3 Questions). Ix"></span></div><div class="ec-hub-item">[[Question 45->Upper GI bleed - Rx]]<span class="ec-status" data-case="Upper GI bleed. Rx"></span></div><div class="ec-hub-item">[[Question 46->Peptic ulcer bleed - Ix]]<span class="ec-status" data-case="Peptic ulcer bleed. Ix"></span></div><div class="ec-hub-item">[[Question 47->Variceal bleed - Ix]]<span class="ec-status" data-case="Variceal bleed. Ix"></span></div><div class="ec-hub-item">[[Question 48->Mesenteric ischemia - Dx]]<span class="ec-status" data-case="Mesenteric ischemia. Dx"></span></div><div class="ec-hub-item">[[Question 49->Acute appendicitis - Rx]]<span class="ec-status" data-case="Acute appendicitis. Rx"></span></div><div class="ec-hub-item">[[Question 50->Ulcerative colitis - Rx]]<span class="ec-status" data-case="Ulcerative colitis. Rx"></span></div><div class="ec-hub-item">[[Question 51->Celiac disease - Dx]]<span class="ec-status" data-case="Celiac disease. Dx"></span></div><div class="ec-hub-item">[[Question 52->C difficile - Rx]]<span class="ec-status" data-case="C difficile. Rx"></span></div><div class="ec-hub-item">[[Question 53->Pancreatitis - Ix]]<span class="ec-status" data-case="Pancreatitis. Ix"></span></div><div class="ec-hub-item">[[Question 54->Pancreatic insufficiency - Mech]]<span class="ec-status" data-case="Pancreatic insufficiency. Mech"></span></div><div class="ec-hub-item">[[Question 55->Cholangitis - Ix]]<span class="ec-status" data-case="Cholangitis. Ix"></span></div><div class="ec-hub-item">[[Question 56->Esophageal manometry - Ix]]<span class="ec-status" data-case="Esophageal manometry. Ix"></span></div><div class="ec-hub-item">[[Question 57->Acute liver failure - Dx]]<span class="ec-status" data-case="Acute liver failure. Dx"></span></div><div class="ec-hub-item">[[Question 58->Hepatic encephalopathy - Rx]]<span class="ec-status" data-case="Hepatic encephalopathy. Rx"></span></div><div class="ec-hub-item">[[Question 59->SBP - Ix]]<span class="ec-status" data-case="SBP. Ix"></span></div><div class="ec-hub-item">[[Question 60->SBP recurrence - Prog]]<span class="ec-status" data-case="SBP recurrence. Prog"></span></div><div class="ec-hub-item">[[Question 61->MELD score - Dx]]<span class="ec-status" data-case="MELD score. Dx"></span></div><div class="ec-hub-item">[[Question 62->Pyloric stenosis - Rx]]<span class="ec-status" data-case="Pyloric stenosis. Rx"></span></div><div class="ec-hub-item">[[Question 63->Intussusception - Dx]]<span class="ec-status" data-case="Intussusception. Dx"></span></div><div class="ec-hub-item">[[Question 64->Enteral nutrition - Opening]]<span class="ec-status" data-case="Enteral nutrition. Opening"></span></div><div class="ec-hub-item">[[Question 65->Ascites SAAG - Ix]]<span class="ec-status" data-case="Ascites SAAG. Ix"></span></div><div class="ec-hub-item">[[Question 66->Pancreatitis severity - Prog]]<span class="ec-status" data-case="Pancreatitis severity. Prog"></span></div><div class="ec-hub-item">[[Question 67->Cirrhosis surgical risk - Prog]]<span class="ec-status" data-case="Cirrhosis surgical risk. Prog"></span></div><div class="ec-hub-item">[[Question 68->Acute kidney injury - Ix]]<span class="ec-status" data-case="Acute kidney injury. Ix"></span></div><div class="ec-hub-item">[[Question 69->Rhabdomyolysis - Ix]]<span class="ec-status" data-case="Rhabdomyolysis. Ix"></span></div><div class="ec-hub-item">[[Question 70->Hyperkalemia - Rx]]<span class="ec-status" data-case="Hyperkalemia. Rx"></span></div><div class="ec-hub-item">[[Question 71->Contraction alkalosis - Mech]]<span class="ec-status" data-case="Contraction alkalosis. Mech"></span></div><div class="ec-hub-item">[[Question 72->PTH phosphaturia - Mech]]<span class="ec-status" data-case="PTH phosphaturia. Mech"></span></div><div class="ec-hub-item">[[Question 73->Nephrolithiasis - Ix]]<span class="ec-status" data-case="Nephrolithiasis. Ix"></span></div><div class="ec-hub-item">[[Question 74->Nephrotic syndrome - Dx]]<span class="ec-status" data-case="Nephrotic syndrome. Dx"></span></div><div class="ec-hub-item">[[Question 75->Glomerular hematuria - Ix]]<span class="ec-status" data-case="Glomerular hematuria. Ix"></span></div><div class="ec-hub-item">[[Question 76->Poststreptococcal GN - Dx]]<span class="ec-status" data-case="Poststreptococcal GN. Dx"></span></div><div class="ec-hub-item">[[Question 77->Lupus nephritis - Mech]]<span class="ec-status" data-case="Lupus nephritis. Mech"></span></div><div class="ec-hub-item">[[Question 78->Albuminuria progression - Prog]]<span class="ec-status" data-case="Albuminuria progression. Prog"></span></div><div class="ec-hub-item">[[Question 79->Testicular torsion - Ix]]<span class="ec-status" data-case="Testicular torsion. Ix"></span></div><div class="ec-hub-item">[[Question 80->Testicular torsion 2 - Rx]]<span class="ec-status" data-case="Testicular torsion 2. Rx"></span></div><div class="ec-hub-item">[[Question 81->Microscopic hematuria - Ix]]<span class="ec-status" data-case="Microscopic hematuria. Ix"></span></div><div class="ec-hub-item">[[Question 82->DKA - Ix]]<span class="ec-status" data-case="DKA. Ix"></span></div><div class="ec-hub-item">[[Question 83->DKA management - Rx]]<span class="ec-status" data-case="DKA management. Rx"></span></div><div class="ec-hub-item">[[Question 84->Diabetic emergency (Sequential - 2 Questions) - Dx]]<span class="ec-status" data-case="Diabetic emergency (Sequential, 2 Questions). Dx"></span></div><div class="ec-hub-item">[[Question 85->Diabetic foot - Rx]]<span class="ec-status" data-case="Diabetic foot. Rx"></span></div><div class="ec-hub-item">[[Question 86->Diabetic retinopathy - Opening]]<span class="ec-status" data-case="Diabetic retinopathy. Opening"></span></div><div class="ec-hub-item">[[Question 87->Gestational diabetes - Rx]]<span class="ec-status" data-case="Gestational diabetes. Rx"></span></div><div class="ec-hub-item">[[Question 88->Thyroid storm - Dx]]<span class="ec-status" data-case="Thyroid storm. Dx"></span></div><div class="ec-hub-item">[[Question 89->Myxedema coma - Dx]]<span class="ec-status" data-case="Myxedema coma. Dx"></span></div><div class="ec-hub-item">[[Question 90->Graves TRAb - Ix]]<span class="ec-status" data-case="Graves TRAb. Ix"></span></div><div class="ec-hub-item">[[Question 91->Papillary thyroid prognosis - Prog]]<span class="ec-status" data-case="Papillary thyroid prognosis. Prog"></span></div><div class="ec-hub-item">[[Question 92->Adrenal crisis - Dx]]<span class="ec-status" data-case="Adrenal crisis. Dx"></span></div><div class="ec-hub-item">[[Question 93->Adrenal crisis 2 - Rx]]<span class="ec-status" data-case="Adrenal crisis 2. Rx"></span></div><div class="ec-hub-item">[[Question 94->Primary aldosteronism - Ix]]<span class="ec-status" data-case="Primary aldosteronism. Ix"></span></div><div class="ec-hub-item">[[Question 95->Vitamin D deficiency - Opening]]<span class="ec-status" data-case="Vitamin D deficiency. Opening"></span></div><div class="ec-hub-item">[[Question 96->B12 deficiency - Opening]]<span class="ec-status" data-case="B12 deficiency. Opening"></span></div><div class="ec-hub-item">[[Question 97->Folate pregnancy - Opening]]<span class="ec-status" data-case="Folate pregnancy. Opening"></span></div><div class="ec-hub-item">[[Question 98->Bariatric deficiency - Opening]]<span class="ec-status" data-case="Bariatric deficiency. Opening"></span></div><div class="ec-hub-item">[[Question 99->Malnutrition assessment - Opening]]<span class="ec-status" data-case="Malnutrition assessment. Opening"></span></div><div class="ec-hub-item">[[Question 100->Refeeding syndrome - Dx]]<span class="ec-status" data-case="Refeeding syndrome. Dx"></span></div><div class="ec-hub-item">[[Question 101->Thyroid nodule workup - Ix]]<span class="ec-status" data-case="Thyroid nodule workup. Ix"></span></div><div class="ec-hub-item">[[Question 102->Diabetes screening - Prevention]]<span class="ec-status" data-case="Diabetes screening. Prevention"></span></div><div class="ec-hub-item">[[Question 103->Refeeding electrolyte shift - Mech]]<span class="ec-status" data-case="Refeeding electrolyte shift. Mech"></span></div><div class="ec-hub-item">[[Question 104->Iron deficiency - Rx]]<span class="ec-status" data-case="Iron deficiency. Rx"></span></div><div class="ec-hub-item">[[Question 105->RBC transfusion - Rx]]<span class="ec-status" data-case="RBC transfusion. Rx"></span></div><div class="ec-hub-item">[[Question 106->Hereditary spherocytosis - Ix]]<span class="ec-status" data-case="Hereditary spherocytosis. Ix"></span></div><div class="ec-hub-item">[[Question 107->HbS polymerization - Mech]]<span class="ec-status" data-case="HbS polymerization. Mech"></span></div><div class="ec-hub-item">[[Question 108->Acute chest syndrome - Dx]]<span class="ec-status" data-case="Acute chest syndrome. Dx"></span></div><div class="ec-hub-item">[[Question 109->TTP - Dx]]<span class="ec-status" data-case="TTP. Dx"></span></div><div class="ec-hub-item">[[Question 110->Myeloma light chains - Ix]]<span class="ec-status" data-case="Myeloma light chains. Ix"></span></div><div class="ec-hub-item">[[Question 111->ALL high risk - Dx]]<span class="ec-status" data-case="ALL high risk. Dx"></span></div><div class="ec-hub-item">[[Question 112->ALL prognosis - Dx]]<span class="ec-status" data-case="ALL prognosis. Dx"></span></div><div class="ec-hub-item">[[Question 113->AML MRD relapse - Prog]]<span class="ec-status" data-case="AML MRD relapse. Prog"></span></div><div class="ec-hub-item">[[Question 114->Hodgkin lymphoma - Dx]]<span class="ec-status" data-case="Hodgkin lymphoma. Dx"></span></div><div class="ec-hub-item">[[Question 115->Tumor lysis - Ix]]<span class="ec-status" data-case="Tumor lysis. Ix"></span></div><div class="ec-hub-item">[[Question 116->TLS prophylaxis - Rx]]<span class="ec-status" data-case="TLS prophylaxis. Rx"></span></div><div class="ec-hub-item">[[Question 117->Neutropenic fever - Dx]]<span class="ec-status" data-case="Neutropenic fever. Dx"></span></div><div class="ec-hub-item">[[Question 118->Cord compression - Rx]]<span class="ec-status" data-case="Cord compression. Rx"></span></div><div class="ec-hub-item">[[Question 119->Breast cancer prognosis - Dx]]<span class="ec-status" data-case="Breast cancer prognosis. Dx"></span></div><div class="ec-hub-item">[[Question 120->Triple negative breast - Dx]]<span class="ec-status" data-case="Triple negative breast. Dx"></span></div><div class="ec-hub-item">[[Question 121->Heparin-induced thrombocytopenia mechanism - Mech]]<span class="ec-status" data-case="Heparin-induced thrombocytopenia mechanism. Mech"></span></div><div class="ec-hub-item">[[Question 122->Warfarin skin necrosis - Mech]]<span class="ec-status" data-case="Warfarin skin necrosis. Mech"></span></div><div class="ec-hub-item">[[Question 123->Tumor lysis syndrome - Mech]]<span class="ec-status" data-case="Tumor lysis syndrome. Mech"></span></div><div class="ec-hub-item">[[Question 124->Sepsis - Ix]]<span class="ec-status" data-case="Sepsis. Ix"></span></div><div class="ec-hub-item">[[Question 125->Meningitis - Ix]]<span class="ec-status" data-case="Meningitis. Ix"></span></div><div class="ec-hub-item">[[Question 126->Meningitis GCS prognosis - Prog]]<span class="ec-status" data-case="Meningitis GCS prognosis. Prog"></span></div><div class="ec-hub-item">[[Question 127->N meningitidis - Micro]]<span class="ec-status" data-case="N meningitidis. Micro"></span></div><div class="ec-hub-item">[[Question 128->Neonatal meningitis - Opening]]<span class="ec-status" data-case="Neonatal meningitis. Opening"></span></div><div class="ec-hub-item">[[Question 129->Mononucleosis - Rx]]<span class="ec-status" data-case="Mononucleosis. Rx"></span></div><div class="ec-hub-item">[[Question 130->Toxoplasma AIDS - Dx]]<span class="ec-status" data-case="Toxoplasma AIDS. Dx"></span></div><div class="ec-hub-item">[[Question 131->Gonorrhea treatment - Rx]]<span class="ec-status" data-case="Gonorrhea treatment. Rx"></span></div><div class="ec-hub-item">[[Question 132->Syphilis pregnancy - Rx]]<span class="ec-status" data-case="Syphilis pregnancy. Rx"></span></div><div class="ec-hub-item">[[Question 133->Pelvic inflammatory disease - Rx]]<span class="ec-status" data-case="Pelvic inflammatory disease. Rx"></span></div><div class="ec-hub-item">[[Question 134->Otitis media - Rx]]<span class="ec-status" data-case="Otitis media. Rx"></span></div><div class="ec-hub-item">[[Question 135->Peritonsillar abscess - Rx]]<span class="ec-status" data-case="Peritonsillar abscess. Rx"></span></div><div class="ec-hub-item">[[Question 136->Necrotizing fasciitis - Dx]]<span class="ec-status" data-case="Necrotizing fasciitis. Dx"></span></div><div class="ec-hub-item">[[Question 137->Septic arthritis - Dx]]<span class="ec-status" data-case="Septic arthritis. Dx"></span></div><div class="ec-hub-item">[[Question 138->Campylobacter - Micro]]<span class="ec-status" data-case="Campylobacter. Micro"></span></div><div class="ec-hub-item">[[Question 139->Kawasaki treatment - Rx]]<span class="ec-status" data-case="Kawasaki treatment. Rx"></span></div><div class="ec-hub-item">[[Question 140->Febrile infant - Ix]]<span class="ec-status" data-case="Febrile infant. Ix"></span></div><div class="ec-hub-item">[[Question 141->Partner notification - Ethics]]<span class="ec-status" data-case="Partner notification. Ethics"></span></div><div class="ec-hub-item">[[Question 142->Hepatitis C screening - Prevention]]<span class="ec-status" data-case="Hepatitis C screening. Prevention"></span></div><div class="ec-hub-item">[[Question 143->HIV preexposure prophylaxis - Prevention]]<span class="ec-status" data-case="HIV preexposure prophylaxis. Prevention"></span></div><div class="ec-hub-item">[[Question 144->Zoster vaccination - Prevention]]<span class="ec-status" data-case="Zoster vaccination. Prevention"></span></div><div class="ec-hub-item">[[Question 145->Rabies postexposure prophylaxis - Prevention]]<span class="ec-status" data-case="Rabies postexposure prophylaxis. Prevention"></span></div><div class="ec-hub-item">[[Question 146->Latent tuberculosis - Prevention]]<span class="ec-status" data-case="Latent tuberculosis. Prevention"></span></div><div class="ec-hub-item">[[Question 147->Sepsis risk stratification - Prog]]<span class="ec-status" data-case="Sepsis risk stratification. Prog"></span></div><div class="ec-hub-item">[[Question 148->Stroke - Ix]]<span class="ec-status" data-case="Stroke. Ix"></span></div><div class="ec-hub-item">[[Question 149->Large vessel stroke - Rx]]<span class="ec-status" data-case="Large vessel stroke. Rx"></span></div><div class="ec-hub-item">[[Question 150->Malignant MCA edema - Prog]]<span class="ec-status" data-case="Malignant MCA edema. Prog"></span></div><div class="ec-hub-item">[[Question 151->Status epilepticus - Opening]]<span class="ec-status" data-case="Status epilepticus. Opening"></span></div><div class="ec-hub-item">[[Question 152->Refractory SE - Rx]]<span class="ec-status" data-case="Refractory SE. Rx"></span></div><div class="ec-hub-item">[[Question 153->Febrile seizure - Dx]]<span class="ec-status" data-case="Febrile seizure. Dx"></span></div><div class="ec-hub-item">[[Question 154->Guillain-Barre - Dx]]<span class="ec-status" data-case="Guillain-Barre. Dx"></span></div><div class="ec-hub-item">[[Question 155->MS MRI findings - Ix]]<span class="ec-status" data-case="MS MRI findings. Ix"></span></div><div class="ec-hub-item">[[Question 156->Wernicke - Dx]]<span class="ec-status" data-case="Wernicke. Dx"></span></div><div class="ec-hub-item">[[Question 157->Parkinson treatment - Rx]]<span class="ec-status" data-case="Parkinson treatment. Rx"></span></div><div class="ec-hub-item">[[Question 158->Parkinson basal ganglia - Mech]]<span class="ec-status" data-case="Parkinson basal ganglia. Mech"></span></div><div class="ec-hub-item">[[Question 159->Delirium - Dx]]<span class="ec-status" data-case="Delirium. Dx"></span></div><div class="ec-hub-item">[[Question 160->Meniere disease - Dx]]<span class="ec-status" data-case="Meniere disease. Dx"></span></div><div class="ec-hub-item">[[Question 161->Post-arrest neuroprognostication - Prog]]<span class="ec-status" data-case="Post-arrest neuroprognostication. Prog"></span></div><div class="ec-hub-item">[[Question 162->Suicide risk - Opening]]<span class="ec-status" data-case="Suicide risk. Opening"></span></div><div class="ec-hub-item">[[Question 163->Psych transition - Opening]]<span class="ec-status" data-case="Psych transition. Opening"></span></div><div class="ec-hub-item">[[Question 164->Panic disorder - Dx]]<span class="ec-status" data-case="Panic disorder. Dx"></span></div><div class="ec-hub-item">[[Question 165->Acute mania - Rx]]<span class="ec-status" data-case="Acute mania. Rx"></span></div><div class="ec-hub-item">[[Question 166->Anorexia nervosa - Opening]]<span class="ec-status" data-case="Anorexia nervosa. Opening"></span></div><div class="ec-hub-item">[[Question 167->Schizophrenia dopamine - Mech]]<span class="ec-status" data-case="Schizophrenia dopamine. Mech"></span></div><div class="ec-hub-item">[[Question 168->Serotonin syndrome - Dx]]<span class="ec-status" data-case="Serotonin syndrome. Dx"></span></div><div class="ec-hub-item">[[Question 169->Alcohol withdrawal - Rx]]<span class="ec-status" data-case="Alcohol withdrawal. Rx"></span></div><div class="ec-hub-item">[[Question 170->Opioid overdose - Rx]]<span class="ec-status" data-case="Opioid overdose. Rx"></span></div><div class="ec-hub-item">[[Question 171->Acetaminophen - Opening]]<span class="ec-status" data-case="Acetaminophen. Opening"></span></div><div class="ec-hub-item">[[Question 172->CCB-BB overdose - Opening]]<span class="ec-status" data-case="CCB-BB overdose. Opening"></span></div><div class="ec-hub-item">[[Question 173->Methemoglobinemia - Dx]]<span class="ec-status" data-case="Methemoglobinemia. Dx"></span></div><div class="ec-hub-item">[[Question 174->Carbon monoxide - Dx]]<span class="ec-status" data-case="Carbon monoxide. Dx"></span></div><div class="ec-hub-item">[[Question 175->Duty to warn - Ethics]]<span class="ec-status" data-case="Duty to warn. Ethics"></span></div><div class="ec-hub-item">[[Question 176->Tobacco cessation pharmacotherapy - Prevention]]<span class="ec-status" data-case="Tobacco cessation pharmacotherapy. Prevention"></span></div><div class="ec-hub-item">[[Question 177->Serotonin syndrome mechanism - Mech]]<span class="ec-status" data-case="Serotonin syndrome mechanism. Mech"></span></div><div class="ec-hub-item">[[Question 178->Ectopic pregnancy - Dx]]<span class="ec-status" data-case="Ectopic pregnancy. Dx"></span></div><div class="ec-hub-item">[[Question 179->Ectopic pregnancy 2 - Dx]]<span class="ec-status" data-case="Ectopic pregnancy 2. Dx"></span></div><div class="ec-hub-item">[[Question 180->Eclampsia - Dx]]<span class="ec-status" data-case="Eclampsia. Dx"></span></div><div class="ec-hub-item">[[Question 181->Severe preeclampsia - Rx]]<span class="ec-status" data-case="Severe preeclampsia. Rx"></span></div><div class="ec-hub-item">[[Question 182->Preeclampsia expectant - Prog]]<span class="ec-status" data-case="Preeclampsia expectant. Prog"></span></div><div class="ec-hub-item">[[Question 183->Placenta previa - Ix]]<span class="ec-status" data-case="Placenta previa. Ix"></span></div><div class="ec-hub-item">[[Question 184->Placental abruption - Dx]]<span class="ec-status" data-case="Placental abruption. Dx"></span></div><div class="ec-hub-item">[[Question 185->Postpartum hemorrhage - Opening]]<span class="ec-status" data-case="Postpartum hemorrhage. Opening"></span></div><div class="ec-hub-item">[[Question 186->PPH management - Rx]]<span class="ec-status" data-case="PPH management. Rx"></span></div><div class="ec-hub-item">[[Question 187->Amenorrhea workup - Ix]]<span class="ec-status" data-case="Amenorrhea workup. Ix"></span></div><div class="ec-hub-item">[[Question 188->Ovarian torsion - Opening]]<span class="ec-status" data-case="Ovarian torsion. Opening"></span></div><div class="ec-hub-item">[[Question 189->Cervical screening - Opening]]<span class="ec-status" data-case="Cervical screening. Opening"></span></div><div class="ec-hub-item">[[Question 190->Adolescent well visit - Opening]]<span class="ec-status" data-case="Adolescent well visit. Opening"></span></div><div class="ec-hub-item">[[Question 191->Tdap in pregnancy - Prevention]]<span class="ec-status" data-case="Tdap in pregnancy. Prevention"></span></div><div class="ec-hub-item">[[Question 192->Preconception folic acid - Prevention]]<span class="ec-status" data-case="Preconception folic acid. Prevention"></span></div><div class="ec-hub-item">[[Question 193->Well child visit - Opening]]<span class="ec-status" data-case="Well child visit. Opening"></span></div><div class="ec-hub-item">[[Question 194->Neonatal jaundice - Rx]]<span class="ec-status" data-case="Neonatal jaundice. Rx"></span></div><div class="ec-hub-item">[[Question 195->Emergency care of a minor - Ethics]]<span class="ec-status" data-case="Emergency care of a minor. Ethics"></span></div><div class="ec-hub-item">[[Question 196->Major burn - Opening]]<span class="ec-status" data-case="Major burn. Opening"></span></div><div class="ec-hub-item">[[Question 197->Compartment syndrome - Ix]]<span class="ec-status" data-case="Compartment syndrome. Ix"></span></div><div class="ec-hub-item">[[Question 198->Compartment syndrome 2 - Rx]]<span class="ec-status" data-case="Compartment syndrome 2. Rx"></span></div><div class="ec-hub-item">[[Question 199->Angle closure glaucoma - Rx]]<span class="ec-status" data-case="Angle closure glaucoma. Rx"></span></div><div class="ec-hub-item">[[Question 200->SJS TEN - Dx]]<span class="ec-status" data-case="SJS TEN. Dx"></span></div><div class="ec-hub-item">[[Question 201->Anti-CCP RA - Ix]]<span class="ec-status" data-case="Anti-CCP RA. Ix"></span></div><div class="ec-hub-item">[[Question 202->Giant cell arteritis - Rx]]<span class="ec-status" data-case="Giant cell arteritis. Rx"></span></div><div class="ec-hub-item">[[Question 203->Acute gout - Rx]]<span class="ec-status" data-case="Acute gout. Rx"></span></div><div class="ec-hub-item">[[Question 204->XLA BTK - Mech]]<span class="ec-status" data-case="XLA BTK. Mech"></span></div><div class="ec-hub-item">[[Question 205->Wound healing phases - Mech]]<span class="ec-status" data-case="Wound healing phases. Mech"></span></div><div class="ec-hub-item">[[Question 206->Goals of care - Opening]]<span class="ec-status" data-case="Goals of care. Opening"></span></div><div class="ec-hub-item">[[Question 207->Screening refusal - Opening]]<span class="ec-status" data-case="Screening refusal. Opening"></span></div><div class="ec-hub-item">[[Question 208->Adolescent confidentiality - Ethics]]<span class="ec-status" data-case="Adolescent confidentiality. Ethics"></span></div><div class="ec-hub-item">[[Question 209->Decision-making capacity - Ethics]]<span class="ec-status" data-case="Decision-making capacity. Ethics"></span></div><div class="ec-hub-item">[[Question 210->Disclosure of medical error - Ethics]]<span class="ec-status" data-case="Disclosure of medical error. Ethics"></span></div><div class="ec-hub-item">[[Question 211->Transfusion refusal - Ethics]]<span class="ec-status" data-case="Transfusion refusal. Ethics"></span></div><div class="ec-hub-item">[[Question 212->Substituted judgment - Ethics]]<span class="ec-status" data-case="Substituted judgment. Ethics"></span></div><div class="ec-hub-item">[[Question 213->Potentially inappropriate treatment - Ethics]]<span class="ec-status" data-case="Potentially inappropriate treatment. Ethics"></span></div><div class="ec-hub-item">[[Question 214->Industry gifts - Ethics]]<span class="ec-status" data-case="Industry gifts. Ethics"></span></div><div class="ec-hub-item">[[Question 215->Medical interpretation - Ethics]]<span class="ec-status" data-case="Medical interpretation. Ethics"></span></div><div class="ec-hub-item">[[Question 216->Advance directive conflict - Ethics]]<span class="ec-status" data-case="Advance directive conflict. Ethics"></span></div><div class="ec-hub-item">[[Question 217->Family request for nondisclosure - Ethics]]<span class="ec-status" data-case="Family request for nondisclosure. Ethics"></span></div><div class="ec-hub-item">[[Question 218->Inappropriate antibiotic request - Ethics]]<span class="ec-status" data-case="Inappropriate antibiotic request. Ethics"></span></div><div class="ec-hub-item">[[Question 219->Diagnostic error - Opening]]<span class="ec-status" data-case="Diagnostic error. Opening"></span></div><div class="ec-hub-item">[[Question 220->Med reconciliation - Opening]]<span class="ec-status" data-case="Med reconciliation. Opening"></span></div><div class="ec-hub-item">[[Question 221->Surgical safety - Opening]]<span class="ec-status" data-case="Surgical safety. Opening"></span></div><div class="ec-hub-item">[[Question 222->SSI prevention - Opening]]<span class="ec-status" data-case="SSI prevention. Opening"></span></div><div class="ec-hub-item">[[Question 223->Hand hygiene - Opening]]<span class="ec-status" data-case="Hand hygiene. Opening"></span></div><div class="ec-hub-item">[[Question 224->Vaccination QI - Opening]]<span class="ec-status" data-case="Vaccination QI. Opening"></span></div><div class="ec-hub-item">[[Question 225->QI PDSA - Opening]]<span class="ec-status" data-case="QI PDSA. Opening"></span></div><div class="ec-hub-item">[[Question 226->Just culture after error - QI]]<span class="ec-status" data-case="Just culture after error. QI"></span></div><div class="ec-hub-item">[[Question 227->Catheter infection bundle - QI]]<span class="ec-status" data-case="Catheter infection bundle. QI"></span></div><div class="ec-hub-item">[[Question 228->Latent system failure - QI]]<span class="ec-status" data-case="Latent system failure. QI"></span></div><div class="ec-hub-item">[[Question 229->Proactive risk analysis - QI]]<span class="ec-status" data-case="Proactive risk analysis. QI"></span></div><div class="ec-hub-item">[[Question 230->Improvement cycle - QI]]<span class="ec-status" data-case="Improvement cycle. QI"></span></div><div class="ec-hub-item">[[Question 231->Hierarchy of controls - QI]]<span class="ec-status" data-case="Hierarchy of controls. QI"></span></div><div class="ec-hub-item">[[Question 232->Care transitions - QI]]<span class="ec-status" data-case="Care transitions. QI"></span></div><div class="ec-hub-item">[[Question 233->Failure to rescue - QI]]<span class="ec-status" data-case="Failure to rescue. QI"></span></div><div class="ec-hub-item">[[Question 234->Handoff standardization - QI]]<span class="ec-status" data-case="Handoff standardization. QI"></span></div><div class="ec-hub-item">[[Question 235->Alarm fatigue - QI]]<span class="ec-status" data-case="Alarm fatigue. QI"></span></div><div class="ec-hub-item">[[Question 236->Catheter-associated infection - QI]]<span class="ec-status" data-case="Catheter-associated infection. QI"></span></div><div class="ec-hub-item">[[Question 237->Second victim - QI]]<span class="ec-status" data-case="Second victim. QI"></span></div><div class="ec-hub-item">[[Question 238->Risk reduction measures - Opening]]<span class="ec-status" data-case="Risk reduction measures. Opening"></span></div><div class="ec-hub-item">[[Question 239->Research abstract - Opening]]<span class="ec-status" data-case="Research abstract. Opening"></span></div><div class="ec-hub-item">[[Question 240->Drug advertisement - Opening]]<span class="ec-status" data-case="Drug advertisement. Opening"></span></div><div class="ec-hub-item">[[Question 241->Statin prevention - Opening]]<span class="ec-status" data-case="Statin prevention. Opening"></span></div><div class="ec-hub-item">[[Question 242->Pneumococcal prevention - Opening]]<span class="ec-status" data-case="Pneumococcal prevention. Opening"></span></div><div class="ec-hub-item">[[Question 243->Lung screening - Opening]]<span class="ec-status" data-case="Lung screening. Opening"></span></div><div class="ec-hub-item">[[Question 244->NNT interpretation - Biostat]]<span class="ec-status" data-case="NNT interpretation. Biostat"></span></div><div class="ec-hub-item">[[Question 245->Predictive value and prevalence - Biostat]]<span class="ec-status" data-case="Predictive value and prevalence. Biostat"></span></div><div class="ec-hub-item">[[Question 246->Lung cancer screening eligibility - Prevention]]<span class="ec-status" data-case="Lung cancer screening eligibility. Prevention"></span></div><div class="ec-hub-item">[[Question 247->Osteoporosis screening - Prevention]]<span class="ec-status" data-case="Osteoporosis screening. Prevention"></span></div><div class="ec-hub-item">[[Question 248->Lead-time bias - Biostat]]<span class="ec-status" data-case="Lead-time bias. Biostat"></span></div><div class="ec-hub-item">[[Question 249->Ruling out with a sensitive test - Biostat]]<span class="ec-status" data-case="Ruling out with a sensitive test. Biostat"></span></div><div class="ec-hub-item">[[Question 250->Type II error - Biostat]]<span class="ec-status" data-case="Type II error. Biostat"></span></div><div class="ec-hub-item">[[Question 251->Confidence interval interpretation - Biostat]]<span class="ec-status" data-case="Confidence interval interpretation. Biostat"></span></div><div class="ec-hub-item">[[Question 252->Intention to treat - Biostat]]<span class="ec-status" data-case="Intention to treat. Biostat"></span></div><div class="ec-hub-item">[[Question 253->Study design selection - Biostat]]<span class="ec-status" data-case="Study design selection. Biostat"></span></div><div class="ec-hub-item">[[Question 254->Selection bias - Biostat]]<span class="ec-status" data-case="Selection bias. Biostat"></span></div><div class="ec-hub-item">[[Question 255->Confounding and effect modification - Biostat]]<span class="ec-status" data-case="Confounding and effect modification. Biostat"></span></div><div class="ec-hub-item">[[Question 256->Hazard ratio - Biostat]]<span class="ec-status" data-case="Hazard ratio. Biostat"></span></div><div class="ec-hub-item">[[Question 257->Recall bias - Biostat]]<span class="ec-status" data-case="Recall bias. Biostat"></span></div><div class="ec-hub-item">[[Question 258->Publication bias - Biostat]]<span class="ec-status" data-case="Publication bias. Biostat"></span></div><div class="ec-hub-item">[[Question 259->Colorectal screening onset - Prevention]]<span class="ec-status" data-case="Colorectal screening onset. Prevention"></span></div><div class="ec-hub-item">[[Question 260->Open tibial fracture - Rx]]<span class="ec-status" data-case="Open tibial fracture. Rx"></span></div><div class="ec-hub-item">[[Question 261->Compartment syndrome fasciotomy - Rx]]<span class="ec-status" data-case="Compartment syndrome fasciotomy. Rx"></span></div><div class="ec-hub-item">[[Question 262->Septic arthritis drainage - Rx]]<span class="ec-status" data-case="Septic arthritis drainage. Rx"></span></div><div class="ec-hub-item">[[Question 263->Necrotizing infection debridement - Rx]]<span class="ec-status" data-case="Necrotizing infection debridement. Rx"></span></div><div class="ec-hub-item">[[Question 264->Hip fracture timing - Rx]]<span class="ec-status" data-case="Hip fracture timing. Rx"></span></div><div class="ec-hub-item">[[Question 265->Cauda equina decompression - Rx]]<span class="ec-status" data-case="Cauda equina decompression. Rx"></span></div><div class="ec-hub-item">[[Question 266->Shoulder dislocation reduction - Rx]]<span class="ec-status" data-case="Shoulder dislocation reduction. Rx"></span></div><div class="ec-hub-item">[[Question 267->Diabetic foot osteomyelitis - Rx]]<span class="ec-status" data-case="Diabetic foot osteomyelitis. Rx"></span></div><div class="ec-hub-item">[[Question 268->Spinal epidural abscess - Rx]]<span class="ec-status" data-case="Spinal epidural abscess. Rx"></span></div><div class="ec-hub-item">[[Question 269->Achilles tendon rupture - Rx]]<span class="ec-status" data-case="Achilles tendon rupture. Rx"></span></div><div class="ec-hub-item">[[Question 270->Gout flare therapy - Rx]]<span class="ec-status" data-case="Gout flare therapy. Rx"></span></div><div class="ec-hub-item">[[Question 271->Rheumatoid arthritis initial DMARD - Rx]]<span class="ec-status" data-case="Rheumatoid arthritis initial DMARD. Rx"></span></div><div class="ec-hub-item">[[Question 272->Osteoporosis pharmacotherapy - Rx]]<span class="ec-status" data-case="Osteoporosis pharmacotherapy. Rx"></span></div><div class="ec-hub-item">[[Question 273->Cellulitis antibiotic choice - Rx]]<span class="ec-status" data-case="Cellulitis antibiotic choice. Rx"></span></div><div class="ec-hub-item">[[Question 274->SJS causative drug withdrawal - Rx]]<span class="ec-status" data-case="SJS causative drug withdrawal. Rx"></span></div><div class="ec-hub-item">[[Question 275->Psoriasis escalation - Rx]]<span class="ec-status" data-case="Psoriasis escalation. Rx"></span></div><div class="ec-hub-item">[[Question 276->Dialysis initiation - Rx]]<span class="ec-status" data-case="Dialysis initiation. Rx"></span></div><div class="ec-hub-item">[[Question 277->Obstructive uropathy decompression - Rx]]<span class="ec-status" data-case="Obstructive uropathy decompression. Rx"></span></div><div class="ec-hub-item">[[Question 278->Hyperkalemia intervention - Rx]]<span class="ec-status" data-case="Hyperkalemia intervention. Rx"></span></div><div class="ec-hub-item">[[Question 279->Urinary retention decompression - Rx]]<span class="ec-status" data-case="Urinary retention decompression. Rx"></span></div><div class="ec-hub-item">[[Question 280->BPH pharmacotherapy - Rx]]<span class="ec-status" data-case="BPH pharmacotherapy. Rx"></span></div><div class="ec-hub-item">[[Question 281->Contrast nephropathy prevention - Prevention]]<span class="ec-status" data-case="Contrast nephropathy prevention. Prevention"></span></div><div class="ec-hub-item">[[Question 282->Transplant rejection - Dx]]<span class="ec-status" data-case="Transplant rejection. Dx"></span></div><div class="ec-hub-item">[[Question 283->Nephrolithiasis intervention - Rx]]<span class="ec-status" data-case="Nephrolithiasis intervention. Rx"></span></div><div class="ec-hub-item">[[Question 284->Rhabdomyolysis intervention - Rx]]<span class="ec-status" data-case="Rhabdomyolysis intervention. Rx"></span></div><div class="ec-hub-item">[[Question 285->Hyponatremia correction rate - Rx]]<span class="ec-status" data-case="Hyponatremia correction rate. Rx"></span></div><div class="ec-hub-item">[[Question 286->Intubation timing - Rx]]<span class="ec-status" data-case="Intubation timing. Rx"></span></div><div class="ec-hub-item">[[Question 287->Chest tube indication - Rx]]<span class="ec-status" data-case="Chest tube indication. Rx"></span></div><div class="ec-hub-item">[[Question 288->Cardioversion versus rate control - Rx]]<span class="ec-status" data-case="Cardioversion versus rate control. Rx"></span></div><div class="ec-hub-item">[[Question 289->Pericardiocentesis indication - Rx]]<span class="ec-status" data-case="Pericardiocentesis indication. Rx"></span></div><div class="ec-hub-item">[[Question 290->Massive transfusion protocol - Rx]]<span class="ec-status" data-case="Massive transfusion protocol. Rx"></span></div><div class="ec-hub-item">[[Question 291->Variceal band ligation - Rx]]<span class="ec-status" data-case="Variceal band ligation. Rx"></span></div><div class="ec-hub-item">[[Question 292->ERCP in cholangitis - Rx]]<span class="ec-status" data-case="ERCP in cholangitis. Rx"></span></div><div class="ec-hub-item">[[Question 293->Central line indication - Rx]]<span class="ec-status" data-case="Central line indication. Rx"></span></div><div class="ec-hub-item">[[Question 294->Tension pneumothorax decompression - Rx]]<span class="ec-status" data-case="Tension pneumothorax decompression. Rx"></span></div><div class="ec-hub-item">[[Question 295->Developmental milestones - Dx]]<span class="ec-status" data-case="Developmental milestones. Dx"></span></div><div class="ec-hub-item">[[Question 296->Geriatric falls assessment - Prevention]]<span class="ec-status" data-case="Geriatric falls assessment. Prevention"></span></div><div class="ec-hub-item">[[Question 297->Childhood immunization catch-up - Prevention]]<span class="ec-status" data-case="Childhood immunization catch-up. Prevention"></span></div><div class="ec-hub-item">[[Question 298->Newborn hyperbilirubinemia threshold - Rx]]<span class="ec-status" data-case="Newborn hyperbilirubinemia threshold. Rx"></span></div><div class="ec-hub-item">[[Question 299->Malignant hyperthermia - Rx]]<span class="ec-status" data-case="Malignant hyperthermia. Rx"></span></div></div><div class="ec-note"><b>Disclaimer</b><br>Critical is free and actively maintained, with more cases planned in the coming weeks. Debrief passages cite a guideline that was current when the case was written, and no physician has formally reviewed the full case bank yet. Treat it as practice, not your primary reference, and if something looks off, <a href="https://github.com/xairu23/Critical/issues" target="_blank" rel="noopener">open an issue on GitHub</a>.<br><br><b>Educational tool only, not medical advice, and not a substitute for UWorld, Amboss, or your other question banks. Critical doesn't treat patients or replace a clinician, it's a study aid, nothing more. Not affiliated with, endorsed by, or sponsored by USMLE, NBME, FSMB, ECFMG, or any other organization.</b></div></div>

<div class="ec-scene">Emergency department · 21:50</div> A 4-year-old boy weighing 17 kg is lethargic after 2 days of fever and vomiting. He is mottled with cool peripheries and a capillary refill of four seconds. Temperature is 39.2°C, blood pressure 72/38 mm Hg, pulse is 178/min, and respirations are 36/min. He responds only to voice. Intravenous access has just been obtained and the physician is about to give antibiotics. <span class="ec-prompt">Which of the following is the most appropriate next step in diagnosis?</span> [[Blood cultures before antibiotics->Sepsis - Ix correct]] [[CT of the abdomen->Sepsis - Ix D3]] [[Lumbar puncture->Sepsis - Ix D1]] [[Repeat serum lactate in 2 hours->Sepsis - Ix D2]] [[Serum procalcitonin->Sepsis - Ix D5]] [[Urine culture by bag specimen->Sepsis - Ix D4]]

<span class="ec-case-marker" hidden data-entry="Sepsis. Ix"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Blood cultures before antibiotics</div> Cultures obtained before antibiotics substantially raise the yield, and a single dose can sterilize them within an hour. Drawing them takes seconds through access that is already in place, so it does not delay treatment, and if obtaining cultures would delay antibiotics, the antibiotics go first. <div class="ec-src"><b>Source:</b> Weiss SL, et al. Surviving Sepsis Campaign International Guidelines for the Management of Septic Shock and Sepsis-Associated Organ Dysfunction in Children. Pediatr Crit Care Med 2020;21(2):e52-e106.</div></div> [[Start another case->Hub]] [[Restart this case->Sepsis - Ix]] [[Next case →->Meningitis - Ix]]

<span class="ec-case-marker" hidden data-entry="Sepsis. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Imaging has a role once a surgical source is suspected and the child is stabilized. Taking a shocked 4-year-old to the scanner before resuscitation is where these patients deteriorate. <div class="ec-teach"><div class="th">What the findings point to</div> Cultures obtained before antibiotics substantially raise the yield, and a single dose can sterilize them within an hour. Drawing them takes seconds through access that is already in place, so it does not delay treatment, and if obtaining cultures would delay antibiotics, the antibiotics go first. <div class="ec-src"><b>Source:</b> Weiss SL, et al. Surviving Sepsis Campaign International Guidelines for the Management of Septic Shock and Sepsis-Associated Organ Dysfunction in Children. Pediatr Crit Care Med 2020;21(2):e52-e106.</div></div></div> [[Try this question again->Sepsis - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Sepsis. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Cerebrospinal fluid is valuable and meningitis is plausible with fever, vomiting and lethargy. He is in shock with a capillary refill of four seconds, and lumbar puncture is deferred in hemodynamic instability, antibiotics and resuscitation come first. <div class="ec-teach"><div class="th">What the findings point to</div> Cultures obtained before antibiotics substantially raise the yield, and a single dose can sterilize them within an hour. Drawing them takes seconds through access that is already in place, so it does not delay treatment, and if obtaining cultures would delay antibiotics, the antibiotics go first. <div class="ec-src"><b>Source:</b> Weiss SL, et al. Surviving Sepsis Campaign International Guidelines for the Management of Septic Shock and Sepsis-Associated Organ Dysfunction in Children. Pediatr Crit Care Med 2020;21(2):e52-e106.</div></div></div> [[Try this question again->Sepsis - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Sepsis. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Procalcitonin can support antibiotic decisions in some settings and has a role in de-escalation. Withholding antibiotics in septic shock pending a biomarker is indefensible. <div class="ec-teach"><div class="th">What the findings point to</div> Cultures obtained before antibiotics substantially raise the yield, and a single dose can sterilize them within an hour. Drawing them takes seconds through access that is already in place, so it does not delay treatment, and if obtaining cultures would delay antibiotics, the antibiotics go first. <div class="ec-src"><b>Source:</b> Weiss SL, et al. Surviving Sepsis Campaign International Guidelines for the Management of Septic Shock and Sepsis-Associated Organ Dysfunction in Children. Pediatr Crit Care Med 2020;21(2):e52-e106.</div></div></div> [[Try this question again->Sepsis - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Sepsis. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Serial lactate is genuinely part of sepsis management and is used to assess response, so this is a real step. It is a monitoring parameter for later, not the sample that must be obtained in the next thirty seconds. <div class="ec-teach"><div class="th">What the findings point to</div> Cultures obtained before antibiotics substantially raise the yield, and a single dose can sterilize them within an hour. Drawing them takes seconds through access that is already in place, so it does not delay treatment, and if obtaining cultures would delay antibiotics, the antibiotics go first. <div class="ec-src"><b>Source:</b> Weiss SL, et al. Surviving Sepsis Campaign International Guidelines for the Management of Septic Shock and Sepsis-Associated Organ Dysfunction in Children. Pediatr Crit Care Med 2020;21(2):e52-e106.</div></div></div> [[Try this question again->Sepsis - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Sepsis. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Urine is a common source in this age group and should be sampled, but a bag specimen is frequently contaminated and unreliable, catheter or suprapubic sampling is used. It does not take priority over blood cultures and antibiotics. <div class="ec-teach"><div class="th">What the findings point to</div> Cultures obtained before antibiotics substantially raise the yield, and a single dose can sterilize them within an hour. Drawing them takes seconds through access that is already in place, so it does not delay treatment, and if obtaining cultures would delay antibiotics, the antibiotics go first. <div class="ec-src"><b>Source:</b> Weiss SL, et al. Surviving Sepsis Campaign International Guidelines for the Management of Septic Shock and Sepsis-Associated Organ Dysfunction in Children. Pediatr Crit Care Med 2020;21(2):e52-e106.</div></div></div> [[Try this question again->Sepsis - Ix]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 19:20</div> A 22-year-old man with type 1 diabetes presents with vomiting, abdominal pain and Kussmaul breathing after 2 days of a febrile illness during which he stopped his insulin. Glucose is 518 mg/dL, venous pH 7.14, bicarbonate 8 mEq/L, potassium 3.1 mEq/L, and urine ketones are strongly positive. He is drowsy but arousable. <span class="ec-prompt">Which of the following is the most appropriate next step in diagnosis?</span> [[CT of the head to exclude intracranial pathology->DKA - Ix D3]] [[Recheck serum glucose hourly->DKA - Ix D1]] [[Recheck serum potassium every 1–2 hours->DKA - Ix correct]] [[Repeat arterial blood gases hourly->DKA - Ix D4]] [[Serum beta-hydroxybutyrate every 4 hours->DKA - Ix D2]] [[Serum lipase to evaluate for pancreatitis->DKA - Ix D5]]

<span class="ec-case-marker" hidden data-entry="DKA. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Direct ketone measurement is more informative than urine ketones, since urine testing detects acetoacetate and can appear to worsen as the patient improves. It is a useful adjunct rather than the parameter that governs the next hour. <div class="ec-teach"><div class="th">What the findings point to</div> Potassium is the measurement that governs this resuscitation. Total body potassium is profoundly depleted despite whatever the serum shows, and insulin drives it further intracellularly, insulin is withheld if potassium is below 3.5 mEq/L and the level is rechecked every one to 2 hours because it moves faster than anything else in the first hours. <div class="ec-src"><b>Source:</b> Umpierrez GE, et al. Hyperglycemic Crises in Adults With Diabetes. Diabetes Care 2024;47(8):1257-1275.</div></div></div> [[Try this question again->DKA - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="DKA. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Cerebral edema is a real complication and imaging is indicated for focal signs or deterioration despite treatment. Drowsiness in a patient with a pH of 7.14 and this degree of dehydration is expected and improves with treatment. <div class="ec-teach"><div class="th">What the findings point to</div> Potassium is the measurement that governs this resuscitation. Total body potassium is profoundly depleted despite whatever the serum shows, and insulin drives it further intracellularly, insulin is withheld if potassium is below 3.5 mEq/L and the level is rechecked every one to 2 hours because it moves faster than anything else in the first hours. <div class="ec-src"><b>Source:</b> Umpierrez GE, et al. Hyperglycemic Crises in Adults With Diabetes. Diabetes Care 2024;47(8):1257-1275.</div></div></div> [[Try this question again->DKA - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="DKA. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Venous pH and bicarbonate track arterial values closely enough for management and avoid repeated arterial punctures. Hourly arterial sampling adds pain and risk without changing decisions. <div class="ec-teach"><div class="th">What the findings point to</div> Potassium is the measurement that governs this resuscitation. Total body potassium is profoundly depleted despite whatever the serum shows, and insulin drives it further intracellularly, insulin is withheld if potassium is below 3.5 mEq/L and the level is rechecked every one to 2 hours because it moves faster than anything else in the first hours. <div class="ec-src"><b>Source:</b> Umpierrez GE, et al. Hyperglycemic Crises in Adults With Diabetes. Diabetes Care 2024;47(8):1257-1275.</div></div></div> [[Try this question again->DKA - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="DKA. Ix"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Recheck serum potassium every 1–2 hours</div> Potassium is the measurement that governs this resuscitation. Total body potassium is profoundly depleted despite whatever the serum shows, and insulin drives it further intracellularly, insulin is withheld if potassium is below 3.5 mEq/L and the level is rechecked every one to 2 hours because it moves faster than anything else in the first hours. <div class="ec-src"><b>Source:</b> Umpierrez GE, et al. Hyperglycemic Crises in Adults With Diabetes. Diabetes Care 2024;47(8):1257-1275.</div></div> [[Start another case->Hub]] [[Restart this case->DKA - Ix]] [[Next case →->DKA management - Rx]]

<span class="ec-case-marker" hidden data-entry="DKA. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Hourly glucose is genuinely done and is needed to time the switch to dextrose-containing fluid, so this is close. Glucose falls well before the ketoacidosis resolves, and treating it as the main parameter is how infusions are stopped too early, the endpoint is closure of the anion gap. <div class="ec-teach"><div class="th">What the findings point to</div> Potassium is the measurement that governs this resuscitation. Total body potassium is profoundly depleted despite whatever the serum shows, and insulin drives it further intracellularly, insulin is withheld if potassium is below 3.5 mEq/L and the level is rechecked every one to 2 hours because it moves faster than anything else in the first hours. <div class="ec-src"><b>Source:</b> Umpierrez GE, et al. Hyperglycemic Crises in Adults With Diabetes. Diabetes Care 2024;47(8):1257-1275.</div></div></div> [[Try this question again->DKA - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="DKA. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Abdominal pain is common in ketoacidosis itself and lipase is frequently raised without pancreatitis, so an early lipase often misleads. Reassess the abdomen once the acidosis has been corrected. <div class="ec-teach"><div class="th">What the findings point to</div> Potassium is the measurement that governs this resuscitation. Total body potassium is profoundly depleted despite whatever the serum shows, and insulin drives it further intracellularly, insulin is withheld if potassium is below 3.5 mEq/L and the level is rechecked every one to 2 hours because it moves faster than anything else in the first hours. <div class="ec-src"><b>Source:</b> Umpierrez GE, et al. Hyperglycemic Crises in Adults With Diabetes. Diabetes Care 2024;47(8):1257-1275.</div></div></div> [[Try this question again->DKA - Ix]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 06:15</div> A 59-year-old man has 50 minutes of crushing central chest pain with diaphoresis. The initial 12-lead ECG shows ST elevation in leads II, III and aVF with reciprocal depression in I and aVL. Temperature is 36.8°C, blood pressure 112/70 mm Hg, pulse is 58/min, and respirations are 16/min. Aspirin has been given and the catheterization laboratory has been alerted. <span class="ec-prompt">Which of the following is the most appropriate next step in diagnosis?</span> [[Bedside echocardiography->STEMI - Ix D2]] [[Chest radiography->STEMI - Ix D5]] [[CT coronary angiography->STEMI - Ix D4]] [[Posterior leads V7 to V9->STEMI - Ix D3]] [[Right-sided ECG leads V4R to V6R->STEMI - Ix correct]] [[Serial troponin measurement->STEMI - Ix D1]]

<span class="ec-case-marker" hidden data-entry="STEMI. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Echocardiography is useful when the ECG is equivocal or to look for mechanical complications and alternative diagnoses such as dissection. The ECG here is diagnostic, so it adds delay rather than information. <div class="ec-teach"><div class="th">What the findings point to</div> Inferior infarction involves the right coronary artery in most cases, and right ventricular infarction accompanies it in a substantial minority. Identifying it changes management immediately: these patients are preload-dependent, so nitrates and diuretics can cause profound hypotension, and they need fluid loading instead. Right-sided leads take under a minute and must not delay reperfusion. <div class="ec-src"><b>Source:</b> Rao SV, et al. 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes. Circulation 2025;151(13):e771-e862.</div></div></div> [[Try this question again->STEMI - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="STEMI. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A film may be obtained if dissection is genuinely suspected, but routine radiography delays reperfusion without changing the decision. <div class="ec-teach"><div class="th">What the findings point to</div> Inferior infarction involves the right coronary artery in most cases, and right ventricular infarction accompanies it in a substantial minority. Identifying it changes management immediately: these patients are preload-dependent, so nitrates and diuretics can cause profound hypotension, and they need fluid loading instead. Right-sided leads take under a minute and must not delay reperfusion. <div class="ec-src"><b>Source:</b> Rao SV, et al. 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes. Circulation 2025;151(13):e771-e862.</div></div></div> [[Try this question again->STEMI - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="STEMI. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This has a role in stable chest pain to exclude coronary disease. It has no place in an evolving ST-elevation infarction, where invasive angiography is both diagnostic and therapeutic. <div class="ec-teach"><div class="th">What the findings point to</div> Inferior infarction involves the right coronary artery in most cases, and right ventricular infarction accompanies it in a substantial minority. Identifying it changes management immediately: these patients are preload-dependent, so nitrates and diuretics can cause profound hypotension, and they need fluid loading instead. Right-sided leads take under a minute and must not delay reperfusion. <div class="ec-src"><b>Source:</b> Rao SV, et al. 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes. Circulation 2025;151(13):e771-e862.</div></div></div> [[Try this question again->STEMI - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="STEMI. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Posterior leads are genuinely valuable and are the right addition when there is ST depression in V1 to V3 suggesting posterior involvement, so this is the strongest wrong answer. His reciprocal changes are in I and aVL, which points to right ventricular rather than posterior extension. <div class="ec-teach"><div class="th">What the findings point to</div> Inferior infarction involves the right coronary artery in most cases, and right ventricular infarction accompanies it in a substantial minority. Identifying it changes management immediately: these patients are preload-dependent, so nitrates and diuretics can cause profound hypotension, and they need fluid loading instead. Right-sided leads take under a minute and must not delay reperfusion. <div class="ec-src"><b>Source:</b> Rao SV, et al. 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes. Circulation 2025;151(13):e771-e862.</div></div></div> [[Try this question again->STEMI - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="STEMI. Ix"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Right-sided ECG leads V4R to V6R.</div> Inferior infarction involves the right coronary artery in most cases, and right ventricular infarction accompanies it in a substantial minority. Identifying it changes management immediately: these patients are preload-dependent, so nitrates and diuretics can cause profound hypotension, and they need fluid loading instead. Right-sided leads take under a minute and must not delay reperfusion. <div class="ec-src"><b>Source:</b> Rao SV, et al. 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes. Circulation 2025;151(13):e771-e862.</div></div> [[Start another case->Hub]] [[Restart this case->STEMI - Ix]] [[Next case →->STEMI prognosis - Dx]]

<span class="ec-case-marker" hidden data-entry="STEMI. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Troponin confirms myocardial injury but is often normal in the first hours, and ST elevation with this history is already an indication for immediate reperfusion. Waiting for a biomarker is the classic way to lose myocardium. <div class="ec-teach"><div class="th">What the findings point to</div> Inferior infarction involves the right coronary artery in most cases, and right ventricular infarction accompanies it in a substantial minority. Identifying it changes management immediately: these patients are preload-dependent, so nitrates and diuretics can cause profound hypotension, and they need fluid loading instead. Right-sided leads take under a minute and must not delay reperfusion. <div class="ec-src"><b>Source:</b> Rao SV, et al. 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes. Circulation 2025;151(13):e771-e862.</div></div></div> [[Try this question again->STEMI - Ix]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 16:50</div> A 42-year-old woman had urticaria, wheeze and hypotension 20 minutes after a restaurant meal. She responded to two doses of intramuscular epinephrine and has been observed for 4 hours with no recurrence. She takes propranolol for migraine. She has eaten at the restaurant before without problems and is unsure what triggered it. <span class="ec-prompt">Which of the following is the most appropriate next step in diagnosis?</span> [[No investigation is required->Anaphylaxis - Ix D5]] [[Serum histamine level drawn at presentation->Anaphylaxis - Ix D3]] [[Serum tryptase now, baseline level after recovery->Anaphylaxis - Ix correct]] [[Skin prick testing before discharge->Anaphylaxis - Ix D1]] [[Specific IgE panel to a broad range of foods->Anaphylaxis - Ix D2]] [[Total serum IgE to assess atopic burden->Anaphylaxis - Ix D4]]

<span class="ec-case-marker" hidden data-entry="Anaphylaxis. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Histamine rises and falls within minutes, so by the time blood is drawn it has usually normalized. Tryptase has a longer window and is the more useful marker. <div class="ec-teach"><div class="th">What the findings point to</div> A tryptase taken within a few hours of onset, compared against a baseline drawn at least 24 hours later once symptoms have fully resolved, supports the diagnosis when it is uncertain, and a persistently raised baseline points to an underlying mast cell disorder. The acute sample must be taken now because tryptase falls within hours. <div class="ec-src"><b>Source:</b> Golden DBK, et al. Anaphylaxis: A 2023 Practice Parameter Update. Ann Allergy Asthma Immunol 2024;132(2):124-176.</div></div></div> [[Try this question again->Anaphylaxis - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Anaphylaxis. Ix"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Serum tryptase now, baseline level after recovery</div> A tryptase taken within a few hours of onset, compared against a baseline drawn at least 24 hours later once symptoms have fully resolved, supports the diagnosis when it is uncertain, and a persistently raised baseline points to an underlying mast cell disorder. The acute sample must be taken now because tryptase falls within hours. <div class="ec-src"><b>Source:</b> Golden DBK, et al. Anaphylaxis: A 2023 Practice Parameter Update. Ann Allergy Asthma Immunol 2024;132(2):124-176.</div></div> [[Start another case->Hub]] [[Restart this case->Anaphylaxis - Ix]] [[Next case →->COPD ventilation - Rx]]

<span class="ec-case-marker" hidden data-entry="Anaphylaxis. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Allergy testing is essential and she should have it, so this is the closest wrong answer. It is performed after several weeks, testing too soon risks false negatives because mast cell mediators are depleted, and it belongs in a specialist setting with resuscitation available. <div class="ec-teach"><div class="th">What the findings point to</div> A tryptase taken within a few hours of onset, compared against a baseline drawn at least 24 hours later once symptoms have fully resolved, supports the diagnosis when it is uncertain, and a persistently raised baseline points to an underlying mast cell disorder. The acute sample must be taken now because tryptase falls within hours. <div class="ec-src"><b>Source:</b> Golden DBK, et al. Anaphylaxis: A 2023 Practice Parameter Update. Ann Allergy Asthma Immunol 2024;132(2):124-176.</div></div></div> [[Try this question again->Anaphylaxis - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Anaphylaxis. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Untargeted panels generate false positives and sensitizations of no clinical relevance, which lead to unnecessary avoidance. Testing is directed by a careful history taken at allergy follow-up. <div class="ec-teach"><div class="th">What the findings point to</div> A tryptase taken within a few hours of onset, compared against a baseline drawn at least 24 hours later once symptoms have fully resolved, supports the diagnosis when it is uncertain, and a persistently raised baseline points to an underlying mast cell disorder. The acute sample must be taken now because tryptase falls within hours. <div class="ec-src"><b>Source:</b> Golden DBK, et al. Anaphylaxis: A 2023 Practice Parameter Update. Ann Allergy Asthma Immunol 2024;132(2):124-176.</div></div></div> [[Try this question again->Anaphylaxis - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Anaphylaxis. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Total IgE reflects atopy generally and cannot identify a trigger or confirm anaphylaxis. <div class="ec-teach"><div class="th">What the findings point to</div> A tryptase taken within a few hours of onset, compared against a baseline drawn at least 24 hours later once symptoms have fully resolved, supports the diagnosis when it is uncertain, and a persistently raised baseline points to an underlying mast cell disorder. The acute sample must be taken now because tryptase falls within hours. <div class="ec-src"><b>Source:</b> Golden DBK, et al. Anaphylaxis: A 2023 Practice Parameter Update. Ann Allergy Asthma Immunol 2024;132(2):124-176.</div></div></div> [[Try this question again->Anaphylaxis - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Anaphylaxis. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Resolution is not the end of the episode. She needs the acute tryptase now, epinephrine autoinjectors with training, a written action plan, and allergy referral, and her propranolol should be reviewed, since beta-blockade predicts a harder course if it recurs. <div class="ec-teach"><div class="th">What the findings point to</div> A tryptase taken within a few hours of onset, compared against a baseline drawn at least 24 hours later once symptoms have fully resolved, supports the diagnosis when it is uncertain, and a persistently raised baseline points to an underlying mast cell disorder. The acute sample must be taken now because tryptase falls within hours. <div class="ec-src"><b>Source:</b> Golden DBK, et al. Anaphylaxis: A 2023 Practice Parameter Update. Ann Allergy Asthma Immunol 2024;132(2):124-176.</div></div></div> [[Try this question again->Anaphylaxis - Ix]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 23:15</div> A 6-year-old girl with known epilepsy is brought in generalized tonic-clonic and still convulsing after eight continuous minutes. Her parents report she missed her evening medication. She weighs 21 kg. Intravenous access has been established and a bedside glucose is 96 mg/dL. <span class="ec-prompt">Which of the following is the most appropriate pharmacotherapy?</span> [[CT head and labs first->Status epilepticus - Workup trap]] [[Give Intravenous levetiracetam->Status epilepticus - Levetiracetam first]] [[Intravenous fosphenytoin as the initial agent->Status epilepticus - Fosphenytoin first trap]] [[Intravenous lorazepam->Status epilepticus - Benzo correct]] [[Rectal diazepam as the initial benzodiazepine->Status epilepticus - Route trap]]

<span class="ec-case-marker" hidden data-entry="Status epilepticus. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ The seizure will not wait for the scanner.</div> This sends an actively seizing patient for imaging before treatment. Prolonged convulsions cause progressive neuronal injury, the drug comes first, the workup follows once the seizure is controlled (glucose is already checked and normal). <div class="ec-teach"><div class="th">Why not this</div> Active status epilepticus is treated immediately with a benzodiazepine. Imaging and further labs follow seizure control; the one laboratory value needed up front, glucose, is already normal here. <div class="ec-src"><b>Source:</b> Standard status epilepticus algorithms; Kapur J, et al. (ESETT). N Engl J Med 2019.</div></div></div> [[Try this question again->Status epilepticus - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Status epilepticus. Opening"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Intravenous lorazepam</div> IV lorazepam goes in at an adequate weight-based dose. Benzodiazepines are the established first-line abortive for status epilepticus, and adequate dosing is what actually stops the seizure. <div class="ec-teach"><div class="th">Why a benzodiazepine</div> Benzodiazepines (IV lorazepam, or IM midazolam if no IV) are first-line for convulsive status epilepticus. Under-dosing is a common error and is especially common in children, where the weight-based calculation invites hesitancy, give the full dose. If intravenous access had not been available, intramuscular midazolam, or the buccal or rectal route, is effective. The ESETT trial enrolled children as well as adults and found levetiracetam, fosphenytoin and valproate equivalent as second-line agents. <br><br><b>Then:</b> After an adequate benzodiazepine, the second-line options, levetiracetam, fosphenytoin, and valproate, showed no significant difference in seizure cessation or safety in a major randomized trial. Any of the three is a reasonable choice. <div class="ec-src"><b>Source:</b> Kapur J, et al. Randomized Trial of Three Anticonvulsant Medications for Status Epilepticus (ESETT). N Engl J Med 2019;381(22):2103-2113.</div></div></div> <b>Seizure aborted → admitted for monitoring.</b> [[Start another case->Hub]] [[Restart this case->Status epilepticus - Opening]] [[Next case →->Refractory SE - Rx]]

<span class="ec-case-marker" hidden data-entry="Status epilepticus. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Second-line drug in the first-line slot.</div> Levetiracetam is a genuine status epilepticus drug and it will appear later in this algorithm, but it is slower to abort a seizure than a benzodiazepine. The brain keeps seizing while it loads. <div class="ec-teach"><div class="th">The order matters</div> Benzodiazepines are first-line for convulsive status epilepticus. Levetiracetam, fosphenytoin and valproate are second-line, used after an adequate benzodiazepine dose fails. <div class="ec-src"><b>Source:</b> Kapur J, et al. Randomized Trial of Three Anticonvulsant Medications for Status Epilepticus (ESETT). N Engl J Med 2019;381(22):2103-2113.</div></div></div> [[Try this question again->Status epilepticus - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Status epilepticus. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Right drug class, and a route chosen for the wrong reason.</div> Rectal diazepam is a genuine and valuable option in children, it is what parents use at home and what is given when there is no intravenous access. Here access is already established. Choosing a less reliable route when a reliable one is in place delays the effective dose, and being a child is not by itself a reason to avoid the intravenous route. <div class="ec-teach"><div class="th">Why this is wrong</div> Give an intravenous benzodiazepine at the full weight-based dose. Reserve intramuscular midazolam, or the buccal or rectal route, for when intravenous access is unavailable, in that situation they are first-line rather than second-best. <div class="ec-src"><b>Source:</b> Glauser T, et al. Evidence-Based Guideline: Treatment of Convulsive Status Epilepticus. Epilepsy Curr 2016;16(1):48-61.</div></div></div> [[Try this question again->Status epilepticus - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Status epilepticus. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Right family, wrong order.</div> Fosphenytoin is a real status-epilepticus drug, but it is second-line. It takes time to load and will not abort the seizure as fast as a benzodiazepine. Meanwhile the brain keeps seizing. <div class="ec-teach"><div class="th">Where this breaks down</div> Second-line antiseizure medications (fosphenytoin, levetiracetam, valproate) come after a benzodiazepine, not before. The benzodiazepine is the first move. <div class="ec-src"><b>Source:</b> Kapur J, et al. (ESETT). N Engl J Med 2019.</div></div></div> [[Try this question again->Status epilepticus - Opening]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 08:20</div> A 72-year-old man developed right-sided weakness and difficulty speaking 65 minutes ago; the onset was witnessed by his wife. He takes amlodipine and no anticoagulant. Blood pressure is 168/94 mm Hg, glucose is 106 mg/dL. Examination shows a right facial droop, right arm and leg weakness, and expressive dysphasia. NIH Stroke Scale score is 14. He is within the thrombolysis window. <span class="ec-prompt">Which of the following is the most appropriate next step in diagnosis?</span> [[Carotid duplex ultrasonography->Stroke - Ix carotid]] [[CT angiography of the head and neck->Stroke - Ix ct]] [[Diffusion-weighted MRI of the brain->Stroke - Ix diffusion-weighted]] [[Echocardiography with bubble study->Stroke - Ix echocardiography]] [[Lumbar puncture->Stroke - Ix lumbar]] [[Non-contrast CT of the head->Stroke - Ix correct]]

<span class="ec-case-marker" hidden data-entry="Stroke. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Carotid duplex ultrasonography is not the next step.</div> This informs secondary prevention and the timing of endarterectomy. It has no role in the hyperacute decision. <div class="ec-teach"><div class="th">What to do instead</div> The single question that has to be answered before thrombolysis is whether this is hemorrhagic. Non-contrast computed tomography answers it in minutes and is available everywhere, which is why it is the immediate study in every acute stroke pathway. It need not show the infarct, an early ischemic stroke often looks normal, and that is an acceptable result. <div class="ec-src"><b>Source:</b> Powers WJ, et al. AHA/ASA Guidelines for the Early Management of Patients With Acute Ischemic Stroke. Stroke 2019;50(12):e344-e418.</div></div></div> [[Try this question again->Stroke - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Stroke. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ CT angiography of the head and neck is not the next step.</div> Vessel imaging identifies a large-vessel occlusion and is essential for selecting thrombectomy candidates, so it is a genuine and important part of modern stroke care, often performed in the same sitting. It does not replace the non-contrast study, because the decision it informs comes after hemorrhage has been excluded. <div class="ec-teach"><div class="th">What to do instead</div> The single question that has to be answered before thrombolysis is whether this is hemorrhagic. Non-contrast computed tomography answers it in minutes and is available everywhere, which is why it is the immediate study in every acute stroke pathway. It need not show the infarct, an early ischemic stroke often looks normal, and that is an acceptable result. <div class="ec-src"><b>Source:</b> Powers WJ, et al. AHA/ASA Guidelines for the Early Management of Patients With Acute Ischemic Stroke. Stroke 2019;50(12):e344-e418.</div></div></div> [[Try this question again->Stroke - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Stroke. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Diffusion-weighted MRI of the brain is not the next step.</div> MRI is far more sensitive for early ischemia and is the better test for posterior circulation and for wake-up strokes where mismatch imaging guides treatment. It is slower and less available, and taking a thrombolysis candidate to MRI first costs viable brain. <div class="ec-teach"><div class="th">What to do instead</div> The single question that has to be answered before thrombolysis is whether this is hemorrhagic. Non-contrast computed tomography answers it in minutes and is available everywhere, which is why it is the immediate study in every acute stroke pathway. It need not show the infarct, an early ischemic stroke often looks normal, and that is an acceptable result. <div class="ec-src"><b>Source:</b> Powers WJ, et al. AHA/ASA Guidelines for the Early Management of Patients With Acute Ischemic Stroke. Stroke 2019;50(12):e344-e418.</div></div></div> [[Try this question again->Stroke - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Stroke. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Echocardiography with bubble study is not the next step.</div> This looks for a cardioembolic or paradoxical source and belongs to the workup after stabilization, particularly in a younger patient. It does not affect what happens in the next hour. <div class="ec-teach"><div class="th">What to do instead</div> The single question that has to be answered before thrombolysis is whether this is hemorrhagic. Non-contrast computed tomography answers it in minutes and is available everywhere, which is why it is the immediate study in every acute stroke pathway. It need not show the infarct, an early ischemic stroke often looks normal, and that is an acceptable result. <div class="ec-src"><b>Source:</b> Powers WJ, et al. AHA/ASA Guidelines for the Early Management of Patients With Acute Ischemic Stroke. Stroke 2019;50(12):e344-e418.</div></div></div> [[Try this question again->Stroke - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Stroke. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Lumbar puncture is not the next step.</div> This is reserved for suspected subarachnoid hemorrhage with a negative computed tomography, in a patient with thunderclap headache. It is not part of an ischemic stroke pathway and would be dangerous before imaging. <div class="ec-teach"><div class="th">What to do instead</div> The single question that has to be answered before thrombolysis is whether this is hemorrhagic. Non-contrast computed tomography answers it in minutes and is available everywhere, which is why it is the immediate study in every acute stroke pathway. It need not show the infarct, an early ischemic stroke often looks normal, and that is an acceptable result. <div class="ec-src"><b>Source:</b> Powers WJ, et al. AHA/ASA Guidelines for the Early Management of Patients With Acute Ischemic Stroke. Stroke 2019;50(12):e344-e418.</div></div></div> [[Try this question again->Stroke - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Stroke. Ix"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Non-contrast CT of the head.</div> The single question that has to be answered before thrombolysis is whether this is hemorrhagic. Non-contrast computed tomography answers it in minutes and is available everywhere, which is why it is the immediate study in every acute stroke pathway. It need not show the infarct, an early ischemic stroke often looks normal, and that is an acceptable result. <div class="ec-src"><b>Source:</b> Powers WJ, et al. AHA/ASA Guidelines for the Early Management of Patients With Acute Ischemic Stroke. Stroke 2019;50(12):e344-e418.</div></div> [[Start another case->Hub]] [[Restart this case->Stroke - Ix]] [[Next case →->Large vessel stroke - Rx]]

<div class="ec-scene">Emergency department · 21:15</div> A 27-year-old man is brought in 20 minutes after a motorcycle crash with severe breathlessness. Temperature is 36.9°C, blood pressure 76/48 mm Hg, pulse is 138/min, respirations are 34/min, and oxygen saturation 84% on high-flow oxygen. Breath sounds are absent over the left hemithorax, which is hyperresonant to percussion. The trachea is deviated to the right and the jugular venous pressure is raised. He is becoming agitated. <span class="ec-prompt">Which of the following is the most likely diagnosis?</span> [[Cardiac tamponade->Tension pneumothorax - Dx D2]] [[Flail chest with pulmonary contusion->Tension pneumothorax - Dx D3]] [[Massive hemothorax->Tension pneumothorax - Dx D1]] [[Ruptured thoracic aorta->Tension pneumothorax - Dx D5]] [[Tension pneumothorax->Tension pneumothorax - Dx correct]] [[Traumatic diaphragmatic rupture->Tension pneumothorax - Dx D4]]

<span class="ec-case-marker" hidden data-entry="Tension pneumothorax. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Tamponade gives obstructive shock with raised venous pressure and can follow penetrating trauma, so it belongs on the list. Breath sounds are equal and the chest is not hyperresonant, and the trachea is central. <div class="ec-teach"><div class="th">What the findings point to</div> Obstructive shock with absent breath sounds and hyperresonance on one side, contralateral tracheal deviation and raised venous pressure after trauma. Rising intrapleural pressure displaces the mediastinum and obstructs venous return, so the shock is mechanical, this is a clinical diagnosis and imaging must not precede decompression. <div class="ec-src"><b>Source:</b> ATLS Advanced Trauma Life Support, 10th ed.</div></div></div> [[Try this question again->Tension pneumothorax - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Tension pneumothorax. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This causes respiratory distress and hypoxemia after blunt trauma, with paradoxical chest wall movement. It does not produce tracheal deviation or a hyperresonant hemithorax. <div class="ec-teach"><div class="th">What the findings point to</div> Obstructive shock with absent breath sounds and hyperresonance on one side, contralateral tracheal deviation and raised venous pressure after trauma. Rising intrapleural pressure displaces the mediastinum and obstructs venous return, so the shock is mechanical, this is a clinical diagnosis and imaging must not precede decompression. <div class="ec-src"><b>Source:</b> ATLS Advanced Trauma Life Support, 10th ed.</div></div></div> [[Try this question again->Tension pneumothorax - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Tension pneumothorax. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This also gives unilateral absent breath sounds and shock after trauma, so it is the closest alternative. The hemithorax is dull to percussion rather than hyperresonant, and the venous pressure is typically low from blood loss rather than raised. <div class="ec-teach"><div class="th">What the findings point to</div> Obstructive shock with absent breath sounds and hyperresonance on one side, contralateral tracheal deviation and raised venous pressure after trauma. Rising intrapleural pressure displaces the mediastinum and obstructs venous return, so the shock is mechanical, this is a clinical diagnosis and imaging must not precede decompression. <div class="ec-src"><b>Source:</b> ATLS Advanced Trauma Life Support, 10th ed.</div></div></div> [[Try this question again->Tension pneumothorax - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Tension pneumothorax. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Aortic injury after deceleration causes shock and a widened mediastinum on imaging, but with equal breath sounds and no hyperresonance or tracheal deviation. <div class="ec-teach"><div class="th">What the findings point to</div> Obstructive shock with absent breath sounds and hyperresonance on one side, contralateral tracheal deviation and raised venous pressure after trauma. Rising intrapleural pressure displaces the mediastinum and obstructs venous return, so the shock is mechanical, this is a clinical diagnosis and imaging must not precede decompression. <div class="ec-src"><b>Source:</b> ATLS Advanced Trauma Life Support, 10th ed.</div></div></div> [[Try this question again->Tension pneumothorax - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Tension pneumothorax. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Tension pneumothorax.</div> Obstructive shock with absent breath sounds and hyperresonance on one side, contralateral tracheal deviation and raised venous pressure after trauma. Rising intrapleural pressure displaces the mediastinum and obstructs venous return, so the shock is mechanical, this is a clinical diagnosis and imaging must not precede decompression. <div class="ec-src"><b>Source:</b> ATLS Advanced Trauma Life Support, 10th ed.</div></div> [[Start another case->Hub]] [[Restart this case->Tension pneumothorax - Dx]] [[Next case →->Tension PTX - Rx]]

<span class="ec-case-marker" hidden data-entry="Tension pneumothorax. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Herniated bowel can reduce breath sounds on the left and shift the mediastinum, which makes this a genuine consideration in left-sided blunt trauma. It develops less abruptly and gives bowel sounds in the chest with a dull or mixed percussion note. <div class="ec-teach"><div class="th">What the findings point to</div> Obstructive shock with absent breath sounds and hyperresonance on one side, contralateral tracheal deviation and raised venous pressure after trauma. Rising intrapleural pressure displaces the mediastinum and obstructs venous return, so the shock is mechanical, this is a clinical diagnosis and imaging must not precede decompression. <div class="ec-src"><b>Source:</b> ATLS Advanced Trauma Life Support, 10th ed.</div></div></div> [[Try this question again->Tension pneumothorax - Dx]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 01:50</div> A 52-year-old man with known cirrhosis has had two episodes of large-volume hematemesis and melena over the past 6 hours. Temperature is 37.0°C, blood pressure 94/58 mm Hg, pulse is 118/min, and respirations are 20/min. Hemoglobin is 7.4 g/dL. He has spider nevi, palmar erythema and moderate ascites. He has been resuscitated, given octreotide and ceftriaxone, and is now hemodynamically stable. <span class="ec-prompt">Which of the following is the most appropriate next step in diagnosis?</span> [[Abdominal ultrasonography with portal Doppler->Variceal bleed - Ix D5]] [[Balloon tamponade with a Sengstaken-Blakemore tube->Variceal bleed - Ix D3]] [[CT angiography of the abdomen->Variceal bleed - Ix D1]] [[Nasogastric tube and lavage->Variceal bleed - Ix D4]] [[Transjugular intrahepatic portosystemic shunt->Variceal bleed - Ix D2]] [[Upper endoscopy within 12 hours->Variceal bleed - Ix correct]]

<span class="ec-case-marker" hidden data-entry="Variceal bleed. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This assesses portal patency and is part of the wider cirrhosis workup. It does not identify or treat the bleeding lesion. <div class="ec-teach"><div class="th">What the findings point to</div> Endoscopy is diagnostic and therapeutic in variceal bleeding, band ligation controls hemorrhage and reduces rebleeding and mortality. In suspected variceal bleeding it is performed within 12 hours of presentation, sooner than the 24-hour window used for non-variceal upper gastrointestinal bleeding, once the patient has been resuscitated. <div class="ec-src"><b>Source:</b> Garcia-Tsao G, et al. Portal Hypertensive Bleeding in Cirrhosis: AASLD Practice Guidance. Hepatology 2017;65(1):310-335.</div></div></div> [[Try this question again->Variceal bleed - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Variceal bleed. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Tamponade is a temporizing rescue for uncontrolled hemorrhage while definitive therapy is arranged, with serious complications including esophageal rupture. He is stable, so it is not indicated. <div class="ec-teach"><div class="th">What the findings point to</div> Endoscopy is diagnostic and therapeutic in variceal bleeding, band ligation controls hemorrhage and reduces rebleeding and mortality. In suspected variceal bleeding it is performed within 12 hours of presentation, sooner than the 24-hour window used for non-variceal upper gastrointestinal bleeding, once the patient has been resuscitated. <div class="ec-src"><b>Source:</b> Garcia-Tsao G, et al. Portal Hypertensive Bleeding in Cirrhosis: AASLD Practice Guidance. Hepatology 2017;65(1):310-335.</div></div></div> [[Try this question again->Variceal bleed - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Variceal bleed. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This localizes active arterial bleeding and is useful when endoscopy fails or is not feasible. It offers no therapeutic option for varices and requires brisk bleeding to be positive. <div class="ec-teach"><div class="th">What the findings point to</div> Endoscopy is diagnostic and therapeutic in variceal bleeding, band ligation controls hemorrhage and reduces rebleeding and mortality. In suspected variceal bleeding it is performed within 12 hours of presentation, sooner than the 24-hour window used for non-variceal upper gastrointestinal bleeding, once the patient has been resuscitated. <div class="ec-src"><b>Source:</b> Garcia-Tsao G, et al. Portal Hypertensive Bleeding in Cirrhosis: AASLD Practice Guidance. Hepatology 2017;65(1):310-335.</div></div></div> [[Try this question again->Variceal bleed - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Variceal bleed. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A negative aspirate does not exclude an upper source and the result would not change management. Guidelines no longer recommend it routinely. <div class="ec-teach"><div class="th">What the findings point to</div> Endoscopy is diagnostic and therapeutic in variceal bleeding, band ligation controls hemorrhage and reduces rebleeding and mortality. In suspected variceal bleeding it is performed within 12 hours of presentation, sooner than the 24-hour window used for non-variceal upper gastrointestinal bleeding, once the patient has been resuscitated. <div class="ec-src"><b>Source:</b> Garcia-Tsao G, et al. Portal Hypertensive Bleeding in Cirrhosis: AASLD Practice Guidance. Hepatology 2017;65(1):310-335.</div></div></div> [[Try this question again->Variceal bleed - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Variceal bleed. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> TIPS is a genuine and important therapy, early or pre-emptive TIPS improves outcomes in selected high-risk patients, which makes this the strongest wrong answer. It follows endoscopic assessment rather than replacing it, and it is a rescue or early-secondary measure, not the initial diagnostic step. <div class="ec-teach"><div class="th">What the findings point to</div> Endoscopy is diagnostic and therapeutic in variceal bleeding, band ligation controls hemorrhage and reduces rebleeding and mortality. In suspected variceal bleeding it is performed within 12 hours of presentation, sooner than the 24-hour window used for non-variceal upper gastrointestinal bleeding, once the patient has been resuscitated. <div class="ec-src"><b>Source:</b> Garcia-Tsao G, et al. Portal Hypertensive Bleeding in Cirrhosis: AASLD Practice Guidance. Hepatology 2017;65(1):310-335.</div></div></div> [[Try this question again->Variceal bleed - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Variceal bleed. Ix"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Upper endoscopy within 12 hours.</div> Endoscopy is diagnostic and therapeutic in variceal bleeding, band ligation controls hemorrhage and reduces rebleeding and mortality. In suspected variceal bleeding it is performed within 12 hours of presentation, sooner than the 24-hour window used for non-variceal upper gastrointestinal bleeding, once the patient has been resuscitated. <div class="ec-src"><b>Source:</b> Garcia-Tsao G, et al. Portal Hypertensive Bleeding in Cirrhosis: AASLD Practice Guidance. Hepatology 2017;65(1):310-335.</div></div> [[Start another case->Hub]] [[Restart this case->Variceal bleed - Ix]] [[Next case →->Mesenteric ischemia - Dx]]

<div class="ec-scene">Emergency department · 20:15</div> A 16-year-old girl is brought in by her mother after disclosing an intentional acetaminophen overdose about 5 hours ago. She feels well and her examination is unremarkable, which is exactly what early acetaminophen toxicity looks like. She is alert and cooperative, and her mother is with her. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Activated charcoal, reassess in the morning->Acetaminophen - Charcoal late]] [[Base the decision on symptoms and Liver enzymes->Acetaminophen - Symptoms trap]] [[Discharge; she feels well->Acetaminophen - Discharge trap]] [[N-acetylcysteine now, before the level->Acetaminophen - Empiric NAC trap]] [[Timed serum level on the Rumack-Matthew nomogram->Acetaminophen - Level correct]]

<span class="ec-case-marker" hidden data-entry="Acetaminophen. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ By the time she is symptomatic, it is late.</div> Acetaminophen poisoning produces almost no symptoms and normal liver enzymes for the first 24 hours, then the liver fails. Waiting for her to look sick means missing the window when the antidote actually works. <div class="ec-teach"><div class="th">What went wrong</div> Early normal exam and normal transaminases do not reassure. Treatment is decided by the acetaminophen level on the nomogram, not by symptoms. <div class="ec-src"><b>Source:</b> Revised Rumack-Matthew nomogram (150 mcg/mL treatment line at 4 h); Rumack BH, Matthew H. Pediatrics 1975;55(6):871-876.</div></div></div> [[Try this question again->Acetaminophen - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Acetaminophen. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ This patient was discharged with a lethal ingestion in progress.</div> She feels fine because acetaminophen toxicity hides for a day. Discharging her before a level means she may return in fulminant liver failure, after the antidote's window has closed. <div class="ec-teach"><div class="th">Why not this</div> A well-appearing patient after acetaminophen overdose still needs a timed level on the nomogram before any disposition decision. <div class="ec-src"><b>Source:</b> Revised Rumack-Matthew nomogram (150 mcg/mL treatment line at 4 h); Rumack BH, Matthew H. Pediatrics 1975;55(6):871-876.</div></div></div> [[Try this question again->Acetaminophen - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Acetaminophen. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Past the window, and not the treatment.</div> Activated charcoal adsorbs acetaminophen well, but its benefit is greatest within about an hour and falls away after four, she is at five and a half. More importantly, charcoal is decontamination, not an antidote, and reassessing in the morning wastes the window in which NAC works best. <div class="ec-teach"><div class="th">Where this breaks down</div> Charcoal is an early decontamination measure, generally within 1-4 hours of ingestion. It does not replace N-acetylcysteine, and disposition is decided by a timed level on the nomogram, not by overnight observation. <div class="ec-src"><b>Source:</b> Rumack BH, Matthew H. Acetaminophen poisoning and toxicity. Pediatrics 1975; 55(6):871-876.</div></div></div> [[Try this question again->Acetaminophen - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Acetaminophen. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Defensible in some presentations, and not the best answer in this one.</div> Starting the antidote empirically is correct when the timing is unknown, when the ingestion was staggered, or when presentation is beyond 8 hours and the level will not return in time, so this is not a careless answer. Here the ingestion time is known and she is at 5 hours, so an interpretable level will be available well inside the window in which the antidote retains full efficacy. <div class="ec-teach"><div class="th">Why this is wrong</div> Draw a level at 4 hours or later and plot it on the Rumack-Matthew nomogram, which decides who needs treatment. Start the antidote empirically if the level will not return before 8 hours from ingestion, and never delay it past that point waiting for a result. <div class="ec-src"><b>Source:</b> Revised Rumack-Matthew nomogram (150 mcg/mL treatment line at 4 h); Rumack BH, Matthew H. Pediatrics 1975;55(6):871-876.</div></div></div> [[Try this question again->Acetaminophen - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Acetaminophen. Opening"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Timed serum level on the Rumack-Matthew nomogram</div> A serum acetaminophen concentration is drawn, she is past 4 hours, so it is interpretable, and plot it against time on the Rumack-Matthew nomogram. It comes back above the treatment line. <div class="ec-teach"><div class="th">Why the nomogram</div> Acetaminophen toxicity is clinically silent for the first day, so symptoms cannot be waited for. The approach is identical in adolescents, with weight-based dosing of the antidote. Alongside the medical management, an intentional overdose in a minor requires a mental health assessment before discharge and attention to safeguarding, the medical clearance and the psychiatric evaluation run in parallel, and neither substitutes for the other. A level drawn at 4 hours or later, plotted on the Rumack-Matthew nomogram, decides who needs N-acetylcysteine. The US treatment line runs from 150 mcg/mL at 4 hours downward. <br><br><b>Then:</b> N-acetylcysteine replenishes glutathione and is close to 100% hepatoprotective when started within 8 hours of ingestion. Once a level is above the treatment line, it is started immediately and run to full course, without waiting for enzymes to rise. <div class="ec-src"><b>Source:</b> Revised Rumack-Matthew nomogram (150 mcg/mL treatment line at 4 h); Rumack BH, Matthew H. Pediatrics 1975;55(6):871-876.</div></div></div> <b>Hepatotoxicity prevented → psychiatry and medicine admission.</b> [[Start another case->Hub]] [[Restart this case->Acetaminophen - Opening]] [[Next case →->CCB-BB overdose - Opening]]

<div class="ec-scene">Emergency department · 01:40</div> A 44-year-old man has 12 hours of fever, severe headache and neck stiffness. He is drowsy with a Glasgow Coma Scale score of 13 and has a new mild weakness of the right arm. Blood cultures have been drawn and empiric antibiotics with dexamethasone have been given. <span class="ec-prompt">Which of the following is the most appropriate next step in diagnosis?</span> [[Blood cultures and empiric treatment, no lumbar puncture->Meningitis - Ix D3]] [[Coagulation studies before lumbar puncture->Meningitis - Ix D5]] [[CT of the head before lumbar puncture->Meningitis - Ix correct]] [[Immediate lumbar puncture, no imaging->Meningitis - Ix D1]] [[MRI of the brain with contrast->Meningitis - Ix D2]] [[Serum procalcitonin->Meningitis - Ix D4]]

<span class="ec-case-marker" hidden data-entry="Meningitis. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Cultures are already drawn and antibiotics given. Foregoing cerebrospinal fluid entirely loses the organism, the sensitivities, and the ability to distinguish bacterial from viral or other causes, which determines the duration and nature of treatment. <div class="ec-teach"><div class="th">What the findings point to</div> A focal neurological deficit is one of the specific indications for imaging before lumbar puncture, along with a depressed conscious level, new seizure, papilledema and immunocompromise, because of the risk of herniation if a mass lesion or raised pressure is present. He has two of them. Antibiotics and dexamethasone were given first, which is why imaging does not delay treatment. <div class="ec-src"><b>Source:</b> Tunkel AR, et al. IDSA Practice Guidelines for the Management of Bacterial Meningitis. Clin Infect Dis 2004;39(9):1267-1284.</div></div></div> [[Try this question again->Meningitis - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Meningitis. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Checking clotting is sensible if there is bleeding history or anticoagulation, but it is not the pending question here, the focal deficit is. <div class="ec-teach"><div class="th">What the findings point to</div> A focal neurological deficit is one of the specific indications for imaging before lumbar puncture, along with a depressed conscious level, new seizure, papilledema and immunocompromise, because of the risk of herniation if a mass lesion or raised pressure is present. He has two of them. Antibiotics and dexamethasone were given first, which is why imaging does not delay treatment. <div class="ec-src"><b>Source:</b> Tunkel AR, et al. IDSA Practice Guidelines for the Management of Bacterial Meningitis. Clin Infect Dis 2004;39(9):1267-1284.</div></div></div> [[Try this question again->Meningitis - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Meningitis. Ix"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ CT of the head before lumbar puncture.</div> A focal neurological deficit is one of the specific indications for imaging before lumbar puncture, along with a depressed conscious level, new seizure, papilledema and immunocompromise, because of the risk of herniation if a mass lesion or raised pressure is present. He has two of them. Antibiotics and dexamethasone were given first, which is why imaging does not delay treatment. <div class="ec-src"><b>Source:</b> Tunkel AR, et al. IDSA Practice Guidelines for the Management of Bacterial Meningitis. Clin Infect Dis 2004;39(9):1267-1284.</div></div> [[Start another case->Hub]] [[Restart this case->Meningitis - Ix]] [[Next case →->Meningitis GCS prognosis - Prog]]

<span class="ec-case-marker" hidden data-entry="Meningitis. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Prompt cerebrospinal fluid sampling is the priority in most patients with suspected meningitis and delay reduces culture yield, so this is right in the general case, which is what makes it the strongest wrong answer. His focal deficit and reduced conscious level are exactly the exceptions. <div class="ec-teach"><div class="th">What the findings point to</div> A focal neurological deficit is one of the specific indications for imaging before lumbar puncture, along with a depressed conscious level, new seizure, papilledema and immunocompromise, because of the risk of herniation if a mass lesion or raised pressure is present. He has two of them. Antibiotics and dexamethasone were given first, which is why imaging does not delay treatment. <div class="ec-src"><b>Source:</b> Tunkel AR, et al. IDSA Practice Guidelines for the Management of Bacterial Meningitis. Clin Infect Dis 2004;39(9):1267-1284.</div></div></div> [[Try this question again->Meningitis - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Meningitis. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> MRI is more sensitive for complications such as empyema, venous thrombosis and cerebritis, and has a role later. It is slower and less available acutely, and computed tomography answers the herniation question adequately. <div class="ec-teach"><div class="th">What the findings point to</div> A focal neurological deficit is one of the specific indications for imaging before lumbar puncture, along with a depressed conscious level, new seizure, papilledema and immunocompromise, because of the risk of herniation if a mass lesion or raised pressure is present. He has two of them. Antibiotics and dexamethasone were given first, which is why imaging does not delay treatment. <div class="ec-src"><b>Source:</b> Tunkel AR, et al. IDSA Practice Guidelines for the Management of Bacterial Meningitis. Clin Infect Dis 2004;39(9):1267-1284.</div></div></div> [[Try this question again->Meningitis - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Meningitis. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Procalcitonin can support the distinction but does not replace cerebrospinal fluid analysis and would not change immediate management. <div class="ec-teach"><div class="th">What the findings point to</div> A focal neurological deficit is one of the specific indications for imaging before lumbar puncture, along with a depressed conscious level, new seizure, papilledema and immunocompromise, because of the risk of herniation if a mass lesion or raised pressure is present. He has two of them. Antibiotics and dexamethasone were given first, which is why imaging does not delay treatment. <div class="ec-src"><b>Source:</b> Tunkel AR, et al. IDSA Practice Guidelines for the Management of Bacterial Meningitis. Clin Infect Dis 2004;39(9):1267-1284.</div></div></div> [[Try this question again->Meningitis - Ix]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 02:35</div> A 62-year-old man with long-standing hypertension has sudden severe chest pain that he describes as tearing and radiating between his shoulder blades. It was maximal at onset. Systolic pressure differs by nearly 40 mm Hg between arms. A soft early diastolic murmur is heard at the left sternal border. ECG shows left ventricular hypertrophy without ST elevation. Chest radiograph shows a widened mediastinum. <span class="ec-prompt">Which of the following is the most likely diagnosis?</span> [[Acute pericarditis->Aortic dissection - Dx acute]] [[Aortic dissection->Aortic dissection - Dx correct]] [[Esophageal rupture->Aortic dissection - Dx esophageal]] [[ST-elevation myocardial infarction->Aortic dissection - Dx st-elevation]] [[Tension pneumothorax->Aortic dissection - Dx tension]]

<span class="ec-case-marker" hidden data-entry="Aortic dissection. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Acute pericarditis does not fit.</div> Pericarditis gives pleuritic pain that eases on sitting forward, a friction rub, and widespread concave ST elevation with PR depression. It does not produce an interarm pressure difference or a widened mediastinum. <div class="ec-teach"><div class="th">What the findings actually point to</div> Sudden maximal-at-onset tearing pain radiating to the back, an interarm systolic difference, a new diastolic murmur from aortic regurgitation, and a widened mediastinum are the classic combination. Pain that is worst at the very first moment points to a vascular catastrophe rather than to an evolving one. <div class="ec-src"><b>Source:</b> Isselbacher EM, et al. 2022 ACC/AHA Guideline for the Diagnosis and Management of Aortic Disease. Circulation 2022;146(24):e334-e482.</div></div></div> [[Try this question again->Aortic dissection - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Aortic dissection. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Aortic dissection.</div> Sudden maximal-at-onset tearing pain radiating to the back, an interarm systolic difference, a new diastolic murmur from aortic regurgitation, and a widened mediastinum are the classic combination. Pain that is worst at the very first moment points to a vascular catastrophe rather than to an evolving one. <div class="ec-src"><b>Source:</b> Isselbacher EM, et al. 2022 ACC/AHA Guideline for the Diagnosis and Management of Aortic Disease. Circulation 2022;146(24):e334-e482.</div></div> [[Start another case->Hub]] [[Restart this case->Aortic dissection - Dx]] [[Next case →->Ruptured AAA - Ix]]

<span class="ec-case-marker" hidden data-entry="Aortic dissection. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Esophageal rupture does not fit.</div> Boerhaave syndrome follows forceful vomiting and gives pain with subcutaneous emphysema and often a pleural effusion. There is no vomiting history here, and it does not cause aortic regurgitation or unequal arm pressures. <div class="ec-teach"><div class="th">What the findings actually point to</div> Sudden maximal-at-onset tearing pain radiating to the back, an interarm systolic difference, a new diastolic murmur from aortic regurgitation, and a widened mediastinum are the classic combination. Pain that is worst at the very first moment points to a vascular catastrophe rather than to an evolving one. <div class="ec-src"><b>Source:</b> Isselbacher EM, et al. 2022 ACC/AHA Guideline for the Diagnosis and Management of Aortic Disease. Circulation 2022;146(24):e334-e482.</div></div></div> [[Try this question again->Aortic dissection - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Aortic dissection. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ ST-elevation myocardial infarction does not fit.</div> Infarction is the most important thing to distinguish this from, because anticoagulating or lysing a dissection is catastrophic. His ECG shows no ST elevation, and neither the interarm difference nor the widened mediastinum belongs to infarction, though a dissection extending into the right coronary ostium can produce inferior changes. <div class="ec-teach"><div class="th">What the findings actually point to</div> Sudden maximal-at-onset tearing pain radiating to the back, an interarm systolic difference, a new diastolic murmur from aortic regurgitation, and a widened mediastinum are the classic combination. Pain that is worst at the very first moment points to a vascular catastrophe rather than to an evolving one. <div class="ec-src"><b>Source:</b> Isselbacher EM, et al. 2022 ACC/AHA Guideline for the Diagnosis and Management of Aortic Disease. Circulation 2022;146(24):e334-e482.</div></div></div> [[Try this question again->Aortic dissection - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Aortic dissection. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Tension pneumothorax does not fit.</div> This causes acute dyspnea with absent breath sounds, tracheal deviation and hemodynamic collapse. His breath sounds and trachea are not described as abnormal, and it does not cause an interarm gradient. <div class="ec-teach"><div class="th">What the findings actually point to</div> Sudden maximal-at-onset tearing pain radiating to the back, an interarm systolic difference, a new diastolic murmur from aortic regurgitation, and a widened mediastinum are the classic combination. Pain that is worst at the very first moment points to a vascular catastrophe rather than to an evolving one. <div class="ec-src"><b>Source:</b> Isselbacher EM, et al. 2022 ACC/AHA Guideline for the Diagnosis and Management of Aortic Disease. Circulation 2022;146(24):e334-e482.</div></div></div> [[Try this question again->Aortic dissection - Dx]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 17:30</div> A 58-year-old woman has one day of pleuritic chest pain and breathlessness, 3 weeks after a total knee replacement. Temperature is 37.4°C, blood pressure 118/74 mm Hg, pulse is 112/min, respirations are 22/min, and oxygen saturation 91% on room air. There is mild right calf swelling and tenderness. She has no hemoptysis. Chest radiograph is clear and the ECG shows sinus tachycardia. She has no contrast allergy and renal function is normal. Pulmonary embolism is the leading diagnosis. <span class="ec-prompt">Which of the following is the most appropriate next step in diagnosis?</span> [[CT pulmonary angiography->Pulmonary embolism - Ix correct]] [[D-dimer measurement->Pulmonary embolism - Ix d-dimer]] [[Echocardiography->Pulmonary embolism - Ix echocardiography]] [[Lower extremity compression ultrasonography->Pulmonary embolism - Ix lower]] [[Repeat chest radiography in 6 hours->Pulmonary embolism - Ix repeat]] [[Ventilation-perfusion scanning->Pulmonary embolism - Ix ventilation-perfusion]]

<span class="ec-case-marker" hidden data-entry="Pulmonary embolism. Ix"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ CT pulmonary angiography.</div> She has a high pretest probability, recent major orthopedic surgery, signs of deep venous thrombosis, tachycardia, hypoxemia, and pulmonary embolism as the most likely diagnosis. At high probability, imaging is the next step: a negative D-dimer does not lower the post-test probability enough to be safe, and a positive one changes nothing one were not already going to do. With normal renal function and no contrast allergy, CT pulmonary angiography is the test of choice. <div class="ec-src"><b>Source:</b> 2026 AHA/ACC/ACCP/ACEP/CHEST/SCAI/SHM/SIR/SVM/SVN Guideline for the Evaluation and Management of Acute Pulmonary Embolism in Adults. Circulation 2026;153:e977-e1051; van der Hulle T, et al. Lancet 2017 (YEARS).</div></div> [[Start another case->Hub]] [[Restart this case->Pulmonary embolism - Ix]] [[Next case →->Unstable PE - Rx]]

<span class="ec-case-marker" hidden data-entry="Pulmonary embolism. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ D-dimer measurement is not the next step.</div> This is the answer at low or intermediate probability, and it is the most tempting option here. D-dimer earns its place by ruling out disease when the pretest probability is low enough, through PERC, Wells, or a YEARS approach with age-adjusted or 1000 ng/mL thresholds. She meets 2-YEARS criteria and has a high clinical probability, so the test cannot exclude the diagnosis and only delays imaging. <div class="ec-teach"><div class="th">What to do instead</div> She has a high pretest probability, recent major orthopedic surgery, signs of deep venous thrombosis, tachycardia, hypoxemia, and pulmonary embolism as the most likely diagnosis. At high probability, imaging is the next step: a negative D-dimer does not lower the post-test probability enough to be safe, and a positive one changes nothing one were not already going to do. With normal renal function and no contrast allergy, CT pulmonary angiography is the test of choice. <div class="ec-src"><b>Source:</b> 2026 AHA/ACC/ACCP/ACEP/CHEST/SCAI/SHM/SIR/SVM/SVN Guideline for the Evaluation and Management of Acute Pulmonary Embolism in Adults. Circulation 2026;153:e977-e1051; van der Hulle T, et al. Lancet 2017 (YEARS).</div></div></div> [[Try this question again->Pulmonary embolism - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Pulmonary embolism. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Echocardiography is not the next step.</div> Bedside echocardiography is valuable in the hemodynamically unstable patient, where right ventricular strain can justify treatment when the patient is too unwell for the scanner. She is normotensive, so she can be imaged definitively. <div class="ec-teach"><div class="th">What to do instead</div> She has a high pretest probability, recent major orthopedic surgery, signs of deep venous thrombosis, tachycardia, hypoxemia, and pulmonary embolism as the most likely diagnosis. At high probability, imaging is the next step: a negative D-dimer does not lower the post-test probability enough to be safe, and a positive one changes nothing one were not already going to do. With normal renal function and no contrast allergy, CT pulmonary angiography is the test of choice. <div class="ec-src"><b>Source:</b> 2026 AHA/ACC/ACCP/ACEP/CHEST/SCAI/SHM/SIR/SVM/SVN Guideline for the Evaluation and Management of Acute Pulmonary Embolism in Adults. Circulation 2026;153:e977-e1051; van der Hulle T, et al. Lancet 2017 (YEARS).</div></div></div> [[Try this question again->Pulmonary embolism - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Pulmonary embolism. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Lower extremity compression ultrasonography is not the next step.</div> A positive leg ultrasound in this setting would justify anticoagulation without further imaging, so this is a legitimate strategy, particularly in pregnancy or renal failure. A negative result does not exclude pulmonary embolism, and she has neither contraindication to computed tomography. <div class="ec-teach"><div class="th">What to do instead</div> She has a high pretest probability, recent major orthopedic surgery, signs of deep venous thrombosis, tachycardia, hypoxemia, and pulmonary embolism as the most likely diagnosis. At high probability, imaging is the next step: a negative D-dimer does not lower the post-test probability enough to be safe, and a positive one changes nothing one were not already going to do. With normal renal function and no contrast allergy, CT pulmonary angiography is the test of choice. <div class="ec-src"><b>Source:</b> 2026 AHA/ACC/ACCP/ACEP/CHEST/SCAI/SHM/SIR/SVM/SVN Guideline for the Evaluation and Management of Acute Pulmonary Embolism in Adults. Circulation 2026;153:e977-e1051; van der Hulle T, et al. Lancet 2017 (YEARS).</div></div></div> [[Try this question again->Pulmonary embolism - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Pulmonary embolism. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Repeat chest radiography in 6 hours is not the next step.</div> Plain radiography cannot diagnose or exclude embolism. Its role is to identify alternative causes, and it has already done that by being clear. <div class="ec-teach"><div class="th">What to do instead</div> She has a high pretest probability, recent major orthopedic surgery, signs of deep venous thrombosis, tachycardia, hypoxemia, and pulmonary embolism as the most likely diagnosis. At high probability, imaging is the next step: a negative D-dimer does not lower the post-test probability enough to be safe, and a positive one changes nothing one were not already going to do. With normal renal function and no contrast allergy, CT pulmonary angiography is the test of choice. <div class="ec-src"><b>Source:</b> 2026 AHA/ACC/ACCP/ACEP/CHEST/SCAI/SHM/SIR/SVM/SVN Guideline for the Evaluation and Management of Acute Pulmonary Embolism in Adults. Circulation 2026;153:e977-e1051; van der Hulle T, et al. Lancet 2017 (YEARS).</div></div></div> [[Try this question again->Pulmonary embolism - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Pulmonary embolism. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Ventilation-perfusion scanning is not the next step.</div> This is the alternative when iodinated contrast is contraindicated, severe allergy, renal impairment, or in pregnancy where breast radiation matters. Neither applies, and it is less specific and more often non-diagnostic in a patient with any pre-existing lung disease. <div class="ec-teach"><div class="th">What to do instead</div> She has a high pretest probability, recent major orthopedic surgery, signs of deep venous thrombosis, tachycardia, hypoxemia, and pulmonary embolism as the most likely diagnosis. At high probability, imaging is the next step: a negative D-dimer does not lower the post-test probability enough to be safe, and a positive one changes nothing one were not already going to do. With normal renal function and no contrast allergy, CT pulmonary angiography is the test of choice. <div class="ec-src"><b>Source:</b> 2026 AHA/ACC/ACCP/ACEP/CHEST/SCAI/SHM/SIR/SVM/SVN Guideline for the Evaluation and Management of Acute Pulmonary Embolism in Adults. Circulation 2026;153:e977-e1051; van der Hulle T, et al. Lancet 2017 (YEARS).</div></div></div> [[Try this question again->Pulmonary embolism - Ix]] [[Start another case->Hub]]

<div class="ec-scene">Labor and delivery unit · 03:25</div> A 24-year-old primigravida at 34 weeks has a witnessed generalized tonic-clonic seizure lasting 90 seconds. Blood pressure is 172/112 mm Hg with 3+ proteinuria. She had reported headache and visual disturbance the previous day. She has no history of epilepsy, no fever and no neck stiffness. Platelets are 96,000/mm3, aspartate aminotransferase is 88 U/L, and alanine aminotransferase is 76 U/L. <span class="ec-prompt">Which of the following is the most likely diagnosis?</span> [[Amniotic fluid embolism->Eclampsia - Dx D4]] [[Cerebral venous sinus thrombosis->Eclampsia - Dx D2]] [[Eclampsia->Eclampsia - Dx correct]] [[HELLP syndrome without eclampsia->Eclampsia - Dx D1]] [[New-onset idiopathic epilepsy->Eclampsia - Dx D3]]

<span class="ec-case-marker" hidden data-entry="Eclampsia. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This causes sudden cardiorespiratory collapse with coagulopathy, typically during labor or immediately postpartum, and seizure can occur. She is hemodynamically stable and not in labor. <div class="ec-teach"><div class="th">What the findings point to</div> A new generalized seizure in pregnancy beyond 20 weeks with hypertension and proteinuria, preceded by headache and visual symptoms, is eclampsia. The thrombocytopenia and raised transaminases indicate HELLP overlapping with it, which is common and worsens the prognosis for both. <div class="ec-src"><b>Source:</b> American College of Obstetricians and Gynecologists. Gestational Hypertension and Preeclampsia: ACOG Practice Bulletin No. 222. Obstet Gynecol 2020;135(6):e237-e260.</div></div></div> [[Try this question again->Eclampsia - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Eclampsia. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Pregnancy and the puerperium are prothrombotic and this causes headache and seizure, so it stays on the list, particularly if she fails to improve. It does not explain the hypertension with proteinuria and the HELLP laboratory pattern. <div class="ec-teach"><div class="th">What the findings point to</div> A new generalized seizure in pregnancy beyond 20 weeks with hypertension and proteinuria, preceded by headache and visual symptoms, is eclampsia. The thrombocytopenia and raised transaminases indicate HELLP overlapping with it, which is common and worsens the prognosis for both. <div class="ec-src"><b>Source:</b> American College of Obstetricians and Gynecologists. Gestational Hypertension and Preeclampsia: ACOG Practice Bulletin No. 222. Obstet Gynecol 2020;135(6):e237-e260.</div></div></div> [[Try this question again->Eclampsia - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Eclampsia. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Eclampsia.</div> A new generalized seizure in pregnancy beyond 20 weeks with hypertension and proteinuria, preceded by headache and visual symptoms, is eclampsia. The thrombocytopenia and raised transaminases indicate HELLP overlapping with it, which is common and worsens the prognosis for both. <div class="ec-src"><b>Source:</b> American College of Obstetricians and Gynecologists. Gestational Hypertension and Preeclampsia: ACOG Practice Bulletin No. 222. Obstet Gynecol 2020;135(6):e237-e260.</div></div> [[Start another case->Hub]] [[Restart this case->Eclampsia - Dx]] [[Next case →->Severe preeclampsia - Rx]]

<span class="ec-case-marker" hidden data-entry="Eclampsia. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Her platelets and transaminases do meet the pattern, so this is genuinely present, but HELLP does not itself cause seizures. Naming it alone omits the event that has just occurred and the magnesium she needs. <div class="ec-teach"><div class="th">What the findings point to</div> A new generalized seizure in pregnancy beyond 20 weeks with hypertension and proteinuria, preceded by headache and visual symptoms, is eclampsia. The thrombocytopenia and raised transaminases indicate HELLP overlapping with it, which is common and worsens the prognosis for both. <div class="ec-src"><b>Source:</b> American College of Obstetricians and Gynecologists. Gestational Hypertension and Preeclampsia: ACOG Practice Bulletin No. 222. Obstet Gynecol 2020;135(6):e237-e260.</div></div></div> [[Try this question again->Eclampsia - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Eclampsia. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A first seizure in pregnancy is eclampsia until excluded. Diagnosing epilepsy here would omit magnesium and delivery planning in a woman with severe-range hypertension and proteinuria. <div class="ec-teach"><div class="th">What the findings point to</div> A new generalized seizure in pregnancy beyond 20 weeks with hypertension and proteinuria, preceded by headache and visual symptoms, is eclampsia. The thrombocytopenia and raised transaminases indicate HELLP overlapping with it, which is common and worsens the prognosis for both. <div class="ec-src"><b>Source:</b> American College of Obstetricians and Gynecologists. Gestational Hypertension and Preeclampsia: ACOG Practice Bulletin No. 222. Obstet Gynecol 2020;135(6):e237-e260.</div></div></div> [[Try this question again->Eclampsia - Dx]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 12:15</div> A 38-year-old woman with untreated Graves disease presents 2 days after an appendectomy with fever, agitation and palpitations. Temperature is 40.2°C, blood pressure is 148/62 mm Hg, pulse is 168/min and irregularly irregular, and respirations are 26/min. She is tremulous with warm moist skin, a diffusely enlarged thyroid with an audible bruit, and lid lag. She has vomited repeatedly and has diarrhea. She is confused and intermittently combative. <span class="ec-prompt">Which of the following is the most likely diagnosis?</span> [[Alcohol withdrawal->Thyroid storm - Dx alcohol]] [[Malignant hyperthermia->Thyroid storm - Dx malignant]] [[Postoperative sepsis->Thyroid storm - Dx postoperative]] [[Pulmonary embolism->Thyroid storm - Dx pulmonary]] [[Thyroid storm->Thyroid storm - Dx correct]]

<span class="ec-case-marker" hidden data-entry="Thyroid storm. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Alcohol withdrawal does not fit.</div> Withdrawal gives tremor, agitation, fever, tachycardia and diaphoresis and would be a reasonable postoperative thought. It does not produce a goiter with a bruit, lid lag, or atrial fibrillation with a wide pulse pressure, and there is no drinking history. <div class="ec-teach"><div class="th">What the findings actually point to</div> Decompensated thyrotoxicosis with hyperpyrexia, atrial fibrillation with a wide pulse pressure, gastrointestinal upset and central nervous system dysfunction, in a patient with untreated Graves disease and a clear precipitant, recent surgery, is thyroid storm. The goiter with a bruit and lid lag anchor the underlying diagnosis. <div class="ec-src"><b>Source:</b> Ross DS, et al. 2016 American Thyroid Association Guidelines for Diagnosis and Management of Hyperthyroidism. Thyroid 2016;26(10):1343-1421; Burch HB, Wartofsky L. Endocrinol Metab Clin North Am 1993 (diagnostic criteria).</div></div></div> [[Try this question again->Thyroid storm - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Thyroid storm. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Malignant hyperthermia does not fit.</div> This would be the fear after recent anesthesia, so the timing invites it. It presents during or within hours of the anesthetic with masseter spasm, generalized rigidity and a rapidly rising end-tidal carbon dioxide, not 2 days later with a goiter. <div class="ec-teach"><div class="th">What the findings actually point to</div> Decompensated thyrotoxicosis with hyperpyrexia, atrial fibrillation with a wide pulse pressure, gastrointestinal upset and central nervous system dysfunction, in a patient with untreated Graves disease and a clear precipitant, recent surgery, is thyroid storm. The goiter with a bruit and lid lag anchor the underlying diagnosis. <div class="ec-src"><b>Source:</b> Ross DS, et al. 2016 American Thyroid Association Guidelines for Diagnosis and Management of Hyperthyroidism. Thyroid 2016;26(10):1343-1421; Burch HB, Wartofsky L. Endocrinol Metab Clin North Am 1993 (diagnostic criteria).</div></div></div> [[Try this question again->Thyroid storm - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Thyroid storm. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Postoperative sepsis does not fit.</div> Infection is the other major postoperative cause of fever, tachycardia and confusion, and is also a recognized precipitant of storm. It does not explain the goiter, the bruit, the lid lag or the wide pulse pressure, though it should still be sought and treated. <div class="ec-teach"><div class="th">What the findings actually point to</div> Decompensated thyrotoxicosis with hyperpyrexia, atrial fibrillation with a wide pulse pressure, gastrointestinal upset and central nervous system dysfunction, in a patient with untreated Graves disease and a clear precipitant, recent surgery, is thyroid storm. The goiter with a bruit and lid lag anchor the underlying diagnosis. <div class="ec-src"><b>Source:</b> Ross DS, et al. 2016 American Thyroid Association Guidelines for Diagnosis and Management of Hyperthyroidism. Thyroid 2016;26(10):1343-1421; Burch HB, Wartofsky L. Endocrinol Metab Clin North Am 1993 (diagnostic criteria).</div></div></div> [[Try this question again->Thyroid storm - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Thyroid storm. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Pulmonary embolism does not fit.</div> Embolism after abdominal surgery gives dyspnea, pleuritic pain, tachycardia and hypoxemia, and can cause atrial fibrillation. It does not cause a temperature of 40°C with diarrhea and a thyroid bruit. <div class="ec-teach"><div class="th">What the findings actually point to</div> Decompensated thyrotoxicosis with hyperpyrexia, atrial fibrillation with a wide pulse pressure, gastrointestinal upset and central nervous system dysfunction, in a patient with untreated Graves disease and a clear precipitant, recent surgery, is thyroid storm. The goiter with a bruit and lid lag anchor the underlying diagnosis. <div class="ec-src"><b>Source:</b> Ross DS, et al. 2016 American Thyroid Association Guidelines for Diagnosis and Management of Hyperthyroidism. Thyroid 2016;26(10):1343-1421; Burch HB, Wartofsky L. Endocrinol Metab Clin North Am 1993 (diagnostic criteria).</div></div></div> [[Try this question again->Thyroid storm - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Thyroid storm. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Thyroid storm.</div> Decompensated thyrotoxicosis with hyperpyrexia, atrial fibrillation with a wide pulse pressure, gastrointestinal upset and central nervous system dysfunction, in a patient with untreated Graves disease and a clear precipitant, recent surgery, is thyroid storm. The goiter with a bruit and lid lag anchor the underlying diagnosis. <div class="ec-src"><b>Source:</b> Ross DS, et al. 2016 American Thyroid Association Guidelines for Diagnosis and Management of Hyperthyroidism. Thyroid 2016;26(10):1343-1421; Burch HB, Wartofsky L. Endocrinol Metab Clin North Am 1993 (diagnostic criteria).</div></div> [[Start another case->Hub]] [[Restart this case->Thyroid storm - Dx]] [[Next case →->Myxedema coma - Dx]]

<div class="ec-scene">Emergency department · 23:55</div> A 31-year-old man is brought in unresponsive 15 minutes after being found, with a respirations are 5/min, pinpoint pupils, and an oxygen saturation of 82%. Bag-valve-mask ventilation has been started with immediate improvement in saturation. Intravenous access is established. Bystanders report he uses heroin regularly and that the substance may have been mixed with fentanyl. <span class="ec-prompt">Which of the following is the most appropriate pharmacotherapy?</span> [[Intramuscular naloxone as the initial route->Opioid overdose - Rx D3]] [[Intubate without naloxone->Opioid overdose - Rx D5]] [[Large single Intravenous naloxone bolus->Opioid overdose - Rx D1]] [[Naloxone infusion instead of bolus->Opioid overdose - Rx D2]] [[Small titrated Intravenous naloxone doses->Opioid overdose - Rx correct]]

<span class="ec-case-marker" hidden data-entry="Opioid overdose. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best choice.</div> Right antidote, wrong dose. A full reversal bolus in a dependent patient precipitates acute withdrawal with vomiting and combativeness, and the risk of aspiration in someone already obtunded is exactly what one is trying to avoid. <div class="ec-teach"><div class="th">What to give instead</div> The endpoint is adequate respiration, not full alertness. Small titrated doses in an opioid-dependent patient reverse the respiratory depression while avoiding precipitated withdrawal, which causes vomiting, agitation and, in a patient who cannot protect his airway, aspiration. Larger or repeated doses may be needed with fentanyl analogues. <div class="ec-src"><b>Source:</b> Rzasa Lynn R, Galinkin JL. Naloxone dosage for opioid reversal: current evidence and clinical implications. Ther Adv Drug Saf 2018;9(1):63-88.</div></div></div> [[Try this question again->Opioid overdose - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Opioid overdose. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best choice.</div> An infusion is genuinely required for long-acting opioids such as methadone, or where sedation recurs, and it may well follow here given possible fentanyl. It takes time to reach effect while he is not breathing, so it supplements rather than replaces initial titrated dosing. <div class="ec-teach"><div class="th">What to give instead</div> The endpoint is adequate respiration, not full alertness. Small titrated doses in an opioid-dependent patient reverse the respiratory depression while avoiding precipitated withdrawal, which causes vomiting, agitation and, in a patient who cannot protect his airway, aspiration. Larger or repeated doses may be needed with fentanyl analogues. <div class="ec-src"><b>Source:</b> Rzasa Lynn R, Galinkin JL. Naloxone dosage for opioid reversal: current evidence and clinical implications. Ther Adv Drug Saf 2018;9(1):63-88.</div></div></div> [[Try this question again->Opioid overdose - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Opioid overdose. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best choice.</div> Intubation is appropriate if he fails to respond, and airway support is already working by bag-valve-mask. Intubating a reversible poisoning without trying the antidote commits him to ventilation and an intensive care bed unnecessarily. <div class="ec-teach"><div class="th">What to give instead</div> The endpoint is adequate respiration, not full alertness. Small titrated doses in an opioid-dependent patient reverse the respiratory depression while avoiding precipitated withdrawal, which causes vomiting, agitation and, in a patient who cannot protect his airway, aspiration. Larger or repeated doses may be needed with fentanyl analogues. <div class="ec-src"><b>Source:</b> Rzasa Lynn R, Galinkin JL. Naloxone dosage for opioid reversal: current evidence and clinical implications. Ther Adv Drug Saf 2018;9(1):63-88.</div></div></div> [[Try this question again->Opioid overdose - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Opioid overdose. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best choice.</div> The intramuscular route is appropriate in the community and when no access is available, so it is not wrong in principle. He already has intravenous access, which allows titration and onset within a minute or two. <div class="ec-teach"><div class="th">What to give instead</div> The endpoint is adequate respiration, not full alertness. Small titrated doses in an opioid-dependent patient reverse the respiratory depression while avoiding precipitated withdrawal, which causes vomiting, agitation and, in a patient who cannot protect his airway, aspiration. Larger or repeated doses may be needed with fentanyl analogues. <div class="ec-src"><b>Source:</b> Rzasa Lynn R, Galinkin JL. Naloxone dosage for opioid reversal: current evidence and clinical implications. Ther Adv Drug Saf 2018;9(1):63-88.</div></div></div> [[Try this question again->Opioid overdose - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Opioid overdose. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Small titrated Intravenous naloxone doses</div> The endpoint is adequate respiration, not full alertness. Small titrated doses in an opioid-dependent patient reverse the respiratory depression while avoiding precipitated withdrawal, which causes vomiting, agitation and, in a patient who cannot protect his airway, aspiration. Larger or repeated doses may be needed with fentanyl analogues. <div class="ec-src"><b>Source:</b> Rzasa Lynn R, Galinkin JL. Naloxone dosage for opioid reversal: current evidence and clinical implications. Ther Adv Drug Saf 2018;9(1):63-88.</div></div> [[Start another case->Hub]] [[Restart this case->Opioid overdose - Rx]] [[Next case →->Acetaminophen - Opening]]

<div class="ec-scene">Emergency department · 18:40</div> A 54-year-old woman with metastatic breast cancer has 3 days of worsening breathlessness. Blood pressure is 84/62 mm Hg with a 18 mm Hg inspiratory fall in systolic pressure. Jugular venous pressure is raised, heart sounds are muffled, and the lungs are clear. ECG shows low-voltage complexes with beat-to-beat variation in QRS amplitude. <span class="ec-prompt">Which of the following is the most likely diagnosis?</span> [[Cardiac tamponade->Cardiac tamponade - Dx correct]] [[Constrictive pericarditis->Cardiac tamponade - Dx D1]] [[Decompensated left ventricular failure->Cardiac tamponade - Dx D5]] [[Massive pulmonary embolism->Cardiac tamponade - Dx D2]] [[Superior vena cava obstruction->Cardiac tamponade - Dx D3]]

<span class="ec-case-marker" hidden data-entry="Cardiac tamponade. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Cardiac tamponade.</div> Hypotension, raised jugular venous pressure and muffled heart sounds with clear lungs, a pulsus paradoxus above 10 mm Hg, and electrical alternans on a low-voltage ECG. Malignancy is among the commonest causes of a large pericardial effusion, and clear lungs are what separate this from left heart failure. <div class="ec-src"><b>Source:</b> Adler Y, et al. ESC Guidelines for the Diagnosis and Management of Pericardial Diseases. Eur Heart J 2015;36(42):2921-2964.</div></div> [[Start another case->Hub]] [[Restart this case->Cardiac tamponade - Dx]] [[Next case →->Cocaine chest pain - Opening]]

<span class="ec-case-marker" hidden data-entry="Cardiac tamponade. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Constriction gives raised venous pressure with a pericardial knock and Kussmaul sign, developing over months rather than days, and pulsus paradoxus is usually absent. Electrical alternans is not a feature. <div class="ec-teach"><div class="th">What the findings point to</div> Hypotension, raised jugular venous pressure and muffled heart sounds with clear lungs, a pulsus paradoxus above 10 mm Hg, and electrical alternans on a low-voltage ECG. Malignancy is among the commonest causes of a large pericardial effusion, and clear lungs are what separate this from left heart failure. <div class="ec-src"><b>Source:</b> Adler Y, et al. ESC Guidelines for the Diagnosis and Management of Pericardial Diseases. Eur Heart J 2015;36(42):2921-2964.</div></div></div> [[Try this question again->Cardiac tamponade - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Cardiac tamponade. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Left heart failure gives pulmonary crackles and often a third heart sound. Her lungs are clear, which is the finding that redirects attention to a pericardial cause. <div class="ec-teach"><div class="th">What the findings point to</div> Hypotension, raised jugular venous pressure and muffled heart sounds with clear lungs, a pulsus paradoxus above 10 mm Hg, and electrical alternans on a low-voltage ECG. Malignancy is among the commonest causes of a large pericardial effusion, and clear lungs are what separate this from left heart failure. <div class="ec-src"><b>Source:</b> Adler Y, et al. ESC Guidelines for the Diagnosis and Management of Pericardial Diseases. Eur Heart J 2015;36(42):2921-2964.</div></div></div> [[Try this question again->Cardiac tamponade - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Cardiac tamponade. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Embolism gives obstructive shock with raised venous pressure and can mimic this closely, so it is the most important alternative. It typically produces marked hypoxemia and right heart strain on ECG rather than low voltage with electrical alternans. <div class="ec-teach"><div class="th">What the findings point to</div> Hypotension, raised jugular venous pressure and muffled heart sounds with clear lungs, a pulsus paradoxus above 10 mm Hg, and electrical alternans on a low-voltage ECG. Malignancy is among the commonest causes of a large pericardial effusion, and clear lungs are what separate this from left heart failure. <div class="ec-src"><b>Source:</b> Adler Y, et al. ESC Guidelines for the Diagnosis and Management of Pericardial Diseases. Eur Heart J 2015;36(42):2921-2964.</div></div></div> [[Try this question again->Cardiac tamponade - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Cardiac tamponade. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Caval obstruction in malignancy gives facial and upper limb swelling with distended collateral veins and a fixed raised venous pressure. It does not cause pulsus paradoxus or muffled heart sounds. <div class="ec-teach"><div class="th">What the findings point to</div> Hypotension, raised jugular venous pressure and muffled heart sounds with clear lungs, a pulsus paradoxus above 10 mm Hg, and electrical alternans on a low-voltage ECG. Malignancy is among the commonest causes of a large pericardial effusion, and clear lungs are what separate this from left heart failure. <div class="ec-src"><b>Source:</b> Adler Y, et al. ESC Guidelines for the Diagnosis and Management of Pericardial Diseases. Eur Heart J 2015;36(42):2921-2964.</div></div></div> [[Try this question again->Cardiac tamponade - Dx]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 21:05</div> A 61-year-old man has 2 days of melena and one episode of coffee-ground vomiting. He takes naproxen daily for osteoarthritis. Temperature is 37.1°C, blood pressure 112/68 mm Hg, pulse is 104/min, and respirations are 18/min. Hemoglobin is 9.2 g/dL, blood urea nitrogen 42 mg/dL, serum creatinine 1.0 mg/dL, and prothrombin time 12 seconds. He has no stigmata of chronic liver disease. He has been resuscitated with intravenous fluids and a proton pump inhibitor has been started. <span class="ec-prompt">Which of the following is the most appropriate next step in diagnosis?</span> [[CT angiography of the abdomen->Peptic ulcer bleed - Ix ct]] [[Mesenteric angiography with embolization->Peptic ulcer bleed - Ix mesenteric]] [[Nasogastric tube placement and lavage->Peptic ulcer bleed - Ix nasogastric]] [[Technetium-99m labeled red cell scanning->Peptic ulcer bleed - Ix technetium-99m]] [[Upper endoscopy->Peptic ulcer bleed - Ix correct]]

<span class="ec-case-marker" hidden data-entry="Peptic ulcer bleed. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ CT angiography of the abdomen is not the next step.</div> This localizes active arterial bleeding and is useful when endoscopy fails or the source cannot be reached, or in massive bleeding where endoscopy is not feasible. It offers no therapeutic option for a peptic ulcer and requires a brisk rate of bleeding to be positive. <div class="ec-teach"><div class="th">What to do instead</div> Endoscopy is both diagnostic and therapeutic in upper gastrointestinal bleeding: it identifies the lesion, stratifies rebleeding risk by the stigmata seen, and allows immediate hemostatic treatment. In a hemodynamically stable patient it is performed within 24 hours of presentation, after resuscitation. <div class="ec-src"><b>Source:</b> Laine L, et al. ACG Clinical Guideline: Upper Gastrointestinal and Ulcer Bleeding. Am J Gastroenterol 2021;116(5):899-917.</div></div></div> [[Try this question again->Peptic ulcer bleed - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Peptic ulcer bleed. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Mesenteric angiography with embolization is not the next step.</div> This is a rescue therapy for bleeding that endoscopy cannot control. Going there first is an invasive escalation before the first-line procedure has been attempted. <div class="ec-teach"><div class="th">What to do instead</div> Endoscopy is both diagnostic and therapeutic in upper gastrointestinal bleeding: it identifies the lesion, stratifies rebleeding risk by the stigmata seen, and allows immediate hemostatic treatment. In a hemodynamically stable patient it is performed within 24 hours of presentation, after resuscitation. <div class="ec-src"><b>Source:</b> Laine L, et al. ACG Clinical Guideline: Upper Gastrointestinal and Ulcer Bleeding. Am J Gastroenterol 2021;116(5):899-917.</div></div></div> [[Try this question again->Peptic ulcer bleed - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Peptic ulcer bleed. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Nasogastric tube placement and lavage is not the next step.</div> This was traditional practice and remains widely believed in, which is why it is here. A negative aspirate does not exclude an upper gastrointestinal source, a bleeding duodenal ulcer with a competent pylorus can give clear aspirate, and it does not change management. Guidelines no longer recommend it routinely. <div class="ec-teach"><div class="th">What to do instead</div> Endoscopy is both diagnostic and therapeutic in upper gastrointestinal bleeding: it identifies the lesion, stratifies rebleeding risk by the stigmata seen, and allows immediate hemostatic treatment. In a hemodynamically stable patient it is performed within 24 hours of presentation, after resuscitation. <div class="ec-src"><b>Source:</b> Laine L, et al. ACG Clinical Guideline: Upper Gastrointestinal and Ulcer Bleeding. Am J Gastroenterol 2021;116(5):899-917.</div></div></div> [[Try this question again->Peptic ulcer bleed - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Peptic ulcer bleed. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Technetium-99m labeled red cell scanning is not the next step.</div> This detects slow or intermittent bleeding and is used for obscure lower gastrointestinal sources. It localizes poorly and offers no treatment. <div class="ec-teach"><div class="th">What to do instead</div> Endoscopy is both diagnostic and therapeutic in upper gastrointestinal bleeding: it identifies the lesion, stratifies rebleeding risk by the stigmata seen, and allows immediate hemostatic treatment. In a hemodynamically stable patient it is performed within 24 hours of presentation, after resuscitation. <div class="ec-src"><b>Source:</b> Laine L, et al. ACG Clinical Guideline: Upper Gastrointestinal and Ulcer Bleeding. Am J Gastroenterol 2021;116(5):899-917.</div></div></div> [[Try this question again->Peptic ulcer bleed - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Peptic ulcer bleed. Ix"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Upper endoscopy.</div> Endoscopy is both diagnostic and therapeutic in upper gastrointestinal bleeding: it identifies the lesion, stratifies rebleeding risk by the stigmata seen, and allows immediate hemostatic treatment. In a hemodynamically stable patient it is performed within 24 hours of presentation, after resuscitation. <div class="ec-src"><b>Source:</b> Laine L, et al. ACG Clinical Guideline: Upper Gastrointestinal and Ulcer Bleeding. Am J Gastroenterol 2021;116(5):899-917.</div></div> [[Start another case->Hub]] [[Restart this case->Peptic ulcer bleed - Ix]] [[Next case →->Variceal bleed - Ix]]

<div class="ec-scene">Emergency department · 20:35</div> A 28-year-old woman has palpitations that began abruptly while sitting. Temperature is 36.7°C, blood pressure 112/74 mm Hg, pulse is 188/min, and respirations are 18/min. ECG shows a regular narrow-complex tachycardia with no visible P waves and a pseudo-R prime in lead V1. She has had similar self-terminating episodes. She is alert with no chest pain and clear lungs. <span class="ec-prompt">Which of the following is the most likely diagnosis?</span> [[Atrial fibrillation with rapid ventricular response->SVT - Dx D1]] [[Atrial flutter with 2:1 conduction->SVT - Dx D2]] [[AV nodal reentrant tachycardia->SVT - Dx correct]] [[Multifocal atrial tachycardia->SVT - Dx D5]] [[Sinus tachycardia->SVT - Dx D3]]

<span class="ec-case-marker" hidden data-entry="SVT. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Fibrillation gives an irregularly irregular rhythm with absent organized atrial activity. Hers is regular, which is the single most useful discriminator at the bedside. <div class="ec-teach"><div class="th">What the findings point to</div> Abrupt onset and offset, a regular narrow-complex tachycardia around 180 to 200/min with no discernible P waves, and a pseudo-R prime in V1 representing a retrograde P buried in the QRS, in a young patient with recurrent self-terminating episodes. This is the commonest form of paroxysmal supraventricular tachycardia. <div class="ec-src"><b>Source:</b> Page RL, et al. ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia. Circulation 2016;133(14):e506-e574.</div></div></div> [[Try this question again->SVT - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="SVT. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Flutter at 2:1 gives a regular narrow-complex tachycardia around 150/min and is the classic mimic, so it belongs here. The rate of 188/min is faster than typical 2:1 flutter, and flutter waves are usually visible in the inferior leads once the rate is slowed. <div class="ec-teach"><div class="th">What the findings point to</div> Abrupt onset and offset, a regular narrow-complex tachycardia around 180 to 200/min with no discernible P waves, and a pseudo-R prime in V1 representing a retrograde P buried in the QRS, in a young patient with recurrent self-terminating episodes. This is the commonest form of paroxysmal supraventricular tachycardia. <div class="ec-src"><b>Source:</b> Page RL, et al. ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia. Circulation 2016;133(14):e506-e574.</div></div></div> [[Try this question again->SVT - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="SVT. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ AV nodal reentrant tachycardia.</div> Abrupt onset and offset, a regular narrow-complex tachycardia around 180 to 200/min with no discernible P waves, and a pseudo-R prime in V1 representing a retrograde P buried in the QRS, in a young patient with recurrent self-terminating episodes. This is the commonest form of paroxysmal supraventricular tachycardia. <div class="ec-src"><b>Source:</b> Page RL, et al. ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia. Circulation 2016;133(14):e506-e574.</div></div> [[Start another case->Hub]] [[Restart this case->SVT - Dx]] [[Next case →->Unstable bradycardia - Rx]]

<span class="ec-case-marker" hidden data-entry="SVT. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This gives an irregular rhythm with three or more distinct P wave morphologies, typically in severe pulmonary disease. Neither the rhythm nor the context fits. <div class="ec-teach"><div class="th">What the findings point to</div> Abrupt onset and offset, a regular narrow-complex tachycardia around 180 to 200/min with no discernible P waves, and a pseudo-R prime in V1 representing a retrograde P buried in the QRS, in a young patient with recurrent self-terminating episodes. This is the commonest form of paroxysmal supraventricular tachycardia. <div class="ec-src"><b>Source:</b> Page RL, et al. ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia. Circulation 2016;133(14):e506-e574.</div></div></div> [[Try this question again->SVT - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="SVT. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Sinus tachycardia has a gradual onset and offset, an identifiable cause, upright P waves before each QRS, and rarely exceeds about 220 minus age at rest. Hers began abruptly with no P waves visible. <div class="ec-teach"><div class="th">What the findings point to</div> Abrupt onset and offset, a regular narrow-complex tachycardia around 180 to 200/min with no discernible P waves, and a pseudo-R prime in V1 representing a retrograde P buried in the QRS, in a young patient with recurrent self-terminating episodes. This is the commonest form of paroxysmal supraventricular tachycardia. <div class="ec-src"><b>Source:</b> Page RL, et al. ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia. Circulation 2016;133(14):e506-e574.</div></div></div> [[Try this question again->SVT - Dx]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 04:10</div> A 68-year-old woman has had right upper quadrant pain, fever, and jaundice for 2 days. Temperature is 38.9°C, blood pressure 102/60 mm Hg, pulse is 108/min, and respirations are 20/min. Bilirubin is 5.8 mg/dL, alkaline phosphatase is 580 U/L, and the leukocyte count is 18,000/mm3. She has had intermittent biliary colic for months. Fluids and broad-spectrum antibiotics have been started. <span class="ec-prompt">Which of the following is the most appropriate next step in diagnosis?</span> [[Abdominal ultrasonography->Cholangitis - Ix correct]] [[CT of the abdomen with contrast->Cholangitis - Ix ct]] [[Endoscopic retrograde cholangiopancreatography->Cholangitis - Ix endoscopic]] [[Hepatobiliary iminodiacetic acid scanning->Cholangitis - Ix hepatobiliary]] [[Magnetic resonance cholangiopancreatography->Cholangitis - Ix magnetic]]

<span class="ec-case-marker" hidden data-entry="Cholangitis. Ix"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Abdominal ultrasonography.</div> Ultrasonography is the first-line imaging study in suspected biliary obstruction: it is immediate, needs no contrast or radiation, and reliably shows gallstones and bile duct dilatation. It answers the question that determines everything downstream, whether the duct is obstructed and needs drainage. <div class="ec-src"><b>Source:</b> Miura F, et al. Tokyo Guidelines 2018: initial management of acute biliary infection. J Hepatobiliary Pancreat Sci 2018;25(1):31-40.</div></div> [[Start another case->Hub]] [[Restart this case->Cholangitis - Ix]] [[Next case →->Esophageal manometry - Ix]]

<span class="ec-case-marker" hidden data-entry="Cholangitis. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ CT of the abdomen with contrast is not the next step.</div> Computed tomography is useful for complications and alternative diagnoses and detects duct dilatation, but it misses many gallstones, which are often not radio-opaque. It is the second test, not the first. <div class="ec-teach"><div class="th">What to do instead</div> Ultrasonography is the first-line imaging study in suspected biliary obstruction: it is immediate, needs no contrast or radiation, and reliably shows gallstones and bile duct dilatation. It answers the question that determines everything downstream, whether the duct is obstructed and needs drainage. <div class="ec-src"><b>Source:</b> Miura F, et al. Tokyo Guidelines 2018: initial management of acute biliary infection. J Hepatobiliary Pancreat Sci 2018;25(1):31-40.</div></div></div> [[Try this question again->Cholangitis - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Cholangitis. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Endoscopic retrograde cholangiopancreatography is not the next step.</div> ERCP is the definitive drainage procedure and she will very likely need it, which makes this tempting. It is a therapeutic intervention with real complication rates, not a first diagnostic step, and it is arranged once obstruction is confirmed and after resuscitation, urgently, within 24 hours, or sooner if she fails to respond. <div class="ec-teach"><div class="th">What to do instead</div> Ultrasonography is the first-line imaging study in suspected biliary obstruction: it is immediate, needs no contrast or radiation, and reliably shows gallstones and bile duct dilatation. It answers the question that determines everything downstream, whether the duct is obstructed and needs drainage. <div class="ec-src"><b>Source:</b> Miura F, et al. Tokyo Guidelines 2018: initial management of acute biliary infection. J Hepatobiliary Pancreat Sci 2018;25(1):31-40.</div></div></div> [[Try this question again->Cholangitis - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Cholangitis. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Hepatobiliary iminodiacetic acid scanning is not the next step.</div> This assesses cystic duct patency and is used for suspected acute cholecystitis when ultrasonography is equivocal. It does not assess the common bile duct and has no role in acute cholangitis. <div class="ec-teach"><div class="th">What to do instead</div> Ultrasonography is the first-line imaging study in suspected biliary obstruction: it is immediate, needs no contrast or radiation, and reliably shows gallstones and bile duct dilatation. It answers the question that determines everything downstream, whether the duct is obstructed and needs drainage. <div class="ec-src"><b>Source:</b> Miura F, et al. Tokyo Guidelines 2018: initial management of acute biliary infection. J Hepatobiliary Pancreat Sci 2018;25(1):31-40.</div></div></div> [[Try this question again->Cholangitis - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Cholangitis. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Magnetic resonance cholangiopancreatography is not the next step.</div> MRCP images the biliary tree beautifully and is the right test for equivocal cases, especially to exclude choledocholithiasis before surgery. It is slower, less available out of hours, and unnecessary when the clinical picture and ultrasonography will already establish obstruction. <div class="ec-teach"><div class="th">What to do instead</div> Ultrasonography is the first-line imaging study in suspected biliary obstruction: it is immediate, needs no contrast or radiation, and reliably shows gallstones and bile duct dilatation. It answers the question that determines everything downstream, whether the duct is obstructed and needs drainage. <div class="ec-src"><b>Source:</b> Miura F, et al. Tokyo Guidelines 2018: initial management of acute biliary infection. J Hepatobiliary Pancreat Sci 2018;25(1):31-40.</div></div></div> [[Try this question again->Cholangitis - Ix]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 05:30</div> A 43-year-old woman with vitiligo and autoimmune thyroid disease presents with 2 days of vomiting and profound weakness after a febrile illness. Blood pressure is 78/44 mm Hg and does not respond to two liters of saline. Sodium is 126 mEq/L, potassium 5.8 mEq/L, glucose 54 mg/dL. She has hyperpigmentation of the buccal mucosa and palmar creases. <span class="ec-prompt">Which of the following is the most likely diagnosis?</span> [[Diabetic ketoacidosis->Adrenal crisis - Dx D5]] [[Gastroenteritis with dehydration->Adrenal crisis - Dx D4]] [[Primary adrenal insufficiency in crisis->Adrenal crisis - Dx correct]] [[Secondary adrenal insufficiency->Adrenal crisis - Dx D2]] [[Septic shock->Adrenal crisis - Dx D1]]

<span class="ec-case-marker" hidden data-entry="Adrenal crisis. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Ketoacidosis gives vomiting, dehydration and hyperkalemia, but with hyperglycemia and an anion gap acidosis. Her glucose is 54 mg/dL. <div class="ec-teach"><div class="th">What the findings point to</div> Fluid-refractory hypotension with hyponatremia, hyperkalemia and hypoglycemia, in a woman with other autoimmune disease and mucosal hyperpigmentation, is primary adrenal insufficiency. The hyperpigmentation reflects raised ACTH and localizes the lesion to the adrenal rather than the pituitary, and an intercurrent infection is the classic precipitant. <div class="ec-src"><b>Source:</b> Bornstein SR, et al. Diagnosis and Treatment of Primary Adrenal Insufficiency: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2016;101(2):364-389.</div></div></div> [[Try this question again->Adrenal crisis - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Adrenal crisis. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Vomiting and hypotension fit, and this is how the diagnosis is commonly missed. Simple dehydration responds to fluid and does not cause hyperkalemia with hypoglycemia, volume loss typically lowers potassium. <div class="ec-teach"><div class="th">What the findings point to</div> Fluid-refractory hypotension with hyponatremia, hyperkalemia and hypoglycemia, in a woman with other autoimmune disease and mucosal hyperpigmentation, is primary adrenal insufficiency. The hyperpigmentation reflects raised ACTH and localizes the lesion to the adrenal rather than the pituitary, and an intercurrent infection is the classic precipitant. <div class="ec-src"><b>Source:</b> Bornstein SR, et al. Diagnosis and Treatment of Primary Adrenal Insufficiency: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2016;101(2):364-389.</div></div></div> [[Try this question again->Adrenal crisis - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Adrenal crisis. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Primary adrenal insufficiency in crisis.</div> Fluid-refractory hypotension with hyponatremia, hyperkalemia and hypoglycemia, in a woman with other autoimmune disease and mucosal hyperpigmentation, is primary adrenal insufficiency. The hyperpigmentation reflects raised ACTH and localizes the lesion to the adrenal rather than the pituitary, and an intercurrent infection is the classic precipitant. <div class="ec-src"><b>Source:</b> Bornstein SR, et al. Diagnosis and Treatment of Primary Adrenal Insufficiency: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2016;101(2):364-389.</div></div> [[Start another case->Hub]] [[Restart this case->Adrenal crisis - Dx]] [[Next case →->Adrenal crisis 2 - Rx]]

<span class="ec-case-marker" hidden data-entry="Adrenal crisis. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Pituitary failure gives cortisol deficiency with hyponatremia, but aldosterone is preserved by the renin-angiotensin system, so hyperkalemia is absent, and ACTH is low, so there is no hyperpigmentation. <div class="ec-teach"><div class="th">What the findings point to</div> Fluid-refractory hypotension with hyponatremia, hyperkalemia and hypoglycemia, in a woman with other autoimmune disease and mucosal hyperpigmentation, is primary adrenal insufficiency. The hyperpigmentation reflects raised ACTH and localizes the lesion to the adrenal rather than the pituitary, and an intercurrent infection is the classic precipitant. <div class="ec-src"><b>Source:</b> Bornstein SR, et al. Diagnosis and Treatment of Primary Adrenal Insufficiency: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2016;101(2):364-389.</div></div></div> [[Try this question again->Adrenal crisis - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Adrenal crisis. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Infection precipitated this and should be treated, so sepsis is genuinely part of the picture rather than a wrong answer. Septic shock alone does not explain hyperkalemia with hypoglycemia and hyperpigmentation, and the failure to respond to fluids is the clue that a hormone rather than a pathogen is the limiting problem. <div class="ec-teach"><div class="th">What the findings point to</div> Fluid-refractory hypotension with hyponatremia, hyperkalemia and hypoglycemia, in a woman with other autoimmune disease and mucosal hyperpigmentation, is primary adrenal insufficiency. The hyperpigmentation reflects raised ACTH and localizes the lesion to the adrenal rather than the pituitary, and an intercurrent infection is the classic precipitant. <div class="ec-src"><b>Source:</b> Bornstein SR, et al. Diagnosis and Treatment of Primary Adrenal Insufficiency: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2016;101(2):364-389.</div></div></div> [[Try this question again->Adrenal crisis - Dx]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 23:40</div> A 15-year-old boy has 3 hours of sudden severe left scrotal pain that woke him from sleep, with nausea and vomiting. The left testis is high-riding and lies horizontally, is diffusely tender, and the cremasteric reflex is absent on that side. There is no dysuria and he is afebrile. Urinalysis is normal. The urologist is in the hospital and available now. <span class="ec-prompt">Which of the following is the most appropriate next step in diagnosis?</span> [[Bedside manual detorsion, then reassess->Testicular torsion - Ix manual]] [[Doppler ultrasonography of the scrotum->Testicular torsion - Ix doppler]] [[Immediate surgical exploration->Testicular torsion - Ix correct]] [[Radionuclide scrotal scintigraphy->Testicular torsion - Ix radionuclide]] [[Urine culture and antibiotics for epididymitis->Testicular torsion - Ix urine]]

<span class="ec-case-marker" hidden data-entry="Testicular torsion. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Doppler ultrasonography of the scrotum is not the next step.</div> This is the correct test in an equivocal presentation and is the most defensible wrong answer here. Two problems: it takes time this testis does not have, and preserved arterial flow does not exclude torsion, because torsion can be intermittent or incomplete. A negative scan in a patient who looks like this should not be reassuring. <div class="ec-teach"><div class="th">What to do instead</div> The history and examination are diagnostic, and the testicular salvage rate falls steeply after about 6 hours of ischemia. When clinical suspicion is this high and a surgeon is available, exploration is both the diagnostic and the therapeutic step, imaging is what one do when the picture is equivocal, not when it is clear. <div class="ec-src"><b>Source:</b> Sharp VJ, Kieran K, Arlen AM. Testicular torsion: diagnosis, evaluation, and management. Am Fam Physician 2013;88(12):835-840; AUA/EAU guidance on acute scrotum.</div></div></div> [[Try this question again->Testicular torsion - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Testicular torsion. Ix"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Immediate surgical exploration.</div> The history and examination are diagnostic, and the testicular salvage rate falls steeply after about 6 hours of ischemia. When clinical suspicion is this high and a surgeon is available, exploration is both the diagnostic and the therapeutic step, imaging is what one do when the picture is equivocal, not when it is clear. <div class="ec-src"><b>Source:</b> Sharp VJ, Kieran K, Arlen AM. Testicular torsion: diagnosis, evaluation, and management. Am Fam Physician 2013;88(12):835-840; AUA/EAU guidance on acute scrotum.</div></div> [[Start another case->Hub]] [[Restart this case->Testicular torsion - Ix]] [[Next case →->Testicular torsion 2 - Rx]]

<span class="ec-case-marker" hidden data-entry="Testicular torsion. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Manual detorsion at the bedside, then reassess is not the next step.</div> Manual detorsion is a reasonable temporizing measure while theater is prepared, and relief of pain supports the diagnosis. It is not definitive, residual torsion is common and it does not fix the underlying bell-clapper anomaly, so it never replaces exploration and bilateral orchidopexy. <div class="ec-teach"><div class="th">What to do instead</div> The history and examination are diagnostic, and the testicular salvage rate falls steeply after about 6 hours of ischemia. When clinical suspicion is this high and a surgeon is available, exploration is both the diagnostic and the therapeutic step, imaging is what one do when the picture is equivocal, not when it is clear. <div class="ec-src"><b>Source:</b> Sharp VJ, Kieran K, Arlen AM. Testicular torsion: diagnosis, evaluation, and management. Am Fam Physician 2013;88(12):835-840; AUA/EAU guidance on acute scrotum.</div></div></div> [[Try this question again->Testicular torsion - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Testicular torsion. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Radionuclide scrotal scintigraphy is not the next step.</div> This can demonstrate reduced perfusion but is slow, not widely available out of hours, and has been superseded by Doppler ultrasonography. It has no role in an acute presentation. <div class="ec-teach"><div class="th">What to do instead</div> The history and examination are diagnostic, and the testicular salvage rate falls steeply after about 6 hours of ischemia. When clinical suspicion is this high and a surgeon is available, exploration is both the diagnostic and the therapeutic step, imaging is what one do when the picture is equivocal, not when it is clear. <div class="ec-src"><b>Source:</b> Sharp VJ, Kieran K, Arlen AM. Testicular torsion: diagnosis, evaluation, and management. Am Fam Physician 2013;88(12):835-840; AUA/EAU guidance on acute scrotum.</div></div></div> [[Try this question again->Testicular torsion - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Testicular torsion. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Urine culture and empiric antibiotics for epididymitis is not the next step.</div> Epididymitis is the main differential and would be treated this way, but it usually develops gradually with dysuria, fever, a preserved cremasteric reflex and pain relieved by elevating the testis. He has none of those and his urinalysis is normal. <div class="ec-teach"><div class="th">What to do instead</div> The history and examination are diagnostic, and the testicular salvage rate falls steeply after about 6 hours of ischemia. When clinical suspicion is this high and a surgeon is available, exploration is both the diagnostic and the therapeutic step, imaging is what one do when the picture is equivocal, not when it is clear. <div class="ec-src"><b>Source:</b> Sharp VJ, Kieran K, Arlen AM. Testicular torsion: diagnosis, evaluation, and management. Am Fam Physician 2013;88(12):835-840; AUA/EAU guidance on acute scrotum.</div></div></div> [[Try this question again->Testicular torsion - Ix]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 09:45</div> A 27-year-old woman has one day of increasing right-sided pelvic pain and light vaginal spotting. Her last menstrual period was 7 weeks ago. She had chlamydial pelvic infection 3 years ago. Serum hCG is 5,800 mIU/mL. Transvaginal ultrasonography shows no intrauterine gestational sac, a small amount of free fluid in the pouch of Douglas, and a 2 cm right adnexal mass separate from the ovary. <span class="ec-prompt">Which of the following is the most likely diagnosis?</span> [[Acute appendicitis->Ectopic pregnancy - Dx acute]] [[Ectopic pregnancy->Ectopic pregnancy - Dx correct]] [[Ovarian torsion->Ectopic pregnancy - Dx ovarian]] [[Pelvic inflammatory disease->Ectopic pregnancy - Dx pelvic]] [[Ruptured ovarian corpus luteum cyst->Ectopic pregnancy - Dx ruptured]]

<span class="ec-case-marker" hidden data-entry="Ectopic pregnancy. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Acute appendicitis does not fit.</div> Appendicitis gives periumbilical pain migrating to the right lower quadrant with anorexia and localized peritoneal signs. It does not explain the amenorrhea, the positive hCG, or an adnexal mass separate from the ovary. <div class="ec-teach"><div class="th">What the findings actually point to</div> An hCG above the discriminatory threshold with no intrauterine sac, an adnexal mass separate from the ovary, and free fluid is ectopic pregnancy. Prior chlamydial infection with tubal damage is among the strongest risk factors. <div class="ec-src"><b>Source:</b> ACOG Practice Bulletin No. 193: Tubal Ectopic Pregnancy. Obstet Gynecol 2018;131(3):e91-e103.</div></div></div> [[Try this question again->Ectopic pregnancy - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Ectopic pregnancy. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Ectopic pregnancy.</div> An hCG above the discriminatory threshold with no intrauterine sac, an adnexal mass separate from the ovary, and free fluid is ectopic pregnancy. Prior chlamydial infection with tubal damage is among the strongest risk factors. <div class="ec-src"><b>Source:</b> ACOG Practice Bulletin No. 193: Tubal Ectopic Pregnancy. Obstet Gynecol 2018;131(3):e91-e103.</div></div> [[Start another case->Hub]] [[Restart this case->Ectopic pregnancy - Dx]] [[Next case →->Ectopic pregnancy 2 - Dx]]

<span class="ec-case-marker" hidden data-entry="Ectopic pregnancy. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Ovarian torsion does not fit.</div> Torsion gives sudden severe unilateral pain with vomiting and an enlarged edematous ovary. Here the mass is separate from the ovary and the positive hCG with an empty uterus is the finding that decides it. <div class="ec-teach"><div class="th">What the findings actually point to</div> An hCG above the discriminatory threshold with no intrauterine sac, an adnexal mass separate from the ovary, and free fluid is ectopic pregnancy. Prior chlamydial infection with tubal damage is among the strongest risk factors. <div class="ec-src"><b>Source:</b> ACOG Practice Bulletin No. 193: Tubal Ectopic Pregnancy. Obstet Gynecol 2018;131(3):e91-e103.</div></div></div> [[Try this question again->Ectopic pregnancy - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Ectopic pregnancy. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Pelvic inflammatory disease does not fit.</div> Her history of chlamydia makes this tempting. Pelvic infection gives bilateral pain with cervical motion tenderness and discharge, and it does not produce an empty uterus with a positive hCG above the discriminatory level. <div class="ec-teach"><div class="th">What the findings actually point to</div> An hCG above the discriminatory threshold with no intrauterine sac, an adnexal mass separate from the ovary, and free fluid is ectopic pregnancy. Prior chlamydial infection with tubal damage is among the strongest risk factors. <div class="ec-src"><b>Source:</b> ACOG Practice Bulletin No. 193: Tubal Ectopic Pregnancy. Obstet Gynecol 2018;131(3):e91-e103.</div></div></div> [[Try this question again->Ectopic pregnancy - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Ectopic pregnancy. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Ruptured ovarian corpus luteum cyst does not fit.</div> A ruptured cyst gives sudden unilateral pain with free fluid and can occur in early pregnancy, so it is a real consideration. It does not produce a discrete adnexal mass separate from the ovary, and an intrauterine sac should be visible at this hCG. <div class="ec-teach"><div class="th">What the findings actually point to</div> An hCG above the discriminatory threshold with no intrauterine sac, an adnexal mass separate from the ovary, and free fluid is ectopic pregnancy. Prior chlamydial infection with tubal damage is among the strongest risk factors. <div class="ec-src"><b>Source:</b> ACOG Practice Bulletin No. 193: Tubal Ectopic Pregnancy. Obstet Gynecol 2018;131(3):e91-e103.</div></div></div> [[Try this question again->Ectopic pregnancy - Dx]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 22:40</div> A 52-year-old man with daily heavy alcohol use presents 36 hours after his last drink with coarse tremor, sweating, agitation and visual hallucinations. Pulse is 124/min. Clinical Institute Withdrawal Assessment score is 22. He has known cirrhosis with mild coagulopathy. He has had a withdrawal seizure in a previous admission. <span class="ec-prompt">Which of the following is the most appropriate pharmacotherapy?</span> [[Chlordiazepoxide on a fixed tapering schedule->Alcohol withdrawal - Rx D1]] [[Clonidine for autonomic features->Alcohol withdrawal - Rx D4]] [[Haloperidol for hallucinations->Alcohol withdrawal - Rx D2]] [[Lorazepam titrated to symptoms by a validated withdrawal-severity protocol->Alcohol withdrawal - Rx correct]] [[Phenytoin for seizure prevention->Alcohol withdrawal - Rx D3]]

<span class="ec-case-marker" hidden data-entry="Alcohol withdrawal. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best choice.</div> Chlordiazepoxide is a perfectly good agent and fixed schedules are widely used, which makes this the closest wrong answer. Two problems here: it is long-acting and oxidatively metabolized, so it accumulates in cirrhosis, and symptom-triggered dosing outperforms fixed dosing. <div class="ec-teach"><div class="th">What to give instead</div> Benzodiazepines are first-line because they replace the GABAergic tone that alcohol was providing, and symptom-triggered dosing against a validated scale gives less total drug and shorter treatment than fixed schedules. Lorazepam is preferred in significant liver disease because it undergoes glucuronidation without oxidative metabolism, so it does not accumulate. <div class="ec-src"><b>Source:</b> The ASAM Clinical Practice Guideline on Alcohol Withdrawal Management. J Addict Med 2020;14(3S Suppl):1-72.</div></div></div> [[Try this question again->Alcohol withdrawal - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Alcohol withdrawal. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best choice.</div> Alpha-2 agonists do blunt tachycardia and sweating and are sometimes used as adjuncts. Used alone they mask the autonomic signs one is scoring against while leaving the seizure and delirium risk untreated. <div class="ec-teach"><div class="th">What to give instead</div> Benzodiazepines are first-line because they replace the GABAergic tone that alcohol was providing, and symptom-triggered dosing against a validated scale gives less total drug and shorter treatment than fixed schedules. Lorazepam is preferred in significant liver disease because it undergoes glucuronidation without oxidative metabolism, so it does not accumulate. <div class="ec-src"><b>Source:</b> The ASAM Clinical Practice Guideline on Alcohol Withdrawal Management. J Addict Med 2020;14(3S Suppl):1-72.</div></div></div> [[Try this question again->Alcohol withdrawal - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Alcohol withdrawal. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best choice.</div> Alcoholic hallucinosis invites an antipsychotic. Haloperidol lowers the seizure threshold in a man who has already had a withdrawal seizure, prolongs the QT interval, and does not treat the underlying GABA deficit, the hallucinations resolve with adequate benzodiazepine. <div class="ec-teach"><div class="th">What to give instead</div> Benzodiazepines are first-line because they replace the GABAergic tone that alcohol was providing, and symptom-triggered dosing against a validated scale gives less total drug and shorter treatment than fixed schedules. Lorazepam is preferred in significant liver disease because it undergoes glucuronidation without oxidative metabolism, so it does not accumulate. <div class="ec-src"><b>Source:</b> The ASAM Clinical Practice Guideline on Alcohol Withdrawal Management. J Addict Med 2020;14(3S Suppl):1-72.</div></div></div> [[Try this question again->Alcohol withdrawal - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Alcohol withdrawal. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Lorazepam titrated to symptoms by a validated withdrawal-severity protocol</div> Benzodiazepines are first-line because they replace the GABAergic tone that alcohol was providing, and symptom-triggered dosing against a validated scale gives less total drug and shorter treatment than fixed schedules. Lorazepam is preferred in significant liver disease because it undergoes glucuronidation without oxidative metabolism, so it does not accumulate. <div class="ec-src"><b>Source:</b> The ASAM Clinical Practice Guideline on Alcohol Withdrawal Management. J Addict Med 2020;14(3S Suppl):1-72.</div></div> [[Start another case->Hub]] [[Restart this case->Alcohol withdrawal - Rx]] [[Next case →->Opioid overdose - Rx]]

<span class="ec-case-marker" hidden data-entry="Alcohol withdrawal. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best choice.</div> His seizure history makes this tempting. Phenytoin does not prevent withdrawal seizures, trials show no benefit, because these arise from acute GABA and NMDA imbalance rather than a chronic epileptic focus. Benzodiazepines both treat and prevent them. <div class="ec-teach"><div class="th">What to give instead</div> Benzodiazepines are first-line because they replace the GABAergic tone that alcohol was providing, and symptom-triggered dosing against a validated scale gives less total drug and shorter treatment than fixed schedules. Lorazepam is preferred in significant liver disease because it undergoes glucuronidation without oxidative metabolism, so it does not accumulate. <div class="ec-src"><b>Source:</b> The ASAM Clinical Practice Guideline on Alcohol Withdrawal Management. J Addict Med 2020;14(3S Suppl):1-72.</div></div></div> [[Try this question again->Alcohol withdrawal - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Labor & delivery · 03:55</div> Twenty minutes after a prolonged labor and a vaginal delivery, a 31-year-old woman is bleeding heavily. Blood pressure is 84/50 mm Hg and pulse is 128/min. The placenta delivered intact and there are no lacerations, but her uterus is soft and boggy above the umbilicus. Her history includes moderate persistent asthma. This is postpartum hemorrhage from uterine atony. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Bimanual massage and Intravenous oxytocin->Postpartum hemorrhage - First line correct]] [[Emergency hysterectomy for definitive control->Postpartum hemorrhage - Hysterectomy trap]] [[Intramuscular methylergonovine as first uterotonic->Postpartum hemorrhage - Ergot first trap]] [[Manual removal of the placenta->Postpartum hemorrhage - Manual removal]] [[Observe and transfuse if hemoglobin falls->Postpartum hemorrhage - Observe trap]]

<span class="ec-case-marker" hidden data-entry="Postpartum hemorrhage. Opening"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Bimanual massage and Intravenous oxytocin</div> Bimanual massage is started, with IV oxytocin while a second nurse establishes large-bore access and fluids. The uterus firms somewhat, but the bleeding has not stopped. <div class="ec-teach"><div class="th">Why these first</div> Uterine atony causes the large majority of postpartum hemorrhage. Uterine massage and oxytocin are first-line and act quickly, alongside resuscitation. If bleeding continues, escalate to a second-line uterotonic. <br><br><b>Then:</b> Both second-line uterotonics carry a specific contraindication, and the vignette indicates which one applies: <b>methylergonovine is contraindicated in hypertension/preeclampsia</b>, and <b>carboprost is contraindicated in asthma</b>. This patient is asthmatic and normotensive, so methylergonovine is the safe choice. Tranexamic acid is recommended as an adjunct when initial therapy fails.<div class="ec-src"><b>Source:</b> FIGO 2022 recommendations; ACOG Practice Bulletin No. 183: Postpartum Hemorrhage; WOMAN Trial Collaborators. Lancet 2017;389(10084):2105-2116.</div></div></div> <b>Hemorrhage controlled → recovery.</b> [[Start another case->Hub]] [[Restart this case->Postpartum hemorrhage - Opening]] [[Next case →->PPH management - Rx]]

<span class="ec-case-marker" hidden data-entry="Postpartum hemorrhage. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ A real second-line uterotonic, and one with a contraindication worth remembering.</div> Methylergonovine is a genuine uterotonic and it will likely be used if the first-line agent fails. Oxytocin is first-line, and methylergonovine is contraindicated in hypertension and pre-eclampsia because it causes vasoconstriction, which matters in a population where hypertensive disease is common. <div class="ec-teach"><div class="th">Why this is wrong</div> Uterine massage with oxytocin, alongside intravenous access, fluids and crossmatch, is the first move for atony. Escalate to a second uterotonic, methylergonovine if not hypertensive, or a prostaglandin, avoiding carboprost in asthma, then to tamponade and surgical measures. Tranexamic acid within 3 hours reduces death from bleeding. <div class="ec-src"><b>Source:</b> WOMAN Trial Collaborators. Lancet 2017;389(10084):2105-2116; ACOG Practice Bulletin No. 183: Postpartum Hemorrhage.</div></div></div> [[Try this question again->Postpartum hemorrhage - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Postpartum hemorrhage. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Every reversible step was skipped.</div> Hysterectomy ends her fertility and is major surgery in a bleeding, unstable patient. It is the last resort, after uterotonics, tamponade, and uterus-conserving measures have failed. <div class="ec-teach"><div class="th">What this misses</div> Management escalates: massage and uterotonics, then tranexamic acid and tamponade or uterus-conserving procedures, with hysterectomy reserved for refractory hemorrhage. <div class="ec-src"><b>Source:</b> ACOG Practice Bulletin No. 183: Postpartum Hemorrhage; WOMAN Trial Collaborators. Lancet 2017;389(10084):2105-2116.</div></div></div> [[Try this question again->Postpartum hemorrhage - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Postpartum hemorrhage. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ she is exsanguinating while being observed.</div> She is already tachycardic and hypotensive with an atonic uterus. Waiting on a hemoglobin, which lags acute blood loss, while active bleeding continues is how postpartum hemorrhage becomes a maternal death. <div class="ec-teach"><div class="th">The trap</div> Postpartum hemorrhage is treated on clinical findings, immediately. Hemoglobin lags acute loss and must not gate treatment. <div class="ec-src"><b>Source:</b> ACOG Practice Bulletin No. 183: Postpartum Hemorrhage; WOMAN Trial Collaborators. Lancet 2017;389(10084):2105-2116.</div></div></div> [[Try this question again->Postpartum hemorrhage - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Postpartum hemorrhage. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ This looks for a problem she does not have.</div> Retained placental tissue is a genuine cause of postpartum hemorrhage and worth excluding, but the placenta delivered intact and her uterus is soft and boggy, which is atony. Manual exploration delays the massage and uterotonics that would stop the bleeding now. <div class="ec-teach"><div class="th">What this misses</div> Atony causes the large majority of postpartum hemorrhage and is identified by a soft, boggy uterus. Work through the causes systematically, tone, trauma, tissue, thrombin, but treat the one already present first. <div class="ec-src"><b>Source:</b> ACOG Practice Bulletin No. 183: Postpartum Hemorrhage; WOMAN Trial Collaborators. Lancet 2017;389(10084):2105-2116.</div></div></div> [[Try this question again->Postpartum hemorrhage - Opening]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 20:10</div> A 58-year-old man with type 2 diabetes has 18 hours of rapidly worsening left leg pain following a minor scratch. The pain is severe and out of keeping with the appearance of the skin, which shows dusky discoloration with a few hemorrhagic bullae and a poorly demarcated edge. He is febrile and hypotensive. Crepitus is felt over the calf. <span class="ec-prompt">Which of the following is the most likely diagnosis?</span> [[Cellulitis->Necrotizing fasciitis - Dx cellulitis]] [[Compartment syndrome->Necrotizing fasciitis - Dx compartment]] [[Deep venous thrombosis->Necrotizing fasciitis - Dx deep]] [[Necrotizing fasciitis->Necrotizing fasciitis - Dx correct]] [[Pyomyositis->Necrotizing fasciitis - Dx pyomyositis]]

<span class="ec-case-marker" hidden data-entry="Necrotizing fasciitis. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Cellulitis does not fit.</div> Cellulitis gives a warm, erythematous, well-demarcated area that evolves over days and is tender in proportion to its appearance. It does not produce crepitus, hemorrhagic bullae or this degree of systemic toxicity. <div class="ec-teach"><div class="th">What the findings actually point to</div> Pain out of proportion to skin findings, rapid progression over hours, hemorrhagic bullae, dusky poorly demarcated skin, crepitus and systemic toxicity are the recognized features. The diagnosis is clinical and surgical exploration should not wait for imaging. <div class="ec-src"><b>Source:</b> Stevens DL, et al. IDSA Practice Guidelines for the Diagnosis and Management of Skin and Soft Tissue Infections. Clin Infect Dis 2014;59(2):e10-e52.</div></div></div> [[Try this question again->Necrotizing fasciitis - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Necrotizing fasciitis. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Compartment syndrome does not fit.</div> Compartment syndrome also gives pain out of proportion and is a genuine consideration, but it follows trauma, fracture or reperfusion, produces a tense compartment with pain on passive stretch, and does not cause fever, bullae or crepitus. <div class="ec-teach"><div class="th">What the findings actually point to</div> Pain out of proportion to skin findings, rapid progression over hours, hemorrhagic bullae, dusky poorly demarcated skin, crepitus and systemic toxicity are the recognized features. The diagnosis is clinical and surgical exploration should not wait for imaging. <div class="ec-src"><b>Source:</b> Stevens DL, et al. IDSA Practice Guidelines for the Diagnosis and Management of Skin and Soft Tissue Infections. Clin Infect Dis 2014;59(2):e10-e52.</div></div></div> [[Try this question again->Necrotizing fasciitis - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Necrotizing fasciitis. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Deep venous thrombosis does not fit.</div> Thrombosis gives unilateral swelling and calf tenderness without hemorrhagic bullae, crepitus or septic shock. Fever this high and a preceding skin breach point to infection. <div class="ec-teach"><div class="th">What the findings actually point to</div> Pain out of proportion to skin findings, rapid progression over hours, hemorrhagic bullae, dusky poorly demarcated skin, crepitus and systemic toxicity are the recognized features. The diagnosis is clinical and surgical exploration should not wait for imaging. <div class="ec-src"><b>Source:</b> Stevens DL, et al. IDSA Practice Guidelines for the Diagnosis and Management of Skin and Soft Tissue Infections. Clin Infect Dis 2014;59(2):e10-e52.</div></div></div> [[Try this question again->Necrotizing fasciitis - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Necrotizing fasciitis. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Necrotizing fasciitis.</div> Pain out of proportion to skin findings, rapid progression over hours, hemorrhagic bullae, dusky poorly demarcated skin, crepitus and systemic toxicity are the recognized features. The diagnosis is clinical and surgical exploration should not wait for imaging. <div class="ec-src"><b>Source:</b> Stevens DL, et al. IDSA Practice Guidelines for the Diagnosis and Management of Skin and Soft Tissue Infections. Clin Infect Dis 2014;59(2):e10-e52.</div></div> [[Start another case->Hub]] [[Restart this case->Necrotizing fasciitis - Dx]] [[Next case →->Septic arthritis - Dx]]

<span class="ec-case-marker" hidden data-entry="Necrotizing fasciitis. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Pyomyositis does not fit.</div> Pyomyositis gives subacute muscle pain and fever with a localized abscess, usually over days to weeks, and does not produce this rate of progression or the overlying skin necrosis. <div class="ec-teach"><div class="th">What the findings actually point to</div> Pain out of proportion to skin findings, rapid progression over hours, hemorrhagic bullae, dusky poorly demarcated skin, crepitus and systemic toxicity are the recognized features. The diagnosis is clinical and surgical exploration should not wait for imaging. <div class="ec-src"><b>Source:</b> Stevens DL, et al. IDSA Practice Guidelines for the Diagnosis and Management of Skin and Soft Tissue Infections. Clin Infect Dis 2014;59(2):e10-e52.</div></div></div> [[Try this question again->Necrotizing fasciitis - Dx]] [[Start another case->Hub]]

<div class="ec-scene">Oncology ward · 02:20</div> A 61-year-old man is 10 days past cyclophosphamide-based chemotherapy for lymphoma. He develops a single temperature of 38.6°C. Absolute neutrophil count is 300/mm3. He has no cough, dysuria or diarrhea. Examination shows no focus of infection; the skin around his tunneled central line is unremarkable and the chest is clear. <span class="ec-prompt">Which of the following is the most likely diagnosis?</span> [[Central line-associated bloodstream infection->Neutropenic fever - Dx D2]] [[Chemotherapy-induced fever->Neutropenic fever - Dx D1]] [[Community-acquired pneumonia->Neutropenic fever - Dx D5]] [[Febrile neutropenia->Neutropenic fever - Dx correct]] [[Tumor fever from lymphoma->Neutropenic fever - Dx D3]]

<span class="ec-case-marker" hidden data-entry="Neutropenic fever. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This is a leading source and cultures are drawn from the line for exactly this reason, so it is a genuine possibility rather than a wrong answer. It is a specific cause within febrile neutropenia rather than an alternative diagnosis, and the exit site here is unremarkable. <div class="ec-teach"><div class="th">What the findings point to</div> A single temperature of 38.3°C or above, or 38.0°C sustained over an hour, with an absolute neutrophil count below 500/mm3 defines febrile neutropenia. The absence of a focus is expected rather than reassuring, without neutrophils the usual localizing signs and the infiltrate on the chest film may never appear. <div class="ec-src"><b>Source:</b> Freifeld AG, et al. IDSA Clinical Practice Guideline for the Use of Antimicrobial Agents in Neutropenic Patients with Cancer. Clin Infect Dis 2011;52(4):e56-e93.</div></div></div> [[Try this question again->Neutropenic fever - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Neutropenic fever. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Cytotoxic drugs and their infusion reactions can cause fever, and the timing invites this. Attributing fever in a neutropenic patient to the drug is the reasoning that delays antibiotics, and the nadir at 7 to 14 days is precisely when infection is most likely. <div class="ec-teach"><div class="th">What the findings point to</div> A single temperature of 38.3°C or above, or 38.0°C sustained over an hour, with an absolute neutrophil count below 500/mm3 defines febrile neutropenia. The absence of a focus is expected rather than reassuring, without neutrophils the usual localizing signs and the infiltrate on the chest film may never appear. <div class="ec-src"><b>Source:</b> Freifeld AG, et al. IDSA Clinical Practice Guideline for the Use of Antimicrobial Agents in Neutropenic Patients with Cancer. Clin Infect Dis 2011;52(4):e56-e93.</div></div></div> [[Try this question again->Neutropenic fever - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Neutropenic fever. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Pneumonia is a frequent source, but his chest is clear and, importantly, a neutropenic patient may have no infiltrate and no productive cough despite pulmonary infection, so a clear examination does not narrow the diagnosis. <div class="ec-teach"><div class="th">What the findings point to</div> A single temperature of 38.3°C or above, or 38.0°C sustained over an hour, with an absolute neutrophil count below 500/mm3 defines febrile neutropenia. The absence of a focus is expected rather than reassuring, without neutrophils the usual localizing signs and the infiltrate on the chest film may never appear. <div class="ec-src"><b>Source:</b> Freifeld AG, et al. IDSA Clinical Practice Guideline for the Use of Antimicrobial Agents in Neutropenic Patients with Cancer. Clin Infect Dis 2011;52(4):e56-e93.</div></div></div> [[Try this question again->Neutropenic fever - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Neutropenic fever. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Febrile neutropenia.</div> A single temperature of 38.3°C or above, or 38.0°C sustained over an hour, with an absolute neutrophil count below 500/mm3 defines febrile neutropenia. The absence of a focus is expected rather than reassuring, without neutrophils the usual localizing signs and the infiltrate on the chest film may never appear. <div class="ec-src"><b>Source:</b> Freifeld AG, et al. IDSA Clinical Practice Guideline for the Use of Antimicrobial Agents in Neutropenic Patients with Cancer. Clin Infect Dis 2011;52(4):e56-e93.</div></div> [[Start another case->Hub]] [[Restart this case->Neutropenic fever - Dx]] [[Next case →->Cord compression - Rx]]

<span class="ec-case-marker" hidden data-entry="Neutropenic fever. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Lymphoma does cause fever, classically with night sweats and weight loss over weeks. It is a diagnosis of exclusion and never one to make while a patient is neutropenic and newly febrile. <div class="ec-teach"><div class="th">What the findings point to</div> A single temperature of 38.3°C or above, or 38.0°C sustained over an hour, with an absolute neutrophil count below 500/mm3 defines febrile neutropenia. The absence of a focus is expected rather than reassuring, without neutrophils the usual localizing signs and the infiltrate on the chest film may never appear. <div class="ec-src"><b>Source:</b> Freifeld AG, et al. IDSA Clinical Practice Guideline for the Use of Antimicrobial Agents in Neutropenic Patients with Cancer. Clin Infect Dis 2011;52(4):e56-e93.</div></div></div> [[Try this question again->Neutropenic fever - Dx]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 04:05</div> A 24-year-old man had a below-knee cast applied 8 hours ago for a tibial shaft fracture. He now has severe leg pain unrelieved by repeated opioid doses, with agony on passive extension of the toes. The dorsalis pedis pulse is palpable and capillary refill is 2 seconds. Sensation over the first web space is reduced. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Arterial duplex ultrasonography->Compartment syndrome - Ix D2]] [[Elevate the limb and reassess in 1 hour->Compartment syndrome - Ix D5]] [[Measure compartment pressures first->Compartment syndrome - Ix D1]] [[Split the cast to skin and reassess->Compartment syndrome - Ix correct]] [[Urgent MRI of the leg->Compartment syndrome - Ix D3]]

<span class="ec-case-marker" hidden data-entry="Compartment syndrome. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A palpable pulse does not exclude compartment syndrome, compartment pressure rises well above venous but below arterial pressure, so pulses are typically present until very late. Documenting flow would falsely reassure. <div class="ec-teach"><div class="th">What the findings point to</div> Pain out of proportion, unrelieved by opioids, with pain on passive stretch and early sensory loss in the deep peroneal distribution is acute compartment syndrome. The first intervention is to remove the circumferential constriction, splitting the cast and underlying padding down to skin substantially lowers compartment pressure, while orthopedics is called for fasciotomy. <div class="ec-src"><b>Source:</b> McQueen MM, Court-Brown CM. Compartment monitoring in tibial fractures: the pressure threshold for decompression. J Bone Joint Surg Br 1996;78(1):99-104.</div></div></div> [[Try this question again->Compartment syndrome - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Compartment syndrome. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Elevation is intuitive and it is harmful here: raising the limb lowers arterial inflow pressure and reduces perfusion of an already ischemic compartment. Keep the limb at heart level. <div class="ec-teach"><div class="th">What the findings point to</div> Pain out of proportion, unrelieved by opioids, with pain on passive stretch and early sensory loss in the deep peroneal distribution is acute compartment syndrome. The first intervention is to remove the circumferential constriction, splitting the cast and underlying padding down to skin substantially lowers compartment pressure, while orthopedics is called for fasciotomy. <div class="ec-src"><b>Source:</b> McQueen MM, Court-Brown CM. Compartment monitoring in tibial fractures: the pressure threshold for decompression. J Bone Joint Surg Br 1996;78(1):99-104.</div></div></div> [[Try this question again->Compartment syndrome - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Compartment syndrome. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Pressure measurement is valuable where the picture is equivocal or the patient cannot report pain, obtunded, anesthetized, or very young. His examination is unequivocal, delta pressure is more reliable than an absolute threshold, and splitting the cast costs seconds and is itself therapeutic. <div class="ec-teach"><div class="th">What the findings point to</div> Pain out of proportion, unrelieved by opioids, with pain on passive stretch and early sensory loss in the deep peroneal distribution is acute compartment syndrome. The first intervention is to remove the circumferential constriction, splitting the cast and underlying padding down to skin substantially lowers compartment pressure, while orthopedics is called for fasciotomy. <div class="ec-src"><b>Source:</b> McQueen MM, Court-Brown CM. Compartment monitoring in tibial fractures: the pressure threshold for decompression. J Bone Joint Surg Br 1996;78(1):99-104.</div></div></div> [[Try this question again->Compartment syndrome - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Compartment syndrome. Ix"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Split the cast to skin and reassess</div> Pain out of proportion, unrelieved by opioids, with pain on passive stretch and early sensory loss in the deep peroneal distribution is acute compartment syndrome. The first intervention is to remove the circumferential constriction, splitting the cast and underlying padding down to skin substantially lowers compartment pressure, while orthopedics is called for fasciotomy. <div class="ec-src"><b>Source:</b> McQueen MM, Court-Brown CM. Compartment monitoring in tibial fractures: the pressure threshold for decompression. J Bone Joint Surg Br 1996;78(1):99-104.</div></div> [[Start another case->Hub]] [[Restart this case->Compartment syndrome - Ix]] [[Next case →->Compartment syndrome 2 - Rx]]

<span class="ec-case-marker" hidden data-entry="Compartment syndrome. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> MRI cannot diagnose compartment syndrome, takes the patient away from the department, and delays decompression in a condition where muscle necrosis begins within hours. <div class="ec-teach"><div class="th">What the findings point to</div> Pain out of proportion, unrelieved by opioids, with pain on passive stretch and early sensory loss in the deep peroneal distribution is acute compartment syndrome. The first intervention is to remove the circumferential constriction, splitting the cast and underlying padding down to skin substantially lowers compartment pressure, while orthopedics is called for fasciotomy. <div class="ec-src"><b>Source:</b> McQueen MM, Court-Brown CM. Compartment monitoring in tibial fractures: the pressure threshold for decompression. J Bone Joint Surg Br 1996;78(1):99-104.</div></div></div> [[Try this question again->Compartment syndrome - Ix]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 07:50</div> A 34-year-old man and two family members present the same morning with headache, nausea and dizziness. They live in an older home with a gas furnace. He is confused. Pulse oximetry reads 99% on room air and arterial oxygen tension is 280 mm Hg on supplemental oxygen. His skin is normal in color and the chest is clear. Symptoms improve in the two relatives after time outdoors. <span class="ec-prompt">Which of the following is the most likely diagnosis?</span> [[Carbon dioxide narcosis->Carbon monoxide - Dx D4]] [[Carbon monoxide poisoning->Carbon monoxide - Dx correct]] [[Cyanide poisoning->Carbon monoxide - Dx D3]] [[Methemoglobinemia->Carbon monoxide - Dx D1]] [[Viral gastroenteritis->Carbon monoxide - Dx D2]]

<span class="ec-case-marker" hidden data-entry="Carbon monoxide. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Retention causes drowsiness and headache but occurs in patients with severe pulmonary disease and hypoventilation, not in three previously well people in one house. <div class="ec-teach"><div class="th">What the findings point to</div> Multiple household members affected simultaneously in winter with headache, nausea and confusion, improving away from the home, is carbon monoxide until proven otherwise. Pulse oximetry cannot distinguish carboxyhemoglobin from oxyhemoglobin and reads falsely normal, and arterial oxygen tension measures dissolved oxygen and is also normal, both reassure falsely. <div class="ec-src"><b>Source:</b> Weaver LK, et al. Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J Med 2002;347(14):1057-1067.</div></div></div> [[Try this question again->Carbon monoxide - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Carbon monoxide. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Carbon monoxide poisoning.</div> Multiple household members affected simultaneously in winter with headache, nausea and confusion, improving away from the home, is carbon monoxide until proven otherwise. Pulse oximetry cannot distinguish carboxyhemoglobin from oxyhemoglobin and reads falsely normal, and arterial oxygen tension measures dissolved oxygen and is also normal, both reassure falsely. <div class="ec-src"><b>Source:</b> Weaver LK, et al. Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J Med 2002;347(14):1057-1067.</div></div> [[Start another case->Hub]] [[Restart this case->Carbon monoxide - Dx]] [[Next case →->Duty to warn - Ethics]]

<span class="ec-case-marker" hidden data-entry="Carbon monoxide. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Cyanide is a genuine co-exposure in enclosed-space fires and causes severe lactic acidosis with a narrowed arteriovenous oxygen difference. There is no fire here, and it does not affect a household through a furnace. <div class="ec-teach"><div class="th">What the findings point to</div> Multiple household members affected simultaneously in winter with headache, nausea and confusion, improving away from the home, is carbon monoxide until proven otherwise. Pulse oximetry cannot distinguish carboxyhemoglobin from oxyhemoglobin and reads falsely normal, and arterial oxygen tension measures dissolved oxygen and is also normal, both reassure falsely. <div class="ec-src"><b>Source:</b> Weaver LK, et al. Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J Med 2002;347(14):1057-1067.</div></div></div> [[Try this question again->Carbon monoxide - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Carbon monoxide. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This is the other dyshemoglobinemia and shares a falsely reassuring oxygen tension, so it belongs on the list. It gives cyanosis unresponsive to oxygen with an oximeter that plateaus near 85% rather than 99%, and it does not affect a whole household at once. <div class="ec-teach"><div class="th">What the findings point to</div> Multiple household members affected simultaneously in winter with headache, nausea and confusion, improving away from the home, is carbon monoxide until proven otherwise. Pulse oximetry cannot distinguish carboxyhemoglobin from oxyhemoglobin and reads falsely normal, and arterial oxygen tension measures dissolved oxygen and is also normal, both reassure falsely. <div class="ec-src"><b>Source:</b> Weaver LK, et al. Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J Med 2002;347(14):1057-1067.</div></div></div> [[Try this question again->Carbon monoxide - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Carbon monoxide. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Headache, nausea and malaise in several household members in winter is very commonly labeled this way, which is exactly how carbon monoxide is missed. Gastroenteritis does not cause confusion, and symptoms would not improve simply by going outdoors. <div class="ec-teach"><div class="th">What the findings point to</div> Multiple household members affected simultaneously in winter with headache, nausea and confusion, improving away from the home, is carbon monoxide until proven otherwise. Pulse oximetry cannot distinguish carboxyhemoglobin from oxyhemoglobin and reads falsely normal, and arterial oxygen tension measures dissolved oxygen and is also normal, both reassure falsely. <div class="ec-src"><b>Source:</b> Weaver LK, et al. Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J Med 2002;347(14):1057-1067.</div></div></div> [[Try this question again->Carbon monoxide - Dx]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 14:05</div> A 71-year-old man with a 40 pack-year smoking history has sudden severe back and abdominal pain with syncope. Temperature is 36.6°C, blood pressure 82/50 mm Hg, pulse is 124/min, and respirations are 24/min. A pulsatile epigastric mass is palpable. He is pale and diaphoretic but talking. Vascular surgery has been alerted. <span class="ec-prompt">Which of the following is the most appropriate next step in diagnosis?</span> [[Abdominal radiography->Ruptured AAA - Ix D2]] [[Bedside ultrasonography->Ruptured AAA - Ix correct]] [[CT angiography of the abdomen and pelvis->Ruptured AAA - Ix D1]] [[Magnetic resonance angiography of the aorta->Ruptured AAA - Ix D5]] [[Serial hemoglobin measurement->Ruptured AAA - Ix D4]]

<span class="ec-case-marker" hidden data-entry="Ruptured AAA. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A plain film may show calcification of the aneurysm wall but cannot diagnose or exclude rupture, and normal findings would be meaningless here. <div class="ec-teach"><div class="th">What the findings point to</div> Bedside ultrasound identifies an aneurysm within seconds without moving him, and in a hypotensive patient with a pulsatile mass that is all the confirmation required to go to theater. It is highly sensitive for the presence of an aneurysm, and the decision to operate rests on the aneurysm plus the hemodynamics rather than on demonstrating the rupture itself. <div class="ec-src"><b>Source:</b> Chaikof EL, et al. The Society for Vascular Surgery practice guidelines on the care of patients with an abdominal aortic aneurysm. J Vasc Surg 2018;67(1):2-77.e2.</div></div></div> [[Try this question again->Ruptured AAA - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Ruptured AAA. Ix"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Bedside ultrasonography</div> Bedside ultrasound identifies an aneurysm within seconds without moving him, and in a hypotensive patient with a pulsatile mass that is all the confirmation required to go to theater. It is highly sensitive for the presence of an aneurysm, and the decision to operate rests on the aneurysm plus the hemodynamics rather than on demonstrating the rupture itself. <div class="ec-src"><b>Source:</b> Chaikof EL, et al. The Society for Vascular Surgery practice guidelines on the care of patients with an abdominal aortic aneurysm. J Vasc Surg 2018;67(1):2-77.e2.</div></div> [[Start another case->Hub]] [[Restart this case->Ruptured AAA - Ix]] [[Next case →->AAA screening - Opening]]

<span class="ec-case-marker" hidden data-entry="Ruptured AAA. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Computed tomography is the right study in a stable patient, defines the anatomy and determines suitability for endovascular repair, so this is the strongest wrong answer. He is hypotensive, and moving an unstable patient with a ruptured aneurysm to the scanner is where these patients arrest. <div class="ec-teach"><div class="th">What the findings point to</div> Bedside ultrasound identifies an aneurysm within seconds without moving him, and in a hypotensive patient with a pulsatile mass that is all the confirmation required to go to theater. It is highly sensitive for the presence of an aneurysm, and the decision to operate rests on the aneurysm plus the hemodynamics rather than on demonstrating the rupture itself. <div class="ec-src"><b>Source:</b> Chaikof EL, et al. The Society for Vascular Surgery practice guidelines on the care of patients with an abdominal aortic aneurysm. J Vasc Surg 2018;67(1):2-77.e2.</div></div></div> [[Try this question again->Ruptured AAA - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Ruptured AAA. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Magnetic resonance angiography defines aortic anatomy well but takes too long and places an unstable patient somewhere he cannot be resuscitated. <div class="ec-teach"><div class="th">What the findings point to</div> Bedside ultrasound identifies an aneurysm within seconds without moving him, and in a hypotensive patient with a pulsatile mass that is all the confirmation required to go to theater. It is highly sensitive for the presence of an aneurysm, and the decision to operate rests on the aneurysm plus the hemodynamics rather than on demonstrating the rupture itself. <div class="ec-src"><b>Source:</b> Chaikof EL, et al. The Society for Vascular Surgery practice guidelines on the care of patients with an abdominal aortic aneurysm. J Vasc Surg 2018;67(1):2-77.e2.</div></div></div> [[Try this question again->Ruptured AAA - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Ruptured AAA. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Hemoglobin lags acute blood loss and can be near-normal in early exsanguination. Waiting for it to fall is waiting for a change that arrives too late. <div class="ec-teach"><div class="th">What the findings point to</div> Bedside ultrasound identifies an aneurysm within seconds without moving him, and in a hypotensive patient with a pulsatile mass that is all the confirmation required to go to theater. It is highly sensitive for the presence of an aneurysm, and the decision to operate rests on the aneurysm plus the hemodynamics rather than on demonstrating the rupture itself. <div class="ec-src"><b>Source:</b> Chaikof EL, et al. The Society for Vascular Surgery practice guidelines on the care of patients with an abdominal aortic aneurysm. J Vasc Surg 2018;67(1):2-77.e2.</div></div></div> [[Try this question again->Ruptured AAA - Ix]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 15:40</div> A 29-year-old man on long-term sertraline was started on tramadol for back pain yesterday. Over the past 6 hours he has become agitated and tremulous. Temperature is 39.4°C, pulse is 128/min, and he is diaphoretic with dilated pupils. Deep tendon reflexes are brisk throughout and are more marked in the legs than the arms, with inducible ankle clonus. Bowel sounds are hyperactive. He takes no antipsychotic medication. <span class="ec-prompt">Which of the following is the most likely diagnosis?</span> [[Anticholinergic toxicity->Serotonin syndrome - Dx anticholinergic]] [[Neuroleptic malignant syndrome->Serotonin syndrome - Dx neuroleptic]] [[Serotonin syndrome->Serotonin syndrome - Dx correct]] [[Sympathomimetic toxicity->Serotonin syndrome - Dx sympathomimetic]] [[Thyroid storm->Serotonin syndrome - Dx thyroid]]

<span class="ec-case-marker" hidden data-entry="Serotonin syndrome. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Anticholinergic toxicity does not fit.</div> This gives mydriasis, hyperthermia and agitation, so it overlaps. It is distinguished by dry flushed skin, urinary retention and, decisively, absent or reduced bowel sounds. He is diaphoretic with hyperactive bowel sounds, which is the opposite. <div class="ec-teach"><div class="th">What the findings actually point to</div> Rapid onset over hours after adding a second serotonergic agent, with hyperreflexia, inducible clonus greater in the lower limbs than the upper, tremor, mydriasis, hyperactive bowel sounds and hyperthermia, meets the Hunter criteria. Tramadol is serotonergic, which is why it is a frequent culprit alongside a selective serotonin reuptake inhibitor. <div class="ec-src"><b>Source:</b> Dunkley EJC, et al. The Hunter Serotonin Toxicity Criteria. QJM 2003;96(9):635-642; Boyer EW, Shannon M. N Engl J Med 2005;352(11):1112-1120.</div></div></div> [[Try this question again->Serotonin syndrome - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Serotonin syndrome. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Neuroleptic malignant syndrome does not fit.</div> The most important alternative. It evolves over days rather than hours, follows dopamine antagonist exposure or withdrawal of a dopaminergic drug, and produces lead-pipe rigidity with bradyreflexia and normal pupils. He is on no antipsychotic, the onset is hours, and hyperreflexia with clonus is the finding that separates the two. <div class="ec-teach"><div class="th">What the findings actually point to</div> Rapid onset over hours after adding a second serotonergic agent, with hyperreflexia, inducible clonus greater in the lower limbs than the upper, tremor, mydriasis, hyperactive bowel sounds and hyperthermia, meets the Hunter criteria. Tramadol is serotonergic, which is why it is a frequent culprit alongside a selective serotonin reuptake inhibitor. <div class="ec-src"><b>Source:</b> Dunkley EJC, et al. The Hunter Serotonin Toxicity Criteria. QJM 2003;96(9):635-642; Boyer EW, Shannon M. N Engl J Med 2005;352(11):1112-1120.</div></div></div> [[Try this question again->Serotonin syndrome - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Serotonin syndrome. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Serotonin syndrome.</div> Rapid onset over hours after adding a second serotonergic agent, with hyperreflexia, inducible clonus greater in the lower limbs than the upper, tremor, mydriasis, hyperactive bowel sounds and hyperthermia, meets the Hunter criteria. Tramadol is serotonergic, which is why it is a frequent culprit alongside a selective serotonin reuptake inhibitor. <div class="ec-src"><b>Source:</b> Dunkley EJC, et al. The Hunter Serotonin Toxicity Criteria. QJM 2003;96(9):635-642; Boyer EW, Shannon M. N Engl J Med 2005;352(11):1112-1120.</div></div> [[Start another case->Hub]] [[Restart this case->Serotonin syndrome - Dx]] [[Next case →->Alcohol withdrawal - Rx]]

<span class="ec-case-marker" hidden data-entry="Serotonin syndrome. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Sympathomimetic toxicity does not fit.</div> Cocaine or amphetamine toxicity gives agitation, hyperthermia, mydriasis and diaphoresis and can look very similar. It does not produce the neuromuscular signature of clonus and lower-limb-predominant hyperreflexia, and there is a clear temporal link to a new serotonergic drug here. <div class="ec-teach"><div class="th">What the findings actually point to</div> Rapid onset over hours after adding a second serotonergic agent, with hyperreflexia, inducible clonus greater in the lower limbs than the upper, tremor, mydriasis, hyperactive bowel sounds and hyperthermia, meets the Hunter criteria. Tramadol is serotonergic, which is why it is a frequent culprit alongside a selective serotonin reuptake inhibitor. <div class="ec-src"><b>Source:</b> Dunkley EJC, et al. The Hunter Serotonin Toxicity Criteria. QJM 2003;96(9):635-642; Boyer EW, Shannon M. N Engl J Med 2005;352(11):1112-1120.</div></div></div> [[Try this question again->Serotonin syndrome - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Serotonin syndrome. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Thyroid storm does not fit.</div> Storm gives hyperthermia, tachycardia and agitation with a goiter, and typically an identifiable precipitant in a patient with known or suspected thyrotoxicosis. It does not cause clonus, and onset is not tied to a new analgesic. <div class="ec-teach"><div class="th">What the findings actually point to</div> Rapid onset over hours after adding a second serotonergic agent, with hyperreflexia, inducible clonus greater in the lower limbs than the upper, tremor, mydriasis, hyperactive bowel sounds and hyperthermia, meets the Hunter criteria. Tramadol is serotonergic, which is why it is a frequent culprit alongside a selective serotonin reuptake inhibitor. <div class="ec-src"><b>Source:</b> Dunkley EJC, et al. The Hunter Serotonin Toxicity Criteria. QJM 2003;96(9):635-642; Boyer EW, Shannon M. N Engl J Med 2005;352(11):1112-1120.</div></div></div> [[Try this question again->Serotonin syndrome - Dx]] [[Start another case->Hub]]

<div class="ec-scene">Hematology floor · 05:15</div> A 24-year-old woman with homozygous sickle cell disease was admitted 2 days ago with a painful vaso-occlusive crisis affecting her back and thighs, treated with opioids and intravenous fluids. Overnight she develops fever, pleuritic chest pain and increasing dyspnea. Oxygen saturation has fallen to 88% on room air from 97% on admission. Chest radiograph now shows a new infiltrate in the left lower zone that was not present on admission. <span class="ec-prompt">Which of the following is the most likely diagnosis?</span> [[Acute chest syndrome->Acute chest syndrome - Dx correct]] [[Fat embolism syndrome->Acute chest syndrome - Dx fat]] [[Hospital-acquired pneumonia->Acute chest syndrome - Dx hospital-acquired]] [[Pulmonary embolism->Acute chest syndrome - Dx pulmonary]] [[Vaso-occlusive crisis alone->Acute chest syndrome - Dx vaso-occlusive]]

<span class="ec-case-marker" hidden data-entry="Acute chest syndrome. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Acute chest syndrome.</div> A new pulmonary infiltrate with fever and respiratory symptoms in a patient with sickle cell disease is acute chest syndrome by definition. It characteristically appears two to 3 days into an admission for a painful crisis, as opioid-related hypoventilation and splinting from back and rib pain promote atelectasis and local sickling. <div class="ec-src"><b>Source:</b> American Society of Hematology 2020 Guidelines for Sickle Cell Disease: Transfusion Support. Blood Adv 2020;4(2):327; NHLBI Evidence-Based Management of Sickle Cell Disease, 2014.</div></div> [[Start another case->Hub]] [[Restart this case->Acute chest syndrome - Dx]] [[Next case →->TTP - Dx]]

<span class="ec-case-marker" hidden data-entry="Acute chest syndrome. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Fat embolism syndrome does not fit.</div> Marrow fat embolism does complicate sickle crisis and can look similar, so it is a genuine consideration. It typically gives a petechial rash, marked neurologic change and thrombocytopenia, and is far less common than acute chest syndrome. <div class="ec-teach"><div class="th">What the findings actually point to</div> A new pulmonary infiltrate with fever and respiratory symptoms in a patient with sickle cell disease is acute chest syndrome by definition. It characteristically appears two to 3 days into an admission for a painful crisis, as opioid-related hypoventilation and splinting from back and rib pain promote atelectasis and local sickling. <div class="ec-src"><b>Source:</b> American Society of Hematology 2020 Guidelines for Sickle Cell Disease: Transfusion Support. Blood Adv 2020;4(2):327; NHLBI Evidence-Based Management of Sickle Cell Disease, 2014.</div></div></div> [[Try this question again->Acute chest syndrome - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Acute chest syndrome. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Hospital-acquired pneumonia does not fit.</div> Infection is a frequent trigger of acute chest syndrome rather than a competing diagnosis, and the two are treated together. Labeling it pneumonia alone risks omitting transfusion and the specific management this syndrome requires. <div class="ec-teach"><div class="th">What the findings actually point to</div> A new pulmonary infiltrate with fever and respiratory symptoms in a patient with sickle cell disease is acute chest syndrome by definition. It characteristically appears two to 3 days into an admission for a painful crisis, as opioid-related hypoventilation and splinting from back and rib pain promote atelectasis and local sickling. <div class="ec-src"><b>Source:</b> American Society of Hematology 2020 Guidelines for Sickle Cell Disease: Transfusion Support. Blood Adv 2020;4(2):327; NHLBI Evidence-Based Management of Sickle Cell Disease, 2014.</div></div></div> [[Try this question again->Acute chest syndrome - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Acute chest syndrome. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Pulmonary embolism does not fit.</div> Embolism gives pleuritic pain, dyspnea and hypoxemia and is more common in sickle cell disease, but it does not typically cause fever with a new alveolar infiltrate on plain radiograph. <div class="ec-teach"><div class="th">What the findings actually point to</div> A new pulmonary infiltrate with fever and respiratory symptoms in a patient with sickle cell disease is acute chest syndrome by definition. It characteristically appears two to 3 days into an admission for a painful crisis, as opioid-related hypoventilation and splinting from back and rib pain promote atelectasis and local sickling. <div class="ec-src"><b>Source:</b> American Society of Hematology 2020 Guidelines for Sickle Cell Disease: Transfusion Support. Blood Adv 2020;4(2):327; NHLBI Evidence-Based Management of Sickle Cell Disease, 2014.</div></div></div> [[Try this question again->Acute chest syndrome - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Acute chest syndrome. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Vaso-occlusive crisis alone does not fit.</div> Her crisis is ongoing, and chest pain can be part of it. What changes the diagnosis is the new radiographic infiltrate with fever and falling saturation, chest pain in sickle disease is never assumed to be crisis alone once the film changes. <div class="ec-teach"><div class="th">What the findings actually point to</div> A new pulmonary infiltrate with fever and respiratory symptoms in a patient with sickle cell disease is acute chest syndrome by definition. It characteristically appears two to 3 days into an admission for a painful crisis, as opioid-related hypoventilation and splinting from back and rib pain promote atelectasis and local sickling. <div class="ec-src"><b>Source:</b> American Society of Hematology 2020 Guidelines for Sickle Cell Disease: Transfusion Support. Blood Adv 2020;4(2):327; NHLBI Evidence-Based Management of Sickle Cell Disease, 2014.</div></div></div> [[Try this question again->Acute chest syndrome - Dx]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 19:35</div> A 52-year-old woman is found drowsy at home beside an empty bottle of extended-release verapamil and a note. Pulse is 36/min and blood pressure is 68/40 mm Hg. She has received atropine twice and two liters of intravenous fluid, with no meaningful change in heart rate or blood pressure. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[High-dose Intravenous glucagon as primary treatment->CCB-BB overdose - Glucagon primary trap]] [[Intravenous calcium, then high-dose insulin euglycemic therapy->CCB-BB overdose - HIET correct]] [[Intravenous lipid emulsion therapy->CCB-BB overdose - Lipid]] [[Intravenous methylene blue->CCB-BB overdose - Methylene blue trap]] [[Norepinephrine alone, titrated up->CCB-BB overdose - Pressor trap]] [[Standard bradycardia algorithm: atropine, then pacing->CCB-BB overdose - ACLS trap]]

<span class="ec-case-marker" hidden data-entry="CCB-BB overdose. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ The algorithm does not fit the poison.</div> More atropine achieves nothing, the calcium channels are blocked, and no amount of vagal inhibition reopens them. Pacing may capture electrically but often fails to generate a meaningful cardiac output in a myocardium that cannot contract. Meanwhile the antidotal therapies sit unused. <div class="ec-teach"><div class="th">Where the reasoning went wrong</div> The empty verapamil bottle reframes the entire case. In significant CCB or beta-blocker overdose, atropine and pacing are frequently ineffective, the problem is depressed contractility and vasodilation, not vagal tone. Reach for calcium, glucagon (especially for beta-blockers), and high-dose insulin euglycemic therapy. <div class="ec-src"><b>Source:</b> St-Onge M, et al. Experts Consensus Recommendations for the Management of Calcium Channel Blocker Poisoning in Adults. Crit Care Med 2017; 45(3):e306-e315.</div></div></div> [[Try this question again->CCB-BB overdose - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="CCB-BB overdose. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Refractory to vasopressors, that is the point.</div> Climbing the norepinephrine alone chases a shock state that is characteristically resistant to vasopressors in this poisoning. Reported cases require escalating multiple agents with minimal response until high-dose insulin is added. <div class="ec-teach"><div class="th">Where the reasoning went wrong</div> Hemodynamic instability in CCB/beta-blocker overdose is often refractory to initial vasopressor treatment. For a patient on moderate-dose vasopressors, consider early high-dose insulin euglycemic therapy with the goal of weaning the pressors off. <div class="ec-src"><b>Source:</b> St-Onge M, et al. Experts Consensus Recommendations for the Management of Calcium Channel Blocker Poisoning in Adults. Crit Care Med 2017;45(3):e306-e315.</div></div></div> [[Try this question again->CCB-BB overdose - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="CCB-BB overdose. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ The wrong drug for this poison.</div> Glucagon raises intracellular cyclic AMP independently of the beta receptor and is a legitimate agent in beta-blocker toxicity, so reaching for it is not an unreasonable reflex. It is the wrong choice here: she took an extended-release calcium channel blocker, not a beta-blocker, and glucagon does not address calcium channel blockade at all. Supply is often limited, and it reliably causes vomiting in a patient with a depressed conscious level. <div class="ec-teach"><div class="th">Why this is wrong</div> Give calcium first to overcome the channel blockade, then high-dose insulin euglycemic therapy, which improves myocardial contractility and is the intervention with the best supporting evidence in this poisoning. Glucagon has no proven role when only a calcium channel blocker has been taken. <div class="ec-src"><b>Source:</b> St-Onge M, et al. Experts Consensus Recommendations for the Management of Calcium Channel Blocker Poisoning in Adults. Crit Care Med 2017;45(3):e306-e315.</div></div></div> [[Try this question again->CCB-BB overdose - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="CCB-BB overdose. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ A rescue therapy reached for too soon.</div> Lipid emulsion has been used in severe lipophilic drug toxicity and may have a place if everything else fails, but the evidence is largely case reports, and it should not displace calcium and high-dose insulin, which have far better support in this poisoning. <div class="ec-teach"><div class="th">The misstep</div> Work through the established steps first: calcium, then high-dose insulin euglycemic therapy, with glucagon particularly for beta-blocker toxicity. Lipid emulsion, methylene blue and VA-ECMO are salvage options for refractory cases. <div class="ec-src"><b>Source:</b> St-Onge M, et al. Experts Consensus Recommendations for the Management of Calcium Channel Blocker Poisoning in Adults. Crit Care Med 2017;45(3):e306-e315.</div></div></div> [[Try this question again->CCB-BB overdose - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="CCB-BB overdose. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ A genuine rescue therapy, reached for before the first-line ones.</div> Methylene blue inhibits nitric oxide-mediated vasodilation and there are case reports of it reversing shock in calcium channel blocker overdose refractory to everything else. That is the setting it belongs to. The 2023 AHA guideline on management of patients with cardiac arrest or life-threatening toxicity due to poisoning considers its benefit in refractory vasodilatory shock uncertain, and nothing first-line has been tried here yet. <div class="ec-teach"><div class="th">Why this is wrong</div> Give calcium and start high-dose insulin euglycemic therapy with vasopressor support. Keep methylene blue in reserve for shock that persists despite those, and check for G6PD deficiency, in which it is contraindicated. <div class="ec-src"><b>Source:</b> St-Onge M, et al. Crit Care Med 2017;45(3):e306-e315; AHA 2023 Focused Update on Special Circumstances: Cardiac Arrest Associated with Toxic Ingestions.</div></div></div> [[Try this question again->CCB-BB overdose - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="CCB-BB overdose. Opening"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Intravenous calcium, then high-dose insulin euglycemic therapy</div> IV calcium goes in to overcome the channel blockade, and high-dose insulin euglycemic therapy is started with dextrose alongside. Her contractility and pressure begin to recover in a way atropine never achieved. <div class="ec-teach"><div class="th">Where the case turned</div> The clue was the bottle: this is calcium channel blocker poisoning, not primary bradycardia. Atropine works through the vagus and is largely ineffective in significant CCB or beta-blocker toxicity, which produces bradycardia, depressed contractility, and vasodilation that resist standard measures. High-dose insulin has a direct positive inotropic effect and animal data showed it outperformed epinephrine, glucagon, and calcium in verapamil overdose. Glucagon is most useful in beta-blocker toxicity. <div class="ec-src"><b>Source:</b> St-Onge M, et al. Experts Consensus Recommendations for the Management of Calcium Channel Blocker Poisoning in Adults. Crit Care Med 2017; 45(3):e306-e315.</div></div></div> [[Start another case->Hub]] [[Restart this case->CCB-BB overdose - Opening]] [[Next case →->Methemoglobinemia - Dx]]

<div class="ec-scene">Emergency department · 02:20</div> A 31-year-old man arrives with crushing chest pain that began an hour after a night out. He is agitated and diaphoretic with dilated pupils, hypertensive and tachycardic, and admits to snorting cocaine before the pain started. The ECG shows ischemic ST changes. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Intravenous benzodiazepines, plus nitroglycerin and aspirin->Cocaine chest pain - Benzo correct]] [[Intravenous haloperidol for agitation->Cocaine chest pain - Haloperidol trap]] [[Intravenous labetalol for rate and pressure control->Cocaine chest pain - Labetalol]] [[Intravenous metoprolol->Cocaine chest pain - Metoprolol trap]] [[Intravenous phentolamine as the initial agent->Cocaine chest pain - Phentolamine trap]] [[Intravenous sodium nitroprusside->Cocaine chest pain - Nitroprusside trap]]

<span class="ec-case-marker" hidden data-entry="Cocaine chest pain. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ An antipsychotic in a patient at risk of hyperthermia and seizure.</div> Haloperidol settles agitation, and agitation is prominent, so the impulse is understandable. In cocaine toxicity it is a poor choice: butyrophenones lower the seizure threshold, impair heat dissipation in a patient already at risk of hyperthermia, and prolong the QT interval. They also do nothing for the sympathetic drive causing the coronary vasoconstriction. <div class="ec-teach"><div class="th">Why this is wrong</div> Benzodiazepines treat the agitation and the underlying sympathetic surge together, which is why they are first-line. Add nitroglycerin and aspirin for the ischemia. <div class="ec-src"><b>Source:</b> McCord J, et al. Circulation 2008;117(14):1897-1907.</div></div></div> [[Try this question again->Cocaine chest pain - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Cocaine chest pain. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ A contested choice when a clearly safe one exists.</div> Labetalol blocks both alpha and beta receptors, which is why it is sometimes proposed here. But the AHA statement notes it offers no clear advantage and did not reverse cocaine-induced coronary vasoconstriction in humans, and animal models showed increased seizure and death risk. With benzodiazepines and nitrates available and uncontroversial, this is the wrong hill. <div class="ec-teach"><div class="th">Why not this</div> Benzodiazepines are first-line, with nitroglycerin for the vasoconstriction and aspirin for thrombus risk. Beta-blocking agents, including combined alpha-beta blockers, are not the recommended initial approach. <div class="ec-src"><b>Source:</b> AHA Scientific Statement, Management of Cocaine-Associated Chest Pain and Myocardial Infarction (Circulation).</div></div></div> [[Try this question again->Cocaine chest pain - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Cocaine chest pain. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ A recommended drug, placed ahead of the one that comes first.</div> Phentolamine is an alpha-blocker and it is genuinely endorsed for cocaine-associated chest pain, it reverses coronary vasoconstriction directly. That makes this the most defensible wrong answer here. Benzodiazepines come first because they address the central sympathetic drive producing the hypertension, tachycardia and agitation all at once, and they are safer and more available. <div class="ec-teach"><div class="th">Why this is wrong</div> Give benzodiazepines with nitroglycerin and aspirin. Phentolamine is a reasonable addition if hypertension or ongoing ischemia persists despite that, not the opening move. <div class="ec-src"><b>Source:</b> McCord J, et al. Management of Cocaine-Associated Chest Pain and Myocardial Infarction: AHA Scientific Statement. Circulation 2008;117(14):1897-1907.</div></div></div> [[Try this question again->Cocaine chest pain - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Cocaine chest pain. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Effective, and the wrong instrument for this problem.</div> Nitroprusside will lower the pressure, that is not in doubt. It is a non-selective arterial and venous dilator requiring invasive monitoring, it causes reflex tachycardia that worsens myocardial oxygen demand, and it carries cyanide toxicity risk on prolonged infusion. None of that addresses the sympathetic drive that is generating the hypertension. <div class="ec-teach"><div class="th">Why this is wrong</div> Treat the cause with benzodiazepines, and use nitroglycerin for the coronary vasoconstriction and ischemic pain. Reserve nitroprusside for severe hypertension that does not respond to sedation and nitrates. <div class="ec-src"><b>Source:</b> McCord J, et al. Circulation 2008;117(14):1897-1907.</div></div></div> [[Try this question again->Cocaine chest pain - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Cocaine chest pain. Opening"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Intravenous benzodiazepines, plus nitroglycerin and aspirin</div> Benzodiazepines calm the sympathetic surge driving his hypertension, tachycardia, and chest pain, while nitroglycerin reverses the coronary vasoconstriction and aspirin addresses thrombus risk. His pain and pressure settle together. <div class="ec-teach"><div class="th">Where the case turned</div> Take cocaine out of the vignette and this looks like ordinary ACS. With it, the first-line drug changes: <b>benzodiazepines</b> are first-line, with beneficial hemodynamic and neuropsychiatric effects, they treat the sympathetic storm that is the actual driver. Nitroglycerin relieves cocaine-associated chest pain (one case series and two randomized trials) and catheterization studies show it reverses cocaine-induced vasoconstriction. <div class="ec-src"><b>Source:</b> AHA Scientific Statement, Management of Cocaine-Associated Chest Pain and Myocardial Infarction (Circulation); McCord J, et al. Management of Cocaine-Associated Chest Pain and Myocardial Infarction: AHA Scientific Statement. Circulation 2008;117(14):1897-1907.</div></div></div> [[Start another case->Hub]] [[Restart this case->Cocaine chest pain - Opening]] [[Next case →->Exercise stress test - Ix]]

<span class="ec-case-marker" hidden data-entry="Cocaine chest pain. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ The right drug for a different patient.</div> For an ordinary ACS, an early beta-blocker would be reasonable. Here, blocking beta receptors while cocaine keeps stimulating alpha receptors risks worsening coronary vasoconstriction and a further rise in blood pressure, the unopposed alpha phenomenon. His pressure climbs and the pain does not improve. <div class="ec-teach"><div class="th">Where the reasoning went wrong, with an honest caveat</div> The cocaine history is the disambiguating detail. ACC/AHA guidance recommends against beta-blockers in cocaine-precipitated MI, and experimental models show beta-blockade worsens coronary vasoconstriction. The selective beta-1 blocker esmolol raised blood pressure in up to a quarter of patients studied. <br><br>Be aware the evidence is genuinely contested: several recent retrospective studies and meta-analyses found no increase in adverse outcomes with beta-blockers in cocaine users, and the "absolute contraindication" rests on limited, inconsistent clinical data. Labetalol is sometimes proposed as an alternative, but the AHA statement notes it offers no clear advantage and did not reverse coronary vasoconstriction in humans. For exam purposes and the AHA scientific statement on cocaine-associated chest pain, benzodiazepines and nitrates come first. <div class="ec-src"><b>Source:</b> AHA Scientific Statement (Circulation); Richards JR, et al. J Cardiovasc Pharmacol Ther 2017;22:239–249; Lo KB, et al. Am J Med 2019;132:505–509.</div></div></div> [[Try this question again->Cocaine chest pain - Opening]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 11:30</div> A 41-year-old woman has 4 days of fatigue, confusion and a petechial rash. She takes no medications. Hemoglobin is 7.9 g/dL, platelet count is 11,000/mm3, and the blood film shows numerous schistocytes. Lactate dehydrogenase is 1,840 U/L and haptoglobin is undetectable. Prothrombin time and activated partial thromboplastin time are normal. Creatinine is 1.4 mg/dL. Direct antiglobulin test is negative. <span class="ec-prompt">Which of the following is the most likely diagnosis?</span> [[Disseminated intravascular coagulation->TTP - Dx disseminated]] [[Evans syndrome->TTP - Dx evans]] [[Hemolytic uremic syndrome->TTP - Dx hemolytic]] [[Immune thrombocytopenic purpura->TTP - Dx immune]] [[Thrombotic thrombocytopenic purpura->TTP - Dx correct]]

<span class="ec-case-marker" hidden data-entry="TTP. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Disseminated intravascular coagulation does not fit.</div> Consumptive coagulopathy also gives schistocytes and thrombocytopenia, which makes it the closest alternative. It prolongs the prothrombin and partial thromboplastin times, consumes fibrinogen and raises D-dimer, and it occurs in a recognizable clinical context such as sepsis or malignancy. Her clotting times are normal. <div class="ec-teach"><div class="th">What the findings actually point to</div> Microangiopathic hemolysis with schistocytes, severe thrombocytopenia, neurologic change and only mild renal impairment, with normal coagulation times, is thrombotic thrombocytopenic purpura. Normal clotting is the finding that separates it from consumptive coagulopathy. <div class="ec-src"><b>Source:</b> Zheng XL, et al. ISTH guidelines for the diagnosis of thrombotic thrombocytopenic purpura. J Thromb Haemost 2020;18(10):2486-2495.</div></div></div> [[Try this question again->TTP - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="TTP. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Evans syndrome does not fit.</div> Evans syndrome combines autoimmune hemolysis with immune thrombocytopenia. The hemolysis is antibody-mediated, so the direct antiglobulin test is positive and the film shows spherocytes rather than schistocytes. <div class="ec-teach"><div class="th">What the findings actually point to</div> Microangiopathic hemolysis with schistocytes, severe thrombocytopenia, neurologic change and only mild renal impairment, with normal coagulation times, is thrombotic thrombocytopenic purpura. Normal clotting is the finding that separates it from consumptive coagulopathy. <div class="ec-src"><b>Source:</b> Zheng XL, et al. ISTH guidelines for the diagnosis of thrombotic thrombocytopenic purpura. J Thromb Haemost 2020;18(10):2486-2495.</div></div></div> [[Try this question again->TTP - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="TTP. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Hemolytic uremic syndrome does not fit.</div> Hemolytic uremic syndrome shares the microangiopathy but is dominated by acute kidney injury, usually follows a diarrheal illness, and is far more common in children. Her renal impairment is mild and neurologic features predominate. <div class="ec-teach"><div class="th">What the findings actually point to</div> Microangiopathic hemolysis with schistocytes, severe thrombocytopenia, neurologic change and only mild renal impairment, with normal coagulation times, is thrombotic thrombocytopenic purpura. Normal clotting is the finding that separates it from consumptive coagulopathy. <div class="ec-src"><b>Source:</b> Zheng XL, et al. ISTH guidelines for the diagnosis of thrombotic thrombocytopenic purpura. J Thromb Haemost 2020;18(10):2486-2495.</div></div></div> [[Try this question again->TTP - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="TTP. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Immune thrombocytopenia gives isolated severe thrombocytopenia with an otherwise normal blood count and film. It does not cause hemolysis, schistocytes, a raised lactate dehydrogenase or an undetectable haptoglobin. <div class="ec-teach"><div class="th">What the findings actually point to</div> Microangiopathic hemolysis with schistocytes, severe thrombocytopenia, neurologic change and only mild renal impairment, with normal coagulation times, is thrombotic thrombocytopenic purpura. Normal clotting is the finding that separates it from consumptive coagulopathy. <div class="ec-src"><b>Source:</b> Zheng XL, et al. ISTH guidelines for the diagnosis of thrombotic thrombocytopenic purpura. J Thromb Haemost 2020;18(10):2486-2495.</div></div></div> [[Try this question again->TTP - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="TTP. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Thrombotic thrombocytopenic purpura.</div> Microangiopathic hemolysis with schistocytes, severe thrombocytopenia, neurologic change and only mild renal impairment, with normal coagulation times, is thrombotic thrombocytopenic purpura. Normal clotting is the finding that separates it from consumptive coagulopathy. The lactate dehydrogenase of 1,840 U/L and undetectable haptoglobin confirm intravascular hemolysis, and a negative direct antiglobulin test excludes an immune cause. <div class="ec-src"><b>Source:</b> Zheng XL, et al. ISTH guidelines for the diagnosis of thrombotic thrombocytopenic purpura. J Thromb Haemost 2020;18(10):2486-2495.</div></div> [[Start another case->Hub]] [[Restart this case->TTP - Dx]] [[Next case →->Myeloma light chains - Ix]]

<div class="ec-scene">Emergency department · 06:50</div> A 71-year-old woman is brought in during a cold spell after her neighbor found her unresponsive. She has a well-healed anterior neck scar. Temperature is 32.4°C, blood pressure is 92/56 mm Hg, pulse is 46/min, and respirations are 8/min. She is obtunded with non-pitting swelling of the face and hands, dry coarse skin, and delayed relaxation of the ankle reflexes. Sodium is 121 mEq/L, glucose 58 mg/dL, and arterial carbon dioxide tension is raised. She is not on any medication her neighbor knows of. <span class="ec-prompt">Which of the following is the most likely diagnosis?</span> [[Accidental hypothermia->Myxedema coma - Dx accidental]] [[Adrenal crisis->Myxedema coma - Dx adrenal]] [[Myxedema coma->Myxedema coma - Dx correct]] [[Sedative overdose->Myxedema coma - Dx sedative]] [[Sepsis->Myxedema coma - Dx sepsis]]

<span class="ec-case-marker" hidden data-entry="Myxedema coma. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Accidental hypothermia does not fit.</div> Environmental hypothermia is the obvious alternative given the cold spell and would explain the temperature and bradycardia. It does not explain the thyroidectomy scar, the myxedematous swelling, the hyponatremia with hypoglycemia, or the delayed reflex relaxation. <div class="ec-teach"><div class="th">What the findings actually point to</div> Hypothermia, bradycardia, hypoventilation with carbon dioxide retention, hyponatremia, hypoglycemia and depressed consciousness in a patient with a thyroidectomy scar and non-pitting myxedematous swelling is decompensated hypothyroidism. Delayed relaxation of the reflexes is the physical sign that points hardest at it, and cold exposure is a classic precipitant. <div class="ec-src"><b>Source:</b> Jonklaas J, et al. ATA Guidelines for the Treatment of Hypothyroidism. Thyroid 2014;24(12):1670-1751.</div></div></div> [[Try this question again->Myxedema coma - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Myxedema coma. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Adrenal crisis does not fit.</div> This also gives hypotension, hyponatremia and hypoglycemia and genuinely coexists in some patients, which is why glucocorticoid is given before thyroid hormone. It does not produce hypothermia this profound, bradycardia, non-pitting myxedema or delayed reflex relaxation. <div class="ec-teach"><div class="th">What the findings actually point to</div> Hypothermia, bradycardia, hypoventilation with carbon dioxide retention, hyponatremia, hypoglycemia and depressed consciousness in a patient with a thyroidectomy scar and non-pitting myxedematous swelling is decompensated hypothyroidism. Delayed relaxation of the reflexes is the physical sign that points hardest at it, and cold exposure is a classic precipitant. <div class="ec-src"><b>Source:</b> Jonklaas J, et al. ATA Guidelines for the Treatment of Hypothyroidism. Thyroid 2014;24(12):1670-1751.</div></div></div> [[Try this question again->Myxedema coma - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Myxedema coma. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Myxedema coma.</div> Hypothermia, bradycardia, hypoventilation with carbon dioxide retention, hyponatremia, hypoglycemia and depressed consciousness in a patient with a thyroidectomy scar and non-pitting myxedematous swelling is decompensated hypothyroidism. Delayed relaxation of the reflexes is the physical sign that points hardest at it, and cold exposure is a classic precipitant. <div class="ec-src"><b>Source:</b> Jonklaas J, et al. ATA Guidelines for the Treatment of Hypothyroidism. Thyroid 2014;24(12):1670-1751.</div></div> [[Start another case->Hub]] [[Restart this case->Myxedema coma - Dx]] [[Next case →->Graves TRAb - Ix]]

<span class="ec-case-marker" hidden data-entry="Myxedema coma. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Sedative overdose does not fit.</div> Sedative or opioid toxicity would explain the depressed consciousness and hypoventilation, and is worth excluding. It does not cause hypothermia to 32°C with bradycardia, hyponatremia and myxedematous skin changes, and her neighbor reports no medications. <div class="ec-teach"><div class="th">What the findings actually point to</div> Hypothermia, bradycardia, hypoventilation with carbon dioxide retention, hyponatremia, hypoglycemia and depressed consciousness in a patient with a thyroidectomy scar and non-pitting myxedematous swelling is decompensated hypothyroidism. Delayed relaxation of the reflexes is the physical sign that points hardest at it, and cold exposure is a classic precipitant. <div class="ec-src"><b>Source:</b> Jonklaas J, et al. ATA Guidelines for the Treatment of Hypothyroidism. Thyroid 2014;24(12):1670-1751.</div></div></div> [[Try this question again->Myxedema coma - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Myxedema coma. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Sepsis does not fit.</div> Infection is a common precipitant of this presentation and should be sought, so it is a reasonable thought. Sepsis usually gives fever or a lesser degree of hypothermia with tachycardia and vasodilation, not bradycardia at 46/min. <div class="ec-teach"><div class="th">What the findings actually point to</div> Hypothermia, bradycardia, hypoventilation with carbon dioxide retention, hyponatremia, hypoglycemia and depressed consciousness in a patient with a thyroidectomy scar and non-pitting myxedematous swelling is decompensated hypothyroidism. Delayed relaxation of the reflexes is the physical sign that points hardest at it, and cold exposure is a classic precipitant. <div class="ec-src"><b>Source:</b> Jonklaas J, et al. ATA Guidelines for the Treatment of Hypothyroidism. Thyroid 2014;24(12):1670-1751.</div></div></div> [[Try this question again->Myxedema coma - Dx]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 15:10</div> An 8-year-old boy with known asthma is brought in after 2 days of worsening cough and wheeze despite regular albuterol at home. He is sitting forward, speaking in single words, with marked subcostal and intercostal recession and tracheal tug. Respirations are 42/min and oxygen saturation is 90% on room air. There is loud expiratory wheeze throughout. He weighs 26 kg. He has been admitted twice before, once to intensive care. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Intravenous aminophylline with nebulized bronchodilators->Status asthmaticus - Aminophylline trap]] [[Intravenous magnesium sulfate as initial treatment->Status asthmaticus - Mag first]] [[Nebulized albuterol, ipratropium, corticosteroids, oxygen->Status asthmaticus - Initial correct]] [[Oral corticosteroids alone->Status asthmaticus - Oral only trap]] [[Supplemental oxygen with a benzodiazepine for anxiety->Status asthmaticus - Sedation trap]]

<span class="ec-case-marker" hidden data-entry="Status asthmaticus. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Standard therapy once, withdrawn on the evidence.</div> Methylxanthines were used in acute asthma for decades, which is why they still appear plausible. Trials show no additional benefit when added to inhaled beta-2 agonists and corticosteroids, with significantly more vomiting, tremor and arrhythmia, and a narrow therapeutic window requiring level monitoring. They are specifically listed among therapies to avoid. <div class="ec-teach"><div class="th">Why this is wrong</div> High-dose inhaled beta-2 agonist with ipratropium, systemic corticosteroids and oxygen, given together with weight-based dosing. Magnesium is the adjunct for refractory cases. Avoid theophylline, sedatives, mucolytics and chest physiotherapy. <div class="ec-src"><b>Source:</b> GINA 2024 Global Strategy for Asthma Management and Prevention; Mitra AAD, et al. Intravenous aminophylline for acute severe asthma in children over two years receiving inhaled bronchodilators. Cochrane Database Syst Rev 2005;(2):CD001276.</div></div></div> [[Try this question again->Status asthmaticus - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Status asthmaticus. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ A useful adjunct promoted to first-line.</div> Magnesium has a real role in severe asthma and appears later in this algorithm, but it is an adjunct for exacerbations refractory to initial therapy, not the opening move. Giving it first delays the bronchodilators and steroids that do the work. Magnesium is used in children too, at weight-based dosing, and in the same refractory position in the algorithm. <div class="ec-teach"><div class="th">Where this breaks down</div> Initial management is high-dose inhaled beta-2 agonist with ipratropium, systemic corticosteroids and oxygen, given together. IV magnesium is added for severe or refractory cases. <div class="ec-src"><b>Source:</b> GINA 2024 Global Strategy for Asthma Management and Prevention.</div></div></div> [[Try this question again->Status asthmaticus - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Status asthmaticus. Opening"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Nebulized albuterol, ipratropium, corticosteroids, oxygen</div> Continuous nebulized albuterol with ipratropium runs alongside systemic corticosteroids and supplemental oxygen, all started simultaneously rather than in sequence. <div class="ec-teach"><div class="th">The initial bundle</div> Severe exacerbation is treated with high-dose inhaled beta-2 agonists plus ipratropium, systemic corticosteroids and oxygen, started together, the same bundle in children as in adults, with weight-based dosing. A prior intensive care admission marks him as high risk for a fatal attack. In children a silent chest, drowsiness or a falling respiratory rate signals exhaustion rather than improvement. Therapies to <b>avoid</b> because risk outweighs benefit include theophylline, aminophylline, mucolytics, sedatives, and chest physiotherapy. <br><br><b>Then:</b> <b>The gas:</b> asthma exacerbations start with a low PCO2 from hyperventilation. A "false-normal" PCO2 means ventilation has fallen from that hyperventilating baseline, a serious sign of respiratory muscle fatigue and impending failure. <br><br><b>The chest:</b> a quiet or silent chest does not mean the bronchospasm resolved; it means he can no longer move enough air to generate a wheeze. Together with drowsiness and a weakening effort, these signal imminent respiratory arrest. IV magnesium is added for refractory cases, and intubation should not be delayed once indicated.<div class="ec-src"><b>Source:</b> GINA 2024 Global Strategy for Asthma Management and Prevention.</div></div></div> <b>Escalated in time → ICU.</b> [[Start another case->Hub]] [[Restart this case->Status asthmaticus - Opening]] [[Next case →->Asthma ICS - Rx]]

<span class="ec-case-marker" hidden data-entry="Status asthmaticus. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Too little, too slowly.</div> Steroids are essential but take hours to work, and he needs bronchodilation now. A child speaking in single words with recession and tracheal tug cannot wait an hour for reassessment. <div class="ec-teach"><div class="th">Where this breaks down</div> Severe exacerbations require immediate high-dose inhaled bronchodilators with ipratropium and oxygen alongside systemic corticosteroids, not corticosteroids alone with delayed reassessment. <div class="ec-src"><b>Source:</b> GINA 2024 Global Strategy for Asthma Management and Prevention.</div></div></div> [[Try this question again->Status asthmaticus - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Status asthmaticus. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ This suppresses the only thing keeping him ventilated.</div> His respiratory drive is the compensation holding him together. Sedating him blunts it, worsens hypercapnia, and can precipitate respiratory arrest in an airway that is already critically obstructed. Children compensate well and then decompensate abruptly, so the margin here is narrower than it looks. <div class="ec-teach"><div class="th">The trap</div> Sedatives are specifically listed among therapies to avoid in acute asthma. Treat the bronchospasm; do not suppress the respiratory drive. <div class="ec-src"><b>Source:</b> GINA 2024 Global Strategy for Asthma Management and Prevention.</div></div></div> [[Try this question again->Status asthmaticus - Opening]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 13:20</div> A 74-year-old woman with atrial fibrillation, not taking anticoagulation, has 3 hours of severe, poorly localized central abdominal pain. She has vomited twice. The pain is far more severe than the examination suggests, her abdomen is soft with only minimal tenderness and no guarding. Lactate is 4.6 mmol/L and the leukocyte count is 19,400/mm3. <span class="ec-prompt">Which of the following is the most likely diagnosis?</span> [[Acute mesenteric ischemia->Mesenteric ischemia - Dx correct]] [[Perforated peptic ulcer->Mesenteric ischemia - Dx perforated]] [[Ruptured abdominal aortic aneurysm->Mesenteric ischemia - Dx ruptured]] [[Sigmoid diverticulitis->Mesenteric ischemia - Dx sigmoid]] [[Small-bowel obstruction->Mesenteric ischemia - Dx small-bowel]]

<span class="ec-case-marker" hidden data-entry="Mesenteric ischemia. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Acute mesenteric ischemia.</div> Pain out of proportion to a soft abdomen, in a patient with atrial fibrillation and no anticoagulation, with a raised lactate, is embolic mesenteric ischemia until proven otherwise. The examination stays deceptively benign until transmural infarction and peritonitis develop, by which point mortality is very high. <div class="ec-src"><b>Source:</b> Bala M, et al. Acute mesenteric ischemia: WSES guidelines. World J Emerg Surg 2017;12:38.</div></div> [[Start another case->Hub]] [[Restart this case->Mesenteric ischemia - Dx]] [[Next case →->Acute appendicitis - Rx]]

<span class="ec-case-marker" hidden data-entry="Mesenteric ischemia. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Perforated peptic ulcer does not fit.</div> Perforation produces sudden pain with a rigid abdomen, board-like guarding and free air under the diaphragm. Her abdomen is soft, which is the opposite of the expected finding. <div class="ec-teach"><div class="th">What the findings actually point to</div> Pain out of proportion to a soft abdomen, in a patient with atrial fibrillation and no anticoagulation, with a raised lactate, is embolic mesenteric ischemia until proven otherwise. The examination stays deceptively benign until transmural infarction and peritonitis develop, by which point mortality is very high. <div class="ec-src"><b>Source:</b> Bala M, et al. Acute mesenteric ischemia: WSES guidelines. World J Emerg Surg 2017;12:38.</div></div></div> [[Try this question again->Mesenteric ischemia - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Mesenteric ischemia. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Ruptured abdominal aortic aneurysm does not fit.</div> Rupture gives abdominal or back pain with hypotension and often a pulsatile mass. She is tachycardic but the presentation lacks the hemodynamic collapse and the atrial fibrillation points to embolism. <div class="ec-teach"><div class="th">What the findings actually point to</div> Pain out of proportion to a soft abdomen, in a patient with atrial fibrillation and no anticoagulation, with a raised lactate, is embolic mesenteric ischemia until proven otherwise. The examination stays deceptively benign until transmural infarction and peritonitis develop, by which point mortality is very high. <div class="ec-src"><b>Source:</b> Bala M, et al. Acute mesenteric ischemia: WSES guidelines. World J Emerg Surg 2017;12:38.</div></div></div> [[Try this question again->Mesenteric ischemia - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Mesenteric ischemia. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Sigmoid diverticulitis does not fit.</div> Diverticulitis gives left lower quadrant pain with localized tenderness and fever, developing over days. The pain here is central, sudden, and out of proportion to a soft abdomen. <div class="ec-teach"><div class="th">What the findings actually point to</div> Pain out of proportion to a soft abdomen, in a patient with atrial fibrillation and no anticoagulation, with a raised lactate, is embolic mesenteric ischemia until proven otherwise. The examination stays deceptively benign until transmural infarction and peritonitis develop, by which point mortality is very high. <div class="ec-src"><b>Source:</b> Bala M, et al. Acute mesenteric ischemia: WSES guidelines. World J Emerg Surg 2017;12:38.</div></div></div> [[Try this question again->Mesenteric ischemia - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Mesenteric ischemia. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Small-bowel obstruction does not fit.</div> Obstruction gives colicky pain with distension, vomiting and absent flatus, with dilated loops on imaging. Vomiting is present, but the disproportionate pain and the raised lactate with an embolic source point to ischemia. <div class="ec-teach"><div class="th">What the findings actually point to</div> Pain out of proportion to a soft abdomen, in a patient with atrial fibrillation and no anticoagulation, with a raised lactate, is embolic mesenteric ischemia until proven otherwise. The examination stays deceptively benign until transmural infarction and peritonitis develop, by which point mortality is very high. <div class="ec-src"><b>Source:</b> Bala M, et al. Acute mesenteric ischemia: WSES guidelines. World J Emerg Surg 2017;12:38.</div></div></div> [[Try this question again->Mesenteric ischemia - Dx]] [[Start another case->Hub]]

<div class="ec-scene">Labor and delivery unit · 02:50</div> A 31-year-old woman at 32 weeks in her third pregnancy has painless bright red vaginal bleeding that began an hour ago and is now slowing. The uterus is soft and non-tender. She is hemodynamically stable and the fetal heart rate tracing is reassuring. She had a cesarean delivery 2 years ago. No vaginal examination has been performed. <span class="ec-prompt">Which of the following is the most appropriate next step in diagnosis?</span> [[Digital cervical examination to assess dilation->Placenta previa - Ix D1]] [[Kleihauer-Betke test for fetomaternal hemorrhage->Placenta previa - Ix D3]] [[MRI of the pelvis to characterize placental location->Placenta previa - Ix D4]] [[Speculum examination to inspect the cervix->Placenta previa - Ix D2]] [[Transabdominal, then transvaginal ultrasound->Placenta previa - Ix correct]]

<span class="ec-case-marker" hidden data-entry="Placenta previa. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This is the one examination that is contraindicated. With the placenta over the os, a finger can disrupt placental vessels and convert slowing bleeding into catastrophic hemorrhage. <div class="ec-teach"><div class="th">What the findings point to</div> Imaging locates the placenta before any internal examination, and that answer determines everything downstream. Transvaginal scanning is safe in previa, the probe sits in the anterior fornix and does not enter the cervix, and is substantially more accurate than the transabdominal view, particularly for a posterior placenta. <div class="ec-src"><b>Source:</b> SMFM Consult Series: Placenta previa; ACOG Practice Bulletin No. 232: Placenta Accreta Spectrum.</div></div></div> [[Try this question again->Placenta previa - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Placenta previa. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This quantifies fetomaternal hemorrhage and is genuinely relevant, if she is Rh(D)-negative she may need additional anti-D immune globulin. It does not locate the placenta or determine immediate management. <div class="ec-teach"><div class="th">What the findings point to</div> Imaging locates the placenta before any internal examination, and that answer determines everything downstream. Transvaginal scanning is safe in previa, the probe sits in the anterior fornix and does not enter the cervix, and is substantially more accurate than the transabdominal view, particularly for a posterior placenta. <div class="ec-src"><b>Source:</b> SMFM Consult Series: Placenta previa; ACOG Practice Bulletin No. 232: Placenta Accreta Spectrum.</div></div></div> [[Try this question again->Placenta previa - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Placenta previa. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> She has a prior cesarean with possible previa, so accreta is a real concern and MRI has a role in equivocal cases. Ultrasonography is the first-line study for both previa and accreta, and MRI is not an acute investigation. <div class="ec-teach"><div class="th">What the findings point to</div> Imaging locates the placenta before any internal examination, and that answer determines everything downstream. Transvaginal scanning is safe in previa, the probe sits in the anterior fornix and does not enter the cervix, and is substantially more accurate than the transabdominal view, particularly for a posterior placenta. <div class="ec-src"><b>Source:</b> SMFM Consult Series: Placenta previa; ACOG Practice Bulletin No. 232: Placenta Accreta Spectrum.</div></div></div> [[Try this question again->Placenta previa - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Placenta previa. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A speculum examination is lower risk than a digital one and is performed once placental location is known, which makes it the closest wrong answer. Before imaging, any instrumentation carries risk and it does not answer the question that matters. <div class="ec-teach"><div class="th">What the findings point to</div> Imaging locates the placenta before any internal examination, and that answer determines everything downstream. Transvaginal scanning is safe in previa, the probe sits in the anterior fornix and does not enter the cervix, and is substantially more accurate than the transabdominal view, particularly for a posterior placenta. <div class="ec-src"><b>Source:</b> SMFM Consult Series: Placenta previa; ACOG Practice Bulletin No. 232: Placenta Accreta Spectrum.</div></div></div> [[Try this question again->Placenta previa - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Placenta previa. Ix"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Transabdominal, then transvaginal ultrasound</div> Imaging locates the placenta before any internal examination, and that answer determines everything downstream. Transvaginal scanning is safe in previa, the probe sits in the anterior fornix and does not enter the cervix, and is substantially more accurate than the transabdominal view, particularly for a posterior placenta. <div class="ec-src"><b>Source:</b> SMFM Consult Series: Placenta previa; ACOG Practice Bulletin No. 232: Placenta Accreta Spectrum.</div></div> [[Start another case->Hub]] [[Restart this case->Placenta previa - Ix]] [[Next case →->Placental abruption - Dx]]

<div class="ec-scene">Emergency department · 18:05</div> A 46-year-old man develops headache, dyspnea and dizziness 2 hours after a transesophageal echocardiogram during which benzocaine spray was used. He is centrally cyanotic with a slate-gray discoloration. Pulse oximetry reads 85% and does not rise despite high-flow oxygen. Arterial oxygen tension is 280 mm Hg. A drawn blood sample appears chocolate brown and does not redden on exposure to air. The chest is clear. <span class="ec-prompt">Which of the following is the most likely diagnosis?</span> [[Carbon monoxide poisoning->Methemoglobinemia - Dx D1]] [[Cardiac shunt with right-to-left flow->Methemoglobinemia - Dx D4]] [[Methemoglobinemia->Methemoglobinemia - Dx correct]] [[Pulmonary embolism->Methemoglobinemia - Dx D2]] [[Sulfhemoglobinemia->Methemoglobinemia - Dx D3]]

<span class="ec-case-marker" hidden data-entry="Methemoglobinemia. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This is the other dyshemoglobinemia with a falsely reassuring oxygen tension, so it is the closest alternative. Carboxyhemoglobin drives the oximeter toward falsely high readings near 100% rather than a plateau at 85%, causes cherry-red rather than slate-gray discoloration, and has no link to benzocaine. <div class="ec-teach"><div class="th">What the findings point to</div> Cyanosis unresponsive to oxygen, a pulse oximeter stuck near 85% while the arterial oxygen tension is high, chocolate-brown blood that does not redden in air, and a recent oxidizing exposure, benzocaine is a classic precipitant. The saturation gap between oximetry and the calculated value is the diagnostic signature. <div class="ec-src"><b>Source:</b> Wright RO, Lewander WJ, Woolf AD. Methemoglobinemia: etiology, pharmacology, and clinical management. Ann Emerg Med 1999;34(5):646-656.</div></div></div> [[Try this question again->Methemoglobinemia - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Methemoglobinemia. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A shunt causes cyanosis that does not correct fully with oxygen, and this followed a cardiac procedure. It would not give an arterial oxygen tension of 280 mm Hg or chocolate-brown blood. <div class="ec-teach"><div class="th">What the findings point to</div> Cyanosis unresponsive to oxygen, a pulse oximeter stuck near 85% while the arterial oxygen tension is high, chocolate-brown blood that does not redden in air, and a recent oxidizing exposure, benzocaine is a classic precipitant. The saturation gap between oximetry and the calculated value is the diagnostic signature. <div class="ec-src"><b>Source:</b> Wright RO, Lewander WJ, Woolf AD. Methemoglobinemia: etiology, pharmacology, and clinical management. Ann Emerg Med 1999;34(5):646-656.</div></div></div> [[Try this question again->Methemoglobinemia - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Methemoglobinemia. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Methemoglobinemia.</div> Cyanosis unresponsive to oxygen, a pulse oximeter stuck near 85% while the arterial oxygen tension is high, chocolate-brown blood that does not redden in air, and a recent oxidizing exposure, benzocaine is a classic precipitant. The saturation gap between oximetry and the calculated value is the diagnostic signature. <div class="ec-src"><b>Source:</b> Wright RO, Lewander WJ, Woolf AD. Methemoglobinemia: etiology, pharmacology, and clinical management. Ann Emerg Med 1999;34(5):646-656.</div></div> [[Start another case->Hub]] [[Restart this case->Methemoglobinemia - Dx]] [[Next case →->Carbon monoxide - Dx]]

<span class="ec-case-marker" hidden data-entry="Methemoglobinemia. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Embolism causes acute dyspnea and hypoxemia, but the arterial oxygen tension would be low rather than 280 mm Hg, and cyanosis would improve with oxygen. <div class="ec-teach"><div class="th">What the findings point to</div> Cyanosis unresponsive to oxygen, a pulse oximeter stuck near 85% while the arterial oxygen tension is high, chocolate-brown blood that does not redden in air, and a recent oxidizing exposure, benzocaine is a classic precipitant. The saturation gap between oximetry and the calculated value is the diagnostic signature. <div class="ec-src"><b>Source:</b> Wright RO, Lewander WJ, Woolf AD. Methemoglobinemia: etiology, pharmacology, and clinical management. Ann Emerg Med 1999;34(5):646-656.</div></div></div> [[Try this question again->Methemoglobinemia - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Methemoglobinemia. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This genuinely mimics methemoglobinemia with cyanosis and a low oximeter reading and can follow similar drug exposures, which is why it belongs here. It is far rarer, is distinguished on co-oximetry, and does not respond to methylene blue. <div class="ec-teach"><div class="th">What the findings point to</div> Cyanosis unresponsive to oxygen, a pulse oximeter stuck near 85% while the arterial oxygen tension is high, chocolate-brown blood that does not redden in air, and a recent oxidizing exposure, benzocaine is a classic precipitant. The saturation gap between oximetry and the calculated value is the diagnostic signature. <div class="ec-src"><b>Source:</b> Wright RO, Lewander WJ, Woolf AD. Methemoglobinemia: etiology, pharmacology, and clinical management. Ann Emerg Med 1999;34(5):646-656.</div></div></div> [[Try this question again->Methemoglobinemia - Dx]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 03:30</div> A 4-year-old girl has 6 hours of fever, refusal to swallow and a muffled voice. She sits upright leaning forward on her hands, drooling, with inspiratory stridor and an anxious quiet expression, and will not lie down. There is no barking cough and no coryzal prodrome. Her immunization record shows no Haemophilus influenzae type b doses. <span class="ec-prompt">Which of the following is the most likely diagnosis?</span> [[Acute epiglottitis->Epiglottitis - Dx correct]] [[Bacterial tracheitis->Epiglottitis - Dx D3]] [[Croup->Epiglottitis - Dx D1]] [[Foreign body aspiration->Epiglottitis - Dx D4]] [[Retropharyngeal abscess->Epiglottitis - Dx D2]]

<span class="ec-case-marker" hidden data-entry="Epiglottitis. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Acute epiglottitis.</div> Rapid onset over hours with high fever, drooling, refusal to swallow, a muffled voice and the tripod posture, without a barking cough, in an unimmunized child. The absence of a viral prodrome and of the barking cough is what separates it from the far commoner alternative, and Hib immunization status makes it plausible in the modern era. <div class="ec-src"><b>Source:</b> AAP Red Book, Haemophilus influenzae type b infections.</div></div> [[Start another case->Hub]] [[Restart this case->Epiglottitis - Dx]] [[Next case →->Aspirin-exacerbated respiratory disease - Mech]]

<span class="ec-case-marker" hidden data-entry="Epiglottitis. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Tracheitis produces high fever with stridor and toxicity and can be difficult to distinguish, but it typically follows a viral illness, gives a brassy cough with copious purulent secretions, and drooling is not prominent. <div class="ec-teach"><div class="th">What the findings point to</div> Rapid onset over hours with high fever, drooling, refusal to swallow, a muffled voice and the tripod posture, without a barking cough, in an unimmunized child. The absence of a viral prodrome and of the barking cough is what separates it from the far commoner alternative, and Hib immunization status makes it plausible in the modern era. <div class="ec-src"><b>Source:</b> AAP Red Book, Haemophilus influenzae type b infections.</div></div></div> [[Try this question again->Epiglottitis - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Epiglottitis. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Croup is far commoner and is the reflex answer to a child with stridor, which is what makes it the key alternative. It follows a coryzal prodrome, gives a barking cough and hoarse voice rather than a muffled one, and the child will lie down and is not drooling. <div class="ec-teach"><div class="th">What the findings point to</div> Rapid onset over hours with high fever, drooling, refusal to swallow, a muffled voice and the tripod posture, without a barking cough, in an unimmunized child. The absence of a viral prodrome and of the barking cough is what separates it from the far commoner alternative, and Hib immunization status makes it plausible in the modern era. <div class="ec-src"><b>Source:</b> AAP Red Book, Haemophilus influenzae type b infections.</div></div></div> [[Try this question again->Epiglottitis - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Epiglottitis. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Aspiration causes sudden stridor in a previously well child, without fever, and belongs in the differential at this age. Her fever, drooling and progressive 6-hour course do not fit. <div class="ec-teach"><div class="th">What the findings point to</div> Rapid onset over hours with high fever, drooling, refusal to swallow, a muffled voice and the tripod posture, without a barking cough, in an unimmunized child. The absence of a viral prodrome and of the barking cough is what separates it from the far commoner alternative, and Hib immunization status makes it plausible in the modern era. <div class="ec-src"><b>Source:</b> AAP Red Book, Haemophilus influenzae type b infections.</div></div></div> [[Try this question again->Epiglottitis - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Epiglottitis. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This also causes fever, drooling and neck extension in a young child and belongs on the list. It usually evolves over days with neck stiffness and pain on neck movement rather than over hours. <div class="ec-teach"><div class="th">What the findings point to</div> Rapid onset over hours with high fever, drooling, refusal to swallow, a muffled voice and the tripod posture, without a barking cough, in an unimmunized child. The absence of a viral prodrome and of the barking cough is what separates it from the far commoner alternative, and Hib immunization status makes it plausible in the modern era. <div class="ec-src"><b>Source:</b> AAP Red Book, Haemophilus influenzae type b infections.</div></div></div> [[Try this question again->Epiglottitis - Dx]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 10:15</div> A 48-year-old woman has 12 hours of severe epigastric pain radiating to the back with vomiting. Lipase is 1,240 U/L. She drinks no alcohol. Bilirubin is 0.9 mg/dL, alkaline phosphatase is 180 U/L, AST is 62 U/L, and ALT is 58 U/L. She is hemodynamically stable with a soft abdomen and no fever. The diagnosis of acute pancreatitis is established clinically and biochemically. <span class="ec-prompt">Which of the following is the most appropriate next step in diagnosis?</span> [[Abdominal ultrasonography->Pancreatitis - Ix correct]] [[Contrast-enhanced CT of the abdomen now->Pancreatitis - Ix D1]] [[Endoscopic ultrasonography->Pancreatitis - Ix D2]] [[MRCP of the biliary tree->Pancreatitis - Ix D3]] [[Serum IgG4 and autoimmune markers->Pancreatitis - Ix D4]]

<span class="ec-case-marker" hidden data-entry="Pancreatitis. Ix"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Abdominal ultrasonography.</div> Ultrasonography is recommended in every patient with a first episode of acute pancreatitis, to identify gallstones, the commonest cause, and to assess the bile duct. The answer determines whether she needs cholecystectomy before discharge, which markedly reduces recurrence. <div class="ec-src"><b>Source:</b> Crockett SD, et al. AGA Institute Guideline on Initial Management of Acute Pancreatitis. Gastroenterology 2018;154(4):1096-1101.</div></div> [[Start another case->Hub]] [[Restart this case->Pancreatitis - Ix]] [[Next case →->Pancreatic insufficiency - Mech]]

<span class="ec-case-marker" hidden data-entry="Pancreatitis. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Computed tomography is genuinely important in pancreatitis, but for assessing necrosis and complications, and it is most informative after around 72 hours, performed on day one it commonly underestimates necrosis. It is indicated early only when the diagnosis is uncertain or the patient deteriorates. <div class="ec-teach"><div class="th">What the findings point to</div> Ultrasonography is recommended in every patient with a first episode of acute pancreatitis, to identify gallstones, the commonest cause, and to assess the bile duct. The answer determines whether she needs cholecystectomy before discharge, which markedly reduces recurrence. <div class="ec-src"><b>Source:</b> Crockett SD, et al. AGA Institute Guideline on Initial Management of Acute Pancreatitis. Gastroenterology 2018;154(4):1096-1101.</div></div></div> [[Try this question again->Pancreatitis - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Pancreatitis. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This is excellent for occult microlithiasis and is useful when transabdominal ultrasound is negative and no cause is found. It is a second-line study, not the first. <div class="ec-teach"><div class="th">What the findings point to</div> Ultrasonography is recommended in every patient with a first episode of acute pancreatitis, to identify gallstones, the commonest cause, and to assess the bile duct. The answer determines whether she needs cholecystectomy before discharge, which markedly reduces recurrence. <div class="ec-src"><b>Source:</b> Crockett SD, et al. AGA Institute Guideline on Initial Management of Acute Pancreatitis. Gastroenterology 2018;154(4):1096-1101.</div></div></div> [[Try this question again->Pancreatitis - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Pancreatitis. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> MRCP images the duct beautifully and is the right test when choledocholithiasis is suspected but unproven. Her bilirubin is normal and the duct has not yet been assessed by the simpler, faster, first-line study. <div class="ec-teach"><div class="th">What the findings point to</div> Ultrasonography is recommended in every patient with a first episode of acute pancreatitis, to identify gallstones, the commonest cause, and to assess the bile duct. The answer determines whether she needs cholecystectomy before discharge, which markedly reduces recurrence. <div class="ec-src"><b>Source:</b> Crockett SD, et al. AGA Institute Guideline on Initial Management of Acute Pancreatitis. Gastroenterology 2018;154(4):1096-1101.</div></div></div> [[Try this question again->Pancreatitis - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Pancreatitis. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Autoimmune pancreatitis is a real cause and worth pursuing when common causes are excluded and the course is atypical. It is not a first-line investigation in a first episode. <div class="ec-teach"><div class="th">What the findings point to</div> Ultrasonography is recommended in every patient with a first episode of acute pancreatitis, to identify gallstones, the commonest cause, and to assess the bile duct. The answer determines whether she needs cholecystectomy before discharge, which markedly reduces recurrence. <div class="ec-src"><b>Source:</b> Crockett SD, et al. AGA Institute Guideline on Initial Management of Acute Pancreatitis. Gastroenterology 2018;154(4):1096-1101.</div></div></div> [[Try this question again->Pancreatitis - Ix]] [[Start another case->Hub]]

<div class="ec-scene">Oncology ward · 08:00</div> A 19-year-old man with Burkitt lymphoma is 24 hours into his first cycle of chemotherapy. Uric acid is 14.2 mg/dL, potassium 6.1 mEq/L, phosphate 7.8 mg/dL, corrected calcium 6.6 mg/dL, and creatinine has risen from 0.9 to 2.6 mg/dL. He is asymptomatic. The physician plan to give rasburicase. <span class="ec-prompt">Which of the following is the most appropriate next step in diagnosis?</span> [[12-lead ECG to screen for hyperkalemic changes->Tumor lysis - Ix D1]] [[Glucose-6-phosphate dehydrogenase activity->Tumor lysis - Ix correct]] [[Renal ultrasonography->Tumor lysis - Ix D2]] [[Repeat uric acid in 6 hours->Tumor lysis - Ix D3]] [[Serum ionized calcium->Tumor lysis - Ix D5]]

<span class="ec-case-marker" hidden data-entry="Tumor lysis. Ix"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Glucose-6-phosphate dehydrogenase activity.</div> Rasburicase generates hydrogen peroxide as it degrades urate, and in G6PD deficiency this causes severe hemolysis and methemoglobinemia, the drug is contraindicated. Screening before administration is the check that makes the treatment safe, and it is the single test that could change the plan. <div class="ec-src"><b>Source:</b> Coiffier B, et al. Guidelines for the Management of Pediatric and Adult Tumor Lysis Syndrome. J Clin Oncol 2008;26(16):2767-2778.</div></div> [[Start another case->Hub]] [[Restart this case->Tumor lysis - Ix]] [[Next case →->TLS prophylaxis - Rx]]

<span class="ec-case-marker" hidden data-entry="Tumor lysis. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Obstruction from urate or calcium phosphate crystals is worth considering if he fails to respond, and imaging is reasonable then. His rising creatinine in this setting is explained by the syndrome itself. <div class="ec-teach"><div class="th">What the findings point to</div> Rasburicase generates hydrogen peroxide as it degrades urate, and in G6PD deficiency this causes severe hemolysis and methemoglobinemia, the drug is contraindicated. Screening before administration is the check that makes the treatment safe, and it is the single test that could change the plan. <div class="ec-src"><b>Source:</b> Coiffier B, et al. Guidelines for the Management of Pediatric and Adult Tumor Lysis Syndrome. J Clin Oncol 2008;26(16):2767-2778.</div></div></div> [[Try this question again->Tumor lysis - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Tumor lysis. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Waiting to see whether it climbs further, in a patient who already meets criteria for established tumor lysis with rising creatinine, spends time he does not have. <div class="ec-teach"><div class="th">What the findings point to</div> Rasburicase generates hydrogen peroxide as it degrades urate, and in G6PD deficiency this causes severe hemolysis and methemoglobinemia, the drug is contraindicated. Screening before administration is the check that makes the treatment safe, and it is the single test that could change the plan. <div class="ec-src"><b>Source:</b> Coiffier B, et al. Guidelines for the Management of Pediatric and Adult Tumor Lysis Syndrome. J Clin Oncol 2008;26(16):2767-2778.</div></div></div> [[Try this question again->Tumor lysis - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Tumor lysis. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Confirming true hypocalcemia is reasonable, but asymptomatic hypocalcemia in tumor lysis is deliberately left alone, giving calcium risks calcium phosphate precipitation in the kidney. <div class="ec-teach"><div class="th">What the findings point to</div> Rasburicase generates hydrogen peroxide as it degrades urate, and in G6PD deficiency this causes severe hemolysis and methemoglobinemia, the drug is contraindicated. Screening before administration is the check that makes the treatment safe, and it is the single test that could change the plan. <div class="ec-src"><b>Source:</b> Coiffier B, et al. Guidelines for the Management of Pediatric and Adult Tumor Lysis Syndrome. J Clin Oncol 2008;26(16):2767-2778.</div></div></div> [[Try this question again->Tumor lysis - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Tumor lysis. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> An ECG should be obtained, his potassium is 6.1 mEq/L and cardiac monitoring is part of management. It does not alter the decision about rasburicase, which is the drug about to be given. <div class="ec-teach"><div class="th">What the findings point to</div> Rasburicase generates hydrogen peroxide as it degrades urate, and in G6PD deficiency this causes severe hemolysis and methemoglobinemia, the drug is contraindicated. Screening before administration is the check that makes the treatment safe, and it is the single test that could change the plan. <div class="ec-src"><b>Source:</b> Coiffier B, et al. Guidelines for the Management of Pediatric and Adult Tumor Lysis Syndrome. J Clin Oncol 2008;26(16):2767-2778.</div></div></div> [[Try this question again->Tumor lysis - Ix]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 10:05</div> A 46-year-old man has 5 days of progressive weakness that began in his feet and has ascended to his thighs. He now struggles to climb stairs. He had a diarrheal illness 3 weeks ago. Examination shows symmetric flaccid weakness, worse distally, with absent deep tendon reflexes throughout and mild distal paresthesia but no sensory level. Bladder and bowel function are normal. Cerebrospinal fluid shows protein 96 mg/dL with 2 leukocytes/mm3. <span class="ec-prompt">Which of the following is the most likely diagnosis?</span> [[Acute transverse myelitis->Guillain-Barre - Dx acute]] [[Botulism->Guillain-Barre - Dx botulism]] [[Guillain-Barré syndrome->Guillain-Barre - Dx correct]] [[Myasthenia gravis->Guillain-Barre - Dx myasthenia]] [[Tick paralysis->Guillain-Barre - Dx tick]]

<span class="ec-case-marker" hidden data-entry="Guillain-Barre. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Acute transverse myelitis does not fit.</div> Myelitis gives a discrete sensory level, sphincter involvement, and reflexes that are typically increased once spinal shock passes. He has no sensory level and normal sphincters, which is the distinction that matters most because the imaging and treatment differ entirely. <div class="ec-teach"><div class="th">What the findings actually point to</div> Progressive symmetric ascending flaccid weakness with areflexia, following a diarrheal illness by one to 3 weeks, with albuminocytologic dissociation, raised cerebrospinal fluid protein and a normal cell count, is Guillain-Barré syndrome. Preserved sphincter function and the absence of a sensory level argue against a cord lesion. <div class="ec-src"><b>Source:</b> Willison HJ, Jacobs BC, van Doorn PA. Guillain-Barre syndrome. Lancet 2016;388(10045):717-727.</div></div></div> [[Try this question again->Guillain-Barre - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Guillain-Barre. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Botulism does not fit.</div> Botulism produces descending weakness beginning with cranial nerves, diplopia, ptosis, dysphagia, with fixed dilated pupils and prominent autonomic features. His weakness ascends and the cranial nerves are unaffected. <div class="ec-teach"><div class="th">What the findings actually point to</div> Progressive symmetric ascending flaccid weakness with areflexia, following a diarrheal illness by one to 3 weeks, with albuminocytologic dissociation, raised cerebrospinal fluid protein and a normal cell count, is Guillain-Barré syndrome. Preserved sphincter function and the absence of a sensory level argue against a cord lesion. <div class="ec-src"><b>Source:</b> Willison HJ, Jacobs BC, van Doorn PA. Guillain-Barre syndrome. Lancet 2016;388(10045):717-727.</div></div></div> [[Try this question again->Guillain-Barre - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Guillain-Barre. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Guillain-Barré syndrome.</div> Progressive symmetric ascending flaccid weakness with areflexia, following a diarrheal illness by one to 3 weeks, with albuminocytologic dissociation, raised cerebrospinal fluid protein and a normal cell count, is Guillain-Barré syndrome. Preserved sphincter function and the absence of a sensory level argue against a cord lesion. <div class="ec-src"><b>Source:</b> Willison HJ, Jacobs BC, van Doorn PA. Guillain-Barre syndrome. Lancet 2016;388(10045):717-727.</div></div> [[Start another case->Hub]] [[Restart this case->Guillain-Barre - Dx]] [[Next case →->MS MRI findings - Ix]]

<span class="ec-case-marker" hidden data-entry="Guillain-Barre. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Myasthenia gravis does not fit.</div> Myasthenia gives fatigable weakness that is worse with activity, prominently ocular and bulbar, with preserved reflexes and normal cerebrospinal fluid. His reflexes are absent and there is no diurnal fluctuation. <div class="ec-teach"><div class="th">What the findings actually point to</div> Progressive symmetric ascending flaccid weakness with areflexia, following a diarrheal illness by one to 3 weeks, with albuminocytologic dissociation, raised cerebrospinal fluid protein and a normal cell count, is Guillain-Barré syndrome. Preserved sphincter function and the absence of a sensory level argue against a cord lesion. <div class="ec-src"><b>Source:</b> Willison HJ, Jacobs BC, van Doorn PA. Guillain-Barre syndrome. Lancet 2016;388(10045):717-727.</div></div></div> [[Try this question again->Guillain-Barre - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Guillain-Barre. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Tick paralysis does not fit.</div> Tick paralysis genuinely mimics this with ascending flaccid weakness and areflexia, and is worth remembering because removing the tick is curative. Cerebrospinal fluid protein is normal in tick paralysis, and there is no antecedent diarrheal illness. <div class="ec-teach"><div class="th">What the findings actually point to</div> Progressive symmetric ascending flaccid weakness with areflexia, following a diarrheal illness by one to 3 weeks, with albuminocytologic dissociation, raised cerebrospinal fluid protein and a normal cell count, is Guillain-Barré syndrome. Preserved sphincter function and the absence of a sensory level argue against a cord lesion. <div class="ec-src"><b>Source:</b> Willison HJ, Jacobs BC, van Doorn PA. Guillain-Barre syndrome. Lancet 2016;388(10045):717-727.</div></div></div> [[Try this question again->Guillain-Barre - Dx]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 01:15</div> A 6-year-old boy is pulled from a house fire and arrives 25 minutes later. He has deep partial- and full-thickness burns over roughly 30% of his body surface, assessed using a Lund-Browder chart. His eyebrows and nasal hairs are singed, his voice is hoarse, and he is coughing black sputum. He weighs 21 kg and is currently maintaining his own airway. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Carboxyhemoglobin level; intubate only if elevated->Major burn - Carboxyhemoglobin trap]] [[Early intubation for inhalation injury, before edema->Major burn - Airway correct]] [[Intubate; calculate fluids by rule of nines->Major burn - Rule of nines trap]] [[Parkland fluids; defer the airway since he is breathing->Major burn - Fluids first trap]] [[Topical antibiotics and dressings->Major burn - Dressing trap]]

<span class="ec-case-marker" hidden data-entry="Major burn. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Wound care is not resuscitation.</div> Topical antimicrobials matter later, for infection prevention. They do nothing for an airway about to close or for the massive fluid shift already underway in a 30% burn. <div class="ec-teach"><div class="th">The trap</div> Follow the trauma sequence: airway, breathing, circulation, then fluid resuscitation, then wound care. Burn dressings do not come first. <div class="ec-src"><b>Source:</b> American Burn Association Advanced Burn Life Support Provider Manual, 2023.</div></div></div> [[Try this question again->Major burn - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Major burn. Opening"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Early intubation for inhalation injury, before edema</div> He is intubated early, while the anatomy is still normal. Fluid resuscitation and burn care follow immediately afterward. <div class="ec-teach"><div class="th">Why the airway cannot wait</div> Severely burned patients are trauma patients first, airway, breathing, circulation, then resuscitation. A child's airway is smaller in absolute terms, so the same degree of edema narrows it proportionally more, and the threshold for early intubation is correspondingly lower. Burn surface area in children is estimated with a Lund-Browder chart rather than the rule of nines, because the head accounts for a far greater proportion of surface area and the legs less. Add maintenance fluid containing dextrose to the resuscitation volume, since children have limited glycogen stores, and consider non-accidental injury where the pattern or history does not fit. Suspect inhalation injury with enclosed-space exposure, singed nasal hairs or eyebrows, carbonaceous sputum, hoarse voice, stridor, or facial burns. These patients are intubated <b>early</b>, because airway edema develops rapidly and late intubation becomes extremely difficult or impossible. Inhalation injury also raises fluid requirements roughly 30–50% above the calculated estimate. <br><br><b>Then:</b> Parkland is 4 mL × kg × %TBSA of <b>lactated Ringer's</b> (not normal saline, which causes hyperchloremic acidosis at these volumes) over 24 hours, half in the first 8 hours <b>from the time of injury, not arrival</b>. Count only partial- and full-thickness burns in the TBSA; exclude superficial burns. The formula is a starting estimate, titrate to urine output (0.5 mL/kg/h adults, 1 mL/kg/h children). <br><br>An honest note: field TBSA estimates routinely overshoot, and over-resuscitation causes real harm. Some burn centers now start at 2 mL/kg/%TBSA (Modified Brooke), also endorsed by the American Burn Association, precisely to reduce fluid creep.<div class="ec-src"><b>Source:</b> American Burn Association Advanced Burn Life Support Provider Manual, 2023; ABA transfer criteria.</div></div></div> <b>Resuscitated and transferred → burn center.</b> [[Start another case->Hub]] [[Restart this case->Major burn - Opening]] [[Next case →->Compartment syndrome - Ix]]

<span class="ec-case-marker" hidden data-entry="Major burn. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ The airway call is right, and the estimate is the wrong tool for a child.</div> Intubating early is correct, so this is the closest wrong answer available. The rule of nines is built on adult body proportions. In a 6-year-old the head is a far larger share of surface area and the legs a smaller one, so applying it here materially misestimates the burn and therefore the resuscitation volume. <div class="ec-teach"><div class="th">Why this is wrong</div> Intubate early, then estimate surface area with a Lund-Browder chart, which is age-adjusted. Add maintenance fluid containing dextrose to the resuscitation volume because children have limited glycogen stores, and consider non-accidental injury where the pattern or history does not fit. <div class="ec-src"><b>Source:</b> American Burn Association Advanced Burn Life Support Provider Manual, 2023.</div></div></div> [[Try this question again->Major burn - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Major burn. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ One made an airway decision depend on a test that answers a different question.</div> Carboxyhemoglobin indicates about systemic carbon monoxide exposure. It says nothing about the thermal and chemical injury to his upper airway, and it can be normal in a patient whose larynx is about to swell shut, particularly if oxygen has already been running. His hoarseness, singed nasal hairs and carbonaceous sputum are the findings that matter, and they are already present. <div class="ec-teach"><div class="th">Why this is wrong</div> Intubate early, while the anatomy is still normal. Airway edema in inhalation injury develops over hours and is accelerated by the fluid resuscitation he is about to receive; once it is established, intubation becomes difficult or impossible and a surgical airway through burned neck tissue is a poor alternative. Check carboxyhemoglobin and consider cyanide toxicity in parallel, they change what else the drug is given, not whether one secure the airway. <div class="ec-src"><b>Source:</b> American Burn Association Advanced Burn Life Support Provider Manual, 2023.</div></div></div> [[Try this question again->Major burn - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Major burn. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ One lose the airway an hour later.</div> He is breathing now, but hoarseness and sooty sputum mean the airway is already injured, and progressive edema plus the large-volume resuscitation one is about to start will swell it shut. When one finally try to intubate, the landmarks are gone. <div class="ec-teach"><div class="th">Why not this</div> Fluid creep from burn resuscitation itself exacerbates airway edema. With signs of inhalation injury, intubate early rather than waiting for respiratory distress. <div class="ec-src"><b>Source:</b> American Burn Association Advanced Burn Life Support Provider Manual, 2023.</div></div></div> [[Try this question again->Major burn - Opening]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 09:40</div> A 29-year-old man is found after lying immobile overnight following heavy alcohol use. He has severe bilateral thigh pain and swelling and is passing small volumes of tea-colored urine. Urine dipstick is strongly positive for blood, but microscopy shows no red cells. Potassium is 5.9 mEq/L. <span class="ec-prompt">Which of the following is the most appropriate next step in diagnosis?</span> [[Renal ultrasonography->Rhabdomyolysis - Ix D2]] [[Repeat urinalysis in 6 hours->Rhabdomyolysis - Ix D5]] [[Serum creatine kinase->Rhabdomyolysis - Ix correct]] [[Serum troponin to assess for cardiac injury->Rhabdomyolysis - Ix D4]] [[Urine myoglobin to confirm pigment nephropathy->Rhabdomyolysis - Ix D1]]

<span class="ec-case-marker" hidden data-entry="Rhabdomyolysis. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Imaging excludes obstruction and is reasonable in undifferentiated acute kidney injury. It does not diagnose rhabdomyolysis and must not delay fluid resuscitation, whose benefit is time-dependent. <div class="ec-teach"><div class="th">What the findings point to</div> Creatine kinase is the diagnostic test and the one that stratifies risk, levels above roughly five times the upper limit of normal establish rhabdomyolysis, and the peak correlates with the likelihood of acute kidney injury. The dipstick-positive, microscopy-negative discrepancy has already told one that heme pigment is myoglobin rather than hemoglobin. <div class="ec-src"><b>Source:</b> Bosch X, Poch E, Grau JM. Rhabdomyolysis and Acute Kidney Injury. N Engl J Med 2009;361(1):62-72.</div></div></div> [[Try this question again->Rhabdomyolysis - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Rhabdomyolysis. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Repeating a test that has already given a diagnostic answer wastes the window in which fluid resuscitation determines whether his kidneys recover. <div class="ec-teach"><div class="th">What the findings point to</div> Creatine kinase is the diagnostic test and the one that stratifies risk, levels above roughly five times the upper limit of normal establish rhabdomyolysis, and the peak correlates with the likelihood of acute kidney injury. The dipstick-positive, microscopy-negative discrepancy has already told one that heme pigment is myoglobin rather than hemoglobin. <div class="ec-src"><b>Source:</b> Bosch X, Poch E, Grau JM. Rhabdomyolysis and Acute Kidney Injury. N Engl J Med 2009;361(1):62-72.</div></div></div> [[Try this question again->Rhabdomyolysis - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Rhabdomyolysis. Ix"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Serum creatine kinase.</div> Creatine kinase is the diagnostic test and the one that stratifies risk, levels above roughly five times the upper limit of normal establish rhabdomyolysis, and the peak correlates with the likelihood of acute kidney injury. The dipstick-positive, microscopy-negative discrepancy has already told one that heme pigment is myoglobin rather than hemoglobin. <div class="ec-src"><b>Source:</b> Bosch X, Poch E, Grau JM. Rhabdomyolysis and Acute Kidney Injury. N Engl J Med 2009;361(1):62-72.</div></div> [[Start another case->Hub]] [[Restart this case->Rhabdomyolysis - Ix]] [[Next case →->Hyperkalemia - Rx]]

<span class="ec-case-marker" hidden data-entry="Rhabdomyolysis. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Troponin may be mildly raised in rhabdomyolysis from skeletal muscle injury and can confuse rather than clarify. He has no cardiac symptoms, and an ECG is the immediate cardiac test given his potassium. <div class="ec-teach"><div class="th">What the findings point to</div> Creatine kinase is the diagnostic test and the one that stratifies risk, levels above roughly five times the upper limit of normal establish rhabdomyolysis, and the peak correlates with the likelihood of acute kidney injury. The dipstick-positive, microscopy-negative discrepancy has already told one that heme pigment is myoglobin rather than hemoglobin. <div class="ec-src"><b>Source:</b> Bosch X, Poch E, Grau JM. Rhabdomyolysis and Acute Kidney Injury. N Engl J Med 2009;361(1):62-72.</div></div></div> [[Try this question again->Rhabdomyolysis - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Rhabdomyolysis. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This seems the most direct test and it is unreliable: myoglobin is cleared rapidly and can be negative while muscle is still breaking down. The dipstick discrepancy is effectively the same information, immediately and free. <div class="ec-teach"><div class="th">What the findings point to</div> Creatine kinase is the diagnostic test and the one that stratifies risk, levels above roughly five times the upper limit of normal establish rhabdomyolysis, and the peak correlates with the likelihood of acute kidney injury. The dipstick-positive, microscopy-negative discrepancy has already told one that heme pigment is myoglobin rather than hemoglobin. <div class="ec-src"><b>Source:</b> Bosch X, Poch E, Grau JM. Rhabdomyolysis and Acute Kidney Injury. N Engl J Med 2009;361(1):62-72.</div></div></div> [[Try this question again->Rhabdomyolysis - Ix]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 23:10</div> A 58-year-old man with alcohol-related cirrhosis and known ascites has had fever and worsening confusion for 2 days. He has diffuse abdominal tenderness without guarding. Temperature is 38.2°C. He has grade 2 encephalopathy and creatinine has risen to 1.6 mg/dL. Prothrombin time is prolonged with an INR of 1.8 and platelets are 68,000/mm3. <span class="ec-prompt">Which of the following is the most appropriate next step in diagnosis?</span> [[Blood cultures, then empiric antibiotics->SBP - Ix D3]] [[Correct coagulopathy with fresh frozen plasma before tapping->SBP - Ix D1]] [[CT of the abdomen->SBP - Ix D2]] [[Diagnostic paracentesis (cell count and culture)->SBP - Ix correct]] [[Empiric antibiotics, reassess in 12 hours->SBP - Ix D5]]

<span class="ec-case-marker" hidden data-entry="SBP. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Blood cultures should be sent, but they are positive in only a minority. Without ascitic fluid one cannot confirm the diagnosis, cannot distinguish spontaneous from secondary peritonitis, and lose the one uncontaminated sample once antibiotics start. <div class="ec-teach"><div class="th">What the findings point to</div> Every cirrhotic patient admitted with ascites and fever, abdominal pain, encephalopathy or renal impairment needs a diagnostic tap. Treatment is triggered by an ascitic neutrophil count of 250/mm3 or more, and cultures are inoculated into blood culture bottles at the bedside, which substantially raises yield. <div class="ec-src"><b>Source:</b> Biggins SW, et al. AASLD Practice Guidance on ascites and hepatorenal syndrome. Hepatology 2021;74(2):1014-1048.</div></div></div> [[Try this question again->SBP - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="SBP. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This is the commonest reason a necessary tap is not done. Coagulopathy of cirrhosis is not a contraindication, bleeding complications are rare even with a markedly prolonged prothrombin time and low platelets, and routine correction with plasma is not recommended and delays diagnosis. <div class="ec-teach"><div class="th">What the findings point to</div> Every cirrhotic patient admitted with ascites and fever, abdominal pain, encephalopathy or renal impairment needs a diagnostic tap. Treatment is triggered by an ascitic neutrophil count of 250/mm3 or more, and cultures are inoculated into blood culture bottles at the bedside, which substantially raises yield. <div class="ec-src"><b>Source:</b> Biggins SW, et al. AASLD Practice Guidance on ascites and hepatorenal syndrome. Hepatology 2021;74(2):1014-1048.</div></div></div> [[Try this question again->SBP - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="SBP. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Imaging has a role where secondary peritonitis is suspected, so this is a reasonable thought in a tender abdomen. It does not diagnose spontaneous bacterial peritonitis, exposes an already-injured kidney to contrast, and delays the tap. <div class="ec-teach"><div class="th">What the findings point to</div> Every cirrhotic patient admitted with ascites and fever, abdominal pain, encephalopathy or renal impairment needs a diagnostic tap. Treatment is triggered by an ascitic neutrophil count of 250/mm3 or more, and cultures are inoculated into blood culture bottles at the bedside, which substantially raises yield. <div class="ec-src"><b>Source:</b> Biggins SW, et al. AASLD Practice Guidance on ascites and hepatorenal syndrome. Hepatology 2021;74(2):1014-1048.</div></div></div> [[Try this question again->SBP - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="SBP. Ix"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Diagnostic paracentesis (cell count and culture)</div> Every cirrhotic patient admitted with ascites and fever, abdominal pain, encephalopathy or renal impairment needs a diagnostic tap. Treatment is triggered by an ascitic neutrophil count of 250/mm3 or more, and cultures are inoculated into blood culture bottles at the bedside, which substantially raises yield. <div class="ec-src"><b>Source:</b> Biggins SW, et al. AASLD Practice Guidance on ascites and hepatorenal syndrome. Hepatology 2021;74(2):1014-1048.</div></div> [[Start another case->Hub]] [[Restart this case->SBP - Ix]] [[Next case →->SBP recurrence - Prog]]

<span class="ec-case-marker" hidden data-entry="SBP. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Antibiotics are needed and will be given, but starting them before the tap destroys the culture yield, and 12 hours of observation in a patient with encephalopathy and rising creatinine is a poor substitute for a diagnosis. <div class="ec-teach"><div class="th">What the findings point to</div> Every cirrhotic patient admitted with ascites and fever, abdominal pain, encephalopathy or renal impairment needs a diagnostic tap. Treatment is triggered by an ascitic neutrophil count of 250/mm3 or more, and cultures are inoculated into blood culture bottles at the bedside, which substantially raises yield. <div class="ec-src"><b>Source:</b> Biggins SW, et al. AASLD Practice Guidance on ascites and hepatorenal syndrome. Hepatology 2021;74(2):1014-1048.</div></div></div> [[Try this question again->SBP - Ix]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 05:20</div> A 22-year-old woman has sudden severe right lower quadrant pain with vomiting, waking her from sleep. Pregnancy test is negative. Ultrasound shows a markedly enlarged, edematous right ovary, but Doppler demonstrates preserved arterial flow within it. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[CT abdomen/pelvis before involving surgery->Ovarian torsion - CT trap]] [[hCG and tumor markers before referral->Ovarian torsion - Marker trap]] [[Preserved Doppler flow rules out torsion->Ovarian torsion - Doppler trap]] [[Repeat ultrasound in 6 hours for flow loss->Ovarian torsion - Serial imaging trap]] [[Urgent gynecology referral for laparoscopy->Ovarian torsion - Laparoscopy correct]]

<span class="ec-case-marker" hidden data-entry="Ovarian torsion. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Tests that matter later, ordered ahead of the operation.</div> A pregnancy test is genuinely essential, it changes the differential entirely, and it has already been done and is negative. Quantitative hCG adds nothing beyond that, and tumor markers are for characterizing a mass electively; they are frequently raised non-specifically in torsion and inflammation, and results take days. <div class="ec-teach"><div class="th">Why this is wrong</div> Refer urgently for diagnostic laparoscopy. Ovarian salvage depends on time to detorsion, and preserved Doppler flow does not exclude the diagnosis because of the dual arterial supply. <div class="ec-src"><b>Source:</b> ACOG Committee Opinion No. 783: Adnexal Torsion in Adolescents.</div></div></div> [[Try this question again->Ovarian torsion - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Ovarian torsion. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ More imaging, more ischemic time.</div> CT will not confirm torsion either, no imaging modality can, and the delay costs viable ovarian tissue in a 22-year-old with future fertility at stake. <div class="ec-teach"><div class="th">The misstep</div> Routine investigations should not delay management. Ultrasound is the imaging modality of choice, but torsion remains a surgical diagnosis; when suspicion is high, proceed to diagnostic laparoscopy. <div class="ec-src"><b>Source:</b> ACOG (2019); ACOG Committee Opinion No. 783: Adnexal Torsion in Adolescents.</div></div></div> [[Try this question again->Ovarian torsion - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Ovarian torsion. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ The dual blood supply fooled one.</div> One used a normal Doppler to rule out a diagnosis it cannot rule out. Her ovary is torsed and continues to infarct while she is worked up for something else, and delayed diagnosis is precisely what costs the ovary. <div class="ec-teach"><div class="th">Where the reasoning went wrong</div> A normal Doppler does not exclude ovarian torsion; the ovarian and uterine arteries provide dual supply, so flow persists in partial and intermittent torsion. Relying on it has been shown to delay management. Clinical suspicion alone may warrant laparoscopy. <div class="ec-src"><b>Source:</b> ACOG (2019); "Diagnosis of Ovarian Torsion: Is It Time to Forget About Doppler?" (J Obstet Gynaecol Can); ACOG Committee Opinion No. 783: Adnexal Torsion in Adolescents.</div></div></div> [[Try this question again->Ovarian torsion - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Ovarian torsion. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ One have scheduled a test to tell one the ovary has died.</div> The dual arterial supply from the ovarian and uterine arteries means flow can persist in a torsed ovary, and torsion is often intermittent, so a repeat scan may show flow again even while the ovary is infarcting. If flow is finally absent in 6 hours, that is not a diagnosis arriving on time. It is the finding that appears once the ovary is no longer salvageable. <div class="ec-teach"><div class="th">Why this is wrong</div> The diagnosis is clinical and the confirmation is surgical. Sudden severe unilateral pain with vomiting, a negative pregnancy test, and an enlarged edematous ovary on ultrasound is enough to take her to laparoscopy, where detorsion preserves ovarian function in the great majority of cases even when the ovary looks frankly ischemic. Preserved Doppler flow does not exclude torsion; the enlarged edematous ovary is the more reliable sonographic sign. <div class="ec-src"><b>Source:</b> ACOG Committee Opinion No. 783: Adnexal Torsion in Adolescents (2019, reaffirmed); Bar-On S, et al. Fertil Steril 2010 (conservative laparoscopic management of adnexal torsion).</div></div></div> [[Try this question again->Ovarian torsion - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Ovarian torsion. Opening"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Urgent gynecology referral for laparoscopy</div> Gynecology takes her for diagnostic laparoscopy, which finds the right ovary torsed twice around its pedicle, despite the preserved flow on ultrasound. <div class="ec-teach"><div class="th">Where the case turned</div> Preserved Doppler flow looks like reassurance and is the single most common reason this diagnosis gets missed. The ovary has a <b>dual blood supply</b>, ovarian and uterine arteries, so flow can persist despite torsion; studies report arterial flow in as many as 60% of surgically confirmed cases. Absent flow is highly specific, but its presence excludes nothing. Adnexal torsion is a <b>surgical diagnosis</b>: no clinical or imaging criteria are sufficient to confirm it preoperatively, and Doppler flow alone should not guide decision making. The most common ultrasound finding is simply an enlarged, edematous ovary, which she had. <div class="ec-src"><b>Source:</b> ACOG Committee Opinion, Adnexal Torsion in Adolescents (2019); SAEM CDEM; ACOG Committee Opinion No. 783: Adnexal Torsion in Adolescents.</div></div></div> [[Start another case->Hub]] [[Restart this case->Ovarian torsion - Opening]] [[Next case →->Cervical screening - Opening]]

<div class="ec-scene">Medical ward · 06:30</div> A 61-year-old woman with a BMI of 14 after 12 days of negligible intake was started on nutritional support 4 days ago. She now has worsening weakness, mild confusion and peripheral edema. Phosphate is 1.1 mg/dL, potassium 2.9 mEq/L, magnesium 1.2 mg/dL. She is mildly tachycardic and her jugular venous pressure is raised. <span class="ec-prompt">Which of the following is the most likely diagnosis?</span> [[Congestive cardiac failure->Refeeding syndrome - Dx D4]] [[Hospital-acquired hyponatremia->Refeeding syndrome - Dx D2]] [[Refeeding syndrome->Refeeding syndrome - Dx correct]] [[Sepsis->Refeeding syndrome - Dx D1]] [[Wernicke encephalopathy->Refeeding syndrome - Dx D3]]

<span class="ec-case-marker" hidden data-entry="Refeeding syndrome. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The edema and raised venous pressure fit, and cardiac decompensation is part of the syndrome rather than a separate diagnosis, hypophosphatemia impairs myocardial contractility directly. <div class="ec-teach"><div class="th">What the findings point to</div> Falling phosphate, potassium and magnesium with fluid retention and cardiac and neurological signs, appearing within the first few days of reintroducing nutrition in a severely malnourished patient. Carbohydrate drives an insulin surge that shifts these electrolytes intracellularly at a point when total body stores are already depleted. <div class="ec-src"><b>Source:</b> da Silva JSV, et al. ASPEN Consensus Recommendations for Refeeding Syndrome. Nutr Clin Pract 2020;35(2):178-195.</div></div></div> [[Try this question again->Refeeding syndrome - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Refeeding syndrome. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Sodium disturbance causes confusion and should be checked, but it does not explain hypophosphatemia and hypomagnesemia or the edema and raised venous pressure. <div class="ec-teach"><div class="th">What the findings point to</div> Falling phosphate, potassium and magnesium with fluid retention and cardiac and neurological signs, appearing within the first few days of reintroducing nutrition in a severely malnourished patient. Carbohydrate drives an insulin surge that shifts these electrolytes intracellularly at a point when total body stores are already depleted. <div class="ec-src"><b>Source:</b> da Silva JSV, et al. ASPEN Consensus Recommendations for Refeeding Syndrome. Nutr Clin Pract 2020;35(2):178-195.</div></div></div> [[Try this question again->Refeeding syndrome - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Refeeding syndrome. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Refeeding syndrome.</div> Falling phosphate, potassium and magnesium with fluid retention and cardiac and neurological signs, appearing within the first few days of reintroducing nutrition in a severely malnourished patient. Carbohydrate drives an insulin surge that shifts these electrolytes intracellularly at a point when total body stores are already depleted. <div class="ec-src"><b>Source:</b> da Silva JSV, et al. ASPEN Consensus Recommendations for Refeeding Syndrome. Nutr Clin Pract 2020;35(2):178-195.</div></div> [[Start another case->Hub]] [[Restart this case->Refeeding syndrome - Dx]] [[Next case →->Thyroid nodule workup - Ix]]

<span class="ec-case-marker" hidden data-entry="Refeeding syndrome. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Confusion, tachycardia and weakness in an inpatient reasonably raise infection, and it should be excluded. Sepsis does not produce this specific triad of falling phosphate, potassium and magnesium timed to the start of feeding. <div class="ec-teach"><div class="th">What the findings point to</div> Falling phosphate, potassium and magnesium with fluid retention and cardiac and neurological signs, appearing within the first few days of reintroducing nutrition in a severely malnourished patient. Carbohydrate drives an insulin surge that shifts these electrolytes intracellularly at a point when total body stores are already depleted. <div class="ec-src"><b>Source:</b> da Silva JSV, et al. ASPEN Consensus Recommendations for Refeeding Syndrome. Nutr Clin Pract 2020;35(2):178-195.</div></div></div> [[Try this question again->Refeeding syndrome - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Refeeding syndrome. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This is a genuine concurrent risk, carbohydrate load in a thiamine-deplete patient can precipitate it, which is why thiamine is given before or with feeding. It causes ophthalmoplegia and ataxia and does not cause the electrolyte pattern. <div class="ec-teach"><div class="th">What the findings point to</div> Falling phosphate, potassium and magnesium with fluid retention and cardiac and neurological signs, appearing within the first few days of reintroducing nutrition in a severely malnourished patient. Carbohydrate drives an insulin surge that shifts these electrolytes intracellularly at a point when total body stores are already depleted. <div class="ec-src"><b>Source:</b> da Silva JSV, et al. ASPEN Consensus Recommendations for Refeeding Syndrome. Nutr Clin Pract 2020;35(2):178-195.</div></div></div> [[Try this question again->Refeeding syndrome - Dx]] [[Start another case->Hub]]

<div class="ec-scene">Primary care clinic · 09:30</div> A 68-year-old man with type 2 diabetes on metformin for 9 years reports numbness and tingling in both feet and mild unsteadiness. Hemoglobin is 10.2 g/dL and mean corpuscular volume is 112 fL. He has reduced vibration and position sense in the toes with absent ankle reflexes. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Attribute it to diabetes; optimize glucose->B12 deficiency - Diabetic trap]] [[Check serum vitamin B12 and replace if deficient->B12 deficiency - Correct]] [[Empiric intramuscular vitamin vitamin B12 without measuring a level->B12 deficiency - Empiric trap]] [[Folate for the macrocytic anemia->B12 deficiency - Folate trap]] [[Stop metformin; recheck CBC in 3 months->B12 deficiency - Stop metformin trap]]

<span class="ec-case-marker" hidden data-entry="B12 deficiency. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ The MCV of 112 is not diabetes.</div> Diabetic neuropathy is real and common, but it does not cause a macrocytosis of 112. Anchoring on the diabetes ignores a reversible cause sitting in his medication list. <div class="ec-teach"><div class="th">Why this fails</div> Macrocytic anemia with neuropathy points to B12 deficiency. Metformin is a well-recognized cause and the exam expects one to check it. <div class="ec-src"><b>Source:</b> Aroda VR, et al. Long-term Metformin Use and Vitamin B12 Deficiency in the DPPOS. J Clin Endocrinol Metab 2016;101(4):1754-1761.</div></div></div> [[Try this question again->B12 deficiency - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="B12 deficiency. Opening"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Check serum vitamin B12 and replace if deficient</div> One send a B12 level, which returns low, and start replacement. His anemia corrects and his neuropathy stabilizes. <div class="ec-teach"><div class="th">The drug-nutrient interaction</div> Long-term metformin impairs vitamin B12 absorption and is a recognized cause of deficiency, periodic B12 measurement is recommended in patients on prolonged therapy, particularly those with anemia or neuropathy. B12 deficiency produces macrocytic anemia <b>and</b> neurologic disease (subacute combined degeneration: dorsal column and corticospinal involvement, so vibration and position sense go first). Other drug-nutrient pairs worth knowing: isoniazid depletes pyridoxine (B6), methotrexate depletes folate, phenytoin depletes folate, and proton pump inhibitors impair B12 absorption. <div class="ec-src"><b>Source:</b> ADA Standards of Care (periodic B12 measurement on long-term metformin).</div></div></div> <b>Deficiency identified and replaced.</b> [[Start another case->Hub]] [[Restart this case->B12 deficiency - Opening]] [[Next case →->Folate pregnancy - Opening]]

<span class="ec-case-marker" hidden data-entry="B12 deficiency. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Folate corrects the blood and lets the spinal cord rot.</div> Folate will improve the macrocytosis and anemia, masking the hematologic clue, while the neurologic damage of B12 deficiency progresses. Subacute combined degeneration can become irreversible. <div class="ec-teach"><div class="th">Where the logic fails</div> Never give folate alone for macrocytic anemia without excluding B12 deficiency: it corrects the hematologic picture while neurologic injury advances. <div class="ec-src"><b>Source:</b> AAFP macrocytic anemia review.</div></div></div> [[Try this question again->B12 deficiency - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="B12 deficiency. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Defensible instinct, and it discards information one will need.</div> Treating on strong suspicion is reasonable and replacement is safe, so this is not reckless. Without a baseline one cannot confirm the diagnosis, cannot distinguish deficiency from the other causes of macrocytosis and neuropathy in a diabetic on metformin, and cannot justify lifelong replacement or interpret a poor response later. <div class="ec-teach"><div class="th">Why this is wrong</div> Check a serum B12, using methylmalonic acid if the level is borderline, and replace, the level takes hours and does not delay treatment. Metformin can usually continue with monitoring and supplementation. Neurological recovery depends on how long the deficiency ran, so replacement is not deferred. <div class="ec-src"><b>Source:</b> Aroda VR, et al. Long-term Metformin Use and Vitamin B12 Deficiency in the DPPOS. J Clin Endocrinol Metab 2016;101(4):1754-1761.</div></div></div> [[Try this question again->B12 deficiency - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="B12 deficiency. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ One removed the cause and left the deficit in place.</div> Metformin does impair B12 absorption, and reviewing the drug is reasonable. But stopping it does nothing about the B12 he is already missing, worsens his glycemic control in the meantime, and buys 3 months of watching, during which subacute combined degeneration of the cord can progress. Neurological damage from B12 deficiency becomes irreversible with time, and his posterior column signs say the clock has already started. <div class="ec-teach"><div class="th">Why this is wrong</div> Confirm with a serum B12 level, use methylmalonic acid if the level is borderline, and replace. Metformin can usually be continued with monitoring and supplementation rather than withdrawn. Hematologic recovery is prompt; neurological recovery depends on how long the deficiency ran before replacement. <div class="ec-src"><b>Source:</b> Aroda et al., J Clin Endocrinol Metab 2016 (DPPOS, long-term metformin and B12); ADA Standards of Care 2024, periodic B12 measurement in metformin-treated patients.</div></div></div> [[Try this question again->B12 deficiency - Opening]] [[Start another case->Hub]]

<div class="ec-scene">Surgical intensive care unit · 06:50</div> A 55-year-old man with severe acute pancreatitis has been NPO for 4 days. He is hemodynamically stable, has bowel sounds, and has no obstruction, ischemia, or high-output fistula. The team is deciding how to feed him. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Continue NPO, reassess in 3 days->Enteral nutrition - NPO trap]] [[Enteral nutrition, but withhold if residual >250 mL->Enteral nutrition - Residual volume trap]] [[Start enteral nutrition now->Enteral nutrition - Correct]] [[Start TPN via central line->Enteral nutrition - TPN trap]] [[Wait for a post-pyloric tube; gastric feeding stimulates the pancreas->Enteral nutrition - Post-pyloric trap]]

<span class="ec-case-marker" hidden data-entry="Enteral nutrition. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ A week of starvation in a catabolic illness.</div> Severe pancreatitis is a high-catabolic state. Prolonged fasting worsens muscle loss, immune function, and gut barrier integrity, and early enteral feeding actually reduces morbidity here rather than aggravating the pancreatitis. <div class="ec-teach"><div class="th">The error</div> Early enteral nutrition reduces morbidity in acute pancreatitis; prolonged nil-by-mouth is no longer recommended. <div class="ec-src"><b>Source:</b> ACG Clinical Guideline: Management of Acute Pancreatitis (2024).</div></div></div> [[Try this question again->Enteral nutrition - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Enteral nutrition. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ A monitoring practice that has largely been abandoned.</div> Checking residuals was routine and the reasoning, avoid aspiration, sounds sound. Trials found that not monitoring residual volume did not increase ventilator-associated pneumonia, and that using thresholds to interrupt feeding reduces delivered calories without benefit. Repeated interruptions are a common reason patients never reach nutritional goals. <div class="ec-teach"><div class="th">Why this is wrong</div> Feed enterally now by whichever route is available; nasogastric is acceptable and simpler than waiting for post-pyloric access. Manage intolerance with prokinetics and positioning rather than by stopping, and reserve post-pyloric feeding for genuine gastric failure. <div class="ec-src"><b>Source:</b> Reignier J, et al. JAMA 2013;309(3):249-256 (gastric residual volume monitoring); Crockett SD, et al. AGA Institute Guideline on Initial Management of Acute Pancreatitis. Gastroenterology 2018;154(4):1096-1101.</div></div></div> [[Try this question again->Enteral nutrition - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Enteral nutrition. Opening"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Start enteral nutrition now</div> Enteral feeding is started through a tube. He tolerates it, and one avoid the line and metabolic complications parenteral nutrition would have brought. <div class="ec-teach"><div class="th">The rule and its exceptions</div> The principle is simple: <b>if the gut works, use it.</b> Enteral nutrition preserves gut mucosal integrity, reduces bacterial translocation, costs less, and avoids the complications of central venous access. Parenteral nutrition is reserved for a non-functioning or inaccessible gut, bowel obstruction, ischemia, high-output fistula, short bowel syndrome, or severe malabsorption. TPN complications to know: catheter-related bloodstream infection, hyperglycemia, electrolyte derangement, hepatic steatosis and cholestasis, and refeeding syndrome. <div class="ec-src"><b>Source:</b> McClave SA, et al. SCCM/ASPEN Guidelines for Nutrition Support in the Adult Critically Ill Patient. JPEN 2016;40(2):159-211; Compher C, et al. ASPEN 2022 update. JPEN 2022;46(1):12-41; ACG acute pancreatitis guideline (2024).</div></div></div> <b>Fed enterally, complications avoided.</b> [[Start another case->Hub]] [[Restart this case->Enteral nutrition - Opening]] [[Next case →->Ascites SAAG - Ix]]

<span class="ec-case-marker" hidden data-entry="Enteral nutrition. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ One chose the riskier route for no reason.</div> Parenteral nutrition brings catheter-related bloodstream infection, hyperglycemia, hepatic steatosis and cholestasis, and it lets the gut mucosa atrophy. None of that is necessary in a patient whose gut works. <div class="ec-teach"><div class="th">What went wrong</div> Parenteral nutrition is reserved for a non-functioning or inaccessible gastrointestinal tract. When the gut works, enteral feeding is preferred. <div class="ec-src"><b>Source:</b> McClave SA, et al. SCCM/ASPEN Guidelines for Nutrition Support in the Adult Critically Ill Patient. JPEN 2016;40(2):159-211; Compher C, et al. ASPEN 2022 update. JPEN 2022;46(1):12-41; ACG acute pancreatitis guideline (2024).</div></div></div> [[Try this question again->Enteral nutrition - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Enteral nutrition. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ The rationale is textbook, and the evidence stopped supporting it.</div> Pancreatic rest was the reasoning behind post-pyloric feeding for years, and it is why this option sounds authoritative. Randomized trials and successive meta-analyses have not shown nasojejunal feeding to be superior to nasogastric feeding in severe acute pancreatitis, mortality, organ failure, aspiration and pain are comparable. What post-pyloric placement reliably does add is delay, because it needs endoscopic or fluoroscopic assistance, and on day four the delay is the harm. <div class="ec-teach"><div class="th">Why this is wrong</div> Feed enterally through whichever route is available now; nasogastric is acceptable and simpler. Reserve post-pyloric access for patients who genuinely fail gastric feeding, persistent high residuals, intolerance, or gastric outlet obstruction, rather than making it a precondition for starting. <div class="ec-src"><b>Source:</b> Dutta et al., Cochrane Database Syst Rev 2020, CD010582; ACG Clinical Guideline: Management of Acute Pancreatitis, Am J Gastroenterol 2013 and 2024 update.</div></div></div> [[Try this question again->Enteral nutrition - Opening]] [[Start another case->Hub]]

<div class="ec-scene">Bariatric follow-up clinic · 10:20</div> A 41-year-old woman is 2 years out from Roux-en-Y gastric bypass. She stopped taking her prescribed supplements a year ago. She now reports fatigue and exertional dyspnea. Hemoglobin is 9.4 g/dL, mean corpuscular volume is 72 fL, and ferritin is 8 ng/mL. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Intravenous iron; stop once hemoglobin normalizes->Bariatric deficiency - Stop when normal trap]] [[Iron replacement; screen for other post-bypass deficiencies->Bariatric deficiency - Correct]] [[Oral ferrous sulfate alone, recheck in 3 months->Bariatric deficiency - Oral iron trap]] [[Replace vitamin B12 alone; it is the classic post-bypass deficiency->Bariatric deficiency - B12 only trap]] [[Urgent colonoscopy before replacing anything->Bariatric deficiency - Colonoscopy trap]]

<span class="ec-case-marker" hidden data-entry="Bariatric deficiency. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ One treated the anemia and left the anatomy untreated.</div> Intravenous iron is a perfectly reasonable route here, oral iron is poorly absorbed after bypass and she may not tolerate it. The error is the stopping rule. Roux-en-Y bypass permanently excludes the duodenum and proximal jejunum, where iron is absorbed, and reduces the gastric acid that converts dietary iron to an absorbable form. Normalizing her hemoglobin does not restore any of that; withdraw supplementation and she returns to where she is now. <div class="ec-teach"><div class="th">Why this is wrong</div> Supplementation after bypass is lifelong, together with annual monitoring. Low ferritin 2 years post-operatively with documented non-adherence is an expected consequence and rarely needs a search for occult blood loss first, but it should prompt screening for the deficiencies that travel with it: vitamin B12, folate, vitamin D and calcium, thiamine, and copper and zinc where symptoms suggest them. <div class="ec-src"><b>Source:</b> Mechanick et al., Clinical Practice Guidelines for the Perioperative Nutrition, Metabolic, and Nonsurgical Support of Patients Undergoing Bariatric Procedures, Surg Obes Relat Dis 2020 (AACE/TOS/ASMBS).</div></div></div> [[Try this question again->Bariatric deficiency - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Bariatric deficiency. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ One skipped the obvious cause sitting in the history.</div> Iron deficiency does warrant a search for blood loss in the right patient, but she has a bypass that anatomically excludes the duodenum where iron is absorbed, and she stopped her supplements a year ago. Investigation without replacement also leaves her anemic for weeks. <div class="ec-teach"><div class="th">Where this breaks down</div> Roux-en-Y bypass causes predictable malabsorptive iron deficiency. Replace and screen broadly; pursue gastrointestinal investigation if the picture does not fit or does not respond. <div class="ec-src"><b>Source:</b> Mechanick JI, et al. Perioperative Nutrition, Metabolic, and Nonsurgical Support of Patients Undergoing Bariatric Procedures. Surg Obes Relat Dis 2020 (AACE/TOS/ASMBS).</div></div></div> [[Try this question again->Bariatric deficiency - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Bariatric deficiency. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Right family, wrong deficiency, and too narrow.</div> B12 deficiency after bypass is real, but it causes a <b>macrocytic</b> anemia. Her MCV is 72 with a ferritin of 8, which is iron. And replacing only one nutrient in a patient off all supplements for a year misses the others. <div class="ec-teach"><div class="th">Why not this</div> Match the deficiency to the indices: microcytic with low ferritin is iron. Post-bypass patients need screening across iron, B12, folate, calcium, vitamin D and thiamine. <div class="ec-src"><b>Source:</b> Mechanick JI, et al. Perioperative Nutrition, Metabolic, and Nonsurgical Support of Patients Undergoing Bariatric Procedures. Surg Obes Relat Dis 2020 (AACE/TOS/ASMBS).</div></div></div> [[Try this question again->Bariatric deficiency - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Bariatric deficiency. Opening"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Iron replacement; screen for other post-bypass deficiencies</div> It is started iron and check B12, folate, vitamin D, calcium and thiamine, because bypass anatomy predicts multiple simultaneous deficiencies, and she has been off supplements for a year. <div class="ec-teach"><div class="th">What bypass anatomy predicts</div> Roux-en-Y gastric bypass reduces acid and bypasses the duodenum and proximal jejunum, so it causes predictable deficiencies in <b>iron, vitamin B12, folate, calcium, vitamin D, and thiamine</b>. Lifelong supplementation and periodic monitoring are required. Match the anemia to the indices: microcytic with low ferritin is iron; macrocytic points to B12 or folate. Thiamine deficiency deserves particular respect, persistent vomiting after bariatric surgery can precipitate Wernicke encephalopathy within weeks. <div class="ec-src"><b>Source:</b> ASMBS/AACE/TOS clinical practice guidelines for nutritional support of the bariatric surgery patient (2020).</div></div></div> <b>Deficiencies identified and supplementation restarted.</b> [[Start another case->Hub]] [[Restart this case->Bariatric deficiency - Opening]] [[Next case →->Malnutrition assessment - Opening]]

<span class="ec-case-marker" hidden data-entry="Bariatric deficiency. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ The usual first-line iron, in the one anatomy that defeats it.</div> Oral iron is first-line for iron deficiency almost everywhere, which is what makes this the closest wrong answer. Roux-en-Y bypass excludes the duodenum and proximal jejunum where iron is absorbed and reduces the gastric acid needed to convert dietary iron to an absorbable form, so standard oral dosing frequently fails, and 3 months is a long time to find that out. <div class="ec-teach"><div class="th">Why this is wrong</div> Use higher-dose oral iron with vitamin C, or parenteral iron where oral fails or is not tolerated, and screen for the deficiencies that travel with it. B12, folate, vitamin D and calcium, thiamine. Supplementation after bypass is lifelong with annual monitoring. <div class="ec-src"><b>Source:</b> Mechanick JI, et al. Clinical Practice Guidelines for the Perioperative Nutrition, Metabolic, and Nonsurgical Support of Patients Undergoing Bariatric Procedures. Surg Obes Relat Dis 2020.</div></div></div> [[Try this question again->Bariatric deficiency - Opening]] [[Start another case->Hub]]

<div class="ec-scene">Primary care clinic · 11:15</div> A 62-year-old woman with limited sun exposure and a history of celiac disease has had diffuse bone pain and proximal muscle weakness for 6 months, with difficulty rising from a chair. Alkaline phosphatase is 214 U/L, calcium is 8.4 mg/dL, phosphate is 2.4 mg/dL, parathyroid hormone is 118 pg/mL, and 25-hydroxyvitamin D is 9 ng/mL. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Bisphosphonate without replacing vitamin D or calcium->Vitamin D deficiency - Bisphosphonate trap]] [[Parathyroidectomy instead of replacing vitamin D->Vitamin D deficiency - PTH trap]] [[Recheck parathyroid hormone in 3 months before treating->Vitamin D deficiency - Recheck trap]] [[Replace vitamin D and calcium; treat the malabsorption->Vitamin D deficiency - Correct]] [[Vitamin D alone; recheck calcium in 6 weeks->Vitamin D deficiency - Vitamin D alone trap]]

<span class="ec-case-marker" hidden data-entry="Vitamin D deficiency. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ The PTH is a consequence, not a question.</div> Her parathyroid hormone is elevated because her vitamin D is 9 and her gut is not absorbing calcium, the gland is doing exactly what it should. Repeating the measurement answers nothing one does not already know, and 3 months of untreated osteomalacia is three more months of bone pain, proximal weakness and fracture risk. <div class="ec-teach"><div class="th">Why this is wrong</div> Secondary hyperparathyroidism in this setting resolves with replacement. Give vitamin D at repletion doses with calcium, treat the celiac disease driving the malabsorption, and recheck the 25-hydroxyvitamin D and PTH after replacement to confirm the picture corrects. A PTH that stays high once vitamin D is replete is the finding that would raise primary hyperparathyroidism. <div class="ec-src"><b>Source:</b> Holick MF, et al. Evaluation, Treatment, and Prevention of Vitamin D Deficiency: an Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2011;96(7):1911-1930.</div></div></div> [[Try this question again->Vitamin D deficiency - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Vitamin D deficiency. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ This is secondary, not primary, hyperparathyroidism.</div> Her PTH is high <em>because</em> her vitamin D and calcium are low, the glands are responding appropriately. In primary hyperparathyroidism calcium would be high, not low-normal. Surgery here removes a normal compensatory response. <div class="ec-teach"><div class="th">What this misses</div> Distinguish secondary hyperparathyroidism (low or low-normal calcium, driven by vitamin D deficiency or renal disease) from primary (hypercalcemia). Treat the deficiency. <div class="ec-src"><b>Source:</b> Holick MF, et al. Evaluation, Treatment, and Prevention of Vitamin D Deficiency: Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2011;96(7):1911-1930.</div></div></div> [[Try this question again->Vitamin D deficiency - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Vitamin D deficiency. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Half the replacement, and the half one left out is what her bones need.</div> Replacing the deficient vitamin is the main move and this gets that right. Giving it without calcium in a patient with malabsorption risks hungry bone, as mineralization resumes, calcium is drawn rapidly into bone and serum calcium can fall further, worsening the secondary hyperparathyroidism one is trying to correct. <div class="ec-teach"><div class="th">Why this is wrong</div> Replace vitamin D together with calcium, and treat the celiac disease driving the malabsorption, without that, replacement at standard doses will underperform. Recheck 25-hydroxyvitamin D, calcium and parathyroid hormone after replacement. <div class="ec-src"><b>Source:</b> Holick MF, et al. Evaluation, Treatment, and Prevention of Vitamin D Deficiency: an Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2011;96(7):1911-1930.</div></div></div> [[Try this question again->Vitamin D deficiency - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Vitamin D deficiency. Opening"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Replace vitamin D and calcium; treat the malabsorption</div> It is started vitamin D and calcium replacement and review her celiac disease control, since ongoing malabsorption will keep her deficient no matter what one prescribe. <div class="ec-teach"><div class="th">The pattern to recognize</div> Vitamin D deficiency causing osteomalacia produces bone pain, proximal muscle weakness, low or low-normal calcium and phosphate, <b>elevated alkaline phosphatase</b>, and <b>secondary</b> hyperparathyroidism. Risk factors include malabsorption (celiac disease, inflammatory bowel disease, bariatric surgery), limited sun exposure, darker skin pigmentation, older age, and obesity. In children the same deficiency causes rickets. Replace vitamin D and calcium, and treat the malabsorptive cause or replacement will not hold. <div class="ec-src"><b>Source:</b> Endocrine Society clinical practice guidance on vitamin D.</div></div></div> <b>Deficiency corrected and cause addressed.</b> [[Start another case->Hub]] [[Restart this case->Vitamin D deficiency - Opening]] [[Next case →->B12 deficiency - Opening]]

<span class="ec-case-marker" hidden data-entry="Vitamin D deficiency. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ It would worsen the hypocalcemia.</div> This is osteomalacia from vitamin D deficiency, not osteoporosis. Giving a bisphosphonate to a vitamin D–deficient patient with low-normal calcium risks significant hypocalcemia, and it does nothing about the missing vitamin. <div class="ec-teach"><div class="th">The misstep</div> Correct vitamin D deficiency before starting antiresorptive therapy. Osteomalacia is treated by replacing vitamin D and calcium, not by suppressing bone turnover. <div class="ec-src"><b>Source:</b> Holick MF, et al. Evaluation, Treatment, and Prevention of Vitamin D Deficiency: an Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2011;96(7):1911-1930.</div></div></div> [[Try this question again->Vitamin D deficiency - Opening]] [[Start another case->Hub]]

<div class="ec-scene">Primary care clinic · 13:15</div> A 55-year-old man with hypertension who smokes has no history of cardiovascular disease. His calculated 10-year cardiovascular risk is 12% and his LDL cholesterol is 150 mg/dL. <span class="ec-prompt">Which of the following is the most appropriate health maintenance measure?</span> [[Defer a statin until 10-year risk >20%->Statin prevention - Vitamin K trap]] [[Reserve statins for established cardiovascular disease->Statin prevention - Iron trap]] [[Start a statin for primary prevention->Statin prevention - Correct]] [[Statin only after a coronary calcium score->Statin prevention - Vasculitis trap]] [[Withhold a statin; LDL is below 190->Statin prevention - Platelet trap]]

<span class="ec-case-marker" hidden data-entry="Statin prevention. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ The threshold is 10%, not 20%.</div> Waiting for a 20% risk leaves years of preventable events on the table; the B recommendation begins at a 10-year risk of 10%. <div class="ec-teach"><div class="th">The error</div> USPSTF: prescribe a statin at a 10-year CVD risk of 10% or greater with at least one risk factor. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Statin Use for the Primary Prevention of Cardiovascular Disease in Adults. JAMA 2022;328(8):746-753 (B recommendation).</div></div></div> [[Try this question again->Statin prevention - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Statin prevention. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ That is secondary prevention.</div> Limiting statins to patients who already have cardiovascular disease ignores primary prevention, exactly the situation here. <div class="ec-teach"><div class="th">The error</div> This recommendation is about primary prevention in adults without prior CVD who meet the risk criteria. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Statin Use for the Primary Prevention of Cardiovascular Disease in Adults. JAMA 2022;328(8):746-753 (B recommendation).</div></div></div> [[Try this question again->Statin prevention - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Statin prevention. Opening"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Start a statin for primary prevention</div> It is started a moderate-intensity statin for primary prevention and counsel on smoking cessation. <div class="ec-teach"><div class="th">The 10% threshold does the work</div> The USPSTF gives a B recommendation to prescribe a statin for adults 40 to 75 with at least one cardiovascular risk factor (dyslipidemia, diabetes, hypertension, or smoking) and an estimated 10-year cardiovascular risk of 10% or greater. He has hypertension and smoking and a 12% risk, so a statin is indicated for primary prevention. At 7.5% to under 10% it would be selectively offered; at 76 or older the evidence is insufficient. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Statin Use for the Primary Prevention of Cardiovascular Disease in Adults. JAMA 2022;328(8):746-753 (B recommendation).</div></div></div> <b>Statin started for primary prevention.</b> [[Start another case->Hub]] [[Restart this case->Statin prevention - Opening]] [[Next case →->Pneumococcal prevention - Opening]]

<span class="ec-case-marker" hidden data-entry="Statin prevention. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ A calcium score is not required here.</div> Coronary calcium scoring can refine borderline decisions, but it is not a prerequisite, and at a 12% risk the indication is already clear. <div class="ec-teach"><div class="th">The error</div> The USPSTF pathway uses risk factors plus the estimated 10-year risk; a calcium score is optional, not mandatory. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Statin Use for the Primary Prevention of Cardiovascular Disease in Adults. JAMA 2022;328(8):746-753 (B recommendation).</div></div></div> [[Try this question again->Statin prevention - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Statin prevention. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ LDL below 190 does not exclude a statin.</div> The LDL ≥190 rule is a separate treatment pathway; the USPSTF risk-based criteria are met here regardless of an LDL of 150. <div class="ec-teach"><div class="th">The error</div> Statin indication here rests on risk factors and a 10-year risk ≥10%, not on reaching an LDL of 190. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Statin Use for the Primary Prevention of Cardiovascular Disease in Adults. JAMA 2022;328(8):746-753 (B recommendation).</div></div></div> [[Try this question again->Statin prevention - Opening]] [[Start another case->Hub]]

<div class="ec-scene">Journal club · 07:35</div> A drug lowers the 5-year risk of an outcome from 2.0% to 1.0%. A colleague says it "halves the risk" and should be given to everyone. <span class="ec-prompt">Which of the following is the most appropriate interpretation of this result?</span> [[The absolute risk reduction is 50%, so nearly every treated patient benefits->Risk reduction measures - Admit trap]] [[The number needed to treat is 2->Risk reduction measures - Medication alone trap]] [[The relative and absolute risk reductions are equal in this case->Risk reduction measures - Benzo trap]] [[The relative risk reduction is 50%, but the absolute reduction is only 1%->Risk reduction measures - Correct]] [[The result cannot be judged without the p-value->Risk reduction measures - Follow-up interval trap]]

<span class="ec-case-marker" hidden data-entry="Risk reduction measures. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The 50% is the relative reduction. The absolute risk reduction is 2.0% − 1.0% = 1%, not 50%. <div class="ec-teach"><div class="th">The error</div> ARR = difference in absolute risks = 1%; the 50% figure is the relative risk reduction. <div class="ec-src"><b>Source:</b> Cook RJ, Sackett DL. The number needed to treat: a clinically useful measure of treatment effect. BMJ 1995;310:452-454.</div></div></div> [[Try this question again->Risk reduction measures - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Risk reduction measures. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ The NNT here is 100, not 2.</div> NNT = 1/ARR = 1/0.01 = 100. An NNT of 2 would require a 50% absolute reduction, not a 1% one. <div class="ec-teach"><div class="th">The error</div> Use the absolute reduction: ARR = 0.01, so NNT = 100. <div class="ec-src"><b>Source:</b> Cook RJ, Sackett DL. The number needed to treat: a clinically useful measure of treatment effect. BMJ 1995;310:452-454.</div></div></div> [[Try this question again->Risk reduction measures - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Risk reduction measures. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ They coincide only at 100% baseline risk.</div> Relative and absolute reductions are equal only when the baseline risk is 100%. Here RRR is 50% while ARR is 1%, far apart. <div class="ec-teach"><div class="th">The error</div> The two measures diverge whenever baseline risk is below 100%; report both. <div class="ec-src"><b>Source:</b> Cook RJ, Sackett DL. The number needed to treat: a clinically useful measure of treatment effect. BMJ 1995;310:452-454.</div></div></div> [[Try this question again->Risk reduction measures - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Risk reduction measures. Opening"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ The relative risk reduction is 50%, but the absolute reduction is only 1%</div> Going from 2.0% to 1.0% halves the risk in relative terms (a 50% relative risk reduction) but lowers absolute risk by just 1%. The number needed to treat is 1/0.01 = 100. <div class="ec-teach"><div class="th">A big relative effect on a small baseline</div> When the baseline risk is low, an impressive relative risk reduction can correspond to a tiny absolute benefit. Here the 50% RRR translates to a 1% ARR and an NNT of 100, treat 100 people for 5 years to prevent one event. Reporting the absolute reduction and NNT alongside the relative figure keeps the benefit in proportion. The p-value speaks to whether an effect is real, not to how large it is. <div class="ec-src"><b>Source:</b> Cook RJ, Sackett DL. The number needed to treat: a clinically useful measure of treatment effect. BMJ 1995;310:452-454.</div></div></div> [[Start another case->Hub]] [[Restart this case->Risk reduction measures - Opening]] [[Next case →->Research abstract - Opening]]

<span class="ec-case-marker" hidden data-entry="Risk reduction measures. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ The p-value addresses significance, not size.</div> A p-value indicates whether an effect is likely real, not how large it is. One already have the numbers to quantify the benefit: RRR, ARR, and NNT. <div class="ec-teach"><div class="th">The error</div> Statistical significance and magnitude of benefit are different questions; RRR/ARR/NNT quantify the size. <div class="ec-src"><b>Source:</b> Cook RJ, Sackett DL. The number needed to treat: a clinically useful measure of treatment effect. BMJ 1995;310:452-454.</div></div></div> [[Try this question again->Risk reduction measures - Opening]] [[Start another case->Hub]]

<div class="ec-scene">Adolescent medicine · 08:45</div> A 17-year-old girl with anorexia nervosa is brought in by her parents after 4 months of progressive food restriction and weight loss. Body mass index is 13.8 kg/m2. Temperature is 35.4°C, blood pressure is 78/48 mm Hg, and pulse is 38/min. Serum potassium is 2.8 mEq/L. She is alert and insists she is fine and wants to go home. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Admit and nasogastric feeding because she is refusing food->Anorexia nervosa - Involuntary feeding trap]] [[Admit for stabilization with monitoring and cautious refeeding->Anorexia nervosa - Correct]] [[Admit; high-calorie feeding immediately->Anorexia nervosa - Fast feeding trap]] [[Correct potassium in the emergency department, then outpatient follow-up->Anorexia nervosa - Replete and release trap]] [[Discharge to outpatient psychiatry; she is alert and cooperative->Anorexia nervosa - Outpatient trap]]

<span class="ec-case-marker" hidden data-entry="Anorexia nervosa. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ That is how one cause refeeding syndrome.</div> Admission is right; the feeding rate is not. Aggressive caloric reintroduction in a severely malnourished patient triggers the intracellular shift of phosphate, potassium and magnesium, and her potassium is already 2.8. <div class="ec-teach"><div class="th">What this misses</div> Refeeding must be cautious and monitored, with electrolyte repletion and thiamine. Hypophosphatemia is the hallmark of refeeding syndrome. <div class="ec-src"><b>Source:</b> APA eating disorders guideline (2023); ASPEN refeeding consensus (2020).</div></div></div> [[Try this question again->Anorexia nervosa - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Anorexia nervosa. Opening"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Admit for stabilization with monitoring and cautious refeeding</div> She is admitted for medical stabilization: cardiac monitoring, electrolyte repletion, warming, and a cautious refeeding protocol with daily phosphate monitoring, alongside psychiatric care. <div class="ec-teach"><div class="th">Admission criteria worth knowing</div> Medical instability drives the decision to admit, independent of the patient's insight or preference: marked bradycardia, hypotension, hypothermia, orthostatic changes, electrolyte disturbance, arrhythmia, or very low body weight. Anorexia nervosa has among the highest mortality of psychiatric disorders, from cardiac complications and suicide. Once admitted, feeding is <b>cautious and monitored</b> because these patients are the highest-risk group for refeeding syndrome. Nutritional restoration comes first; psychotherapy is the mainstay of longer-term treatment, and in adolescents family-based treatment has the strongest evidence. <div class="ec-src"><b>Source:</b> APA Practice Guideline for the Treatment of Patients With Eating Disorders (2023); ASPEN refeeding consensus (2020).</div></div></div> <b>Admitted for stabilization and cautious refeeding.</b> [[Start another case->Hub]] [[Restart this case->Anorexia nervosa - Opening]] [[Next case →->Schizophrenia dopamine - Mech]]

<span class="ec-case-marker" hidden data-entry="Anorexia nervosa. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Sometimes necessary, and not the opening move.</div> Nasogastric feeding has a genuine place in severe restrictive eating disorders when oral intake is inadequate and the patient is medically unstable, so this is not invented. Starting there in a cooperative patient bypasses oral refeeding, which is preferred where possible, and turns the admission into a confrontation before any relationship has been built. <div class="ec-teach"><div class="th">Why this is wrong</div> Admit for medical stabilization with continuous cardiac monitoring, correct electrolytes before and during feeding, and reintroduce nutrition cautiously by mouth with close monitoring for refeeding syndrome. Escalate to tube feeding if oral intake proves inadequate. <div class="ec-src"><b>Source:</b> Society for Adolescent Health and Medicine. Medical Management of Restrictive Eating Disorders: Position Paper. J Adolesc Health 2022;71(5):648-654.</div></div></div> [[Try this question again->Anorexia nervosa - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Anorexia nervosa. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ One fixed the number that was easiest to fix.</div> Repleting potassium is necessary and it will happen. It is not what makes her safe. Her bradycardia, hypotension and hypothermia are markers of a starved myocardium, and they persist long after an electrolyte is corrected, the arrhythmia risk in severe anorexia does not resolve with a potassium infusion. Sending her home also means the refeeding that follows happens unmonitored, which is when the dangerous shifts occur. <div class="ec-teach"><div class="th">Why this is wrong</div> She meets criteria for inpatient medical admission on several counts independently: degree of malnutrition, bradycardia, hypotension, hypothermia and electrolyte disturbance. Admit for continuous cardiac monitoring, correct electrolytes before and during feeding, and reintroduce nutrition cautiously with close monitoring for refeeding syndrome. Her insistence that she is fine is characteristic of the illness and does not settle the disposition; capacity should be assessed rather than assumed. <div class="ec-src"><b>Source:</b> Society for Adolescent Health and Medicine. Medical Management of Restrictive Eating Disorders: Position Paper. J Adolesc Health 2022;71(5):648-654.</div></div></div> [[Try this question again->Anorexia nervosa - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Anorexia nervosa. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Alertness is not stability.</div> A heart rate of 38, systolic pressure of 78, temperature of 35.4°C and potassium of 2.8 are markers of medical instability that can precipitate fatal arrhythmia. Anorexia nervosa carries one of the highest mortality rates of any psychiatric illness, and much of it is cardiac. <div class="ec-teach"><div class="th">The misstep</div> Bradycardia, hypotension, hypothermia, and electrolyte disturbance are indications for inpatient medical stabilization regardless of the patient's mental state or wishes. <div class="ec-src"><b>Source:</b> APA Practice Guideline for the Treatment of Patients With Eating Disorders (2023).</div></div></div> [[Try this question again->Anorexia nervosa - Opening]] [[Start another case->Hub]]

<div class="ec-scene">Surgical ward · 23:50</div> A 78-year-old man is 2 days after hemiarthroplasty. Overnight he becomes agitated, pulls at his lines and does not recognize his daughter. His attention fluctuates markedly over minutes and he is drowsy at times and hypervigilant at others. His daughter says his memory was entirely normal at home a week ago. He was started on oxybutynin 2 days ago and has not passed urine since the afternoon. <span class="ec-prompt">Which of the following is the most likely diagnosis?</span> [[Delirium->Delirium - Dx correct]] [[Dementia->Delirium - Dx D1]] [[Postoperative stroke->Delirium - Dx D4]] [[Sundowning in established dementia->Delirium - Dx D2]] [[Wernicke encephalopathy->Delirium - Dx D5]]

<span class="ec-case-marker" hidden data-entry="Delirium. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Delirium.</div> Acute onset over hours to days, a fluctuating course, inattention, and altered level of consciousness, with a clear baseline a week earlier, is delirium. Inattention with a fluctuating conscious level is the feature that distinguishes it from every alternative here, and it is characteristically worse at night. <div class="ec-src"><b>Source:</b> Inouye SK, Westendorp RGJ, Saczynski JS. Delirium in elderly people. Lancet 2014;383(9920):911-922.</div></div> [[Start another case->Hub]] [[Restart this case->Delirium - Dx]] [[Next case →->Meniere disease - Dx]]

<span class="ec-case-marker" hidden data-entry="Delirium. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Dementia is the label most often applied to a confused older inpatient, which is why it is here. It develops over months to years with a stable conscious level and preserved attention until late. His daughter reports a normal baseline a week ago. <div class="ec-teach"><div class="th">What the findings point to</div> Acute onset over hours to days, a fluctuating course, inattention, and altered level of consciousness, with a clear baseline a week earlier, is delirium. Inattention with a fluctuating conscious level is the feature that distinguishes it from every alternative here, and it is characteristically worse at night. <div class="ec-src"><b>Source:</b> Inouye SK, Westendorp RGJ, Saczynski JS. Delirium in elderly people. Lancet 2014;383(9920):911-922.</div></div></div> [[Try this question again->Delirium - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Delirium. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Stroke belongs on the differential and warrants examination for focal signs. It produces a fixed deficit rather than a fluctuating conscious level, and there are no lateralizing findings. <div class="ec-teach"><div class="th">What the findings point to</div> Acute onset over hours to days, a fluctuating course, inattention, and altered level of consciousness, with a clear baseline a week earlier, is delirium. Inattention with a fluctuating conscious level is the feature that distinguishes it from every alternative here, and it is characteristically worse at night. <div class="ec-src"><b>Source:</b> Inouye SK, Westendorp RGJ, Saczynski JS. Delirium in elderly people. Lancet 2014;383(9920):911-922.</div></div></div> [[Try this question again->Delirium - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Delirium. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Evening agitation is a real phenomenon and the timing fits. It requires pre-existing dementia, which he does not have, and it does not produce fluctuating consciousness with inattention over minutes. <div class="ec-teach"><div class="th">What the findings point to</div> Acute onset over hours to days, a fluctuating course, inattention, and altered level of consciousness, with a clear baseline a week earlier, is delirium. Inattention with a fluctuating conscious level is the feature that distinguishes it from every alternative here, and it is characteristically worse at night. <div class="ec-src"><b>Source:</b> Inouye SK, Westendorp RGJ, Saczynski JS. Delirium in elderly people. Lancet 2014;383(9920):911-922.</div></div></div> [[Try this question again->Delirium - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Delirium. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This causes confusion with ophthalmoplegia and ataxia in a thiamine-deplete patient. There is no such history and no eye signs. <div class="ec-teach"><div class="th">What the findings point to</div> Acute onset over hours to days, a fluctuating course, inattention, and altered level of consciousness, with a clear baseline a week earlier, is delirium. Inattention with a fluctuating conscious level is the feature that distinguishes it from every alternative here, and it is characteristically worse at night. <div class="ec-src"><b>Source:</b> Inouye SK, Westendorp RGJ, Saczynski JS. Delirium in elderly people. Lancet 2014;383(9920):911-922.</div></div></div> [[Try this question again->Delirium - Dx]] [[Start another case->Hub]]

<div class="ec-scene">Preventive visit · 10:30</div> A 58-year-old woman has a 30 pack-year smoking history and quit 4 years ago. She is asymptomatic, in good health, and would be a candidate for curative treatment if a cancer were found. She asks whether she should be screened for lung cancer. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Annual chest radiograph instead->Lung screening - CXR trap]] [[Annual low-dose CT after shared decision-making->Lung screening - Correct]] [[Annual low-dose CT indefinitely, regardless of health->Lung screening - Indefinite trap]] [[Screening is unnecessary since she quit->Lung screening - Quit trap]] [[Single baseline low-dose CT, repeat only if abnormal->Lung screening - One-off trap]]

<span class="ec-case-marker" hidden data-entry="Lung screening. Opening"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Annual low-dose CT after shared decision-making</div> One discuss the benefits and harms, including false positives and incidental findings, and arrange annual low-dose CT, along with continued support for staying smoke-free. <div class="ec-teach"><div class="th">The eligibility criteria</div> Annual low-dose CT is recommended for adults aged <b>50 to 80</b> with a <b>20 pack-year or greater</b> smoking history who currently smoke or <b>quit within the past 15 years</b>. Screening stops once a person has not smoked for 15 years or develops a health problem that substantially limits life expectancy or the ability or willingness to have curative lung surgery. The evidence base is the National Lung Screening Trial and the NELSON trial. Shared decision-making is part of the recommendation, because false positives and incidental findings are common. <div class="ec-src"><b>Source:</b> USPSTF Lung Cancer Screening recommendation statement (JAMA 2021); National Lung Screening Trial (N Engl J Med 2011).</div></div></div> <b>Enrolled in annual low-dose CT screening.</b> [[Start another case->Hub]] [[Restart this case->Lung screening - Opening]] [[Next case →->NNT interpretation - Biostat]]

<span class="ec-case-marker" hidden data-entry="Lung screening. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ A baseline scan is a snapshot of a process that runs for years.</div> A normal scan today says there is no visible cancer today. The mortality benefit in the trials came from repeated rounds catching tumors that appeared in the interval between scans, a one-time examination captures prevalent disease and then stops looking. Her risk does not reset because one scan was clear. <div class="ec-teach"><div class="th">Why this is wrong</div> Screening is annual for as long as she remains eligible: while she is aged 50 to 80 years, until 15 years have passed since quitting, and until a health problem would substantially limit life expectancy or her willingness to undergo curative surgery. At 58, with 30 pack-years and 4 years since quitting, she qualifies now and will continue to qualify for another 11 years. <div class="ec-src"><b>Source:</b> USPSTF, Screening for Lung Cancer: Recommendation Statement, JAMA 2021;325(10):962-970; National Lung Screening Trial, N Engl J Med 2011;365:395-409.</div></div></div> [[Try this question again->Lung screening - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Lung screening. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Right test and interval, with no stopping rule.</div> Annual low-dose computed tomography is correct, so this is the closest wrong answer. Screening has a defined endpoint: it stops once she is older than 80, once 15 years have passed since quitting, or when a health problem substantially limits life expectancy or the willingness or ability to undergo curative lung surgery. Screening someone who could not be treated only generates harm. <div class="ec-teach"><div class="th">Why this is wrong</div> Screen annually after shared decision-making, and re-check eligibility each year. Screening also carries real harms, false positives, incidental findings, invasive workup of benign nodules, which is why the conversation is part of the recommendation rather than an optional extra. <div class="ec-src"><b>Source:</b> USPSTF. Screening for Lung Cancer: Recommendation Statement. JAMA 2021;325(10):962-970.</div></div></div> [[Try this question again->Lung screening - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Lung screening. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Chest radiography does not reduce lung cancer mortality.</div> Trials of chest radiograph screening failed to show a mortality benefit. Low-dose CT is the modality that did, and substituting a test that does not work gives false reassurance. <div class="ec-teach"><div class="th">Where this breaks down</div> Low-dose CT is the only lung cancer screening modality shown to reduce mortality. Chest radiography is not recommended for screening. <div class="ec-src"><b>Source:</b> USPSTF Lung Cancer Screening recommendation (2021); National Lung Screening Trial (N Engl J Med 2011).</div></div></div> [[Try this question again->Lung screening - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Lung screening. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Risk persists for years after quitting.</div> Quitting reduces risk over time but does not eliminate it, which is why eligibility extends to former smokers who quit within the past 15 years. She quit 4 years ago and remains squarely eligible. <div class="ec-teach"><div class="th">Why not this</div> Eligibility includes people who currently smoke or quit within the past 15 years. Quitting does not immediately remove screening benefit. <div class="ec-src"><b>Source:</b> USPSTF Lung Cancer Screening recommendation (2021).</div></div></div> [[Try this question again->Lung screening - Opening]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 14:30</div> A 54-year-old man with chronic heavy alcohol use and months of poor intake is brought in confused after 3 days of worsening unsteadiness and double vision. He has horizontal nystagmus on lateral gaze with bilateral lateral rectus weakness, a broad-based ataxic gait, and disorientation to time and place. He is afebrile with no neck stiffness and no focal limb weakness. Glucose is 58 mg/dL and there is no history of head injury. <span class="ec-prompt">Which of the following is the most likely diagnosis?</span> [[Acute alcohol intoxication->Wernicke - Dx D3]] [[Alcohol withdrawal delirium->Wernicke - Dx D1]] [[Hepatic encephalopathy->Wernicke - Dx D2]] [[Subdural hematoma->Wernicke - Dx D4]] [[Wernicke encephalopathy->Wernicke - Dx correct]]

<span class="ec-case-marker" hidden data-entry="Wernicke. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Intoxication causes ataxia, nystagmus and confusion and is genuinely the hardest clinical mimic, which is why Wernicke is missed. It resolves as the level falls, whereas his eye signs and ataxia persist and follow months of poor intake. <div class="ec-teach"><div class="th">What the findings point to</div> Ophthalmoplegia, ataxia and confusion in a thiamine-deplete patient. Only a minority present with the complete triad, so treatment is given on suspicion rather than on completeness, and untreated it progresses to the largely irreversible amnestic syndrome of Korsakoff. <div class="ec-src"><b>Source:</b> Thomson AD, Marshall EJ. Alcohol Alcohol 2006 (treatment of Wernicke-Korsakoff syndrome).</div></div></div> [[Try this question again->Wernicke - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Wernicke. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Delirium tremens is the expected diagnosis in this population and is the closest alternative. It occurs 48 to 96 hours after the last drink with autonomic hyperactivity, tremor and hallucinations, and it does not cause ophthalmoplegia or a broad-based ataxia. <div class="ec-teach"><div class="th">What the findings point to</div> Ophthalmoplegia, ataxia and confusion in a thiamine-deplete patient. Only a minority present with the complete triad, so treatment is given on suspicion rather than on completeness, and untreated it progresses to the largely irreversible amnestic syndrome of Korsakoff. <div class="ec-src"><b>Source:</b> Thomson AD, Marshall EJ. Alcohol Alcohol 2006 (treatment of Wernicke-Korsakoff syndrome).</div></div></div> [[Try this question again->Wernicke - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Wernicke. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This causes confusion with asterixis in a patient with chronic liver disease and is common in the same population. It does not produce nystagmus with lateral rectus palsy or gait ataxia. <div class="ec-teach"><div class="th">What the findings point to</div> Ophthalmoplegia, ataxia and confusion in a thiamine-deplete patient. Only a minority present with the complete triad, so treatment is given on suspicion rather than on completeness, and untreated it progresses to the largely irreversible amnestic syndrome of Korsakoff. <div class="ec-src"><b>Source:</b> Thomson AD, Marshall EJ. Alcohol Alcohol 2006 (treatment of Wernicke-Korsakoff syndrome).</div></div></div> [[Try this question again->Wernicke - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Wernicke. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Chronic subdural bleeding is common in this population from falls and must be considered. It usually gives focal signs, headache and a fluctuating conscious level, and there is no head injury history or lateralizing deficit. <div class="ec-teach"><div class="th">What the findings point to</div> Ophthalmoplegia, ataxia and confusion in a thiamine-deplete patient. Only a minority present with the complete triad, so treatment is given on suspicion rather than on completeness, and untreated it progresses to the largely irreversible amnestic syndrome of Korsakoff. <div class="ec-src"><b>Source:</b> Thomson AD, Marshall EJ. Alcohol Alcohol 2006 (treatment of Wernicke-Korsakoff syndrome).</div></div></div> [[Try this question again->Wernicke - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Wernicke. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Wernicke encephalopathy.</div> Ophthalmoplegia, ataxia and confusion in a thiamine-deplete patient. Only a minority present with the complete triad, so treatment is given on suspicion rather than on completeness, and untreated it progresses to the largely irreversible amnestic syndrome of Korsakoff. <div class="ec-src"><b>Source:</b> Thomson AD, Marshall EJ. Alcohol Alcohol 2006 (treatment of Wernicke-Korsakoff syndrome).</div></div> [[Start another case->Hub]] [[Restart this case->Wernicke - Dx]] [[Next case →->Parkinson treatment - Rx]]

<div class="ec-scene">Primary care clinic · 09:20</div> A 68-year-old man who smoked a pack a day for 30 years and quit at 60 comes in for routine care. He is asymptomatic. The physician review which one-time screening he is due. <span class="ec-prompt">Which of the following is the most appropriate health maintenance measure?</span> [[Abdominal CT instead of ultrasound->AAA screening - Cataract trap]] [[Annual abdominal ultrasounds indefinitely->AAA screening - Single dose trap]] [[Obtain a one-time screening abdominal ultrasound->AAA screening - Correct]] [[Screen only if he develops pain->AAA screening - Lubricant trap]] [[Skip screening now that he quit smoking->AAA screening - Confirmation trap]]

<span class="ec-case-marker" hidden data-entry="AAA screening. Opening"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Obtain a one-time screening abdominal ultrasound</div> One order a single screening abdominal ultrasound and document it as a one-time study. <div class="ec-teach"><div class="th">One scan, the right group</div> The USPSTF gives a B recommendation for one-time abdominal ultrasound screening for aortic aneurysm in men aged 65 to 75 who have ever smoked. He is 68 and a former smoker, so he qualifies. Screening targets asymptomatic men because most aneurysms are silent until rupture, which carries a mortality as high as 80%. It is a single scan, not annual, and ultrasound, not CT, is the screening modality. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Screening for Abdominal Aortic Aneurysm: Recommendation Statement. JAMA 2019;322(22):2211-2218 (B recommendation).</div></div></div> <b>One-time aneurysm screening arranged.</b> [[Start another case->Hub]] [[Restart this case->AAA screening - Opening]] [[Next case →->Infective endocarditis - Rx]]

<span class="ec-case-marker" hidden data-entry="AAA screening. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Screening is one-time, not annual.</div> Repeating ultrasounds every year is not what the recommendation calls for and adds cost and follow-up without added benefit for a negative initial screen. <div class="ec-teach"><div class="th">The error</div> The USPSTF recommends a single screening ultrasound for eligible men, not indefinite annual scans. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Screening for Abdominal Aortic Aneurysm: Recommendation Statement. JAMA 2019;322(22):2211-2218 (B recommendation).</div></div></div> [[Try this question again->AAA screening - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="AAA screening. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Screening is for asymptomatic men.</div> Waiting for pain means waiting for the aneurysm to enlarge or rupture; the whole point is to detect it while silent. <div class="ec-teach"><div class="th">The error</div> AAA screening applies to asymptomatic men in the eligible group; symptoms warrant urgent evaluation, not routine screening. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Screening for Abdominal Aortic Aneurysm: Recommendation Statement. JAMA 2019;322(22):2211-2218 (B recommendation).</div></div></div> [[Try this question again->AAA screening - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="AAA screening. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Ultrasound is the screening test.</div> CT adds radiation and contrast for no screening advantage; ultrasonography is accurate, safe, and the recommended modality. <div class="ec-teach"><div class="th">The error</div> The recommended screening test for AAA is abdominal ultrasonography, not CT. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Screening for Abdominal Aortic Aneurysm: Recommendation Statement. JAMA 2019;322(22):2211-2218 (B recommendation).</div></div></div> [[Try this question again->AAA screening - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="AAA screening. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ "Ever smoked" includes former smokers.</div> Quitting lowers ongoing risk but does not erase the accumulated risk; former smokers remain in the screened group. <div class="ec-teach"><div class="th">The error</div> The eligibility criterion is having ever smoked, which includes those who have since quit. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Screening for Abdominal Aortic Aneurysm: Recommendation Statement. JAMA 2019;322(22):2211-2218 (B recommendation).</div></div></div> [[Try this question again->AAA screening - Opening]] [[Start another case->Hub]]

<div class="ec-scene">Preconception visit · 11:20</div> A 30-year-old woman plans to conceive within the next few months. Her first child was born with spina bifida. She takes no medications and asks what she should do before becoming pregnant. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[High-dose folic acid; check a folate level to confirm->Folate pregnancy - Level trap]] [[Standard low-dose folic acid->Folate pregnancy - Standard dose trap]] [[Start high-dose folic acid now, ahead of pregnancy->Folate pregnancy - Correct]] [[Test methylenetetrahydrofolate reductase genotype and set the dose by the result->Folate pregnancy - MTHFR trap]] [[Wait until pregnancy is confirmed to start->Folate pregnancy - Timing trap]]

<span class="ec-case-marker" hidden data-entry="Folate pregnancy. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ A test that cannot change the recommendation.</div> Measuring folate seems like reasonable stewardship before a tenfold dose. Her indication is not biochemical, it is her obstetric history. High-dose supplementation is recommended after a neural tube defect-affected pregnancy regardless of folate status, because the mechanism is not simply deficiency, and a normal level would not lower the dose. <div class="ec-teach"><div class="th">Why this is wrong</div> Start 4 mg daily at least one month before conception and continue through the first trimester. No test modifies that, not serum folate, not red cell folate, and not MTHFR genotyping, which professional bodies advise against. <div class="ec-src"><b>Source:</b> CDC. Recommendations for the use of folic acid to reduce the number of cases of spina bifida and other neural tube defects. MMWR 1991;40(RR-14).</div></div></div> [[Try this question again->Folate pregnancy - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Folate pregnancy. Opening"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Start high-dose folic acid now, ahead of pregnancy</div> It is started high-dose folic acid before conception and continue it through the first trimester, along with standard preconception counseling. <div class="ec-teach"><div class="th">Doses and timing</div> Folic acid prevents neural tube defects, and the timing matters more than almost any other supplement: the neural tube closes in the first 4 weeks after conception, often before a woman knows she is pregnant. All women capable of pregnancy are advised to take a daily supplement starting <b>at least one month before conception</b> and continuing through the first trimester. The dose is higher in specific situations, a previous NTD-affected pregnancy, and in women taking antiepileptic drugs such as valproate or carbamazepine, which interfere with folate. This is a <b>drug-nutrient interaction</b> pattern worth knowing alongside methotrexate and phenytoin, which also deplete folate. <div class="ec-src"><b>Source:</b> USPSTF Folic Acid Supplementation to Prevent Neural Tube Defects recommendation statement; CDC folic acid guidance.</div></div></div> <b>Supplementation started before conception.</b> [[Start another case->Hub]] [[Restart this case->Folate pregnancy - Opening]] [[Next case →->Bariatric deficiency - Opening]]

<span class="ec-case-marker" hidden data-entry="Folate pregnancy. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Correct vitamin, insufficient dose.</div> The routine dose is for average-risk women. A previous NTD-affected pregnancy substantially raises recurrence risk, and the recommended dose in that situation is roughly ten times higher. <div class="ec-teach"><div class="th">Where this breaks down</div> Women with a prior neural tube defect–affected pregnancy require high-dose folic acid, not the standard dose. <div class="ec-src"><b>Source:</b> CDC folic acid recommendations; USPSTF folic acid supplementation for the prevention of neural tube defects.</div></div></div> [[Try this question again->Folate pregnancy - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Folate pregnancy. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ A test that does not change what one do.</div> MTHFR genotyping has become popular precisely because the biochemistry sounds compelling, the enzyme sits in the folate pathway, so surely the variant should guide dosing. It does not. The polymorphisms are common, weakly penetrant, and have no demonstrated clinical utility for this decision; professional bodies advise against ordering the test. Meanwhile the result takes weeks, and she plans to conceive within months. <div class="ec-teach"><div class="th">Why this is wrong</div> Her indication is her obstetric history, not her genotype. A previous neural tube defect–affected pregnancy calls for high-dose folic acid, 4 mg daily, roughly ten times the average-risk dose, started at least one month before conception and continued through the first trimester. No test modifies that. <div class="ec-src"><b>Source:</b> ACMG Practice Guideline: lack of evidence for MTHFR polymorphism testing, Genet Med 2013;15(2):153-156 (reaffirmed 2020); CDC recommendations for folic acid to prevent recurrence of neural tube defects, MMWR 1991;40(RR-14).</div></div></div> [[Try this question again->Folate pregnancy - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Folate pregnancy. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ By then the neural tube has closed.</div> The neural tube closes within the first 4 weeks after conception, often before a pregnancy is recognized. Supplementation started after a positive test misses the window it exists to protect. <div class="ec-teach"><div class="th">Why not this</div> Folic acid must begin before conception, ideally at least one month prior, and continue through the first trimester. <div class="ec-src"><b>Source:</b> USPSTF folic acid recommendation; CDC guidance.</div></div></div> [[Try this question again->Folate pregnancy - Opening]] [[Start another case->Hub]]

<div class="ec-scene">Pediatric ward · 14:30</div> A 3-year-old child in a food-insecure setting has had pitting edema of the legs and a distended abdomen for 2 months, with thin depigmented hair and irritability. Serum albumin is 1.8 g/dL. Muscle wasting is present but subcutaneous fat is partly preserved. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Broad-spectrum antibiotics alone without nutritional support->Malnutrition assessment - Opening Dx5]] [[Cautious phased refeeding with a high-protein formula->Malnutrition assessment - High protein trap]] [[Cautious phased refeeding, electrolyte monitoring, treat infection->Malnutrition assessment - Correct]] [[Immediate high-calorie feeding to correct quickly->Malnutrition assessment - Rapid feeding trap]] [[Intravenous fluid boluses to correct the deficit->Malnutrition assessment - IV fluid trap]]

<span class="ec-case-marker" hidden data-entry="Malnutrition assessment. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ The edema looks like it should be treated with protein, and that is the trap.</div> Kwashiorkor is associated with hypoalbuminemia, so a high-protein formula seems mechanistically aimed at the edema. Starting there overloads a compromised liver and kidney, worsens the metabolic disturbance, and is associated with higher mortality. The initial formula is deliberately low in protein and sodium. <div class="ec-teach"><div class="th">Why this is wrong</div> Begin phased refeeding with a low-protein, low-sodium, high-potassium formula, advancing only once he is stable, then move to a catch-up formula. Treat presumed infection, correct hypoglycemia, hypothermia and micronutrients, and rehydrate orally or by tube rather than intravenously unless he is shocked. <div class="ec-src"><b>Source:</b> WHO Guideline: Updates on the Management of Severe Acute Malnutrition in Infants and Children, 2013.</div></div></div> [[Try this question again->Malnutrition assessment - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Malnutrition assessment. Opening"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Cautious phased refeeding, electrolyte monitoring, treat infection</div> One begin phased nutritional rehabilitation with micronutrient supplementation, treat intercurrent infection, and monitor electrolytes closely, advancing calories gradually. <div class="ec-teach"><div class="th">Kwashiorkor versus marasmus</div> <b>Kwashiorkor</b> is predominantly protein deficiency with relatively preserved calorie intake: edema, hypoalbuminemia, fatty liver with a distended abdomen, skin and hair changes, and irritability. <b>Marasmus</b> is global calorie deficiency: severe wasting of muscle and subcutaneous fat, a shrunken appearance, and <em>no</em> edema, the presence of edema is the practical distinguishing feature. Both require cautious phased refeeding because both carry high refeeding syndrome risk. A caution on assessment in adults: albumin and prealbumin are heavily influenced by inflammation and are unreliable standalone markers of nutritional status. <div class="ec-src"><b>Source:</b> WHO guideline on the management of severe acute malnutrition; ASPEN refeeding consensus (2020).</div></div></div> <b>Phased rehabilitation begun safely.</b> [[Start another case->Hub]] [[Restart this case->Malnutrition assessment - Opening]] [[Next case →->Refeeding syndrome - Dx]]

<span class="ec-case-marker" hidden data-entry="Malnutrition assessment. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ The edema is not telling one he is fluid-overloaded, and it is not telling one to give a bolus either.</div> Severe acute malnutrition changes how a child handles sodium and volume. Cell membrane pumps fail, sodium is retained intracellularly while total body potassium is depleted, and standard isotonic saline delivers far too much sodium and far too little potassium. Volume boluses in this state carry a real risk of fluid overload and cardiac decompensation, and the clinical signs of dehydration it would normally rely on are unreliable in a child with kwashiorkor. <div class="ec-teach"><div class="th">Why this is wrong</div> Rehydrate orally or by nasogastric tube using a low-sodium, high-potassium solution formulated for malnutrition, given slowly with close monitoring for overload. Reserve intravenous fluids for shock. Alongside this: treat presumed infection, correct hypoglycemia and hypothermia, supply potassium and magnesium, and begin low-energy phased feeding before any catch-up growth phase. It should be said that the evidence behind the fluid restriction is weak and under active trial re-examination, but it remains the standard of care. <div class="ec-src"><b>Source:</b> WHO Guideline: Updates on the Management of Severe Acute Malnutrition in Infants and Children, 2013; WHO Pocket Book of Hospital Care for Children, 2nd ed.</div></div></div> [[Try this question again->Malnutrition assessment - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Malnutrition assessment. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ The fastest way to kill a severely malnourished child.</div> Aggressive caloric loading in severe malnutrition precipitates refeeding syndrome, the intracellular shift of phosphate, potassium and magnesium, and can cause cardiac failure and death. <div class="ec-teach"><div class="th">The misstep</div> Severe malnutrition requires cautious, phased refeeding with electrolyte monitoring. Hypophosphatemia is the hallmark of refeeding syndrome. <div class="ec-src"><b>Source:</b> WHO management of severe acute malnutrition; ASPEN refeeding consensus (2020).</div></div></div> [[Try this question again->Malnutrition assessment - Opening]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 11:45</div> A 68-year-old woman has 4 days of vomiting and poor oral intake. She is orthostatic with dry mucous membranes. Creatinine has risen from a baseline of 0.9 to 3.1 mg/dL, with a blood urea nitrogen to creatinine ratio of 28. Urine sodium and creatinine give a fractional excretion of sodium of 0.4%. She takes lisinopril and ibuprofen. Urinalysis shows no protein, no blood and no casts on dipstick. <span class="ec-prompt">Which of the following is the most appropriate next step in diagnosis?</span> [[Renal biopsy for histologic diagnosis->Acute kidney injury - Ix D5]] [[Renal ultrasonography->Acute kidney injury - Ix D1]] [[Repeat FENa after starting a diuretic->Acute kidney injury - Ix D2]] [[Serum and urine protein electrophoresis->Acute kidney injury - Ix D3]] [[Urine microscopy for sediment->Acute kidney injury - Ix correct]]

<span class="ec-case-marker" hidden data-entry="Acute kidney injury. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Biopsy is reserved for unexplained acute kidney injury after non-invasive evaluation, or where glomerular or interstitial disease is suspected. The cause here is apparent from the history. <div class="ec-teach"><div class="th">What the findings point to</div> Sediment examination is the test that distinguishes prerenal azotemia from established acute tubular necrosis at the bedside, bland sediment with hyaline casts supports a prerenal state that will reverse with volume, whereas muddy brown granular casts indicate tubular injury that will not. That distinction determines whether fluid alone is the treatment. <div class="ec-src"><b>Source:</b> KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney Int Suppl 2012;2(1):1-138.</div></div></div> [[Try this question again->Acute kidney injury - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Acute kidney injury. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Excluding obstruction is part of any acute kidney injury workup and this should be done, but her history, orthostasis, fractional sodium excretion of 0.4% and urea-to-creatinine ratio of 28 all point to a prerenal cause, and imaging must not delay fluid resuscitation. <div class="ec-teach"><div class="th">What the findings point to</div> Sediment examination is the test that distinguishes prerenal azotemia from established acute tubular necrosis at the bedside, bland sediment with hyaline casts supports a prerenal state that will reverse with volume, whereas muddy brown granular casts indicate tubular injury that will not. That distinction determines whether fluid alone is the treatment. <div class="ec-src"><b>Source:</b> KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney Int Suppl 2012;2(1):1-138.</div></div></div> [[Try this question again->Acute kidney injury - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Acute kidney injury. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Fractional sodium excretion is unreliable once a diuretic has been given, the fractional excretion of urea is used instead in that situation. Deliberately confounding the own test is the error. <div class="ec-teach"><div class="th">What the findings point to</div> Sediment examination is the test that distinguishes prerenal azotemia from established acute tubular necrosis at the bedside, bland sediment with hyaline casts supports a prerenal state that will reverse with volume, whereas muddy brown granular casts indicate tubular injury that will not. That distinction determines whether fluid alone is the treatment. <div class="ec-src"><b>Source:</b> KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney Int Suppl 2012;2(1):1-138.</div></div></div> [[Try this question again->Acute kidney injury - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Acute kidney injury. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This screens for myeloma-related kidney disease and is appropriate when the cause is unexplained, particularly with anemia, hypercalcemia or bone pain. It is not the immediate question in a woman with 4 days of vomiting. <div class="ec-teach"><div class="th">What the findings point to</div> Sediment examination is the test that distinguishes prerenal azotemia from established acute tubular necrosis at the bedside, bland sediment with hyaline casts supports a prerenal state that will reverse with volume, whereas muddy brown granular casts indicate tubular injury that will not. That distinction determines whether fluid alone is the treatment. <div class="ec-src"><b>Source:</b> KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney Int Suppl 2012;2(1):1-138.</div></div></div> [[Try this question again->Acute kidney injury - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Acute kidney injury. Ix"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Urine microscopy for sediment.</div> Sediment examination is the test that distinguishes prerenal azotemia from established acute tubular necrosis at the bedside, bland sediment with hyaline casts supports a prerenal state that will reverse with volume, whereas muddy brown granular casts indicate tubular injury that will not. That distinction determines whether fluid alone is the treatment. <div class="ec-src"><b>Source:</b> KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney Int Suppl 2012;2(1):1-138.</div></div> [[Start another case->Hub]] [[Restart this case->Acute kidney injury - Ix]] [[Next case →->Rhabdomyolysis - Ix]]

<div class="ec-scene">Emergency department · 04:20</div> A 39-year-old man has 6 hours of severe colicky left flank pain radiating to the groin, with nausea. He is afebrile and hemodynamically stable. Urinalysis shows microscopic hematuria without nitrites or leukocyte esterase. Creatinine is 0.9 mg/dL. This is his first such episode and analgesia has been given. <span class="ec-prompt">Which of the following is the most appropriate next step in diagnosis?</span> [[CT abdomen/pelvis with Intravenous contrast->Nephrolithiasis - Ix ct]] [[Intravenous pyelography->Nephrolithiasis - Ix intravenous]] [[Non-contrast CT abdomen/pelvis->Nephrolithiasis - Ix correct]] [[Plain abdominal radiography->Nephrolithiasis - Ix plain]] [[Renal and bladder ultrasonography->Nephrolithiasis - Ix renal]]

<span class="ec-case-marker" hidden data-entry="Nephrolithiasis. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Contrast obscures stones within the collecting system, which is precisely what one is looking for, and adds a nephrotoxic and allergy risk for no diagnostic gain. <div class="ec-teach"><div class="th">What to do instead</div> Non-contrast computed tomography is the reference standard for urolithiasis: it detects essentially all stones regardless of composition, gives size and location, which determine whether the stone will pass, and identifies alternative diagnoses in a first presentation of undifferentiated flank pain. <div class="ec-src"><b>Source:</b> Assimos D, et al. AUA/Endourological Society Guideline: Surgical Management of Stones. J Urol 2016 (amended 2019); Smith-Bindman R, et al. N Engl J Med 2014;371(12):1100-1110 (ultrasonography vs CT for suspected nephrolithiasis).</div></div></div> [[Try this question again->Nephrolithiasis - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Nephrolithiasis. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Intravenous pyelography is not the next step.</div> This was the historical standard and has been superseded. It is slower, needs contrast, delivers comparable or greater radiation, and is less sensitive than non-contrast computed tomography. <div class="ec-teach"><div class="th">What to do instead</div> Non-contrast computed tomography is the reference standard for urolithiasis: it detects essentially all stones regardless of composition, gives size and location, which determine whether the stone will pass, and identifies alternative diagnoses in a first presentation of undifferentiated flank pain. <div class="ec-src"><b>Source:</b> Assimos D, et al. AUA/Endourological Society Guideline: Surgical Management of Stones. J Urol 2016 (amended 2019); Smith-Bindman R, et al. N Engl J Med 2014;371(12):1100-1110 (ultrasonography vs CT for suspected nephrolithiasis).</div></div></div> [[Try this question again->Nephrolithiasis - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Nephrolithiasis. Ix"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Non-contrast CT abdomen/pelvis</div> Non-contrast computed tomography is the reference standard for urolithiasis: it detects essentially all stones regardless of composition, gives size and location, which determine whether the stone will pass, and identifies alternative diagnoses in a first presentation of undifferentiated flank pain. <div class="ec-src"><b>Source:</b> Assimos D, et al. AUA/Endourological Society Guideline: Surgical Management of Stones. J Urol 2016 (amended 2019); Smith-Bindman R, et al. N Engl J Med 2014;371(12):1100-1110 (ultrasonography vs CT for suspected nephrolithiasis).</div></div> [[Start another case->Hub]] [[Restart this case->Nephrolithiasis - Ix]] [[Next case →->Nephrotic syndrome - Dx]]

<span class="ec-case-marker" hidden data-entry="Nephrolithiasis. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Plain abdominal radiography is not the next step.</div> A plain film shows only radio-opaque stones, misses uric acid stones entirely, and cannot reliably localize or size a ureteral stone. Its main use is following a stone already known to be visible. <div class="ec-teach"><div class="th">What to do instead</div> Non-contrast computed tomography is the reference standard for urolithiasis: it detects essentially all stones regardless of composition, gives size and location, which determine whether the stone will pass, and identifies alternative diagnoses in a first presentation of undifferentiated flank pain. <div class="ec-src"><b>Source:</b> Assimos D, et al. AUA/Endourological Society Guideline: Surgical Management of Stones. J Urol 2016 (amended 2019); Smith-Bindman R, et al. N Engl J Med 2014;371(12):1100-1110 (ultrasonography vs CT for suspected nephrolithiasis).</div></div></div> [[Try this question again->Nephrolithiasis - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Nephrolithiasis. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Renal and bladder ultrasonography is not the next step.</div> This is the right first test in pregnancy, in children, and in patients with recurrent known stone disease where limiting cumulative radiation matters, so it is a real and increasingly favored option. It is less sensitive for small and mid-ureteral stones and gives less reliable sizing, and this is a first presentation where an alternative diagnosis has not yet been excluded. <div class="ec-teach"><div class="th">What to do instead</div> Non-contrast computed tomography is the reference standard for urolithiasis: it detects essentially all stones regardless of composition, gives size and location, which determine whether the stone will pass, and identifies alternative diagnoses in a first presentation of undifferentiated flank pain. <div class="ec-src"><b>Source:</b> Assimos D, et al. AUA/Endourological Society Guideline: Surgical Management of Stones. J Urol 2016 (amended 2019); Smith-Bindman R, et al. N Engl J Med 2014;371(12):1100-1110 (ultrasonography vs CT for suspected nephrolithiasis).</div></div></div> [[Try this question again->Nephrolithiasis - Ix]] [[Start another case->Hub]]

<div class="ec-scene">Outpatient clinic · 11:20</div> A 23-year-old woman has 5 days of lower abdominal pain with cervical motion and adnexal tenderness. Temperature is 37.8°C. Pregnancy test is negative and there is no adnexal mass. She tolerates oral intake, is hemodynamically stable, and has no allergies. She has a new sexual partner and inconsistent condom use. <span class="ec-prompt">Which of the following is the most appropriate pharmacotherapy?</span> [[Ceftriaxone once, then doxycycline and metronidazole->Pelvic inflammatory disease - Rx correct]] [[Intramuscular ceftriaxone once; oral doxycycline 14 days->Pelvic inflammatory disease - Rx D1]] [[Intravenous cefoxitin and doxycycline, inpatient->Pelvic inflammatory disease - Rx D5]] [[Oral doxycycline alone for a full 14-day course->Pelvic inflammatory disease - Rx D4]] [[Oral levofloxacin and metronidazole 14 days->Pelvic inflammatory disease - Rx D3]]

<span class="ec-case-marker" hidden data-entry="Pelvic inflammatory disease. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best choice.</div> This was the standard regimen for years and is what most people remember, which makes it the closest wrong answer. The 2021 update moved metronidazole from optional to recommended for all patients rather than only for suspected abscess or bacterial vaginosis. <div class="ec-teach"><div class="th">What to give instead</div> The recommended outpatient regimen. Ceftriaxone covers gonorrhea, doxycycline covers chlamydia and is given for a full 14 days, and metronidazole was added for all patients in the 2021 guidelines because anaerobes are recovered from the upper genital tract in a substantial proportion of cases and are implicated in the tubal damage that causes infertility. <div class="ec-src"><b>Source:</b> Workowski KA, et al. Sexually Transmitted Infections Treatment Guidelines, 2021. MMWR Recomm Rep 2021;70(4):1-187.</div></div></div> [[Try this question again->Pelvic inflammatory disease - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Pelvic inflammatory disease. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Ceftriaxone once, then doxycycline and metronidazole</div> The recommended outpatient regimen. Ceftriaxone covers gonorrhea, doxycycline covers chlamydia and is given for a full 14 days, and metronidazole was added for all patients in the 2021 guidelines because anaerobes are recovered from the upper genital tract in a substantial proportion of cases and are implicated in the tubal damage that causes infertility. <div class="ec-src"><b>Source:</b> Workowski KA, et al. Sexually Transmitted Infections Treatment Guidelines, 2021. MMWR Recomm Rep 2021;70(4):1-187.</div></div> [[Start another case->Hub]] [[Restart this case->Pelvic inflammatory disease - Rx]] [[Next case →->Otitis media - Rx]]

<span class="ec-case-marker" hidden data-entry="Pelvic inflammatory disease. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best choice.</div> This is the correct parenteral regimen, but admission is reserved for pregnancy, tubo-ovarian abscess, inability to tolerate oral therapy, failed outpatient treatment, severe illness, or a surgical emergency. She has none of these. <div class="ec-teach"><div class="th">What to give instead</div> The recommended outpatient regimen. Ceftriaxone covers gonorrhea, doxycycline covers chlamydia and is given for a full 14 days, and metronidazole was added for all patients in the 2021 guidelines because anaerobes are recovered from the upper genital tract in a substantial proportion of cases and are implicated in the tubal damage that causes infertility. <div class="ec-src"><b>Source:</b> Workowski KA, et al. Sexually Transmitted Infections Treatment Guidelines, 2021. MMWR Recomm Rep 2021;70(4):1-187.</div></div></div> [[Try this question again->Pelvic inflammatory disease - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Pelvic inflammatory disease. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best choice.</div> Doxycycline is essential but treats chlamydia and some atypicals only. Omitting gonococcal and anaerobic cover leaves the two organism groups most associated with tubal damage untreated. <div class="ec-teach"><div class="th">What to give instead</div> The recommended outpatient regimen. Ceftriaxone covers gonorrhea, doxycycline covers chlamydia and is given for a full 14 days, and metronidazole was added for all patients in the 2021 guidelines because anaerobes are recovered from the upper genital tract in a substantial proportion of cases and are implicated in the tubal damage that causes infertility. <div class="ec-src"><b>Source:</b> Workowski KA, et al. Sexually Transmitted Infections Treatment Guidelines, 2021. MMWR Recomm Rep 2021;70(4):1-187.</div></div></div> [[Try this question again->Pelvic inflammatory disease - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Pelvic inflammatory disease. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best choice.</div> Fluoroquinolone-based regimens are alternatives where cephalosporins cannot be used, so this is not invented. Widespread gonococcal fluoroquinolone resistance means they are no longer recommended as first-line, and they carry boxed warnings. <div class="ec-teach"><div class="th">What to give instead</div> The recommended outpatient regimen. Ceftriaxone covers gonorrhea, doxycycline covers chlamydia and is given for a full 14 days, and metronidazole was added for all patients in the 2021 guidelines because anaerobes are recovered from the upper genital tract in a substantial proportion of cases and are implicated in the tubal damage that causes infertility. <div class="ec-src"><b>Source:</b> Workowski KA, et al. Sexually Transmitted Infections Treatment Guidelines, 2021. MMWR Recomm Rep 2021;70(4):1-187.</div></div></div> [[Try this question again->Pelvic inflammatory disease - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 19:50</div> A 64-year-old man with type 2 diabetes has 36 hours of increasing pain and swelling in his right knee. He now refuses to move it at all. Temperature is 38.6°C and the leukocyte count is 17,000/mm3. The knee is hot, swollen and exquisitely tender, with a large effusion and pain through any arc of movement. He has had two previous episodes of first metatarsophalangeal joint pain that settled with indomethacin. Serum uric acid is 7.6 mg/dL. <span class="ec-prompt">Which of the following is the most likely diagnosis?</span> [[Acute gout flare->Septic arthritis - Dx acute]] [[Lyme arthritis->Septic arthritis - Dx lyme]] [[Pseudogout->Septic arthritis - Dx pseudogout]] [[Reactive arthritis->Septic arthritis - Dx reactive]] [[Septic arthritis->Septic arthritis - Dx correct]]

<span class="ec-case-marker" hidden data-entry="Septic arthritis. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Acute gout flare does not fit.</div> His previous podagra and raised uric acid make this the most tempting answer, and it is why the case exists. Serum uric acid is normal or low in a substantial minority of acute flares and raised in many people who never flare, so it cannot distinguish them. Only synovial fluid can, and treating this as gout while it is infected destroys the joint within days. <div class="ec-teach"><div class="th">What the findings actually point to</div> A hot swollen joint with fever, a raised leukocyte count and pain through the entire range of movement is septic arthritis until synovial fluid proves otherwise. Diabetes is a risk factor, and the history of gout neither excludes infection nor explains refusal to move the joint at all, the two can coexist. <div class="ec-src"><b>Source:</b> Margaretten ME, et al. Does this adult patient have septic arthritis? JAMA 2007;297(13):1478-1488.</div></div></div> [[Try this question again->Septic arthritis - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Septic arthritis. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Lyme arthritis does not fit.</div> Lyme gives a large-joint monoarthritis, often the knee, but it evolves over weeks to months with less systemic toxicity and requires exposure in an endemic area. <div class="ec-teach"><div class="th">What the findings actually point to</div> A hot swollen joint with fever, a raised leukocyte count and pain through the entire range of movement is septic arthritis until synovial fluid proves otherwise. Diabetes is a risk factor, and the history of gout neither excludes infection nor explains refusal to move the joint at all, the two can coexist. <div class="ec-src"><b>Source:</b> Margaretten ME, et al. Does this adult patient have septic arthritis? JAMA 2007;297(13):1478-1488.</div></div></div> [[Try this question again->Septic arthritis - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Septic arthritis. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Pseudogout does not fit.</div> Calcium pyrophosphate arthritis affects the knee, can be acutely inflammatory with fever, and shows chondrocalcinosis on radiographs, so it is a real consideration. It is still diagnosed on the same synovial fluid that must be sent to exclude infection. <div class="ec-teach"><div class="th">What the findings actually point to</div> A hot swollen joint with fever, a raised leukocyte count and pain through the entire range of movement is septic arthritis until synovial fluid proves otherwise. Diabetes is a risk factor, and the history of gout neither excludes infection nor explains refusal to move the joint at all, the two can coexist. <div class="ec-src"><b>Source:</b> Margaretten ME, et al. Does this adult patient have septic arthritis? JAMA 2007;297(13):1478-1488.</div></div></div> [[Try this question again->Septic arthritis - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Septic arthritis. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Reactive arthritis does not fit.</div> Reactive arthritis follows a genitourinary or enteric infection by one to 4 weeks, is usually oligoarticular and asymmetric with enthesitis, and does not present as a single acutely septic-appearing joint. <div class="ec-teach"><div class="th">What the findings actually point to</div> A hot swollen joint with fever, a raised leukocyte count and pain through the entire range of movement is septic arthritis until synovial fluid proves otherwise. Diabetes is a risk factor, and the history of gout neither excludes infection nor explains refusal to move the joint at all, the two can coexist. <div class="ec-src"><b>Source:</b> Margaretten ME, et al. Does this adult patient have septic arthritis? JAMA 2007;297(13):1478-1488.</div></div></div> [[Try this question again->Septic arthritis - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Septic arthritis. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Septic arthritis.</div> A hot swollen joint with fever, a raised leukocyte count and pain through the entire range of movement is septic arthritis until synovial fluid proves otherwise. Diabetes is a risk factor, and the history of gout neither excludes infection nor explains refusal to move the joint at all, the two can coexist. <div class="ec-src"><b>Source:</b> Margaretten ME, et al. Does this adult patient have septic arthritis? JAMA 2007;297(13):1478-1488.</div></div> [[Start another case->Hub]] [[Restart this case->Septic arthritis - Dx]] [[Next case →->Campylobacter - Micro]]

<div class="ec-scene">Dermatology consult · 14:20</div> A 34-year-old woman started lamotrigine eighteen days ago. She had 4 days of fever and malaise, then a painful eruption beginning on the trunk and face that has spread. There are dusky purpuric macules with flaccid blisters, and gentle lateral pressure extends the blister, about 12% of body surface is detached. She has painful oral erosions and conjunctival injection with crusting. The palms and soles are largely spared. There is no facial edema and the eosinophil count is normal. <span class="ec-prompt">Which of the following is the most likely diagnosis?</span> [[Acute generalized exanthematous pustulosis->SJS TEN - Dx acute]] [[Drug reaction with eosinophilia and systemic symptoms->SJS TEN - Dx drug]] [[Erythema multiforme major->SJS TEN - Dx erythema]] [[Staphylococcal scalded skin syndrome->SJS TEN - Dx staphylococcal]] [[Stevens-Johnson syndrome / toxic epidermal necrolysis overlap->SJS TEN - Dx correct]]

<span class="ec-case-marker" hidden data-entry="SJS TEN. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Acute generalized exanthematous pustulosis does not fit.</div> This gives dozens of small non-follicular sterile pustules on edematous erythema, appears within days rather than weeks, is usually febrile with neutrophilia, and resolves with desquamation. There are no pustules here, and mucosal erosions are uncommon. <div class="ec-teach"><div class="th">What the findings actually point to</div> Dusky purpuric macules progressing to flaccid blisters with a positive Nikolsky sign, involvement of two or more mucosal surfaces, a central trunk-and-face distribution, and onset within a few weeks of starting a known culprit drug is SJS/TEN. Detachment between 10% and 30% of body surface defines the overlap band. <div class="ec-src"><b>Source:</b> Bastuji-Garin S, et al. Arch Dermatol 1993 (clinical classification of epidermal necrolysis).</div></div></div> [[Try this question again->SJS TEN - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="SJS TEN. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Drug reaction with eosinophilia and systemic symptoms does not fit.</div> DRESS is the other severe drug reaction to know and has a comparable latency, so it is the closest alternative. It gives facial edema, a morbilliform eruption, marked eosinophilia, lymphadenopathy and hepatitis, not epidermal detachment. Her eosinophil count is normal and there is no facial edema. <div class="ec-teach"><div class="th">What the findings actually point to</div> Dusky purpuric macules progressing to flaccid blisters with a positive Nikolsky sign, involvement of two or more mucosal surfaces, a central trunk-and-face distribution, and onset within a few weeks of starting a known culprit drug is SJS/TEN. Detachment between 10% and 30% of body surface defines the overlap band. <div class="ec-src"><b>Source:</b> Bastuji-Garin S, et al. Arch Dermatol 1993 (clinical classification of epidermal necrolysis).</div></div></div> [[Try this question again->SJS TEN - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="SJS TEN. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Erythema multiforme major does not fit.</div> This produces typical target lesions with three concentric rings, distributed acrally on the hands, feet and limbs, and is usually triggered by herpes simplex rather than a drug. Her lesions are central and truncal without true targets. <div class="ec-teach"><div class="th">What the findings actually point to</div> Dusky purpuric macules progressing to flaccid blisters with a positive Nikolsky sign, involvement of two or more mucosal surfaces, a central trunk-and-face distribution, and onset within a few weeks of starting a known culprit drug is SJS/TEN. Detachment between 10% and 30% of body surface defines the overlap band. <div class="ec-src"><b>Source:</b> Bastuji-Garin S, et al. Arch Dermatol 1993 (clinical classification of epidermal necrolysis).</div></div></div> [[Try this question again->SJS TEN - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="SJS TEN. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Staphylococcal scalded skin syndrome does not fit.</div> This is the classic mimic and also gives a positive Nikolsky sign, so it deserves consideration. The split is subcorneal rather than full-thickness, mucous membranes are spared, and it occurs mainly in young children or adults with renal failure or immunosuppression. <div class="ec-teach"><div class="th">What the findings actually point to</div> Dusky purpuric macules progressing to flaccid blisters with a positive Nikolsky sign, involvement of two or more mucosal surfaces, a central trunk-and-face distribution, and onset within a few weeks of starting a known culprit drug is SJS/TEN. Detachment between 10% and 30% of body surface defines the overlap band. <div class="ec-src"><b>Source:</b> Bastuji-Garin S, et al. Arch Dermatol 1993 (clinical classification of epidermal necrolysis).</div></div></div> [[Try this question again->SJS TEN - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="SJS TEN. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Stevens-Johnson syndrome / toxic epidermal necrolysis overlap.</div> Dusky purpuric macules progressing to flaccid blisters with a positive Nikolsky sign, involvement of two or more mucosal surfaces, a central trunk-and-face distribution, and onset within a few weeks of starting a known culprit drug is SJS/TEN. Detachment between 10% and 30% of body surface defines the overlap band. <div class="ec-src"><b>Source:</b> Bastuji-Garin S, et al. Arch Dermatol 1993 (clinical classification of epidermal necrolysis).</div></div> [[Start another case->Hub]] [[Restart this case->SJS TEN - Dx]] [[Next case →->Anti-CCP RA - Ix]]

<div class="ec-scene">Primary care clinic · 10:15</div> A 58-year-old man returns for routine care after recovering from community-acquired pneumonia. He has no chronic illness and has never received a pneumococcal vaccine. He asks how to lower his risk of future pneumococcal disease. <span class="ec-prompt">Which of the following is the most appropriate health maintenance measure?</span> [[23-valent polysaccharide alone, no conjugate->Pneumococcal prevention - Culture trap]] [[Administer a pneumococcal conjugate vaccine now->Pneumococcal prevention - Correct]] [[Defer vaccination until age 65->Pneumococcal prevention - Macrolide trap]] [[Repeat chest radiography every 6 months to detect recurrence->Pneumococcal prevention - Opening Dx5]] [[Standby home antibiotics if symptoms recur->Pneumococcal prevention - Fluoroquinolone trap]]

<span class="ec-case-marker" hidden data-entry="Pneumococcal prevention. Opening"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Administer a pneumococcal conjugate vaccine now</div> One administer a pneumococcal conjugate vaccine at this visit and document it. <div class="ec-teach"><div class="th">The age threshold moved to 50</div> In October 2024 ACIP lowered the age for routine pneumococcal vaccination from 65 to 50: every PCV-naive adult 50 or older should receive a single conjugate vaccine (PCV20 or PCV21 alone, or PCV15 followed by PPSV23 at least a year later). At 58 and PCV-naive, he is due now. Annual influenza vaccination also matters, because influenza predisposes to secondary bacterial pneumonia. <div class="ec-src"><b>Source:</b> Kobayashi M, et al. Expanded Recommendations for Use of Pneumococcal Conjugate Vaccines Among Adults Aged ≥50 Years: ACIP, United States, 2024. MMWR Morb Mortal Wkly Rep 2025.</div></div></div> <b>Vaccinated at the visit; no further pneumococcal dose owed now.</b> [[Start another case->Hub]] [[Restart this case->Pneumococcal prevention - Opening]] [[Next case →->Lung screening - Opening]]

<span class="ec-case-marker" hidden data-entry="Pneumococcal prevention. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ The threshold is 50, not 65.</div> Waiting until 65 leaves him unprotected through his highest-incidence years for the age band that prompted the change. <div class="ec-teach"><div class="th">The error</div> ACIP lowered the routine pneumococcal vaccination age to 50 in October 2024; a PCV-naive 58-year-old qualifies now. <div class="ec-src"><b>Source:</b> Kobayashi M, et al. Expanded Recommendations for Use of Pneumococcal Conjugate Vaccines Among Adults Aged ≥50 Years: ACIP, United States, 2024. MMWR Morb Mortal Wkly Rep 2025.</div></div></div> [[Try this question again->Pneumococcal prevention - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Pneumococcal prevention. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ The current schedule is conjugate-based.</div> Polysaccharide vaccine alone is no longer the primary strategy for adults; the recommendation is a conjugate vaccine (PCV20 or PCV21 alone, or PCV15 then PPSV23). <div class="ec-teach"><div class="th">The error</div> Give a conjugate vaccine as the foundation; PPSV23 has a role only in series after PCV15, not as stand-alone primary vaccination. <div class="ec-src"><b>Source:</b> Kobayashi M, et al. Expanded Recommendations for Use of Pneumococcal Conjugate Vaccines Among Adults Aged ≥50 Years: ACIP, United States, 2024. MMWR Morb Mortal Wkly Rep 2025.</div></div></div> [[Try this question again->Pneumococcal prevention - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Pneumococcal prevention. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Standby antibiotics are not prevention.</div> Handing a patient antibiotics to start on his own is not a preventive measure and encourages inappropriate use and resistance. <div class="ec-teach"><div class="th">The error</div> Prevention here means vaccination, not self-started antibiotics. Reserve antibiotics for evaluated, indicated infection. <div class="ec-src"><b>Source:</b> CDC Core Elements of Outpatient Antibiotic Stewardship.</div></div></div> [[Try this question again->Pneumococcal prevention - Opening]] [[Start another case->Hub]]

<div class="ec-scene">Operating room · 08:05</div> The physician is about to begin an elective operation. The patient is anesthetized and draped and the team is assembled. Wrong-site surgery is rare but catastrophic, and the hospital wants a reliable way to prevent it. <span class="ec-prompt">Which of the following is the most appropriate systems-level response?</span> [[Confirm the site only for lateralized procedures->Surgical safety - Professional standard trap]] [[One member checks the chart without pausing->Surgical safety - Delegation trap]] [[Proceed on the surgeon's recollection, no pause->Surgical safety - Selective trap]] [[Require the surgeon to mark the site without a team pause->Surgical safety - Opening Dx5]] [[Whole-team time-out: verify patient, procedure, site->Surgical safety - Correct]]

<span class="ec-case-marker" hidden data-entry="Surgical safety. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ The protocol covers all procedures.</div> Limiting verification to paired structures leaves every other procedure without the safeguard; wrong-site and wrong-procedure events are not confined to laterality. <div class="ec-teach"><div class="th">The error</div> Preprocedure verification and the time-out apply to all operative and invasive procedures, not only lateralized ones. <div class="ec-src"><b>Source:</b> The Joint Commission. Universal Protocol for Preventing Wrong Site, Wrong Procedure, Wrong Person Surgery.</div></div></div> [[Try this question again->Surgical safety - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Surgical safety. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ A silent solo check is not a time-out.</div> One person quietly reviewing the chart bypasses the shared cross-check that catches the errors an individual would miss. <div class="ec-teach"><div class="th">The error</div> The time-out requires active involvement of the whole team, not a silent single-person confirmation. <div class="ec-src"><b>Source:</b> The Joint Commission. Universal Protocol for Preventing Wrong Site, Wrong Procedure, Wrong Person Surgery.</div></div></div> [[Try this question again->Surgical safety - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Surgical safety. Opening"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Whole-team time-out: verify patient, procedure, site</div> The team pauses; everyone actively confirms the correct patient, the correct procedure, and the correct site before the incision is made. <div class="ec-teach"><div class="th">Three steps, one active pause</div> The Joint Commission's Universal Protocol has three components: a preprocedure verification process, marking of the operative site with the patient involved where possible, and a time-out immediately before starting in which the <b>entire team actively</b> confirms patient, procedure, and site. It applies to all operative and invasive procedures, and compliance is an accreditation requirement, a deliberate barrier placed exactly where memory fails. <div class="ec-src"><b>Source:</b> The Joint Commission. Universal Protocol for Preventing Wrong Site, Wrong Procedure, Wrong Person Surgery.</div></div></div> <b>Correct patient, procedure, and site confirmed as a team.</b> [[Start another case->Hub]] [[Restart this case->Surgical safety - Opening]] [[Next case →->SSI prevention - Opening]]

<span class="ec-case-marker" hidden data-entry="Surgical safety. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Relying on memory is the failure mode.</div> Individual recollection is precisely what wrong-site events arise from; skipping the formal pause removes the barrier meant to catch the slip. <div class="ec-teach"><div class="th">The error</div> The Universal Protocol exists because memory and assumption fail; an active, documented time-out is mandatory. <div class="ec-src"><b>Source:</b> The Joint Commission. Universal Protocol for Preventing Wrong Site, Wrong Procedure, Wrong Person Surgery.</div></div></div> [[Try this question again->Surgical safety - Opening]] [[Start another case->Hub]]

<div class="ec-scene">Oncology ward · 16:00</div> A 71-year-old man with widely metastatic pancreatic cancer progressing through third-line therapy has an estimated prognosis of weeks. He has capacity. During the visit he asks what would happen if his heart stopped, and says he does not want to die on a machine. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Ask his family to decide about resuscitation on his behalf->Goals of care - Opening Dx5]] [[Avoid the topic to preserve hope->Goals of care - Avoid trap]] [[Explore his values, discuss what CPR achieves, and recommend->Goals of care - Correct]] [[Explore values, then call CPR futile and not offer it->Goals of care - Futility trap]] [[Write the DNR order now on what he just said->Goals of care - Premature order trap]]

<span class="ec-case-marker" hidden data-entry="Goals of care. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ He asked. Deflecting takes the decision away from him.</div> Avoiding the conversation while he still has capacity means the decision will eventually be made by someone else, in a crisis, without knowing his wishes. Honest prognostic information does not remove hope; it lets him direct the time he has. <div class="ec-teach"><div class="th">The misstep</div> Patients have a right to prognostic information and to participate in decisions about their care. Avoidance forfeits the window in which the patient can speak for himself. <div class="ec-src"><b>Source:</b> Bernacki RE, Block SD. Communication About Serious Illness Care Goals. JAMA Intern Med 2014;174(12):1994-2003.</div></div></div> [[Try this question again->Goals of care - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Goals of care. Opening"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Explore his values, discuss what CPR achieves, and recommend</div> One explore what he understands and what matters to him, give an honest account of his prognosis and what CPR would and would not achieve, make a clear recommendation, document the resulting order, and involve palliative care. <div class="ec-teach"><div class="th">How the conversation is structured</div> Goals-of-care discussions start by exploring what the patient understands and what matters to him, then give honest prognostic information, including what CPR realistically achieves in advanced metastatic cancer, where survival to discharge is very low, and then make a <b>recommendation</b> aligned with his stated values. A do-not-resuscitate order limits resuscitation only; it does not mean withdrawal of other treatment, and it must not reduce symptom control, nursing attention, or disease-directed therapy the patient still wants. Involve palliative care early. Document the decision, and revisit it if his condition or wishes change. <div class="ec-src"><b>Source:</b> AMA Code of Medical Ethics (withholding or withdrawing life-sustaining treatment); serious illness communication standards.</div></div></div> <b>Wishes documented while he could express them.</b> [[Start another case->Hub]] [[Restart this case->Goals of care - Opening]] [[Next case →->Screening refusal - Opening]]

<span class="ec-case-marker" hidden data-entry="Goals of care. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Right conversation, and a word that ends it.</div> Exploring values first is correct and a recommendation is appropriate, so this is the closest wrong answer. Declaring treatment futile is a contested judgment that patients hear as a decision made without them, and strict physiological futility is rare. It also forecloses the discussion at the point where his understanding of CPR was about to be explored. <div class="ec-teach"><div class="th">Why this is wrong</div> Explore what he understands and hopes for, give honest information about what CPR achieves in advanced metastatic cancer, then make a recommendation and check whether he agrees. A recommendation invites a response; a declaration of futility does not. <div class="ec-src"><b>Source:</b> Bernacki RE, Block SD. Communication About Serious Illness Care Goals. JAMA Intern Med 2014;174(12):1994-2003.</div></div></div> [[Try this question again->Goals of care - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Goals of care. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ He opened a conversation; one closed it.</div> "I do not want to die on a machine" is a value, not an order set. It may well end in a DNR, it probably should, but converting one sentence into a signed order skips the part that makes the decision his: what he understands CPR to involve, what outcomes he is picturing, what he is hoping for in the weeks he has, and whether he means resuscitation only or also intubation, pressors, and transfer to intensive care. <div class="ec-teach"><div class="th">Why this is wrong</div> Code status follows from a goals-of-care discussion rather than substituting for one. Explore understanding and values first, provide honest information about what CPR achieves in advanced metastatic cancer, then make a recommendation and check agreement. Documenting immediately also forfeits the chance to identify a surrogate and address the rest of the plan while he still has capacity. <div class="ec-src"><b>Source:</b> Bernacki & Block, JAMA Intern Med 2014 (serious illness communication); AAHPM position on physician recommendations in code status discussions; VitalTalk REMAP framework.</div></div></div> [[Try this question again->Goals of care - Opening]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 23:47</div> A 47-year-old man is brought in by a friend after 2 weeks of worsening hopelessness and saying goodbye to family members. He describes active suicidal ideation with a specific plan, has a firearm at home, made an attempt last year, lives alone, and has been drinking heavily. He says he does not want to be here and asks to leave. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Allow him to leave once a family member agrees to supervise him->Suicide risk - Opening Dx5]] [[Discharge with outpatient psychiatry and a crisis line->Suicide risk - Discharge trap]] [[Hold for evaluation; start an antidepressant in the emergency department->Suicide risk - Immediate medication trap]] [[Hold for psychiatric evaluation and restrict access to means->Suicide risk - Correct]] [[No-suicide contract and outpatient follow-up->Suicide risk - Contract trap]]

<span class="ec-case-marker" hidden data-entry="Suicide risk. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ The document protects the anxiety, not his life.</div> No-suicide contracts became common practice and have no evidence base, there are no randomized trials showing they prevent suicide or attempts, and the reviews are consistent on this. They put the burden of the crisis on the patient at exactly the moment his judgment is most impaired, and they can make patients less willing to disclose what they are thinking. They also offer no legal protection, and arguably the reverse: they document that risk was recognized and that little was done about it. <div class="ec-teach"><div class="th">Why this is wrong</div> The evidence-based alternative is a collaborative safety plan, warning signs, coping steps, people to contact, and restricting access to the means he has described, but a safety plan is an outpatient tool and it does not substitute for admission in a patient who meets criteria this clearly. Active ideation with a specific plan, a prior attempt within a year, living alone, heavy drinking, and available means is a presentation for psychiatric hold and evaluation. His request to leave does not settle it; capacity to refuse care must be assessed, not assumed from the absence of a prior determination. <div class="ec-src"><b>Source:</b> Rudd MD, Mandrusiak M, Joiner TE. The case against no-suicide contracts. J Clin Psychol 2006;62(2):243-251; Stanley B, Brown GK. Safety Planning Intervention. Cogn Behav Pract 2012;19(2):256-264.</div></div></div> [[Try this question again->Suicide risk - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Suicide risk. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Every risk factor is present at once.</div> Active ideation with a specific plan, immediately available lethal means, a prior attempt, social isolation and acute intoxication is the highest-risk combination there is. A follow-up appointment does not protect him tonight. <div class="ec-teach"><div class="th">Why this is wrong</div> Active suicidal ideation with plan, intent and available means requires immediate protection and psychiatric evaluation, not outpatient referral. <div class="ec-src"><b>Source:</b> APA Practice Guideline for the Assessment and Treatment of Patients with Suicidal Behaviors; SAMHSA guidance.</div></div></div> [[Try this question again->Suicide risk - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Suicide risk. Opening"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Hold for psychiatric evaluation and restrict access to means</div> One keep him in a safe observation area with one-to-one supervision, arrange urgent psychiatric evaluation, initiate an involuntary hold when he tries to leave, and work with his friend and family on removing access to the firearm. <div class="ec-teach"><div class="th">What raises risk, and what actually lowers it</div> The features that mark imminent risk: <b>active ideation with a specific plan</b>, <b>intent</b>, <b>access to lethal means</b>, a prior attempt (the strongest single predictor), acute intoxication, hopelessness, recent loss, and social isolation. Giving away possessions and saying goodbye are behavioral warning signs. <b>Means restriction</b> is among the most effective interventions available, firearm access in particular, since firearm attempts have the highest case fatality, and it should be discussed with the patient and family. So-called no-suicide contracts have no evidence base and should not substitute for a structured safety plan. This is a topic where local statutes govern the mechanics of involuntary evaluation. <div class="ec-src"><b>Source:</b> APA Practice Guideline for the Assessment and Treatment of Patients With Suicidal Behaviors; SAMHSA suicide prevention guidance.</div></div></div> <b>Protected, evaluated, means restricted.</b> [[Start another case->Hub]] [[Restart this case->Suicide risk - Opening]] [[Next case →->Psych transition - Opening]]

<span class="ec-case-marker" hidden data-entry="Suicide risk. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ The hold is right; the prescription is not this visit's decision.</div> He will likely need pharmacotherapy and starting early seems efficient, so the instinct is not wrong. Antidepressants take weeks to work and do nothing for acute risk, the choice belongs with the clinician who will follow him, and starting one in the emergency department without that continuity risks an unmonitored early period. <div class="ec-teach"><div class="th">Why this is wrong</div> Hold for psychiatric evaluation, restrict access to means, and ensure he is not left alone. Treatment decisions follow the specialist assessment. Capacity to refuse care must be assessed rather than assumed from the absence of a prior determination. <div class="ec-src"><b>Source:</b> The Joint Commission National Patient Safety Goal 15.01.01 on suicide risk reduction.</div></div></div> [[Try this question again->Suicide risk - Opening]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 04:40</div> A 3-week-old boy, born at term after an uncomplicated pregnancy, is brought in for a day of poor feeding and irritability. His mother says he has been difficult to rouse for feeds and feels hot. He has no cough, vomiting or diarrhea. Temperature is 38.6°C, pulse is 186/min, and the anterior fontanelle is full. He is irritable when handled and consolable only briefly. There is no rash and no focal neurologic deficit. Maternal group B streptococcus status was not documented. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Empiric oral amoxicillin pending culture results->Neonatal meningitis - Opening Dx5]] [[Intravenous ampicillin and cefotaxime, after cultures and lumbar puncture->Neonatal meningitis - Correct]] [[Intravenous ceftriaxone and vancomycin, after cultures and lumbar puncture->Neonatal meningitis - Ceftriaxone trap]] [[Intravenous dexamethasone with the first antibiotic dose->Neonatal meningitis - Dexamethasone trap]] [[Observe; treat only if cerebrospinal fluid is abnormal->Neonatal meningitis - Observe trap]]

<span class="ec-case-marker" hidden data-entry="Neonatal meningitis. Opening"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Intravenous ampicillin and cefotaxime, after cultures and lumbar puncture</div> Blood cultures and a lumbar puncture are obtained without delay, and ampicillin with cefotaxime goes in immediately afterward. Cerebrospinal fluid shows a raised leukocyte count with neutrophil predominance, low glucose and raised protein. <div class="ec-teach"><div class="th">Why this is right</div> Under one month the pathogens are group B streptococcus, Escherichia coli and Listeria monocytogenes. Ampicillin is what covers Listeria, cephalosporins do not, and cefotaxime covers the gram-negative enterics. A febrile infant this age with no clear source gets a full sepsis evaluation including lumbar puncture, and antibiotics follow immediately; if the tap cannot be done promptly or he becomes unstable, antibiotics go in first and the tap follows.<div class="ec-src"><b>Source:</b> Tunkel AR, et al. IDSA Practice Guidelines for the Management of Bacterial Meningitis. Clin Infect Dis 2004;39(9):1267-1284; AAP Red Book, Meningitis.</div></div></div> [[Start another case->Hub]] [[Restart this case->Neonatal meningitis - Opening]] [[Next case →->Mononucleosis - Rx]]

<span class="ec-case-marker" hidden data-entry="Neonatal meningitis. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ The adult regimen, and two problems with it in a neonate.</div> Vancomycin plus a third-generation cephalosporin is correct empiric therapy for an adult, so this is the closest wrong answer. Two things change under a month. Ceftriaxone displaces bilirubin from albumin and is avoided in neonates because of the risk of kernicterus, and it precipitates with calcium-containing intravenous fluids, cefotaxime is used instead. The bigger omission is Listeria: no cephalosporin covers it, which is why ampicillin is in the regimen at this age. <div class="ec-teach"><div class="th">Why this is wrong</div> Cover by age. Under one month: ampicillin plus cefotaxime. One to 3 months: ampicillin with ceftriaxone or cefotaxime, plus vancomycin. Over 3 months: vancomycin plus ceftriaxone or cefotaxime. Vancomycin is directed at resistant pneumococcus, which is not a neonatal pathogen. <div class="ec-src"><b>Source:</b> Tunkel AR, et al. Clin Infect Dis 2004;39(9):1267-1284; AAP Red Book, antimicrobial therapy by age.</div></div></div> [[Try this question again->Neonatal meningitis - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Neonatal meningitis. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ A real adjunct, and it is not indicated at this age.</div> Adjunctive dexamethasone reduces hearing loss in Haemophilus influenzae type b meningitis and is considered in older infants and children, so reaching for it shows one know the adjunct exists. It is specifically not indicated in neonates and infants younger than 6 weeks, the trials excluded them and there is no evidence of benefit. It also reduces cerebrospinal fluid penetration of vancomycin. <div class="ec-teach"><div class="th">Why this is wrong</div> Give the antibiotics. Dexamethasone is considered from 6 weeks of age, given just before or with the first antibiotic dose, with the strongest evidence in Hib and continued controversy in pneumococcal disease. It is never given instead of, or ahead of, antimicrobial therapy. <div class="ec-src"><b>Source:</b> Odio CM, et al. N Engl J Med 1991;324(22):1525-1531; AAP Pediatric Care Online, Meningitis; Tunkel AR, et al. Clin Infect Dis 2004;39(9):1267-1284.</div></div></div> [[Try this question again->Neonatal meningitis - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Neonatal meningitis. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Waiting is the one thing a febrile neonate cannot afford.</div> Serial examination is reasonable in an older, well-appearing child with a clear viral source. It is not reasonable here. A neonate has an immature immune response and few localizing signs, invasive bacterial infection progresses over hours, and irritability with a full fontanelle is already the presentation rather than a warning of one. <div class="ec-teach"><div class="th">Why this is wrong</div> Fever without a source under one month is a full sepsis evaluation, blood, urine and cerebrospinal fluid cultures, with admission and empiric parenteral antibiotics started without waiting for results. Treatment is de-escalated when cultures return, not withheld until they do. <div class="ec-src"><b>Source:</b> AAP Clinical Practice Guideline: Evaluation and Management of Well-Appearing Febrile Infants 8 to 60 Days Old. Pediatrics 2021;148(2):e2021052228.</div></div></div> [[Try this question again->Neonatal meningitis - Opening]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 22:25</div> A 7-month-old boy, born at term and previously well, has 3 days of coryza and cough now with noisy breathing and reduced feeding. Respirations are 58/min with subcostal recession and nasal flaring. Auscultation reveals diffuse wheeze and fine inspiratory crackles. He has a low-grade temperature of 38.1°C, alert and consolable, and is taking two-thirds of his usual feeds. This is his first episode of wheeze. <span class="ec-prompt">Which of the following is the most likely diagnosis?</span> [[Bacterial pneumonia->Bronchiolitis - Dx D2]] [[Bronchiolitis->Bronchiolitis - Dx correct]] [[Congestive cardiac failure from an undiagnosed cardiac lesion->Bronchiolitis - Dx D4]] [[Foreign body aspiration->Bronchiolitis - Dx D3]] [[Viral-induced wheeze or early asthma->Bronchiolitis - Dx D1]]

<span class="ec-case-marker" hidden data-entry="Bronchiolitis. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Pneumonia typically gives higher fever with focal findings and a focal infiltrate. His findings are diffuse and bilateral, and routine radiography in bronchiolitis frequently shows atelectasis that is misread as consolidation. <div class="ec-teach"><div class="th">What the findings point to</div> A first episode of wheeze in an infant under 12 months, preceded by two to 3 days of coryza, with diffuse wheeze and crackles and increased work of breathing, in the winter season. The crackles are the feature that distinguishes it from asthma, the obstruction is small-airway plugging and edema rather than reversible bronchospasm. <div class="ec-src"><b>Source:</b> Ralston SL, et al. AAP Clinical Practice Guideline: The Diagnosis, Management, and Prevention of Bronchiolitis. Pediatrics 2014;134(5):e1474-e1502.</div></div></div> [[Try this question again->Bronchiolitis - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Bronchiolitis. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Bronchiolitis.</div> A first episode of wheeze in an infant under 12 months, preceded by two to 3 days of coryza, with diffuse wheeze and crackles and increased work of breathing, in the winter season. The crackles are the feature that distinguishes it from asthma, the obstruction is small-airway plugging and edema rather than reversible bronchospasm. <div class="ec-src"><b>Source:</b> Ralston SL, et al. AAP Clinical Practice Guideline: The Diagnosis, Management, and Prevention of Bronchiolitis. Pediatrics 2014;134(5):e1474-e1502.</div></div> [[Start another case->Hub]] [[Restart this case->Bronchiolitis - Dx]] [[Next case →->Epiglottitis - Dx]]

<span class="ec-case-marker" hidden data-entry="Bronchiolitis. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Heart failure in infancy causes tachypnea, poor feeding and crackles and can be mistaken for this, so it is worth considering. It usually presents with hepatomegaly, a murmur, poor growth and sweating on feeding, none of which is described. <div class="ec-teach"><div class="th">What the findings point to</div> A first episode of wheeze in an infant under 12 months, preceded by two to 3 days of coryza, with diffuse wheeze and crackles and increased work of breathing, in the winter season. The crackles are the feature that distinguishes it from asthma, the obstruction is small-airway plugging and edema rather than reversible bronchospasm. <div class="ec-src"><b>Source:</b> Ralston SL, et al. AAP Clinical Practice Guideline: The Diagnosis, Management, and Prevention of Bronchiolitis. Pediatrics 2014;134(5):e1474-e1502.</div></div></div> [[Try this question again->Bronchiolitis - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Bronchiolitis. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Aspiration causes sudden onset in a previously well child with unilateral wheeze and reduced air entry, and belongs on the list at this age. His onset was gradual over 3 days with a viral prodrome and bilateral findings. <div class="ec-teach"><div class="th">What the findings point to</div> A first episode of wheeze in an infant under 12 months, preceded by two to 3 days of coryza, with diffuse wheeze and crackles and increased work of breathing, in the winter season. The crackles are the feature that distinguishes it from asthma, the obstruction is small-airway plugging and edema rather than reversible bronchospasm. <div class="ec-src"><b>Source:</b> Ralston SL, et al. AAP Clinical Practice Guideline: The Diagnosis, Management, and Prevention of Bronchiolitis. Pediatrics 2014;134(5):e1474-e1502.</div></div></div> [[Try this question again->Bronchiolitis - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Bronchiolitis. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Recurrent wheeze without crackles, often with a family history of atopy and a bronchodilator response, in a child usually older than 12 months. This is his first episode with crackles, and the distinction matters because it determines whether albuterol and steroids have any role. <div class="ec-teach"><div class="th">What the findings point to</div> A first episode of wheeze in an infant under 12 months, preceded by two to 3 days of coryza, with diffuse wheeze and crackles and increased work of breathing, in the winter season. The crackles are the feature that distinguishes it from asthma, the obstruction is small-airway plugging and edema rather than reversible bronchospasm. <div class="ec-src"><b>Source:</b> Ralston SL, et al. AAP Clinical Practice Guideline: The Diagnosis, Management, and Prevention of Bronchiolitis. Pediatrics 2014;134(5):e1474-e1502.</div></div></div> [[Try this question again->Bronchiolitis - Dx]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 16:20</div> An 11-month-old boy has 6 hours of episodic severe crying during which he draws his knees up, each episode lasting minutes and separated by intervals in which he is quiet, pale and settled. He has vomited three times and passed dark red mucoid stool. A sausage-shaped mass is palpable in the right upper quadrant. Between episodes his abdomen is soft without peritoneal signs. <span class="ec-prompt">Which of the following is the most likely diagnosis?</span> [[Acute gastroenteritis->Intussusception - Dx D2]] [[Intussusception->Intussusception - Dx correct]] [[Malrotation with midgut volvulus->Intussusception - Dx D1]] [[Meckel diverticulum with bleeding->Intussusception - Dx D3]] [[Testicular torsion->Intussusception - Dx D5]]

<span class="ec-case-marker" hidden data-entry="Intussusception. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Vomiting and abnormal stool fit, and this is the usual initial label. Gastroenteritis causes continuous rather than paroxysmal pain, watery stool rather than mucoid blood, and no palpable mass. <div class="ec-teach"><div class="th">What the findings point to</div> Episodic colicky pain with well intervals in an infant, vomiting, red currant jelly stool and a palpable sausage-shaped mass is ileocolic intussusception. The peak incidence is between 6 and 36 months, and the deceptively normal child between episodes is why the diagnosis is missed. <div class="ec-src"><b>Source:</b> Applegate KE. Intussusception in children: evidence-based diagnosis and treatment. Pediatr Radiol 2009;39(Suppl 2):S140-S143.</div></div></div> [[Try this question again->Intussusception - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Intussusception. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Intussusception.</div> Episodic colicky pain with well intervals in an infant, vomiting, red currant jelly stool and a palpable sausage-shaped mass is ileocolic intussusception. The peak incidence is between 6 and 36 months, and the deceptively normal child between episodes is why the diagnosis is missed. <div class="ec-src"><b>Source:</b> Applegate KE. Intussusception in children: evidence-based diagnosis and treatment. Pediatr Radiol 2009;39(Suppl 2):S140-S143.</div></div> [[Start another case->Hub]] [[Restart this case->Intussusception - Dx]] [[Next case →->Enteral nutrition - Opening]]

<span class="ec-case-marker" hidden data-entry="Intussusception. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This is the diagnosis one cannot afford to miss and it belongs on the list. It presents with bilious vomiting and a rapidly deteriorating, often peritonitic child, usually in the first month of life, rather than with episodic pain and well intervals. <div class="ec-teach"><div class="th">What the findings point to</div> Episodic colicky pain with well intervals in an infant, vomiting, red currant jelly stool and a palpable sausage-shaped mass is ileocolic intussusception. The peak incidence is between 6 and 36 months, and the deceptively normal child between episodes is why the diagnosis is missed. <div class="ec-src"><b>Source:</b> Applegate KE. Intussusception in children: evidence-based diagnosis and treatment. Pediatr Radiol 2009;39(Suppl 2):S140-S143.</div></div></div> [[Try this question again->Intussusception - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Intussusception. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A Meckel diverticulum causes painless rectal bleeding, sometimes brisk. It can also act as a lead point for intussusception, but bleeding alone does not produce colicky episodes and a mass. <div class="ec-teach"><div class="th">What the findings point to</div> Episodic colicky pain with well intervals in an infant, vomiting, red currant jelly stool and a palpable sausage-shaped mass is ileocolic intussusception. The peak incidence is between 6 and 36 months, and the deceptively normal child between episodes is why the diagnosis is missed. <div class="ec-src"><b>Source:</b> Applegate KE. Intussusception in children: evidence-based diagnosis and treatment. Pediatr Radiol 2009;39(Suppl 2):S140-S143.</div></div></div> [[Try this question again->Intussusception - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Intussusception. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Torsion causes inconsolable crying and vomiting in an infant and the scrotum must be examined in any irritable baby, but it does not cause a right upper quadrant mass or bloody stool. <div class="ec-teach"><div class="th">What the findings point to</div> Episodic colicky pain with well intervals in an infant, vomiting, red currant jelly stool and a palpable sausage-shaped mass is ileocolic intussusception. The peak incidence is between 6 and 36 months, and the deceptively normal child between episodes is why the diagnosis is missed. <div class="ec-src"><b>Source:</b> Applegate KE. Intussusception in children: evidence-based diagnosis and treatment. Pediatr Radiol 2009;39(Suppl 2):S140-S143.</div></div></div> [[Try this question again->Intussusception - Dx]] [[Start another case->Hub]]

<div class="ec-scene">Pediatric clinic · 11:00</div> A 9-month-old girl is brought for a routine health supervision visit. She was born at term and has been well. She sits without support, crawls, pulls to stand, transfers objects hand to hand, babbles with consonants, and shows stranger anxiety. Growth is tracking along the 50th percentile. Immunizations are up to date. She is breastfed with complementary foods introduced at 6 months. Her mother asks what should be done today. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Developmental surveillance and screening for anemia->Well child visit - Correct]] [[Formal audiometry and acuity testing->Well child visit - vision trap]] [[Lead and TB testing regardless of risk->Well child visit - lead trap]] [[No screening needed; she is thriving->Well child visit - no trap]] [[Refer for developmental eval; she is not walking yet->Well child visit - referral trap]]

<span class="ec-case-marker" hidden data-entry="Well child visit. Opening"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Developmental surveillance and screening for anemia.</div> At 9 months the schedule calls for a structured developmental screen using a validated instrument, and screening for iron deficiency anemia is recommended at around this age given the transition from milk-based to complementary feeding. Her milestones are all age-appropriate, which is documented rather than assumed. <div class="ec-src"><b>Source:</b> Hagan JF, Shaw JS, Duncan PM, eds. Bright Futures: Guidelines for Health Supervision of Infants, Children, and Adolescents, 4th ed. AAP, 2017; AAP Recommendations for Preventive Pediatric Health Care (Periodicity Schedule).</div></div> [[Start another case->Hub]] [[Restart this case->Well child visit - Opening]] [[Next case →->Neonatal jaundice - Rx]]

<span class="ec-case-marker" hidden data-entry="Well child visit. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the next step.</div> Both are recommended, but as risk-based screening guided by a structured risk assessment, housing age, immigration and travel history, known exposures, rather than universally at this visit. Testing every infant irrespective of risk is not the recommendation. <div class="ec-teach"><div class="th">What to do instead</div> At 9 months the schedule calls for a structured developmental screen using a validated instrument, and screening for iron deficiency anemia is recommended at around this age given the transition from milk-based to complementary feeding. Her milestones are all age-appropriate, which is documented rather than assumed. <div class="ec-src"><b>Source:</b> Hagan JF, Shaw JS, Duncan PM, eds. Bright Futures: Guidelines for Health Supervision of Infants, Children, and Adolescents, 4th ed. AAP, 2017; AAP Recommendations for Preventive Pediatric Health Care (Periodicity Schedule).</div></div></div> [[Try this question again->Well child visit - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Well child visit. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the next step.</div> Independent walking typically appears between about 12 and 15 months, and many children walk later than that normally. Pulling to stand at 9 months is exactly on track, and referring here would generate unnecessary alarm. <div class="ec-teach"><div class="th">What to do instead</div> At 9 months the schedule calls for a structured developmental screen using a validated instrument, and screening for iron deficiency anemia is recommended at around this age given the transition from milk-based to complementary feeding. Her milestones are all age-appropriate, which is documented rather than assumed. <div class="ec-src"><b>Source:</b> Hagan JF, Shaw JS, Duncan PM, eds. Bright Futures: Guidelines for Health Supervision of Infants, Children, and Adolescents, 4th ed. AAP, 2017; AAP Recommendations for Preventive Pediatric Health Care (Periodicity Schedule).</div></div></div> [[Try this question again->Well child visit - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Well child visit. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the next step.</div> Formal audiometry and chart-based acuity require cooperation not present at this age. Vision and hearing are assessed at this visit by risk assessment and by observation, with objective testing at older ages or where risk is identified. <div class="ec-teach"><div class="th">What to do instead</div> At 9 months the schedule calls for a structured developmental screen using a validated instrument, and screening for iron deficiency anemia is recommended at around this age given the transition from milk-based to complementary feeding. Her milestones are all age-appropriate, which is documented rather than assumed. <div class="ec-src"><b>Source:</b> Hagan JF, Shaw JS, Duncan PM, eds. Bright Futures: Guidelines for Health Supervision of Infants, Children, and Adolescents, 4th ed. AAP, 2017; AAP Recommendations for Preventive Pediatric Health Care (Periodicity Schedule).</div></div></div> [[Try this question again->Well child visit - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Well child visit. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the next step.</div> A well-child visit is not an absence of action. It is the structured opportunity for developmental screening, anemia screening, anticipatory guidance on nutrition, sleep, safety and injury prevention, and review of the immunization schedule. <div class="ec-teach"><div class="th">What to do instead</div> At 9 months the schedule calls for a structured developmental screen using a validated instrument, and screening for iron deficiency anemia is recommended at around this age given the transition from milk-based to complementary feeding. Her milestones are all age-appropriate, which is documented rather than assumed. <div class="ec-src"><b>Source:</b> Hagan JF, Shaw JS, Duncan PM, eds. Bright Futures: Guidelines for Health Supervision of Infants, Children, and Adolescents, 4th ed. AAP, 2017; AAP Recommendations for Preventive Pediatric Health Care (Periodicity Schedule).</div></div></div> [[Try this question again->Well child visit - Opening]] [[Start another case->Hub]]

<div class="ec-scene">Pediatric clinic · 15:20</div> A 16-year-old girl attends for a routine health supervision visit, accompanied by her mother. She has no complaints and is doing well at school. Her immunizations are complete except for the human papillomavirus vaccine series, which her family deferred. Her mother mentions in passing that she has a new boyfriend and stays in the room expecting to be present throughout. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Begin cervical cytology; she is sexually active->Adolescent well visit - begin trap]] [[Defer HPV vaccine; she is already sexually active->Adolescent well visit - defer trap]] [[Get mother's consent before discussing sexual health->Adolescent well visit - obtain trap]] [[Interview her confidentially without her mother present->Adolescent well visit - Correct]] [[No screening needed; she is healthy->Adolescent well visit - no trap]] [[Screen for depression only if mother reports concerns->Adolescent well visit - screen trap]]

<span class="ec-case-marker" hidden data-entry="Adolescent well visit. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the next step.</div> This is the most tempting option because it links a real risk to a real test. Cervical cancer screening begins at age 21 regardless of the age of sexual debut or the number of partners, because cervical cancer is vanishingly rare before 21 and HPV infection in adolescents usually clears spontaneously. Screening earlier finds transient abnormalities and leads to procedures that can compromise later pregnancies. <div class="ec-teach"><div class="th">What to do instead</div> Adolescents are seen alone for part of every health supervision visit. Confidential time is what makes an accurate psychosocial history possible, sexual activity, substance use, mood, safety, and it is the single practice most associated with adolescents disclosing risk. Explain the limits of confidentiality up front: disclosure is required for imminent danger to self or others, or abuse. A structured psychosocial screen such as HEEADSSS, depression screening, and review of the immunization schedule follow. <div class="ec-src"><b>Source:</b> Hagan JF, Shaw JS, Duncan PM, eds. Bright Futures: Guidelines for Health Supervision of Infants, Children, and Adolescents, 4th ed. AAP, 2017; USPSTF cervical cancer screening (2018); CDC/ACIP HPV vaccination recommendations.</div></div></div> [[Try this question again->Adolescent well visit - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Adolescent well visit. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the next step.</div> Vaccination is still recommended and still beneficial, she is unlikely to have been exposed to every vaccine type, and protection against the remaining types is worthwhile. Catch-up vaccination is recommended through age 26, and shared decision-making applies from 27 to 45. Prior activity is a reason to vaccinate promptly, not to withhold. <div class="ec-teach"><div class="th">What to do instead</div> Adolescents are seen alone for part of every health supervision visit. Confidential time is what makes an accurate psychosocial history possible, sexual activity, substance use, mood, safety, and it is the single practice most associated with adolescents disclosing risk. Explain the limits of confidentiality up front: disclosure is required for imminent danger to self or others, or abuse. A structured psychosocial screen such as HEEADSSS, depression screening, and review of the immunization schedule follow. <div class="ec-src"><b>Source:</b> Hagan JF, Shaw JS, Duncan PM, eds. Bright Futures: Guidelines for Health Supervision of Infants, Children, and Adolescents, 4th ed. AAP, 2017; USPSTF cervical cancer screening (2018); CDC/ACIP HPV vaccination recommendations.</div></div></div> [[Try this question again->Adolescent well visit - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Adolescent well visit. Opening"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Interview her confidentially without her mother present.</div> Adolescents are seen alone for part of every health supervision visit. Confidential time is what makes an accurate psychosocial history possible, sexual activity, substance use, mood, safety, and it is the single practice most associated with adolescents disclosing risk. Explain the limits of confidentiality up front: disclosure is required for imminent danger to self or others, or abuse. A structured psychosocial screen such as HEEADSSS, depression screening, and review of the immunization schedule follow. <div class="ec-src"><b>Source:</b> Hagan JF, Shaw JS, Duncan PM, eds. Bright Futures: Guidelines for Health Supervision of Infants, Children, and Adolescents, 4th ed. AAP, 2017; USPSTF cervical cancer screening (2018); CDC/ACIP HPV vaccination recommendations.</div></div> [[Start another case->Hub]] [[Restart this case->Adolescent well visit - Opening]] [[Next case →->Tdap in pregnancy - Prevention]]

<span class="ec-case-marker" hidden data-entry="Adolescent well visit. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the next step.</div> Adolescent confidentiality and consent rules vary by jurisdiction and by service; in most states minors may consent independently to STI care, and many states extend that to contraception and substance use treatment. Requiring parental consent for the conversation itself defeats the purpose of the confidential interview and is the reliable way to ensure she discloses nothing. <div class="ec-teach"><div class="th">What to do instead</div> Adolescents are seen alone for part of every health supervision visit. Confidential time is what makes an accurate psychosocial history possible, sexual activity, substance use, mood, safety, and it is the single practice most associated with adolescents disclosing risk. Explain the limits of confidentiality up front: disclosure is required for imminent danger to self or others, or abuse. A structured psychosocial screen such as HEEADSSS, depression screening, and review of the immunization schedule follow. <div class="ec-src"><b>Source:</b> Hagan JF, Shaw JS, Duncan PM, eds. Bright Futures: Guidelines for Health Supervision of Infants, Children, and Adolescents, 4th ed. AAP, 2017; USPSTF cervical cancer screening (2018); CDC/ACIP HPV vaccination recommendations.</div></div></div> [[Try this question again->Adolescent well visit - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Adolescent well visit. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the next step.</div> Universal annual depression screening is recommended for adolescents from age 12, not screening triggered by parental concern. Parents frequently do not recognize adolescent depression, and the adolescent is the more reliable informant, which is another reason the confidential interview comes first. <div class="ec-teach"><div class="th">What to do instead</div> Adolescents are seen alone for part of every health supervision visit. Confidential time is what makes an accurate psychosocial history possible, sexual activity, substance use, mood, safety, and it is the single practice most associated with adolescents disclosing risk. Explain the limits of confidentiality up front: disclosure is required for imminent danger to self or others, or abuse. A structured psychosocial screen such as HEEADSSS, depression screening, and review of the immunization schedule follow. <div class="ec-src"><b>Source:</b> Hagan JF, Shaw JS, Duncan PM, eds. Bright Futures: Guidelines for Health Supervision of Infants, Children, and Adolescents, 4th ed. AAP, 2017; USPSTF cervical cancer screening (2018); CDC/ACIP HPV vaccination recommendations.</div></div></div> [[Try this question again->Adolescent well visit - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Adolescent well visit. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the next step.</div> A well adolescent visit is where the screening happens precisely because there are no complaints. Depression and suicide risk, substance use, sexual health, immunizations, blood pressure, and a once-between-9-and-11 lipid screen all belong to the asymptomatic visit. <div class="ec-teach"><div class="th">What to do instead</div> Adolescents are seen alone for part of every health supervision visit. Confidential time is what makes an accurate psychosocial history possible, sexual activity, substance use, mood, safety, and it is the single practice most associated with adolescents disclosing risk. Explain the limits of confidentiality up front: disclosure is required for imminent danger to self or others, or abuse. A structured psychosocial screen such as HEEADSSS, depression screening, and review of the immunization schedule follow. <div class="ec-src"><b>Source:</b> Hagan JF, Shaw JS, Duncan PM, eds. Bright Futures: Guidelines for Health Supervision of Infants, Children, and Adolescents, 4th ed. AAP, 2017; USPSTF cervical cancer screening (2018); CDC/ACIP HPV vaccination recommendations.</div></div></div> [[Try this question again->Adolescent well visit - Opening]] [[Start another case->Hub]]

<div class="ec-scene">Primary care clinic · 09:40</div> A 33-year-old woman attends for a routine visit. Her last cervical cytology was 3 years ago and was normal, so she is due for screening. She declines, saying she completed the human papillomavirus vaccine series as a teenager and understands she no longer needs to be screened. She is well, has no symptoms, and has full capacity. She is otherwise engaged and asks good questions about her care. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Accept the refusal and document, no discussion->Screening refusal - D1]] [[Ask her husband to persuade her->Screening refusal - D3]] [[Call it negligent and threaten to drop her->Screening refusal - D2]] [[Explore her reasons and correct misunderstandings->Screening refusal - Correct]] [[Order the test anyway->Screening refusal - D4]] [[Screening is unnecessary; she had the HPV vaccine->Screening refusal - D5]]

<span class="ec-case-marker" hidden data-entry="Screening refusal. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the next step.</div> Respecting autonomy is right and this is the closest wrong answer, because the endpoint may well be the same. Autonomy requires information: a refusal based on the belief that vaccination replaces screening is not an informed choice, it is an uncorrected error. Exploring first is what makes the eventual refusal valid. <div class="ec-teach"><div class="th">What to do instead</div> An informed refusal is only informed if one know what it rests on. Most declines come from a correctable belief, that the HPV vaccine removes the need to screen, that screening is unnecessary without symptoms, or fear of discomfort or of a previous bad experience. Explore, correct what is factually wrong, offer the alternatives, and if she still declines, respect it and document the discussion with a plan to revisit. <div class="ec-src"><b>Source:</b> AMA Code of Medical Ethics Opinion 2.1.1; USPSTF. Screening for Cervical Cancer: Recommendation Statement. JAMA 2018;320(7):674-686.</div></div></div> [[Try this question again->Screening refusal - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Screening refusal. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the next step.</div> Recruiting a family member to apply pressure bypasses her decision-making rather than supporting it, and it breaches the confidentiality of a consultation she has not consented to share. <div class="ec-teach"><div class="th">What to do instead</div> An informed refusal is only informed if one know what it rests on. Most declines come from a correctable belief, that the HPV vaccine removes the need to screen, that screening is unnecessary without symptoms, or fear of discomfort or of a previous bad experience. Explore, correct what is factually wrong, offer the alternatives, and if she still declines, respect it and document the discussion with a plan to revisit. <div class="ec-src"><b>Source:</b> AMA Code of Medical Ethics Opinion 2.1.1; USPSTF. Screening for Cervical Cancer: Recommendation Statement. JAMA 2018;320(7):674-686.</div></div></div> [[Try this question again->Screening refusal - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Screening refusal. Opening"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Explore her reasons and correct misunderstandings</div> An informed refusal is only informed if one know what it rests on. Most declines come from a correctable belief, that the HPV vaccine removes the need to screen, that screening is unnecessary without symptoms, or fear of discomfort or of a previous bad experience. Explore, correct what is factually wrong, offer the alternatives, and if she still declines, respect it and document the discussion with a plan to revisit. <div class="ec-src"><b>Source:</b> AMA Code of Medical Ethics Opinion 2.1.1; USPSTF. Screening for Cervical Cancer: Recommendation Statement. JAMA 2018;320(7):674-686.</div></div> [[Start another case->Hub]] [[Restart this case->Screening refusal - Opening]] [[Next case →->Adolescent confidentiality - Ethics]]

<span class="ec-case-marker" hidden data-entry="Screening refusal. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the next step.</div> Performing a test a competent adult has declined is battery, regardless of intent. It also destroys the trust that any future screening conversation depends on. <div class="ec-teach"><div class="th">What to do instead</div> An informed refusal is only informed if one know what it rests on. Most declines come from a correctable belief, that the HPV vaccine removes the need to screen, that screening is unnecessary without symptoms, or fear of discomfort or of a previous bad experience. Explore, correct what is factually wrong, offer the alternatives, and if she still declines, respect it and document the discussion with a plan to revisit. <div class="ec-src"><b>Source:</b> AMA Code of Medical Ethics Opinion 2.1.1; USPSTF. Screening for Cervical Cancer: Recommendation Statement. JAMA 2018;320(7):674-686.</div></div></div> [[Try this question again->Screening refusal - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Screening refusal. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the next step.</div> This is the misconception most likely to be behind her refusal, and endorsing it makes it permanent. The vaccine covers the highest-risk types but not all oncogenic types, and vaccinated women continue screening on the same schedule, cytology every 3 years, or high-risk HPV testing or cotesting every 5 years, from 30 to 65. <div class="ec-teach"><div class="th">What to do instead</div> An informed refusal is only informed if one know what it rests on. Most declines come from a correctable belief, that the HPV vaccine removes the need to screen, that screening is unnecessary without symptoms, or fear of discomfort or of a previous bad experience. Explore, correct what is factually wrong, offer the alternatives, and if she still declines, respect it and document the discussion with a plan to revisit. <div class="ec-src"><b>Source:</b> AMA Code of Medical Ethics Opinion 2.1.1; USPSTF. Screening for Cervical Cancer: Recommendation Statement. JAMA 2018;320(7):674-686.</div></div></div> [[Try this question again->Screening refusal - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Screening refusal. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the next step.</div> Framing a refusal as negligence is coercive and factually wrong, screening is a recommendation, not an obligation. Threatening to end the relationship over a declined preventive service abandons a patient who will now be screened by no one. <div class="ec-teach"><div class="th">What to do instead</div> An informed refusal is only informed if one know what it rests on. Most declines come from a correctable belief, that the HPV vaccine removes the need to screen, that screening is unnecessary without symptoms, or fear of discomfort or of a previous bad experience. Explore, correct what is factually wrong, offer the alternatives, and if she still declines, respect it and document the discussion with a plan to revisit. <div class="ec-src"><b>Source:</b> AMA Code of Medical Ethics Opinion 2.1.1; USPSTF. Screening for Cervical Cancer: Recommendation Statement. JAMA 2018;320(7):674-686.</div></div></div> [[Try this question again->Screening refusal - Opening]] [[Start another case->Hub]]

<div class="ec-scene">Journal club · 07:15</div> <div class="ec-abstract"><b>BACKGROUND.</b> Intravenous iron is used for iron-deficiency anemia in chronic kidney disease, but its effect on cardiovascular outcomes is uncertain.<br><b>METHODS.</b> In a multicenter, open-label, randomized trial, 2,141 adults with stage 3-4 chronic kidney disease and ferritin below 100 ng/mL were assigned to high-dose intravenous iron or oral iron. The primary outcome was a composite of nonfatal myocardial infarction, nonfatal stroke, hospitalization for heart failure, or death from any cause. Median follow-up was 2.1 years.<br><b>RESULTS.</b> The primary outcome occurred in 214 of 1,070 patients (20.0%) in the intravenous group and 251 of 1,071 (23.4%) in the oral group (hazard ratio 0.85; 95% CI 0.71-1.02; P=0.08). Hospitalization for heart failure occurred in 4.1% versus 6.3% (hazard ratio 0.65; 95% CI 0.45-0.94; P=0.02). Hemoglobin rose by 0.9 g/dL versus 0.4 g/dL. Serious infections occurred in 9.2% versus 8.8%.<br><b>CONCLUSIONS.</b> High-dose intravenous iron reduced hospitalization for heart failure in patients with chronic kidney disease.</div> <span class="ec-prompt">Which of the following is the most appropriate interpretation of this abstract?</span> [[Serious infections were more common with intravenous iron, which outweighs any benefit->Research abstract - D4]] [[The absolute risk reduction of 3.4% is too small to be clinically meaningful->Research abstract - D3]] [[The conclusion overstates a nonsignificant primary outcome->Research abstract - Correct]] [[The hemoglobin difference confirms that intravenous iron improves cardiovascular outcomes->Research abstract - D5]] [[The open-label design invalidates the mortality component of the composite->Research abstract - D2]] [[The trial was underpowered, since the confidence interval for the primary outcome is wide->Research abstract - D1]]

<span class="ec-case-marker" hidden data-entry="Research abstract. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best interpretation.</div> Infection risk is a legitimate concern with intravenous iron and worth examining. The reported figures are 9.2% versus 8.8%, a difference of 0.4% with no significance test given, too small and too uncertain to support this claim. <div class="ec-teach"><div class="th">What the abstract actually shows</div> The primary composite outcome had a hazard ratio of 0.85 with a 95% confidence interval of 0.71 to 1.02 and P=0.08, the interval crosses 1.0, so the result is not statistically significant. The heart failure result is a secondary outcome, and a conclusion drawn from a significant secondary endpoint when the primary endpoint is negative is hypothesis-generating rather than confirmatory. This is one of the commonest ways trial abstracts overstate what was shown. <div class="ec-src"><b>Source:</b> Guyatt G, et al. Users' Guides to the Medical Literature, 3rd ed; Schulz KF, Altman DG, Moher D. CONSORT 2010 Statement. BMJ 2010;340:c332.</div></div></div> [[Try this question again->Research abstract - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Research abstract. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best interpretation.</div> A 3.4% absolute reduction over 2 years would be clinically meaningful if it were real, that is a number needed to treat of about 29. The problem is not the size of the effect but that the result is compatible with no effect at all. <div class="ec-teach"><div class="th">What the abstract actually shows</div> The primary composite outcome had a hazard ratio of 0.85 with a 95% confidence interval of 0.71 to 1.02 and P=0.08, the interval crosses 1.0, so the result is not statistically significant. The heart failure result is a secondary outcome, and a conclusion drawn from a significant secondary endpoint when the primary endpoint is negative is hypothesis-generating rather than confirmatory. This is one of the commonest ways trial abstracts overstate what was shown. <div class="ec-src"><b>Source:</b> Guyatt G, et al. Users' Guides to the Medical Literature, 3rd ed; Schulz KF, Altman DG, Moher D. CONSORT 2010 Statement. BMJ 2010;340:c332.</div></div></div> [[Try this question again->Research abstract - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Research abstract. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best interpretation.</div> Hemoglobin is a surrogate marker. A drug can move a surrogate convincingly without improving the outcome that matters, which is precisely why the trial measured clinical events, and why the negative primary endpoint is the finding that counts. <div class="ec-teach"><div class="th">What the abstract actually shows</div> The primary composite outcome had a hazard ratio of 0.85 with a 95% confidence interval of 0.71 to 1.02 and P=0.08, the interval crosses 1.0, so the result is not statistically significant. The heart failure result is a secondary outcome, and a conclusion drawn from a significant secondary endpoint when the primary endpoint is negative is hypothesis-generating rather than confirmatory. This is one of the commonest ways trial abstracts overstate what was shown. <div class="ec-src"><b>Source:</b> Guyatt G, et al. Users' Guides to the Medical Literature, 3rd ed; Schulz KF, Altman DG, Moher D. CONSORT 2010 Statement. BMJ 2010;340:c332.</div></div></div> [[Try this question again->Research abstract - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Research abstract. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best interpretation.</div> Open-label design is a genuine limitation and does bias subjective outcomes such as hospitalization decisions, worth noting. Death from any cause is a hard endpoint largely resistant to ascertainment bias, so this criticism is misdirected at the one component least affected. <div class="ec-teach"><div class="th">What the abstract actually shows</div> The primary composite outcome had a hazard ratio of 0.85 with a 95% confidence interval of 0.71 to 1.02 and P=0.08, the interval crosses 1.0, so the result is not statistically significant. The heart failure result is a secondary outcome, and a conclusion drawn from a significant secondary endpoint when the primary endpoint is negative is hypothesis-generating rather than confirmatory. This is one of the commonest ways trial abstracts overstate what was shown. <div class="ec-src"><b>Source:</b> Guyatt G, et al. Users' Guides to the Medical Literature, 3rd ed; Schulz KF, Altman DG, Moher D. CONSORT 2010 Statement. BMJ 2010;340:c332.</div></div></div> [[Try this question again->Research abstract - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Research abstract. Opening"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ The conclusion overstates a nonsignificant primary outcome</div> The primary composite outcome had a hazard ratio of 0.85 with a 95% confidence interval of 0.71 to 1.02 and P=0.08, the interval crosses 1.0, so the result is not statistically significant. The heart failure result is a secondary outcome, and a conclusion drawn from a significant secondary endpoint when the primary endpoint is negative is hypothesis-generating rather than confirmatory. This is one of the commonest ways trial abstracts overstate what was shown. <div class="ec-src"><b>Source:</b> Guyatt G, et al. Users' Guides to the Medical Literature, 3rd ed; Schulz KF, Altman DG, Moher D. CONSORT 2010 Statement. BMJ 2010;340:c332.</div></div> [[Start another case->Hub]] [[Restart this case->Research abstract - Opening]] [[Next case →->Drug advertisement - Opening]]

<span class="ec-case-marker" hidden data-entry="Research abstract. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best interpretation.</div> The interval of 0.71 to 1.02 is reasonably tight for an event-driven trial of this size, and 2,141 patients with 465 events is not obviously underpowered. Power is a design question answered by the pre-specified sample size calculation, not inferred from a non-significant result, concluding "underpowered" whenever P exceeds 0.05 is circular. <div class="ec-teach"><div class="th">What the abstract actually shows</div> The primary composite outcome had a hazard ratio of 0.85 with a 95% confidence interval of 0.71 to 1.02 and P=0.08, the interval crosses 1.0, so the result is not statistically significant. The heart failure result is a secondary outcome, and a conclusion drawn from a significant secondary endpoint when the primary endpoint is negative is hypothesis-generating rather than confirmatory. This is one of the commonest ways trial abstracts overstate what was shown. <div class="ec-src"><b>Source:</b> Guyatt G, et al. Users' Guides to the Medical Literature, 3rd ed; Schulz KF, Altman DG, Moher D. CONSORT 2010 Statement. BMJ 2010;340:c332.</div></div></div> [[Try this question again->Research abstract - Opening]] [[Start another case->Hub]]

<div class="ec-scene">Pharmaceutical advertisement · 12:40</div> <div class="ec-ad"><div class="ec-adhead">CARDIVEX<sup>®</sup> (velsartan calcium)</div><div class="ec-adtag">CUT MAJOR CARDIAC EVENTS BY 38%<sup>1</sup></div><p>In the landmark VECTOR-HF trial, CARDIVEX delivered a <b>38% relative reduction</b> in the primary composite endpoint versus placebo in patients with stable heart failure.<sup>1</sup></p><p><b>Proven to lower NT-proBNP by 41%</b> at 12 weeks.<sup>1</sup> Once-daily dosing. Now approved for adults with NYHA class II-III heart failure.</p><p class="ec-adfine">1. VECTOR-HF: randomized, double-blind, placebo-controlled trial; n=4,210; median follow-up 18 months. Primary composite endpoint (cardiovascular death, heart failure hospitalization, or urgent heart failure visit) occurred in 2.1% of CARDIVEX patients vs 3.4% of placebo patients (HR 0.62; 95% CI 0.44-0.87; P=0.006). The composite result was driven predominantly by urgent heart failure visits; cardiovascular death occurred in 1.1% vs 1.2% (P=0.71). Study funded by the manufacturer. Most common adverse events: dizziness (11%), hyperkalemia (7%).</p></div> <span class="ec-prompt">Which of the following is the most appropriate basis for criticizing its central claim?</span> [[The 41% reduction in NT-proBNP is the strongest evidence of benefit in the advertisement->Drug advertisement - D3]] [[The composite endpoint was driven by its softest component, so the headline overstates hard outcomes->Drug advertisement - D1]] [[The headline reports a relative risk reduction; the absolute reduction is 1.3%->Drug advertisement - Correct]] [[The result is not statistically significant, since the confidence interval is wide->Drug advertisement - D4]] [[The trial was funded by the manufacturer, so the results cannot be relied upon->Drug advertisement - D2]]

<span class="ec-case-marker" hidden data-entry="Drug advertisement. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the central problem.</div> This inverts the hierarchy. NT-proBNP is a surrogate marker, and drugs have repeatedly moved surrogates convincingly while failing on outcomes that matter, which is exactly why the trial measured events. Leading with a biomarker is itself a warning sign in an advertisement. <div class="ec-teach"><div class="th">What the advertisement is actually doing</div> Events fell from 3.4% to 2.1%, an absolute risk reduction of 1.3 percentage points, meaning about 77 patients must be treated for 18 months to prevent one event. The same result expressed as "38%" sounds roughly thirty times larger. Relative risk reduction is the standard way advertising inflates a modest benefit, because it is a true number that describes almost nothing about what an individual patient gains. <div class="ec-src"><b>Source:</b> Guyatt G, et al. Users' Guides to the Medical Literature, 3rd ed; Schwartz LM, Woloshin S. Communicating Uncertainties About Prescription Drugs to the Public. Arch Intern Med 2011;171(16):1463-1468; FDA Guidance for Industry: Consumer-Directed Broadcast Advertisements.</div></div></div> [[Try this question again->Drug advertisement - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Drug advertisement. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the central problem.</div> This is a genuinely good critique and the second-best answer here, the footnote admits the result was driven by urgent heart failure visits, a subjective, physician-determined outcome, while cardiovascular death was 1.1% versus 1.2% with P=0.71. But it identifies a second flaw layered on top of the first. The headline number itself is misleading before one even reach what it was made of. <div class="ec-teach"><div class="th">What the advertisement is actually doing</div> Events fell from 3.4% to 2.1%, an absolute risk reduction of 1.3 percentage points, meaning about 77 patients must be treated for 18 months to prevent one event. The same result expressed as "38%" sounds roughly thirty times larger. Relative risk reduction is the standard way advertising inflates a modest benefit, because it is a true number that describes almost nothing about what an individual patient gains. <div class="ec-src"><b>Source:</b> Guyatt G, et al. Users' Guides to the Medical Literature, 3rd ed; Schwartz LM, Woloshin S. Communicating Uncertainties About Prescription Drugs to the Public. Arch Intern Med 2011;171(16):1463-1468; FDA Guidance for Industry: Consumer-Directed Broadcast Advertisements.</div></div></div> [[Try this question again->Drug advertisement - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Drug advertisement. Opening"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ The headline reports a relative risk reduction; the absolute reduction is 1.3%.</div> Events fell from 3.4% to 2.1%, an absolute risk reduction of 1.3 percentage points, meaning about 77 patients must be treated for 18 months to prevent one event. The same result expressed as "38%" sounds roughly thirty times larger. Relative risk reduction is the standard way advertising inflates a modest benefit, because it is a true number that describes almost nothing about what an individual patient gains. <div class="ec-src"><b>Source:</b> Guyatt G, et al. Users' Guides to the Medical Literature, 3rd ed; Schwartz LM, Woloshin S. Communicating Uncertainties About Prescription Drugs to the Public. Arch Intern Med 2011;171(16):1463-1468; FDA Guidance for Industry: Consumer-Directed Broadcast Advertisements.</div></div> [[Start another case->Hub]] [[Restart this case->Drug advertisement - Opening]] [[Next case →->Statin prevention - Opening]]

<span class="ec-case-marker" hidden data-entry="Drug advertisement. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the central problem.</div> The interval is 0.44 to 0.87 and does not cross 1.0, with P=0.006, this is statistically significant. The problem with the advertisement is not that the effect might be absent, but that a real and modest effect is being presented as a large one. <div class="ec-teach"><div class="th">What the advertisement is actually doing</div> Events fell from 3.4% to 2.1%, an absolute risk reduction of 1.3 percentage points, meaning about 77 patients must be treated for 18 months to prevent one event. The same result expressed as "38%" sounds roughly thirty times larger. Relative risk reduction is the standard way advertising inflates a modest benefit, because it is a true number that describes almost nothing about what an individual patient gains. <div class="ec-src"><b>Source:</b> Guyatt G, et al. Users' Guides to the Medical Literature, 3rd ed; Schwartz LM, Woloshin S. Communicating Uncertainties About Prescription Drugs to the Public. Arch Intern Med 2011;171(16):1463-1468; FDA Guidance for Industry: Consumer-Directed Broadcast Advertisements.</div></div></div> [[Try this question again->Drug advertisement - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Drug advertisement. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the central problem.</div> Industry funding is a real source of bias and is associated with more favorable published conclusions, so noticing it is right. It does not by itself invalidate a randomized, double-blind, placebo-controlled trial, dismissing results on funding alone is as uncritical as accepting them on the headline alone. Judge the design and the numbers. <div class="ec-teach"><div class="th">What the advertisement is actually doing</div> Events fell from 3.4% to 2.1%, an absolute risk reduction of 1.3 percentage points, meaning about 77 patients must be treated for 18 months to prevent one event. The same result expressed as "38%" sounds roughly thirty times larger. Relative risk reduction is the standard way advertising inflates a modest benefit, because it is a true number that describes almost nothing about what an individual patient gains. <div class="ec-src"><b>Source:</b> Guyatt G, et al. Users' Guides to the Medical Literature, 3rd ed; Schwartz LM, Woloshin S. Communicating Uncertainties About Prescription Drugs to the Public. Arch Intern Med 2011;171(16):1463-1468; FDA Guidance for Industry: Consumer-Directed Broadcast Advertisements.</div></div></div> [[Try this question again->Drug advertisement - Opening]] [[Start another case->Hub]]

<div class="ec-scene">Coronary care unit · 03:40</div> A 67-year-old man presented with 90 minutes of crushing substernal chest pain. ECG showed ST-segment elevations in V1–V4. He underwent successful primary PCI with restoration of coronary flow. Several hours later, despite adequate volume resuscitation, his blood pressure is 76/48 mm Hg. He has cool extremities, altered mental status, and lactate is 4.1 mmol/L. <span class="ec-prompt">Which of the following findings is most strongly associated with increased short-term mortality?</span> [[LDL cholesterol of 138 mg/dL->STEMI prognosis - D1]] [[Left ventricular ejection fraction of 42%->STEMI prognosis - D5]] [[Persistent hemodynamic instability->STEMI prognosis - Correct]] [[Previous stable angina->STEMI prognosis - D2]] [[Sinus tachycardia at 102/min->STEMI prognosis - D4]] [[Successful coronary reperfusion->STEMI prognosis - D3]]

<span class="ec-case-marker" hidden data-entry="STEMI prognosis. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Persistent hemodynamic instability.</div> Persistent hypotension with signs of hypoperfusion defines cardiogenic shock, the most powerful short-term mortality predictor after acute MI. Even after successful reperfusion, cardiogenic shock carries in-hospital mortality of 40–50%. Recognition triggers consideration of mechanical circulatory support and shock-team activation. <div class="ec-src"><b>Source:</b> Hochman JS, Buller CE, Sleeper LA, et al. Cardiogenic Shock Complicating Acute Myocardial Infarction. Etiologies, Management and Outcome: A Report from the SHOCK Trial Registry. J Am Coll Cardiol 2000;36(3 Suppl 1):1063-1070; ACC/AHA STEMI/Cardiogenic Shock Guidelines.</div></div> [[Start another case->Hub]] [[Restart this case->STEMI prognosis - Dx]] [[Next case →->AF anticoagulation - Rx]]

<span class="ec-case-marker" hidden data-entry="STEMI prognosis. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ LDL cholesterol is not a short-term predictor.</div> Elevated LDL is a long-term cardiovascular risk factor but does not predict acute post-MI mortality in a patient who has already infarcted. <div class="ec-teach"><div class="th">What to do instead</div> Persistent hypotension with signs of hypoperfusion defines cardiogenic shock, the most powerful short-term mortality predictor after acute MI. Even after successful reperfusion, cardiogenic shock carries in-hospital mortality of 40–50%. Recognition triggers consideration of mechanical circulatory support and shock-team activation. <div class="ec-src"><b>Source:</b> Hochman JS, Buller CE, Sleeper LA, et al. Cardiogenic Shock Complicating Acute Myocardial Infarction. Etiologies, Management and Outcome: A Report from the SHOCK Trial Registry. J Am Coll Cardiol 2000;36(3 Suppl 1):1063-1070; ACC/AHA STEMI/Cardiogenic Shock Guidelines.</div></div></div> [[Try this question again->STEMI prognosis - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="STEMI prognosis. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Previous stable angina is not the strongest predictor.</div> A history of stable angina may reflect chronic coronary disease, but it does not carry the prognostic weight of hemodynamic collapse after infarction. <div class="ec-teach"><div class="th">What to do instead</div> Persistent hypotension with signs of hypoperfusion defines cardiogenic shock, the most powerful short-term mortality predictor after acute MI. Even after successful reperfusion, cardiogenic shock carries in-hospital mortality of 40–50%. Recognition triggers consideration of mechanical circulatory support and shock-team activation. <div class="ec-src"><b>Source:</b> Hochman JS, Buller CE, Sleeper LA, et al. Cardiogenic Shock Complicating Acute Myocardial Infarction. Etiologies, Management and Outcome: A Report from the SHOCK Trial Registry. J Am Coll Cardiol 2000;36(3 Suppl 1):1063-1070; ACC/AHA STEMI/Cardiogenic Shock Guidelines.</div></div></div> [[Try this question again->STEMI prognosis - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="STEMI prognosis. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Successful reperfusion improves prognosis.</div> Successful reperfusion is a favorable finding. The ongoing hemodynamic instability despite reperfusion is the ominous sign. <div class="ec-teach"><div class="th">What to do instead</div> Persistent hypotension with signs of hypoperfusion defines cardiogenic shock, the most powerful short-term mortality predictor after acute MI. Even after successful reperfusion, cardiogenic shock carries in-hospital mortality of 40–50%. Recognition triggers consideration of mechanical circulatory support and shock-team activation. <div class="ec-src"><b>Source:</b> Hochman JS, Buller CE, Sleeper LA, et al. Cardiogenic Shock Complicating Acute Myocardial Infarction. Etiologies, Management and Outcome: A Report from the SHOCK Trial Registry. J Am Coll Cardiol 2000;36(3 Suppl 1):1063-1070; ACC/AHA STEMI/Cardiogenic Shock Guidelines.</div></div></div> [[Try this question again->STEMI prognosis - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="STEMI prognosis. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Tachycardia alone is not the strongest predictor.</div> Sinus tachycardia at 102/min is a compensatory response and may accompany shock, but is far less ominous than frank hypoperfusion with rising lactate and altered mental status. <div class="ec-teach"><div class="th">What to do instead</div> Persistent hypotension with signs of hypoperfusion defines cardiogenic shock, the most powerful short-term mortality predictor after acute MI. Even after successful reperfusion, cardiogenic shock carries in-hospital mortality of 40–50%. Recognition triggers consideration of mechanical circulatory support and shock-team activation. <div class="ec-src"><b>Source:</b> Hochman JS, Buller CE, Sleeper LA, et al. Cardiogenic Shock Complicating Acute Myocardial Infarction. Etiologies, Management and Outcome: A Report from the SHOCK Trial Registry. J Am Coll Cardiol 2000;36(3 Suppl 1):1063-1070; ACC/AHA STEMI/Cardiogenic Shock Guidelines.</div></div></div> [[Try this question again->STEMI prognosis - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="STEMI prognosis. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ LVEF of 42% is reduced but not the strongest predictor here.</div> An LVEF of 42% after anterior STEMI is reduced but not in the cardiogenic shock range. The hemodynamic picture, not the ejection fraction alone, drives prognosis. <div class="ec-teach"><div class="th">What to do instead</div> Persistent hypotension with signs of hypoperfusion defines cardiogenic shock, the most powerful short-term mortality predictor after acute MI. Even after successful reperfusion, cardiogenic shock carries in-hospital mortality of 40–50%. Recognition triggers consideration of mechanical circulatory support and shock-team activation. <div class="ec-src"><b>Source:</b> Hochman JS, Buller CE, Sleeper LA, et al. Cardiogenic Shock Complicating Acute Myocardial Infarction. Etiologies, Management and Outcome: A Report from the SHOCK Trial Registry. J Am Coll Cardiol 2000;36(3 Suppl 1):1063-1070; ACC/AHA STEMI/Cardiogenic Shock Guidelines.</div></div></div> [[Try this question again->STEMI prognosis - Dx]] [[Start another case->Hub]]

<div class="ec-scene">Hepatology clinic · 14:20</div> A 54-year-old man with alcohol-associated cirrhosis is evaluated for liver transplantation. He has ascites requiring large-volume paracentesis and recurrent hepatic encephalopathy. Laboratory studies show total bilirubin 4.1 mg/dL, INR 2.0, creatinine 1.5 mg/dL, and sodium 131 mEq/L. <span class="ec-prompt">Which of the following measures is most appropriate for estimating short-term mortality and prioritizing transplant allocation?</span> [[APRI score->MELD score - D3]] [[Child-Pugh score->MELD score - D1]] [[Glasgow-Blatchford score->MELD score - D4]] [[Maddrey discriminant function->MELD score - D2]] [[MELD-Na score->MELD score - Correct]]

<span class="ec-case-marker" hidden data-entry="MELD score. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ MELD-Na score.</div> The Model for End-stage Liver Disease with sodium (MELD-Na) uses objective laboratory variables, bilirubin, INR, creatinine, and sodium, to estimate 90-day mortality and is the basis for liver-transplant organ allocation in the United States. Unlike the Child-Pugh score, it avoids subjective assessments of ascites and encephalopathy severity. <div class="ec-src"><b>Source:</b> Kamath PS, et al. A Model to Predict Survival in Patients With End-Stage Liver Disease. Hepatology 2001;33(2):464-470; Kim WR, et al. Hyponatremia and Mortality Among Patients on the Liver-Transplant Waiting List. N Engl J Med 2008;359(10):1018-1026; UNOS/OPTN allocation policy.</div></div> [[Start another case->Hub]] [[Restart this case->MELD score - Dx]] [[Next case →->Pyloric stenosis - Rx]]

<span class="ec-case-marker" hidden data-entry="MELD score. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Child-Pugh is not the allocation standard.</div> Child-Pugh was the earlier staging system but includes subjective assessments of ascites and encephalopathy. MELD-Na replaced it for transplant allocation because of its superior objectivity and predictive accuracy. <div class="ec-teach"><div class="th">What to do instead</div> The Model for End-stage Liver Disease with sodium (MELD-Na) uses objective laboratory variables, bilirubin, INR, creatinine, and sodium, to estimate 90-day mortality and is the basis for liver-transplant organ allocation in the United States. Unlike the Child-Pugh score, it avoids subjective assessments of ascites and encephalopathy severity. <div class="ec-src"><b>Source:</b> Kamath PS, et al. A Model to Predict Survival in Patients With End-Stage Liver Disease. Hepatology 2001;33(2):464-470; Kim WR, et al. Hyponatremia and Mortality Among Patients on the Liver-Transplant Waiting List. N Engl J Med 2008;359(10):1018-1026; UNOS/OPTN allocation policy.</div></div></div> [[Try this question again->MELD score - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="MELD score. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Maddrey discriminant function is for alcoholic hepatitis.</div> The Maddrey discriminant function predicts mortality specifically in acute alcoholic hepatitis and guides corticosteroid therapy. It is not used for transplant allocation. <div class="ec-teach"><div class="th">What to do instead</div> The Model for End-stage Liver Disease with sodium (MELD-Na) uses objective laboratory variables, bilirubin, INR, creatinine, and sodium, to estimate 90-day mortality and is the basis for liver-transplant organ allocation in the United States. Unlike the Child-Pugh score, it avoids subjective assessments of ascites and encephalopathy severity. <div class="ec-src"><b>Source:</b> Kamath PS, et al. A Model to Predict Survival in Patients With End-Stage Liver Disease. Hepatology 2001;33(2):464-470; Kim WR, et al. Hyponatremia and Mortality Among Patients on the Liver-Transplant Waiting List. N Engl J Med 2008;359(10):1018-1026; UNOS/OPTN allocation policy.</div></div></div> [[Try this question again->MELD score - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="MELD score. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ APRI estimates fibrosis, not transplant priority.</div> The AST-to-platelet ratio index estimates hepatic fibrosis severity but does not predict short-term mortality or drive transplant allocation. <div class="ec-teach"><div class="th">What to do instead</div> The Model for End-stage Liver Disease with sodium (MELD-Na) uses objective laboratory variables, bilirubin, INR, creatinine, and sodium, to estimate 90-day mortality and is the basis for liver-transplant organ allocation in the United States. Unlike the Child-Pugh score, it avoids subjective assessments of ascites and encephalopathy severity. <div class="ec-src"><b>Source:</b> Kamath PS, et al. A Model to Predict Survival in Patients With End-Stage Liver Disease. Hepatology 2001;33(2):464-470; Kim WR, et al. Hyponatremia and Mortality Among Patients on the Liver-Transplant Waiting List. N Engl J Med 2008;359(10):1018-1026; UNOS/OPTN allocation policy.</div></div></div> [[Try this question again->MELD score - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="MELD score. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Glasgow-Blatchford is for upper GI bleeding.</div> The Glasgow-Blatchford score stratifies risk in upper gastrointestinal bleeding, not chronic liver disease prognosis. <div class="ec-teach"><div class="th">What to do instead</div> The Model for End-stage Liver Disease with sodium (MELD-Na) uses objective laboratory variables, bilirubin, INR, creatinine, and sodium, to estimate 90-day mortality and is the basis for liver-transplant organ allocation in the United States. Unlike the Child-Pugh score, it avoids subjective assessments of ascites and encephalopathy severity. <div class="ec-src"><b>Source:</b> Kamath PS, et al. A Model to Predict Survival in Patients With End-Stage Liver Disease. Hepatology 2001;33(2):464-470; Kim WR, et al. Hyponatremia and Mortality Among Patients on the Liver-Transplant Waiting List. N Engl J Med 2008;359(10):1018-1026; UNOS/OPTN allocation policy.</div></div></div> [[Try this question again->MELD score - Dx]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 16:35</div> A 72-year-old man presents with fever, productive cough, and dyspnea for 2 days. Chest radiography shows a right lower-lobe infiltrate. He is alert but intermittently confused about the date. Blood pressure is 88/56 mm Hg, respirations are 32/min, and BUN is 24 mg/dL. Oxygen saturation is 91% on room air. <span class="ec-prompt">Which of the following severity tools do current US guidelines recommend to support the admission decision?</span> [[APACHE II score->CAP CURB-65 - D3]] [[CURB-65->CAP CURB-65 - D1]] [[NEWS-2->CAP CURB-65 - D4]] [[Pneumonia Severity Index->CAP CURB-65 - Correct]] [[qSOFA score->CAP CURB-65 - D2]]

<span class="ec-case-marker" hidden data-entry="CAP CURB-65. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Pneumonia Severity Index</div> The 2019 ATS/IDSA community-acquired pneumonia guideline recommends the Pneumonia Severity Index in preference to CURB-65 to determine the need for hospitalization, because it has been more extensively validated and identifies a larger proportion of patients who can be treated safely as outpatients. CURB-65 remains a reasonable bedside alternative where the Index is impractical, but it is not the recommended primary tool. Either score supports, and does not replace, clinical judgment. <div class="ec-src"><b>Source:</b> Metlay JP, Waterer GW, Long AC, et al. Diagnosis and Treatment of Adults with Community-acquired Pneumonia. An Official Clinical Practice Guideline of the American Thoracic Society and Infectious Diseases Society of America. Am J Respir Crit Care Med 2019;200(7):e45-e67.</div></div> [[Start another case->Hub]] [[Restart this case->CAP CURB-65 - Dx]] [[Next case →->Tension pneumothorax - Dx]]

<span class="ec-case-marker" hidden data-entry="CAP CURB-65. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> CURB-65 is validated and widely used, and it correctly identifies this patient as severe. It is not, however, the tool the current US guideline recommends first for the admission decision. <div class="ec-teach"><div class="th">What the findings point to</div> The 2019 ATS/IDSA community-acquired pneumonia guideline recommends the Pneumonia Severity Index in preference to CURB-65 to determine the need for hospitalization, because it has been more extensively validated and identifies a larger proportion of patients who can be treated safely as outpatients. CURB-65 remains a reasonable bedside alternative where the Index is impractical, but it is not the recommended primary tool. Either score supports, and does not replace, clinical judgment. <div class="ec-src"><b>Source:</b> Metlay JP, Waterer GW, Long AC, et al. Diagnosis and Treatment of Adults with Community-acquired Pneumonia. An Official Clinical Practice Guideline of the American Thoracic Society and Infectious Diseases Society of America. Am J Respir Crit Care Med 2019;200(7):e45-e67.</div></div></div> [[Try this question again->CAP CURB-65 - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="CAP CURB-65. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ qSOFA screens for sepsis, not CAP disposition specifically.</div> The quick Sequential Organ Failure Assessment uses systolic BP ≤100, respiratory rate ≥22, and altered mental status to screen for sepsis risk. While it identifies sick patients, it was not designed or validated specifically for pneumonia disposition decisions and was downgraded from a screening tool in the 2021 Surviving Sepsis Campaign update. <div class="ec-teach"><div class="th">What to do instead</div> CURB-65 incorporates Confusion, BUN greater than 19 mg/dL (or BUN >19 mg/dL), Respiratory rate ≥30/min, Blood pressure systolic <90 or diastolic ≤60, and age ≥65. This patient scores at least 4 (confusion, elevated BUN, tachypnea, hypotension, age), indicating severe pneumonia requiring hospital admission and likely intensive care assessment. <div class="ec-src"><b>Source:</b> Lim WS, et al. Defining Community Acquired Pneumonia Severity on Presentation to Hospital. Thorax 2003;58(5):377-382; ATS/IDSA CAP Guideline 2019.</div></div></div> [[Try this question again->CAP CURB-65 - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="CAP CURB-65. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ APACHE II is for ICU mortality prediction.</div> APACHE II is a general ICU severity score using 12 physiologic variables, age, and chronic health status. It is not designed for the ED disposition question of whether a patient with community-acquired pneumonia requires hospitalization. <div class="ec-teach"><div class="th">What to do instead</div> CURB-65 incorporates Confusion, BUN greater than 19 mg/dL (or BUN >19 mg/dL), Respiratory rate ≥30/min, Blood pressure systolic <90 or diastolic ≤60, and age ≥65. This patient scores at least 4 (confusion, elevated BUN, tachypnea, hypotension, age), indicating severe pneumonia requiring hospital admission and likely intensive care assessment. <div class="ec-src"><b>Source:</b> Lim WS, et al. Defining Community Acquired Pneumonia Severity on Presentation to Hospital. Thorax 2003;58(5):377-382; ATS/IDSA CAP Guideline 2019.</div></div></div> [[Try this question again->CAP CURB-65 - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="CAP CURB-65. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ NEWS-2 is a general early warning score.</div> The National Early Warning Score 2 is a bedside track-and-trigger tool for detecting clinical deterioration in hospitalized patients. It is not specific to pneumonia and was not designed for the inpatient-vs-outpatient disposition decision. <div class="ec-teach"><div class="th">What to do instead</div> CURB-65 incorporates Confusion, BUN greater than 19 mg/dL (or BUN >19 mg/dL), Respiratory rate ≥30/min, Blood pressure systolic <90 or diastolic ≤60, and age ≥65. This patient scores at least 4 (confusion, elevated BUN, tachypnea, hypotension, age), indicating severe pneumonia requiring hospital admission and likely intensive care assessment. <div class="ec-src"><b>Source:</b> Lim WS, et al. Defining Community Acquired Pneumonia Severity on Presentation to Hospital. Thorax 2003;58(5):377-382; ATS/IDSA CAP Guideline 2019.</div></div></div> [[Try this question again->CAP CURB-65 - Dx]] [[Start another case->Hub]]

<div class="ec-scene">Surgical oncology clinic · 09:45</div> A 49-year-old woman undergoes lumpectomy for a 1.8-cm invasive ductal carcinoma. The tumor is ER-positive, PR-positive, and HER2-negative. Sentinel lymph node biopsy reveals metastatic disease in four of twelve axillary lymph nodes. <span class="ec-prompt">Which of the following findings most strongly indicates a less favorable prognosis?</span> [[Estrogen receptor positivity->Breast cancer prognosis - D1]] [[Extensive axillary nodal involvement->Breast cancer prognosis - Correct]] [[HER2-negative tumor status->Breast cancer prognosis - D3]] [[Progesterone receptor positivity->Breast cancer prognosis - D2]] [[Upper outer quadrant tumor location->Breast cancer prognosis - D4]]

<span class="ec-case-marker" hidden data-entry="Breast cancer prognosis. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Extensive axillary nodal involvement.</div> The number of involved axillary lymph nodes is the single most powerful prognostic factor in operable breast cancer. Four positive nodes places this patient in a substantially higher risk category. Hormone-receptor positivity is generally a favorable finding because it provides a therapeutic target for endocrine therapy. <div class="ec-src"><b>Source:</b> Carter CL, et al. Relation of Tumor Size, Lymph Node Status, and Survival in 24,740 Breast Cancer Cases. Cancer 1989;63(1):181-187; NCCN Clinical Practice Guidelines in Oncology: Breast Cancer.</div></div> [[Start another case->Hub]] [[Restart this case->Breast cancer prognosis - Dx]] [[Next case →->Triple negative breast - Dx]]

<span class="ec-case-marker" hidden data-entry="Breast cancer prognosis. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ ER positivity is a favorable finding.</div> Estrogen receptor positivity predicts response to endocrine therapy and is associated with a more favorable prognosis, not a worse one. <div class="ec-teach"><div class="th">What to do instead</div> The number of involved axillary lymph nodes is the single most powerful prognostic factor in operable breast cancer. Four positive nodes places this patient in a substantially higher risk category. Hormone-receptor positivity is generally a favorable finding because it provides a therapeutic target for endocrine therapy. <div class="ec-src"><b>Source:</b> Carter CL, et al. Relation of Tumor Size, Lymph Node Status, and Survival in 24,740 Breast Cancer Cases. Cancer 1989;63(1):181-187; NCCN Clinical Practice Guidelines in Oncology: Breast Cancer.</div></div></div> [[Try this question again->Breast cancer prognosis - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Breast cancer prognosis. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ PR positivity is favorable.</div> Progesterone receptor expression reinforces the likelihood of endocrine responsiveness and is not an adverse prognostic factor. <div class="ec-teach"><div class="th">What to do instead</div> The number of involved axillary lymph nodes is the single most powerful prognostic factor in operable breast cancer. Four positive nodes places this patient in a substantially higher risk category. Hormone-receptor positivity is generally a favorable finding because it provides a therapeutic target for endocrine therapy. <div class="ec-src"><b>Source:</b> Carter CL, et al. Relation of Tumor Size, Lymph Node Status, and Survival in 24,740 Breast Cancer Cases. Cancer 1989;63(1):181-187; NCCN Clinical Practice Guidelines in Oncology: Breast Cancer.</div></div></div> [[Try this question again->Breast cancer prognosis - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Breast cancer prognosis. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ HER2 negativity is not the strongest adverse factor here.</div> While HER2-positive tumors are more aggressive, effective targeted therapies exist. In this case, the dominant adverse factor is nodal burden. <div class="ec-teach"><div class="th">What to do instead</div> The number of involved axillary lymph nodes is the single most powerful prognostic factor in operable breast cancer. Four positive nodes places this patient in a substantially higher risk category. Hormone-receptor positivity is generally a favorable finding because it provides a therapeutic target for endocrine therapy. <div class="ec-src"><b>Source:</b> Carter CL, et al. Relation of Tumor Size, Lymph Node Status, and Survival in 24,740 Breast Cancer Cases. Cancer 1989;63(1):181-187; NCCN Clinical Practice Guidelines in Oncology: Breast Cancer.</div></div></div> [[Try this question again->Breast cancer prognosis - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Breast cancer prognosis. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Tumor location does not strongly predict outcome.</div> Quadrant location has minimal independent prognostic significance compared with nodal status, tumor size, and biologic subtype. <div class="ec-teach"><div class="th">What to do instead</div> The number of involved axillary lymph nodes is the single most powerful prognostic factor in operable breast cancer. Four positive nodes places this patient in a substantially higher risk category. Hormone-receptor positivity is generally a favorable finding because it provides a therapeutic target for endocrine therapy. <div class="ec-src"><b>Source:</b> Carter CL, et al. Relation of Tumor Size, Lymph Node Status, and Survival in 24,740 Breast Cancer Cases. Cancer 1989;63(1):181-187; NCCN Clinical Practice Guidelines in Oncology: Breast Cancer.</div></div></div> [[Try this question again->Breast cancer prognosis - Dx]] [[Start another case->Hub]]

<div class="ec-scene">Pediatric oncology clinic · 11:00</div> A 5-year-old boy is diagnosed with B-cell acute lymphoblastic leukemia. His presenting white blood cell count is 18,000/mm3. Cytogenetic analysis reveals t(12;21)/ETV6-RUNX1 fusion. He begins induction chemotherapy. Bone marrow examination on day 29 demonstrates fewer than 0.01% residual blasts by flow cytometry. <span class="ec-prompt">Which of the following findings is most strongly associated with a favorable prognosis?</span> [[Age of 15 years or older at initial diagnosis->ALL prognosis - D1]] [[CNS leukemia at presentation->ALL prognosis - D2]] [[Negative minimal residual disease after induction->ALL prognosis - Correct]] [[Persistent measurable residual disease after induction->ALL prognosis - D5]] [[T-cell phenotype with WBC above 100,000/mm3->ALL prognosis - D4]] [[WBC count of 150,000/mm3 at diagnosis->ALL prognosis - D3]]

<span class="ec-case-marker" hidden data-entry="ALL prognosis. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Negative minimal residual disease after induction</div> Measurable residual disease (MRD) assessment after induction is the single most powerful prognostic factor in childhood ALL, superseding presenting features. Negative MRD at end of induction identifies patients with an excellent prognosis. In contrast, persistent MRD predicts higher relapse risk and may trigger treatment intensification. <div class="ec-src"><b>Source:</b> Hunger SP, Mullighan CG. Acute Lymphoblastic Leukemia in Children. N Engl J Med 2015;373(16):1541-1552; NCI Childhood ALL Treatment Guidance.</div></div> [[Start another case->Hub]] [[Restart this case->ALL prognosis - Dx]] [[Next case →->AML MRD relapse - Prog]]

<span class="ec-case-marker" hidden data-entry="ALL prognosis. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Older age is an adverse prognostic factor.</div> Age ≥10 years (particularly adolescents) is associated with worse outcomes in childhood ALL. The favorable age range is 1–9 years. <div class="ec-teach"><div class="th">What to do instead</div> Measurable residual disease (MRD) assessment after induction is the single most powerful prognostic factor in childhood ALL, superseding presenting features. Negative MRD at end of induction identifies patients with an excellent prognosis. In contrast, persistent MRD predicts higher relapse risk and may trigger treatment intensification. <div class="ec-src"><b>Source:</b> Hunger SP, Mullighan CG. Acute Lymphoblastic Leukemia in Children. N Engl J Med 2015;373(16):1541-1552; NCI Childhood ALL Treatment Guidance.</div></div></div> [[Try this question again->ALL prognosis - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="ALL prognosis. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ CNS involvement at diagnosis is adverse.</div> CNS leukemia at presentation is an adverse feature requiring additional CNS-directed therapy. <div class="ec-teach"><div class="th">What to do instead</div> Measurable residual disease (MRD) assessment after induction is the single most powerful prognostic factor in childhood ALL, superseding presenting features. Negative MRD at end of induction identifies patients with an excellent prognosis. In contrast, persistent MRD predicts higher relapse risk and may trigger treatment intensification. <div class="ec-src"><b>Source:</b> Hunger SP, Mullighan CG. Acute Lymphoblastic Leukemia in Children. N Engl J Med 2015;373(16):1541-1552; NCI Childhood ALL Treatment Guidance.</div></div></div> [[Try this question again->ALL prognosis - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="ALL prognosis. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Very high WBC is an adverse factor.</div> A presenting WBC count ≥100,000/mm3 is a high-risk feature associated with worse outcomes. <div class="ec-teach"><div class="th">What to do instead</div> Measurable residual disease (MRD) assessment after induction is the single most powerful prognostic factor in childhood ALL, superseding presenting features. Negative MRD at end of induction identifies patients with an excellent prognosis. In contrast, persistent MRD predicts higher relapse risk and may trigger treatment intensification. <div class="ec-src"><b>Source:</b> Hunger SP, Mullighan CG. Acute Lymphoblastic Leukemia in Children. N Engl J Med 2015;373(16):1541-1552; NCI Childhood ALL Treatment Guidance.</div></div></div> [[Try this question again->ALL prognosis - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="ALL prognosis. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ T-cell ALL with high WBC is higher risk.</div> T-cell phenotype with very high presenting WBC count is associated with a more aggressive clinical course. <div class="ec-teach"><div class="th">What to do instead</div> Measurable residual disease (MRD) assessment after induction is the single most powerful prognostic factor in childhood ALL, superseding presenting features. Negative MRD at end of induction identifies patients with an excellent prognosis. In contrast, persistent MRD predicts higher relapse risk and may trigger treatment intensification. <div class="ec-src"><b>Source:</b> Hunger SP, Mullighan CG. Acute Lymphoblastic Leukemia in Children. N Engl J Med 2015;373(16):1541-1552; NCI Childhood ALL Treatment Guidance.</div></div></div> [[Try this question again->ALL prognosis - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="ALL prognosis. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Persistent MRD is an adverse finding.</div> Persistent measurable residual disease after induction is the strongest adverse prognostic indicator, often leading to treatment intensification or transplant consideration. <div class="ec-teach"><div class="th">What to do instead</div> Measurable residual disease (MRD) assessment after induction is the single most powerful prognostic factor in childhood ALL, superseding presenting features. Negative MRD at end of induction identifies patients with an excellent prognosis. In contrast, persistent MRD predicts higher relapse risk and may trigger treatment intensification. <div class="ec-src"><b>Source:</b> Hunger SP, Mullighan CG. Acute Lymphoblastic Leukemia in Children. N Engl J Med 2015;373(16):1541-1552; NCI Childhood ALL Treatment Guidance.</div></div></div> [[Try this question again->ALL prognosis - Dx]] [[Start another case->Hub]]

<div class="ec-scene">Trauma bay · 19:22</div> A 23-year-old man is seen 15 minutes after a high-speed motor vehicle collision, in severe respiratory distress. Blood pressure is 78/50 mm Hg and pulse is 132/min. Breath sounds are absent on the right with hyperresonance to percussion. The trachea is deviated to the left. Jugular venous pressure is elevated. Tension pneumothorax has been recognized clinically, and needle decompression is chosen as the immediate intervention. <span class="ec-prompt">Which of the following is the most appropriate needle insertion site?</span> [[Fifth intercostal space, midaxillary line->Tension PTX - D2]] [[Fourth or fifth intercostal space, anterior axillary line->Tension PTX - Correct]] [[Second intercostal space, anterior axillary line->Tension PTX - D3]] [[Second intercostal space, midclavicular line->Tension PTX - D1]] [[Sixth intercostal space, posterior axillary line->Tension PTX - D4]]

<span class="ec-case-marker" hidden data-entry="Tension PTX. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Fourth or fifth intercostal space, anterior axillary line</div> A cadaver-based comparison found the chest wall at the traditional second intercostal space, midclavicular line site is significantly thicker than at the fourth or fifth intercostal space, anterior axillary line, the same landmark used for tube thoracostomy. Standard 5 to 8 cm decompression needles fail to reach the pleural space at the classic anterior site in a meaningful proportion of adults, which is why current trauma guidance now favors the lateral position. <div class="ec-src"><b>Source:</b> Inaba K, Branco BC, Eckstein M, Shatz DV, Martin MJ, Green DJ, Noguchi TT, Demetriades D. Optimal positioning for emergent needle thoracostomy: a cadaver-based study. J Trauma 2011;71(5):1099-1103; ACS Committee on Trauma, ATLS 10th ed, 2018.</div></div> [[Start another case->Hub]] [[Restart this case->Tension PTX - Rx]] [[Next case →->Status asthmaticus - Opening]]

<span class="ec-case-marker" hidden data-entry="Tension PTX. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Chest wall is too thick here in most adults. The second intercostal space, midclavicular line is the traditional teaching site, but a standard needle frequently fails to reach the pleural space there.</div> <div class="ec-teach"><div class="th">What to do instead</div> A cadaver-based comparison found the chest wall at the traditional second intercostal space, midclavicular line site is significantly thicker than at the fourth or fifth intercostal space, anterior axillary line, the same landmark used for tube thoracostomy. Standard 5 to 8 cm decompression needles fail to reach the pleural space at the classic anterior site in a meaningful proportion of adults, which is why current trauma guidance now favors the lateral position. <div class="ec-src"><b>Source:</b> Inaba K, Branco BC, Eckstein M, Shatz DV, Martin MJ, Green DJ, Noguchi TT, Demetriades D. Optimal positioning for emergent needle thoracostomy: a cadaver-based study. J Trauma 2011;71(5):1099-1103; ACS Committee on Trauma, ATLS 10th ed, 2018.</div></div></div> [[Try this question again->Tension PTX - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Tension PTX. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Too far posterior and low for a first attempt. The midaxillary line at the fifth space risks the latissimus dorsi and long thoracic neurovascular bundle and is not the preferred landmark.</div> <div class="ec-teach"><div class="th">What to do instead</div> A cadaver-based comparison found the chest wall at the traditional second intercostal space, midclavicular line site is significantly thicker than at the fourth or fifth intercostal space, anterior axillary line, the same landmark used for tube thoracostomy. Standard 5 to 8 cm decompression needles fail to reach the pleural space at the classic anterior site in a meaningful proportion of adults, which is why current trauma guidance now favors the lateral position. <div class="ec-src"><b>Source:</b> Inaba K, Branco BC, Eckstein M, Shatz DV, Martin MJ, Green DJ, Noguchi TT, Demetriades D. Optimal positioning for emergent needle thoracostomy: a cadaver-based study. J Trauma 2011;71(5):1099-1103; ACS Committee on Trauma, ATLS 10th ed, 2018.</div></div></div> [[Try this question again->Tension PTX - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Tension PTX. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Still anterior, but at the wrong level. The second intercostal space remains over the thicker anterior chest wall regardless of whether the line used is midclavicular or anterior axillary.</div> <div class="ec-teach"><div class="th">What to do instead</div> A cadaver-based comparison found the chest wall at the traditional second intercostal space, midclavicular line site is significantly thicker than at the fourth or fifth intercostal space, anterior axillary line, the same landmark used for tube thoracostomy. Standard 5 to 8 cm decompression needles fail to reach the pleural space at the classic anterior site in a meaningful proportion of adults, which is why current trauma guidance now favors the lateral position. <div class="ec-src"><b>Source:</b> Inaba K, Branco BC, Eckstein M, Shatz DV, Martin MJ, Green DJ, Noguchi TT, Demetriades D. Optimal positioning for emergent needle thoracostomy: a cadaver-based study. J Trauma 2011;71(5):1099-1103; ACS Committee on Trauma, ATLS 10th ed, 2018.</div></div></div> [[Try this question again->Tension PTX - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Tension PTX. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Too posterior and too low. The posterior axillary line at the sixth space is well away from the recommended landmark and risks the diaphragm and abdominal viscera on the lower rib margin.</div> <div class="ec-teach"><div class="th">What to do instead</div> A cadaver-based comparison found the chest wall at the traditional second intercostal space, midclavicular line site is significantly thicker than at the fourth or fifth intercostal space, anterior axillary line, the same landmark used for tube thoracostomy. Standard 5 to 8 cm decompression needles fail to reach the pleural space at the classic anterior site in a meaningful proportion of adults, which is why current trauma guidance now favors the lateral position. <div class="ec-src"><b>Source:</b> Inaba K, Branco BC, Eckstein M, Shatz DV, Martin MJ, Green DJ, Noguchi TT, Demetriades D. Optimal positioning for emergent needle thoracostomy: a cadaver-based study. J Trauma 2011;71(5):1099-1103; ACS Committee on Trauma, ATLS 10th ed, 2018.</div></div></div> [[Try this question again->Tension PTX - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Coronary care unit · 02:15</div> A 71-year-old man with an acute inferior myocardial infarction develops confusion and near-syncope 3 hours into his hospital stay. Pulse is 28/min with high-grade second-degree AV block. Blood pressure is 76/42 mm Hg. Atropine 1 mg IV has been administered without improvement in heart rate or hemodynamics. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Carotid sinus massage->Unstable bradycardia - D4]] [[Intravenous adenosine->Unstable bradycardia - D3]] [[Intravenous amiodarone->Unstable bradycardia - D1]] [[Oral metoprolol->Unstable bradycardia - D2]] [[Transcutaneous pacing->Unstable bradycardia - Correct]]

<span class="ec-case-marker" hidden data-entry="Unstable bradycardia. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Transcutaneous pacing.</div> Severe symptomatic bradycardia with hemodynamic instability that fails to respond to atropine requires transcutaneous pacing as a bridge to transvenous pacing. High-grade AV block complicating inferior MI frequently does not respond to atropine because the block is often at or below the bundle of His. Dopamine or epinephrine infusions are alternatives while pacing is prepared. <div class="ec-src"><b>Source:</b> Panchal AR, et al. 2020 AHA Guidelines for CPR and Emergency Cardiovascular Care: Adult Bradycardia. Circulation 2020;142(16 Suppl 2):S366-S368.</div></div> [[Start another case->Hub]] [[Restart this case->Unstable bradycardia - Rx]] [[Next case →->Aortic stenosis - Rx]]

<span class="ec-case-marker" hidden data-entry="Unstable bradycardia. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Amiodarone does not treat bradycardia.</div> Amiodarone is an antiarrhythmic used for tachyarrhythmias. It can worsen bradycardia and AV block. <div class="ec-teach"><div class="th">What to do instead</div> Severe symptomatic bradycardia with hemodynamic instability that fails to respond to atropine requires transcutaneous pacing as a bridge to transvenous pacing. High-grade AV block complicating inferior MI frequently does not respond to atropine because the block is often at or below the bundle of His. Dopamine or epinephrine infusions are alternatives while pacing is prepared. <div class="ec-src"><b>Source:</b> Panchal AR, et al. 2020 AHA Guidelines for CPR and Emergency Cardiovascular Care: Adult Bradycardia. Circulation 2020;142(16 Suppl 2):S366-S368.</div></div></div> [[Try this question again->Unstable bradycardia - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Unstable bradycardia. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Metoprolol will worsen the bradycardia.</div> Beta-blockers slow heart rate and AV conduction. Giving metoprolol to a patient with high-grade AV block and hemodynamic instability is directly harmful. <div class="ec-teach"><div class="th">What to do instead</div> Severe symptomatic bradycardia with hemodynamic instability that fails to respond to atropine requires transcutaneous pacing as a bridge to transvenous pacing. High-grade AV block complicating inferior MI frequently does not respond to atropine because the block is often at or below the bundle of His. Dopamine or epinephrine infusions are alternatives while pacing is prepared. <div class="ec-src"><b>Source:</b> Panchal AR, et al. 2020 AHA Guidelines for CPR and Emergency Cardiovascular Care: Adult Bradycardia. Circulation 2020;142(16 Suppl 2):S366-S368.</div></div></div> [[Try this question again->Unstable bradycardia - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Unstable bradycardia. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Adenosine slows AV conduction.</div> Adenosine transiently blocks AV conduction and is used for SVT. It would worsen high-grade AV block. <div class="ec-teach"><div class="th">What to do instead</div> Severe symptomatic bradycardia with hemodynamic instability that fails to respond to atropine requires transcutaneous pacing as a bridge to transvenous pacing. High-grade AV block complicating inferior MI frequently does not respond to atropine because the block is often at or below the bundle of His. Dopamine or epinephrine infusions are alternatives while pacing is prepared. <div class="ec-src"><b>Source:</b> Panchal AR, et al. 2020 AHA Guidelines for CPR and Emergency Cardiovascular Care: Adult Bradycardia. Circulation 2020;142(16 Suppl 2):S366-S368.</div></div></div> [[Try this question again->Unstable bradycardia - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Unstable bradycardia. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Carotid sinus massage slows the heart rate.</div> Carotid sinus massage increases vagal tone and slows AV conduction. It is used to diagnose or terminate SVT, not to treat bradycardia. <div class="ec-teach"><div class="th">What to do instead</div> Severe symptomatic bradycardia with hemodynamic instability that fails to respond to atropine requires transcutaneous pacing as a bridge to transvenous pacing. High-grade AV block complicating inferior MI frequently does not respond to atropine because the block is often at or below the bundle of His. Dopamine or epinephrine infusions are alternatives while pacing is prepared. <div class="ec-src"><b>Source:</b> Panchal AR, et al. 2020 AHA Guidelines for CPR and Emergency Cardiovascular Care: Adult Bradycardia. Circulation 2020;142(16 Suppl 2):S366-S368.</div></div></div> [[Try this question again->Unstable bradycardia - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 05:37</div> A 63-year-old man with a history of NSAID use for chronic back pain presents with three episodes of melena and lightheadedness over 12 hours. Blood pressure is 88/54 mm Hg and pulse is 118/min. Hemoglobin is 7.1 g/dL. Nasogastric aspirate returns coffee-ground material. BUN-to-creatinine ratio is elevated at 36. After intravenous crystalloid resuscitation and packed red blood cell transfusion, his blood pressure improves to 108/68 mm Hg. <span class="ec-prompt">Which of the following interventions is most appropriate next?</span> [[Capsule endoscopy->Upper GI bleed - D2]] [[CT angiography of the abdomen->Upper GI bleed - D1]] [[CT colonography->Upper GI bleed - D3]] [[Elective outpatient abdominal MRI->Upper GI bleed - D4]] [[Upper endoscopy within 24 hours->Upper GI bleed - Correct]]

<span class="ec-case-marker" hidden data-entry="Upper GI bleed. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Upper endoscopy within 24 hours.</div> Melena, coffee-ground nasogastric aspirate, NSAID use, and an elevated BUN-to-creatinine ratio all point to an upper gastrointestinal source. After hemodynamic stabilization, upper endoscopy within 24 hours is the standard of care: it identifies the bleeding source, allows risk stratification, and provides therapeutic intervention such as clipping or thermal coagulation. <div class="ec-src"><b>Source:</b> Laine L, et al. ACG Clinical Guideline: Upper Gastrointestinal and Ulcer Bleeding. Am J Gastroenterol 2021;116(5):899-917.</div></div> [[Start another case->Hub]] [[Restart this case->Upper GI bleed - Rx]] [[Next case →->Peptic ulcer bleed - Ix]]

<span class="ec-case-marker" hidden data-entry="Upper GI bleed. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ CT angiography is premature.</div> CT angiography can identify active bleeding but does not allow therapeutic intervention. With clinical evidence of an upper GI source, upper endoscopy provides both diagnosis and treatment in a single procedure. <div class="ec-teach"><div class="th">What to do instead</div> Melena, coffee-ground nasogastric aspirate, NSAID use, and an elevated BUN-to-creatinine ratio all point to an upper gastrointestinal source. After hemodynamic stabilization, upper endoscopy within 24 hours is the standard of care: it identifies the bleeding source, allows risk stratification, and provides therapeutic intervention such as clipping or thermal coagulation. <div class="ec-src"><b>Source:</b> Laine L, et al. ACG Clinical Guideline: Upper Gastrointestinal and Ulcer Bleeding. Am J Gastroenterol 2021;116(5):899-917.</div></div></div> [[Try this question again->Upper GI bleed - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Upper GI bleed. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Capsule endoscopy is for obscure GI bleeding.</div> Video capsule endoscopy is used when upper and lower endoscopy have failed to identify a source. It is not the first-line investigation for overt upper GI bleeding. <div class="ec-teach"><div class="th">What to do instead</div> Melena, coffee-ground nasogastric aspirate, NSAID use, and an elevated BUN-to-creatinine ratio all point to an upper gastrointestinal source. After hemodynamic stabilization, upper endoscopy within 24 hours is the standard of care: it identifies the bleeding source, allows risk stratification, and provides therapeutic intervention such as clipping or thermal coagulation. <div class="ec-src"><b>Source:</b> Laine L, et al. ACG Clinical Guideline: Upper Gastrointestinal and Ulcer Bleeding. Am J Gastroenterol 2021;116(5):899-917.</div></div></div> [[Try this question again->Upper GI bleed - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Upper GI bleed. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ CT colonography evaluates the colon.</div> CT colonography is a screening tool for colonic polyps and is not indicated for acute upper gastrointestinal hemorrhage. <div class="ec-teach"><div class="th">What to do instead</div> Melena, coffee-ground nasogastric aspirate, NSAID use, and an elevated BUN-to-creatinine ratio all point to an upper gastrointestinal source. After hemodynamic stabilization, upper endoscopy within 24 hours is the standard of care: it identifies the bleeding source, allows risk stratification, and provides therapeutic intervention such as clipping or thermal coagulation. <div class="ec-src"><b>Source:</b> Laine L, et al. ACG Clinical Guideline: Upper Gastrointestinal and Ulcer Bleeding. Am J Gastroenterol 2021;116(5):899-917.</div></div></div> [[Try this question again->Upper GI bleed - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Upper GI bleed. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Elective MRI is inappropriate in acute bleeding.</div> An elective outpatient study in a patient who just presented with hemodynamic instability from acute bleeding would be a dangerous delay in definitive management. <div class="ec-teach"><div class="th">What to do instead</div> Melena, coffee-ground nasogastric aspirate, NSAID use, and an elevated BUN-to-creatinine ratio all point to an upper gastrointestinal source. After hemodynamic stabilization, upper endoscopy within 24 hours is the standard of care: it identifies the bleeding source, allows risk stratification, and provides therapeutic intervention such as clipping or thermal coagulation. <div class="ec-src"><b>Source:</b> Laine L, et al. ACG Clinical Guideline: Upper Gastrointestinal and Ulcer Bleeding. Am J Gastroenterol 2021;116(5):899-917.</div></div></div> [[Try this question again->Upper GI bleed - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Orthopedic ward · 23:10</div> A 25-year-old man sustained a closed tibial shaft fracture in a fall 6 hours ago and now has severe, progressive lower-leg pain not adequately controlled by parenteral opioids. Temperature is 37.0°C (98.6°F), blood pressure is 132/82 mm Hg, and pulse is 96/min. The anterior compartment is tense and swollen, and passive extension of the toes produces severe pain. Distal pulses are palpable, capillary refill is under 2 seconds, and pulse oximetry on the toes reads 98%. <span class="ec-prompt">Which of the following is the most appropriate next step?</span> [[Ankle-brachial index measurement->Compartment syndrome 2 - D1]] [[Doppler ultrasonography of the distal vessels->Compartment syndrome 2 - D2]] [[Formal compartment pressure measurement before proceeding to surgery->Compartment syndrome 2 - D3]] [[Reassurance, since palpable pulses and normal capillary refill exclude compartment syndrome->Compartment syndrome 2 - D4]] [[Urgent four-compartment fasciotomy without further testing->Compartment syndrome 2 - Correct]]

<span class="ec-case-marker" hidden data-entry="Compartment syndrome 2. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Urgent four-compartment fasciotomy without further testing.</div> Acute compartment syndrome is diagnosed clinically: pain out of proportion to the injury and pain with passive stretch of the compartment muscles. Distal pulses, capillary refill, and pulse oximetry remain normal until very late, because compartment pressure rises well above the level needed to occlude venous and then arterial outflow before it exceeds systemic arterial pressure; a palpable pulse never excludes the diagnosis. Fasciotomy should proceed on clinical grounds alone once suspicion is this high, since any confirmatory test only delays a time-critical decision. <div class="ec-src"><b>Source:</b> Schmidt AH. Acute Compartment Syndrome. Injury 2017;48 Suppl 1:S22-S25; AAOS Clinical Practice Guidelines.</div></div> [[Start another case->Hub]] [[Restart this case->Compartment syndrome 2 - Rx]] [[Next case →->Angle closure glaucoma - Rx]]

<span class="ec-case-marker" hidden data-entry="Compartment syndrome 2. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Ankle-brachial index tests for large-vessel arterial injury, not compartment syndrome. A normal index does not address the microvascular and myoneural ischemia of a closed compartment and would only delay definitive treatment.</div> <div class="ec-teach"><div class="th">What to do instead</div> Acute compartment syndrome is diagnosed clinically: pain out of proportion to the injury and pain with passive stretch of the compartment muscles. Distal pulses, capillary refill, and pulse oximetry remain normal until very late, because compartment pressure rises well above the level needed to occlude venous and then arterial outflow before it exceeds systemic arterial pressure; a palpable pulse never excludes the diagnosis. Fasciotomy should proceed on clinical grounds alone once suspicion is this high, since any confirmatory test only delays a time-critical decision. <div class="ec-src"><b>Source:</b> Schmidt AH. Acute Compartment Syndrome. Injury 2017;48 Suppl 1:S22-S25; AAOS Clinical Practice Guidelines.</div></div></div> [[Try this question again->Compartment syndrome 2 - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Compartment syndrome 2. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Doppler flow in a named artery does not reflect compartment pressure. Major vessels remain patent long after muscle and nerve are already ischemic; a normal study offers false reassurance.</div> <div class="ec-teach"><div class="th">What to do instead</div> Acute compartment syndrome is diagnosed clinically: pain out of proportion to the injury and pain with passive stretch of the compartment muscles. Distal pulses, capillary refill, and pulse oximetry remain normal until very late, because compartment pressure rises well above the level needed to occlude venous and then arterial outflow before it exceeds systemic arterial pressure; a palpable pulse never excludes the diagnosis. Fasciotomy should proceed on clinical grounds alone once suspicion is this high, since any confirmatory test only delays a time-critical decision. <div class="ec-src"><b>Source:</b> Schmidt AH. Acute Compartment Syndrome. Injury 2017;48 Suppl 1:S22-S25; AAOS Clinical Practice Guidelines.</div></div></div> [[Try this question again->Compartment syndrome 2 - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Compartment syndrome 2. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Confirmatory pressure measurement is unnecessary when the clinical picture is this classic. Obtaining and waiting on a formal reading only consumes the narrow window in which fasciotomy still prevents irreversible necrosis.</div> <div class="ec-teach"><div class="th">What to do instead</div> Acute compartment syndrome is diagnosed clinically: pain out of proportion to the injury and pain with passive stretch of the compartment muscles. Distal pulses, capillary refill, and pulse oximetry remain normal until very late, because compartment pressure rises well above the level needed to occlude venous and then arterial outflow before it exceeds systemic arterial pressure; a palpable pulse never excludes the diagnosis. Fasciotomy should proceed on clinical grounds alone once suspicion is this high, since any confirmatory test only delays a time-critical decision. <div class="ec-src"><b>Source:</b> Schmidt AH. Acute Compartment Syndrome. Injury 2017;48 Suppl 1:S22-S25; AAOS Clinical Practice Guidelines.</div></div></div> [[Try this question again->Compartment syndrome 2 - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Compartment syndrome 2. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ A palpable pulse does not exclude the diagnosis. Pulses are preserved until compartment pressure finally exceeds systemic arterial pressure, a very late and near-terminal finding.</div> <div class="ec-teach"><div class="th">What to do instead</div> Acute compartment syndrome is diagnosed clinically: pain out of proportion to the injury and pain with passive stretch of the compartment muscles. Distal pulses, capillary refill, and pulse oximetry remain normal until very late, because compartment pressure rises well above the level needed to occlude venous and then arterial outflow before it exceeds systemic arterial pressure; a palpable pulse never excludes the diagnosis. Fasciotomy should proceed on clinical grounds alone once suspicion is this high, since any confirmatory test only delays a time-critical decision. <div class="ec-src"><b>Source:</b> Schmidt AH. Acute Compartment Syndrome. Injury 2017;48 Suppl 1:S22-S25; AAOS Clinical Practice Guidelines.</div></div></div> [[Try this question again->Compartment syndrome 2 - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 08:45</div> A 68-year-old woman develops sudden-onset aphasia and dense right hemiplegia 90 minutes ago. Blood pressure is 174/96 mm Hg, pulse is 88/min, and oxygen saturation 97% on room air. NIHSS score is 18. Non-contrast CT shows no hemorrhage. CT angiography demonstrates complete occlusion of the left proximal middle cerebral artery. CT perfusion shows a large ischemic penumbra with a small infarct core. IV alteplase is being administered. <span class="ec-prompt">Which of the following is the most appropriate additional intervention?</span> [[Endovascular mechanical thrombectomy->Large vessel stroke - Correct]] [[Full-dose therapeutic anticoagulation with heparin->Large vessel stroke - D1]] [[High-dose intravenous corticosteroids->Large vessel stroke - D3]] [[Immediate carotid endarterectomy->Large vessel stroke - D2]] [[Observation and repeat CT in 24 hours->Large vessel stroke - D4]]

<span class="ec-case-marker" hidden data-entry="Large vessel stroke. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Endovascular mechanical thrombectomy.</div> This patient meets all criteria for mechanical thrombectomy: large-vessel anterior-circulation occlusion, a disabling deficit (this patient's NIHSS of 18 is well above the NIHSS ≥6 eligibility threshold used in the pivotal endovascular thrombectomy trials), small infarct core with salvageable penumbra, and presentation within the treatment window. Thrombectomy reduces disability in eligible patients with a number needed to treat of approximately 2.6 for improved functional outcome. It is performed in addition to IV thrombolysis, not instead of it. <div class="ec-src"><b>Source:</b> Powers WJ, et al. 2019 Guideline for the Early Management of Patients With Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke 2019;50(12):e344-e418; Goyal M, et al. Endovascular Thrombectomy After Large-Vessel Ischaemic Stroke: A Meta-analysis (HERMES). Lancet 2016;387(10029):1723-1731.</div></div> [[Start another case->Hub]] [[Restart this case->Large vessel stroke - Rx]] [[Next case →->Malignant MCA edema - Prog]]

<span class="ec-case-marker" hidden data-entry="Large vessel stroke. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Anticoagulation is not the acute stroke treatment.</div> Therapeutic anticoagulation with heparin is not recommended in acute ischemic stroke. It does not improve outcomes and increases hemorrhagic risk, particularly after thrombolysis. <div class="ec-teach"><div class="th">What to do instead</div> This patient meets all criteria for mechanical thrombectomy: large-vessel anterior-circulation occlusion, a disabling deficit (this patient's NIHSS of 18 is well above the NIHSS ≥6 eligibility threshold used in the pivotal endovascular thrombectomy trials), small infarct core with salvageable penumbra, and presentation within the treatment window. Thrombectomy reduces disability in eligible patients with a number needed to treat of approximately 2.6 for improved functional outcome. It is performed in addition to IV thrombolysis, not instead of it. <div class="ec-src"><b>Source:</b> Powers WJ, et al. 2019 Guideline for the Early Management of Patients With Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke 2019;50(12):e344-e418; Goyal M, et al. Endovascular Thrombectomy After Large-Vessel Ischaemic Stroke: A Meta-analysis (HERMES). Lancet 2016;387(10029):1723-1731.</div></div></div> [[Try this question again->Large vessel stroke - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Large vessel stroke. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Carotid endarterectomy is not the acute intervention.</div> Carotid endarterectomy treats extracranial carotid stenosis and is performed in a non-emergent setting. The acute intracranial occlusion requires endovascular retrieval. <div class="ec-teach"><div class="th">What to do instead</div> This patient meets all criteria for mechanical thrombectomy: large-vessel anterior-circulation occlusion, a disabling deficit (this patient's NIHSS of 18 is well above the NIHSS ≥6 eligibility threshold used in the pivotal endovascular thrombectomy trials), small infarct core with salvageable penumbra, and presentation within the treatment window. Thrombectomy reduces disability in eligible patients with a number needed to treat of approximately 2.6 for improved functional outcome. It is performed in addition to IV thrombolysis, not instead of it. <div class="ec-src"><b>Source:</b> Powers WJ, et al. 2019 Guideline for the Early Management of Patients With Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke 2019;50(12):e344-e418; Goyal M, et al. Endovascular Thrombectomy After Large-Vessel Ischaemic Stroke: A Meta-analysis (HERMES). Lancet 2016;387(10029):1723-1731.</div></div></div> [[Try this question again->Large vessel stroke - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Large vessel stroke. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Corticosteroids have no role in acute ischemic stroke.</div> There is no evidence supporting corticosteroids in acute ischemic stroke. They do not reduce infarct size or improve outcomes. <div class="ec-teach"><div class="th">What to do instead</div> This patient meets all criteria for mechanical thrombectomy: large-vessel anterior-circulation occlusion, a disabling deficit (this patient's NIHSS of 18 is well above the NIHSS ≥6 eligibility threshold used in the pivotal endovascular thrombectomy trials), small infarct core with salvageable penumbra, and presentation within the treatment window. Thrombectomy reduces disability in eligible patients with a number needed to treat of approximately 2.6 for improved functional outcome. It is performed in addition to IV thrombolysis, not instead of it. <div class="ec-src"><b>Source:</b> Powers WJ, et al. 2019 Guideline for the Early Management of Patients With Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke 2019;50(12):e344-e418; Goyal M, et al. Endovascular Thrombectomy After Large-Vessel Ischaemic Stroke: A Meta-analysis (HERMES). Lancet 2016;387(10029):1723-1731.</div></div></div> [[Try this question again->Large vessel stroke - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Large vessel stroke. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Observation wastes the treatment window.</div> With a large penumbra and proximal occlusion, delay allows the penumbra to convert to completed infarct. The evidence strongly favors emergent thrombectomy within the eligible window. <div class="ec-teach"><div class="th">What to do instead</div> This patient meets all criteria for mechanical thrombectomy: large-vessel anterior-circulation occlusion, a disabling deficit (this patient's NIHSS of 18 is well above the NIHSS ≥6 eligibility threshold used in the pivotal endovascular thrombectomy trials), small infarct core with salvageable penumbra, and presentation within the treatment window. Thrombectomy reduces disability in eligible patients with a number needed to treat of approximately 2.6 for improved functional outcome. It is performed in addition to IV thrombolysis, not instead of it. <div class="ec-src"><b>Source:</b> Powers WJ, et al. 2019 Guideline for the Early Management of Patients With Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke 2019;50(12):e344-e418; Goyal M, et al. Endovascular Thrombectomy After Large-Vessel Ischaemic Stroke: A Meta-analysis (HERMES). Lancet 2016;387(10029):1723-1731.</div></div></div> [[Try this question again->Large vessel stroke - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Labor and delivery unit · 14:50</div> A 29-year-old woman has heavy vaginal bleeding beginning 10 minutes after spontaneous vaginal delivery of a term infant. Blood pressure is 92/58 mm Hg and pulse is 116/min. Her uterus is enlarged, soft, and boggy on palpation. Estimated blood loss is 800 mL and increasing. <span class="ec-prompt">Which of the following is the most appropriate initial treatment?</span> [[Bimanual uterine massage plus a uterotonic agent->PPH management - Correct]] [[Immediate peripartum hysterectomy for hemorrhage->PPH management - D2]] [[Manual exploration for retained placenta before any other intervention->PPH management - D3]] [[Observation with repeat hemoglobin in 4 hours->PPH management - D4]] [[Tranexamic acid alone without uterotonics->PPH management - D1]] [[Volume resuscitation alone without uterotonics->PPH management - D5]]

<span class="ec-case-marker" hidden data-entry="PPH management. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Bimanual uterine massage plus a uterotonic agent.</div> Uterine atony is the most common cause of immediate postpartum hemorrhage. Initial management is bimanual uterine massage and administration of a uterotonic, typically oxytocin, with methylergonovine, carboprost, or misoprostol as second-line agents. Simultaneous resuscitation with crystalloid and blood products is essential. Hysterectomy is reserved for refractory hemorrhage after medical and procedural measures fail. <div class="ec-src"><b>Source:</b> ACOG Practice Bulletin No. 183: Postpartum Hemorrhage. Obstet Gynecol 2017;130(4):e168-e186.</div></div> [[Start another case->Hub]] [[Restart this case->PPH management - Rx]] [[Next case →->Amenorrhea workup - Ix]]

<span class="ec-case-marker" hidden data-entry="PPH management. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Tranexamic acid alone is insufficient.</div> Tranexamic acid (TXA) is recommended within 3 hours of PPH onset as an adjunct, the WOMAN trial showed reduced bleeding-related death. However, TXA does not contract the uterus. When the cause is uterine atony, uterotonics and bimanual massage must come first. <div class="ec-teach"><div class="th">What to do instead</div> Uterine atony is the most common cause of immediate postpartum hemorrhage. Initial management is bimanual uterine massage and administration of a uterotonic, typically oxytocin, with methylergonovine, carboprost, or misoprostol as second-line agents. Simultaneous resuscitation with crystalloid and blood products is essential. Hysterectomy is reserved for refractory hemorrhage after medical and procedural measures fail. <div class="ec-src"><b>Source:</b> ACOG Practice Bulletin No. 183: Postpartum Hemorrhage. Obstet Gynecol 2017;130(4):e168-e186.</div></div></div> [[Try this question again->PPH management - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="PPH management. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Hysterectomy is a last resort.</div> Peripartum hysterectomy is definitive but is reserved for life-threatening hemorrhage refractory to uterotonics, compression sutures, and uterine tamponade. It is not the initial step. <div class="ec-teach"><div class="th">What to do instead</div> Uterine atony is the most common cause of immediate postpartum hemorrhage. Initial management is bimanual uterine massage and administration of a uterotonic, typically oxytocin, with methylergonovine, carboprost, or misoprostol as second-line agents. Simultaneous resuscitation with crystalloid and blood products is essential. Hysterectomy is reserved for refractory hemorrhage after medical and procedural measures fail. <div class="ec-src"><b>Source:</b> ACOG Practice Bulletin No. 183: Postpartum Hemorrhage. Obstet Gynecol 2017;130(4):e168-e186.</div></div></div> [[Try this question again->PPH management - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="PPH management. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Manual exploration is not the first step for atony.</div> If the placenta has already been delivered intact, the boggy uterus points to atony, not retained products. Massage and uterotonics come first. <div class="ec-teach"><div class="th">What to do instead</div> Uterine atony is the most common cause of immediate postpartum hemorrhage. Initial management is bimanual uterine massage and administration of a uterotonic, typically oxytocin, with methylergonovine, carboprost, or misoprostol as second-line agents. Simultaneous resuscitation with crystalloid and blood products is essential. Hysterectomy is reserved for refractory hemorrhage after medical and procedural measures fail. <div class="ec-src"><b>Source:</b> ACOG Practice Bulletin No. 183: Postpartum Hemorrhage. Obstet Gynecol 2017;130(4):e168-e186.</div></div></div> [[Try this question again->PPH management - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="PPH management. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Volume resuscitation alone does not stop the bleeding.</div> Crystalloid and blood product resuscitation are essential for maintaining perfusion but do not address the source of hemorrhage. Without uterotonic therapy and mechanical uterine compression, atonic bleeding will continue. <div class="ec-teach"><div class="th">What to do instead</div> Uterine atony is the most common cause of immediate postpartum hemorrhage. Initial management is bimanual uterine massage and administration of a uterotonic, typically oxytocin, with methylergonovine, carboprost, or misoprostol as second-line agents. Simultaneous resuscitation with crystalloid and blood products is essential. Hysterectomy is reserved for refractory hemorrhage after medical and procedural measures fail. <div class="ec-src"><b>Source:</b> ACOG Practice Bulletin No. 183: Postpartum Hemorrhage. Obstet Gynecol 2017;130(4):e168-e186.</div></div></div> [[Try this question again->PPH management - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 21:40</div> A 19-year-old man presents with severe unilateral throat pain worsening over 3 days, muffled voice, and difficulty swallowing. Temperature is 39.2°C. He has trismus and is drooling. Examination shows unilateral tonsillar bulging with uvular deviation to the contralateral side. <span class="ec-prompt">Which of the following is the most appropriate management?</span> [[Drainage of the abscess plus intravenous antibiotics->Peritonsillar abscess - Correct]] [[Elective interval tonsillectomy in 6 weeks without acute drainage->Peritonsillar abscess - D1]] [[Intravenous antibiotics alone without drainage->Peritonsillar abscess - D3]] [[Observation alone->Peritonsillar abscess - D2]] [[Oral corticosteroid monotherapy->Peritonsillar abscess - D4]]

<span class="ec-case-marker" hidden data-entry="Peritonsillar abscess. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Drainage of the abscess plus intravenous antibiotics</div> Peritonsillar abscess requires drainage, by needle aspiration, incision and drainage, or peritonsillar abscess tonsillectomy, combined with appropriate antibiotics. Antibiotics alone are insufficient because they do not adequately penetrate the abscess cavity. Airway assessment is essential, and trismus with drooling suggests significant pharyngeal compromise. <div class="ec-src"><b>Source:</b> Johnson RF, Stewart MG. The Contemporary Approach to Diagnosis and Management of Peritonsillar Abscess. Curr Opin Otolaryngol Head Neck Surg 2005;13(3):157-160.</div></div> [[Start another case->Hub]] [[Restart this case->Peritonsillar abscess - Rx]] [[Next case →->Necrotizing fasciitis - Dx]]

<span class="ec-case-marker" hidden data-entry="Peritonsillar abscess. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Interval tonsillectomy does not address the acute abscess.</div> Immediate tonsillectomy is a legitimate option, but performing it acutely or draining now is what achieves source control. Deferring all intervention for 6 weeks leaves a drainable pus collection in a compromised airway, the collection must be evacuated now, and interval tonsillectomy is a later consideration for recurrent disease. <div class="ec-teach"><div class="th">What to do instead</div> Peritonsillar abscess requires drainage, by needle aspiration, incision and drainage, or peritonsillar abscess tonsillectomy, combined with appropriate antibiotics. Antibiotics alone are insufficient because they do not adequately penetrate the abscess cavity. Airway assessment is essential, and trismus with drooling suggests significant pharyngeal compromise. <div class="ec-src"><b>Source:</b> Johnson RF, Stewart MG. The Contemporary Approach to Diagnosis and Management of Peritonsillar Abscess. Curr Opin Otolaryngol Head Neck Surg 2005;13(3):157-160.</div></div></div> [[Try this question again->Peritonsillar abscess - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Peritonsillar abscess. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Observation risks airway compromise.</div> An untreated peritonsillar abscess can extend into the parapharyngeal or retropharyngeal space, causing airway obstruction or mediastinitis. <div class="ec-teach"><div class="th">What to do instead</div> Peritonsillar abscess requires drainage, by needle aspiration, incision and drainage, or peritonsillar abscess tonsillectomy, combined with appropriate antibiotics. Antibiotics alone are insufficient because they do not adequately penetrate the abscess cavity. Airway assessment is essential, and trismus with drooling suggests significant pharyngeal compromise. <div class="ec-src"><b>Source:</b> Johnson RF, Stewart MG. The Contemporary Approach to Diagnosis and Management of Peritonsillar Abscess. Curr Opin Otolaryngol Head Neck Surg 2005;13(3):157-160.</div></div></div> [[Try this question again->Peritonsillar abscess - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Peritonsillar abscess. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Antibiotics alone are insufficient for a formed abscess.</div> Once an abscess has formed, antibiotics alone cannot adequately penetrate the walled-off collection. Drainage, by needle aspiration, incision, or peritonsillar abscess tonsillectomy, is required for source control. Antibiotics are administered concurrently but are not sufficient alone. <div class="ec-teach"><div class="th">What to do instead</div> Peritonsillar abscess requires drainage, by needle aspiration, incision and drainage, or peritonsillar abscess tonsillectomy, combined with appropriate antibiotics. Antibiotics alone are insufficient because they do not adequately penetrate the abscess cavity. Airway assessment is essential, and trismus with drooling suggests significant pharyngeal compromise. <div class="ec-src"><b>Source:</b> Johnson RF, Stewart MG. The Contemporary Approach to Diagnosis and Management of Peritonsillar Abscess. Curr Opin Otolaryngol Head Neck Surg 2005;13(3):157-160.</div></div></div> [[Try this question again->Peritonsillar abscess - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Peritonsillar abscess. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Corticosteroids alone are insufficient.</div> Systemic corticosteroids may reduce inflammation and edema as an adjunct, but without drainage, the abscess will not resolve and risks airway compromise or extension into deeper neck spaces. <div class="ec-teach"><div class="th">What to do instead</div> Peritonsillar abscess requires drainage, by needle aspiration, incision and drainage, or peritonsillar abscess tonsillectomy, combined with appropriate antibiotics. Antibiotics alone are insufficient because they do not adequately penetrate the abscess cavity. Airway assessment is essential, and trismus with drooling suggests significant pharyngeal compromise. <div class="ec-src"><b>Source:</b> Johnson RF, Stewart MG. The Contemporary Approach to Diagnosis and Management of Peritonsillar Abscess. Curr Opin Otolaryngol Head Neck Surg 2005;13(3):157-160.</div></div></div> [[Try this question again->Peritonsillar abscess - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 00:02</div> A 67-year-old woman develops sudden severe left eye pain, nausea, and vomiting. She sees halos around lights and her vision is markedly blurred. Blood pressure is 158/92 mm Hg and pulse is 96/min. Examination shows the left pupil is mid-dilated and poorly reactive. The cornea appears hazy. Intraocular pressure measured by tonometry is 58 mm Hg. The right eye is normal. <span class="ec-prompt">Which of the following is the most appropriate initial management?</span> [[Firm eye patching with discharge and reassurance->Angle closure glaucoma - D2]] [[Oral diphenhydramine for ocular discomfort relief->Angle closure glaucoma - D4]] [[Reassurance with routine ophthalmology in one week->Angle closure glaucoma - D3]] [[Topical antibiotic eye drops and outpatient follow-up->Angle closure glaucoma - D1]] [[Urgent intraocular pressure reduction with topical and systemic agents->Angle closure glaucoma - Correct]]

<span class="ec-case-marker" hidden data-entry="Angle closure glaucoma. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Urgent intraocular pressure reduction with topical and systemic agents</div> Acute angle closure is an ophthalmologic emergency. Intraocular pressures above 40–50 mm Hg can cause rapid, irreversible optic nerve damage. Immediate treatment includes topical beta-blocker, alpha-agonist, and pilocarpine to constrict the pupil; systemic agents (IV acetazolamide, oral or IV mannitol) to reduce aqueous production; and urgent ophthalmology consultation for definitive laser peripheral iridotomy. <div class="ec-src"><b>Source:</b> AAO Preferred Practice Pattern: Primary Angle Closure Disease. American Academy of Ophthalmology; 2020.</div></div> [[Start another case->Hub]] [[Restart this case->Angle closure glaucoma - Rx]] [[Next case →->SJS TEN - Dx]]

<span class="ec-case-marker" hidden data-entry="Angle closure glaucoma. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This is not an infection. The acute rise in intraocular pressure requires pressure-lowering agents, not antibiotics. <div class="ec-teach"><div class="th">What to do instead</div> Acute angle closure is an ophthalmologic emergency. Intraocular pressures above 40–50 mm Hg can cause rapid, irreversible optic nerve damage. Immediate treatment includes topical beta-blocker, alpha-agonist, and pilocarpine to constrict the pupil; systemic agents (IV acetazolamide, oral or IV mannitol) to reduce aqueous production; and urgent ophthalmology consultation for definitive laser peripheral iridotomy. <div class="ec-src"><b>Source:</b> AAO Preferred Practice Pattern: Primary Angle Closure Disease. American Academy of Ophthalmology; 2020.</div></div></div> [[Try this question again->Angle closure glaucoma - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Angle closure glaucoma. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Patching delays treatment and may worsen pressure.</div> A pressure patch does not treat the underlying pupillary block. Delay in reducing IOP risks permanent vision loss. <div class="ec-teach"><div class="th">What to do instead</div> Acute angle closure is an ophthalmologic emergency. Intraocular pressures above 40–50 mm Hg can cause rapid, irreversible optic nerve damage. Immediate treatment includes topical beta-blocker, alpha-agonist, and pilocarpine to constrict the pupil; systemic agents (IV acetazolamide, oral or IV mannitol) to reduce aqueous production; and urgent ophthalmology consultation for definitive laser peripheral iridotomy. <div class="ec-src"><b>Source:</b> AAO Preferred Practice Pattern: Primary Angle Closure Disease. American Academy of Ophthalmology; 2020.</div></div></div> [[Try this question again->Angle closure glaucoma - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Angle closure glaucoma. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Delay risks permanent blindness.</div> Acute angle closure at an IOP of 58 mm Hg can cause irreversible optic nerve and retinal damage within hours. One-week follow-up is dangerously inadequate. <div class="ec-teach"><div class="th">What to do instead</div> Acute angle closure is an ophthalmologic emergency. Intraocular pressures above 40–50 mm Hg can cause rapid, irreversible optic nerve damage. Immediate treatment includes topical beta-blocker, alpha-agonist, and pilocarpine to constrict the pupil; systemic agents (IV acetazolamide, oral or IV mannitol) to reduce aqueous production; and urgent ophthalmology consultation for definitive laser peripheral iridotomy. <div class="ec-src"><b>Source:</b> AAO Preferred Practice Pattern: Primary Angle Closure Disease. American Academy of Ophthalmology; 2020.</div></div></div> [[Try this question again->Angle closure glaucoma - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Angle closure glaucoma. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Antihistamines are contraindicated.</div> Antihistamines have anticholinergic properties that can worsen pupillary dilation and further raise intraocular pressure in an eye with angle closure. <div class="ec-teach"><div class="th">What to do instead</div> Acute angle closure is an ophthalmologic emergency. Intraocular pressures above 40–50 mm Hg can cause rapid, irreversible optic nerve damage. Immediate treatment includes topical beta-blocker, alpha-agonist, and pilocarpine to constrict the pupil; systemic agents (IV acetazolamide, oral or IV mannitol) to reduce aqueous production; and urgent ophthalmology consultation for definitive laser peripheral iridotomy. <div class="ec-src"><b>Source:</b> AAO Preferred Practice Pattern: Primary Angle Closure Disease. American Academy of Ophthalmology; 2020.</div></div></div> [[Try this question again->Angle closure glaucoma - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Operating room · 01:55</div> A 15-year-old boy underwent immediate surgical exploration for a 3-hour history of left testicular torsion. At operation the left testis is detorsed and, after 10 minutes of observation wrapped in warm saline-soaked gauze, regains a normal pink color and bleeds briskly on incision. <span class="ec-prompt">Which of the following is the most appropriate next step?</span> [[Bilateral scrotal orchiopexy, fixing both the salvaged left testis and the asymptomatic right testis->Testicular torsion 2 - Correct]] [[Biopsy of the contralateral right testis to assess for a bell-clapper anomaly->Testicular torsion 2 - D1]] [[Left orchiectomy regardless of the testis now appearing viable->Testicular torsion 2 - D2]] [[No fixation of either testis, since detorsion alone is curative->Testicular torsion 2 - D3]] [[Unilateral orchiopexy of the left testis only, leaving the right testis unfixed->Testicular torsion 2 - D4]]

<span class="ec-case-marker" hidden data-entry="Testicular torsion 2. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Bilateral scrotal orchiopexy, fixing both the salvaged left testis and the asymptomatic right testis.</div> The bell-clapper deformity that predisposes to torsion is usually bilateral, so a testis explored and found viable after detorsion is fixed in place, and the contralateral, asymptomatic testis is fixed at the same operation to prevent a future torsion on that side. Deferring contralateral fixation leaves a substantial, avoidable risk of losing the only remaining testis to a later torsion. <div class="ec-src"><b>Source:</b> Sharp VJ, Kieran K, Arlen AM. Testicular torsion: diagnosis, evaluation, and management. Am Fam Physician 2013;88(12):835-840; AUA Clinical Guidance.</div></div> [[Start another case->Hub]] [[Restart this case->Testicular torsion 2 - Rx]] [[Next case →->Microscopic hematuria - Ix]]

<span class="ec-case-marker" hidden data-entry="Testicular torsion 2. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ The anomaly is diagnosed by its anatomy at exploration, not by biopsy. A biopsy adds risk to a normal testis and answers a question that fixation already addresses without it.</div> <div class="ec-teach"><div class="th">What to do instead</div> The bell-clapper deformity that predisposes to torsion is usually bilateral, so a testis explored and found viable after detorsion is fixed in place, and the contralateral, asymptomatic testis is fixed at the same operation to prevent a future torsion on that side. Deferring contralateral fixation leaves a substantial, avoidable risk of losing the only remaining testis to a later torsion. <div class="ec-src"><b>Source:</b> Sharp VJ, Kieran K, Arlen AM. Testicular torsion: diagnosis, evaluation, and management. Am Fam Physician 2013;88(12):835-840; AUA Clinical Guidance.</div></div></div> [[Try this question again->Testicular torsion 2 - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Testicular torsion 2. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ A testis that has regained color and bleeds on incision is viable and should be salvaged. Orchiectomy is reserved for a testis that remains dusky and non-bleeding after detorsion and warm packing, not one that has recovered.</div> <div class="ec-teach"><div class="th">What to do instead</div> The bell-clapper deformity that predisposes to torsion is usually bilateral, so a testis explored and found viable after detorsion is fixed in place, and the contralateral, asymptomatic testis is fixed at the same operation to prevent a future torsion on that side. Deferring contralateral fixation leaves a substantial, avoidable risk of losing the only remaining testis to a later torsion. <div class="ec-src"><b>Source:</b> Sharp VJ, Kieran K, Arlen AM. Testicular torsion: diagnosis, evaluation, and management. Am Fam Physician 2013;88(12):835-840; AUA Clinical Guidance.</div></div></div> [[Try this question again->Testicular torsion 2 - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Testicular torsion 2. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Detorsion alone leaves both testes at risk of recurrent torsion. The same predisposing anatomy that twisted the left testis is almost always present on the right as well.</div> <div class="ec-teach"><div class="th">What to do instead</div> The bell-clapper deformity that predisposes to torsion is usually bilateral, so a testis explored and found viable after detorsion is fixed in place, and the contralateral, asymptomatic testis is fixed at the same operation to prevent a future torsion on that side. Deferring contralateral fixation leaves a substantial, avoidable risk of losing the only remaining testis to a later torsion. <div class="ec-src"><b>Source:</b> Sharp VJ, Kieran K, Arlen AM. Testicular torsion: diagnosis, evaluation, and management. Am Fam Physician 2013;88(12):835-840; AUA Clinical Guidance.</div></div></div> [[Try this question again->Testicular torsion 2 - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Testicular torsion 2. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ This leaves the asymptomatic testis unprotected. Because the anomaly is typically bilateral, only fixing the side that already torsed leaves the other testis exposed to the same risk.</div> <div class="ec-teach"><div class="th">What to do instead</div> The bell-clapper deformity that predisposes to torsion is usually bilateral, so a testis explored and found viable after detorsion is fixed in place, and the contralateral, asymptomatic testis is fixed at the same operation to prevent a future torsion on that side. Deferring contralateral fixation leaves a substantial, avoidable risk of losing the only remaining testis to a later torsion. <div class="ec-src"><b>Source:</b> Sharp VJ, Kieran K, Arlen AM. Testicular torsion: diagnosis, evaluation, and management. Am Fam Physician 2013;88(12):835-840; AUA Clinical Guidance.</div></div></div> [[Try this question again->Testicular torsion 2 - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Pediatric Emergency Department · 10:15</div> A 4-week-old full-term boy presents with 3 days of progressively worsening projectile, non-bilious vomiting immediately after feeds. He remains hungry between episodes. Temperature is 37.0°C (98.6°F), pulse is 168/min, and capillary refill is 3 seconds. He appears moderately dehydrated. Laboratory studies show sodium 133 mEq/L, potassium 2.9 mEq/L, chloride 88 mEq/L, bicarbonate 32 mEq/L, and pH 7.52. Ultrasound reveals pyloric muscle thickness of 5 mm and pyloric channel length of 18 mm. <span class="ec-prompt">Which of the following is the most appropriate next step before pyloromyotomy?</span> [[Broad-spectrum intravenous antibiotics->Pyloric stenosis - D1]] [[Correct dehydration and electrolytes before surgery->Pyloric stenosis - Correct]] [[Immediate surgery without metabolic correction->Pyloric stenosis - D2]] [[Intravenous corticosteroids to reduce pyloric muscle edema->Pyloric stenosis - D3]] [[Prokinetic agents to improve gastric emptying->Pyloric stenosis - D4]]

<span class="ec-case-marker" hidden data-entry="Pyloric stenosis. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Correct dehydration and electrolytes before surgery</div> Pyloric stenosis causes hypochloremic, hypokalemic metabolic alkalosis from loss of gastric acid. The metabolic derangements increase anesthetic risk, particularly hypokalemia, which predisposes to cardiac arrhythmias, and alkalosis, which depresses ventilatory drive. Standard practice is to rehydrate and correct the chloride, potassium, and acid-base status over 24–48 hours before proceeding to pyloromyotomy. <div class="ec-src"><b>Source:</b> Aspelund G, Langer JC. Current Management of Hypertrophic Pyloric Stenosis. Semin Pediatr Surg 2007;16(1):27-33; AAP/ACS Guidelines on Perioperative Management of Pyloric Stenosis.</div></div> [[Start another case->Hub]] [[Restart this case->Pyloric stenosis - Rx]] [[Next case →->Intussusception - Dx]]

<span class="ec-case-marker" hidden data-entry="Pyloric stenosis. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Antibiotics are not indicated.</div> Pyloric stenosis is a mechanical obstruction, not an infection. Antibiotics do not address the hypertrophied pylorus or the metabolic derangement. <div class="ec-teach"><div class="th">What to do instead</div> Pyloric stenosis causes hypochloremic, hypokalemic metabolic alkalosis from loss of gastric acid. The metabolic derangements increase anesthetic risk, particularly hypokalemia, which predisposes to cardiac arrhythmias, and alkalosis, which depresses ventilatory drive. Standard practice is to rehydrate and correct the chloride, potassium, and acid-base status over 24–48 hours before proceeding to pyloromyotomy. <div class="ec-src"><b>Source:</b> Aspelund G, Langer JC. Current Management of Hypertrophic Pyloric Stenosis. Semin Pediatr Surg 2007;16(1):27-33; AAP/ACS Guidelines on Perioperative Management of Pyloric Stenosis.</div></div></div> [[Try this question again->Pyloric stenosis - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Pyloric stenosis. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Surgery before correction is dangerous.</div> Operating on a hypokalemic, alkalotic, dehydrated infant substantially increases anesthetic risk. Pyloric stenosis is not a time-critical emergency, the metabolic correction takes priority. <div class="ec-teach"><div class="th">What to do instead</div> Pyloric stenosis causes hypochloremic, hypokalemic metabolic alkalosis from loss of gastric acid. The metabolic derangements increase anesthetic risk, particularly hypokalemia, which predisposes to cardiac arrhythmias, and alkalosis, which depresses ventilatory drive. Standard practice is to rehydrate and correct the chloride, potassium, and acid-base status over 24–48 hours before proceeding to pyloromyotomy. <div class="ec-src"><b>Source:</b> Aspelund G, Langer JC. Current Management of Hypertrophic Pyloric Stenosis. Semin Pediatr Surg 2007;16(1):27-33; AAP/ACS Guidelines on Perioperative Management of Pyloric Stenosis.</div></div></div> [[Try this question again->Pyloric stenosis - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Pyloric stenosis. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Corticosteroids have no role.</div> There is no indication for corticosteroids in pyloric stenosis. The treatment is surgical after metabolic optimization. <div class="ec-teach"><div class="th">What to do instead</div> Pyloric stenosis causes hypochloremic, hypokalemic metabolic alkalosis from loss of gastric acid. The metabolic derangements increase anesthetic risk, particularly hypokalemia, which predisposes to cardiac arrhythmias, and alkalosis, which depresses ventilatory drive. Standard practice is to rehydrate and correct the chloride, potassium, and acid-base status over 24–48 hours before proceeding to pyloromyotomy. <div class="ec-src"><b>Source:</b> Aspelund G, Langer JC. Current Management of Hypertrophic Pyloric Stenosis. Semin Pediatr Surg 2007;16(1):27-33; AAP/ACS Guidelines on Perioperative Management of Pyloric Stenosis.</div></div></div> [[Try this question again->Pyloric stenosis - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Pyloric stenosis. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Prokinetic agents do not treat pyloric stenosis.</div> The hypertrophied pylorus creates a fixed mechanical obstruction. Prokinetic agents cannot overcome it and do not address the metabolic derangement that must be corrected before anesthesia. <div class="ec-teach"><div class="th">What to do instead</div> Pyloric stenosis causes hypochloremic, hypokalemic metabolic alkalosis from loss of gastric acid. The metabolic derangements increase anesthetic risk, particularly hypokalemia, which predisposes to cardiac arrhythmias, and alkalosis, which depresses ventilatory drive. Standard practice is to rehydrate and correct the chloride, potassium, and acid-base status over 24–48 hours before proceeding to pyloromyotomy. <div class="ec-src"><b>Source:</b> Aspelund G, Langer JC. Current Management of Hypertrophic Pyloric Stenosis. Semin Pediatr Surg 2007;16(1):27-33; AAP/ACS Guidelines on Perioperative Management of Pyloric Stenosis.</div></div></div> [[Try this question again->Pyloric stenosis - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Cardiology clinic · 09:00</div> A 64-year-old man with New York Heart Association class III symptoms has a left ventricular ejection fraction of 30% on echocardiography. His blood pressure is 118/74 mm Hg, pulse is 72/min, potassium 4.3 mEq/L, and eGFR 58 mL/min/1.73 m2. He is euvolemic on current loop diuretic therapy. <span class="ec-prompt">Which of the following is the most appropriate combination of disease-modifying pharmacotherapy?</span> [[A loop diuretic, warfarin, amiodarone, and digoxin->HFrEF pillars - D3]] [[A thiazide, an alpha-blocker, a nitrate, and a calcium channel blocker->HFrEF pillars - D4]] [[Amlodipine, a long-acting nitrate, a statin, and aspirin->HFrEF pillars - D2]] [[An ARNI or ACE inhibitor, a beta-blocker, an MRA, and an SGLT2 inhibitor->HFrEF pillars - Correct]] [[Digoxin, aspirin, isosorbide dinitrate, and a loop diuretic->HFrEF pillars - D1]]

<span class="ec-case-marker" hidden data-entry="HFrEF pillars. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ An ARNI or ACE inhibitor, a beta-blocker, an MRA, and an SGLT2 inhibitor</div> The 2022 AHA/ACC/HFSA Heart Failure Guideline establishes four pillars of disease-modifying therapy for HFrEF, each proven to reduce mortality independently: (1) renin-angiotensin system inhibition (ARNI preferred over ACE inhibitor), (2) an evidence-based beta-blocker (carvedilol, metoprolol succinate, or bisoprolol), (3) a mineralocorticoid receptor antagonist (spironolactone or eplerenone), and (4) an SGLT2 inhibitor (dapagliflozin or empagliflozin). Diuretics manage congestion but are not disease-modifying. <div class="ec-src"><b>Source:</b> Heidenreich PA, et al. 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. Circulation 2022;145(18):e895-e1032.</div></div> [[Start another case->Hub]] [[Restart this case->HFrEF pillars - Rx]] [[Next case →->HFrEF cardiac output - Prog]]

<span class="ec-case-marker" hidden data-entry="HFrEF pillars. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ This is not the modern standard.</div> Digoxin reduces hospitalizations but does not reduce mortality. Aspirin, nitrates, and loop diuretics are either adjunctive or symptomatic but are not the disease-modifying pillars. <div class="ec-teach"><div class="th">What to do instead</div> The 2022 AHA/ACC/HFSA Heart Failure Guideline establishes four pillars of disease-modifying therapy for HFrEF, each proven to reduce mortality independently: (1) renin-angiotensin system inhibition (ARNI preferred over ACE inhibitor), (2) an evidence-based beta-blocker (carvedilol, metoprolol succinate, or bisoprolol), (3) a mineralocorticoid receptor antagonist (spironolactone or eplerenone), and (4) an SGLT2 inhibitor (dapagliflozin or empagliflozin). Diuretics manage congestion but are not disease-modifying. <div class="ec-src"><b>Source:</b> Heidenreich PA, et al. 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. Circulation 2022;145(18):e895-e1032.</div></div></div> [[Try this question again->HFrEF pillars - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="HFrEF pillars. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ These agents are not HFrEF pillars.</div> Amlodipine is safe in HFrEF but is not disease-modifying. Statins, nitrates, and aspirin do not constitute the guideline-directed framework. <div class="ec-teach"><div class="th">What to do instead</div> The 2022 AHA/ACC/HFSA Heart Failure Guideline establishes four pillars of disease-modifying therapy for HFrEF, each proven to reduce mortality independently: (1) renin-angiotensin system inhibition (ARNI preferred over ACE inhibitor), (2) an evidence-based beta-blocker (carvedilol, metoprolol succinate, or bisoprolol), (3) a mineralocorticoid receptor antagonist (spironolactone or eplerenone), and (4) an SGLT2 inhibitor (dapagliflozin or empagliflozin). Diuretics manage congestion but are not disease-modifying. <div class="ec-src"><b>Source:</b> Heidenreich PA, et al. 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. Circulation 2022;145(18):e895-e1032.</div></div></div> [[Try this question again->HFrEF pillars - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="HFrEF pillars. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ None of these are disease-modifying pillars.</div> Loop diuretics manage congestion, warfarin treats atrial fibrillation, amiodarone controls arrhythmias, and digoxin reduces symptoms, but none reduce HFrEF mortality as part of the four-pillar framework. <div class="ec-teach"><div class="th">What to do instead</div> The 2022 AHA/ACC/HFSA Heart Failure Guideline establishes four pillars of disease-modifying therapy for HFrEF, each proven to reduce mortality independently: (1) renin-angiotensin system inhibition (ARNI preferred over ACE inhibitor), (2) an evidence-based beta-blocker (carvedilol, metoprolol succinate, or bisoprolol), (3) a mineralocorticoid receptor antagonist (spironolactone or eplerenone), and (4) an SGLT2 inhibitor (dapagliflozin or empagliflozin). Diuretics manage congestion but are not disease-modifying. <div class="ec-src"><b>Source:</b> Heidenreich PA, et al. 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. Circulation 2022;145(18):e895-e1032.</div></div></div> [[Try this question again->HFrEF pillars - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="HFrEF pillars. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ These agents are not indicated for HFrEF.</div> Non-dihydropyridine calcium channel blockers and alpha-blockers are not recommended in HFrEF. Thiazides may be added for diuretic resistance but are not disease-modifying. <div class="ec-teach"><div class="th">What to do instead</div> The 2022 AHA/ACC/HFSA Heart Failure Guideline establishes four pillars of disease-modifying therapy for HFrEF, each proven to reduce mortality independently: (1) renin-angiotensin system inhibition (ARNI preferred over ACE inhibitor), (2) an evidence-based beta-blocker (carvedilol, metoprolol succinate, or bisoprolol), (3) a mineralocorticoid receptor antagonist (spironolactone or eplerenone), and (4) an SGLT2 inhibitor (dapagliflozin or empagliflozin). Diuretics manage congestion but are not disease-modifying. <div class="ec-src"><b>Source:</b> Heidenreich PA, et al. 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. Circulation 2022;145(18):e895-e1032.</div></div></div> [[Try this question again->HFrEF pillars - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 07:20</div> A 22-year-old woman with type 1 diabetes has had vomiting and diffuse abdominal pain for 1 day and now has Kussmaul breathing. Blood pressure is 94/62 mm Hg and pulse is 118/min. Glucose is 480 mg/dL, arterial pH 7.12, serum bicarbonate 8 mEq/L, and β-hydroxybutyrate is 5.8 mmol/L. Serum potassium is 4.8 mEq/L. She has received 1 L of normal saline. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Aggressive Intravenous fluid resuscitation alone without insulin->DKA management - D2]] [[Continuous Intravenous insulin with potassium and fluid management->DKA management - Correct]] [[Intravenous furosemide 40 mg for osmotic diuresis->DKA management - D1]] [[Intravenous sodium bicarbonate in all DKA patients->DKA management - D4]] [[Subcutaneous long-acting insulin glargine alone->DKA management - D3]]

<span class="ec-case-marker" hidden data-entry="DKA management. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Continuous Intravenous insulin with potassium and fluid management</div> Insulin is the only treatment that directly suppresses lipolysis and hepatic ketogenesis, the pathophysiologic engine of DKA. However, insulin cannot be given safely without addressing the potassium: insulin drives potassium intracellularly, and hypokalemia kills before acidosis does. With this patient's potassium at 4.8 mEq/L, insulin can be started immediately with potassium replacement running concurrently. If potassium were below 3.5 mEq/L, insulin would be withheld and potassium repleted (about 10 mEq/h) until it rises above that threshold. Aggressive isotonic fluid resuscitation corrects dehydration and improves renal perfusion. <div class="ec-src"><b>Source:</b> Umpierrez GE, et al. Hyperglycemic Crises in Adults With Diabetes: A Consensus Report (ADA/EASD/AACE/JBDS/DTS). Diabetes Care 2024;47(8):1257-1275; ADA Standards of Care 2026.</div></div> [[Start another case->Hub]] [[Restart this case->DKA management - Rx]] [[Next case →->Diabetic emergency (Sequential - 2 Questions) - Dx]]

<span class="ec-case-marker" hidden data-entry="DKA management. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Furosemide worsens dehydration.</div> DKA patients are profoundly volume-depleted from osmotic diuresis. Furosemide would worsen dehydration and electrolyte losses. <div class="ec-teach"><div class="th">What to do instead</div> Insulin is the only treatment that directly suppresses lipolysis and hepatic ketogenesis, the pathophysiologic engine of DKA. However, insulin cannot be given safely without addressing the potassium: insulin drives potassium intracellularly, and hypokalemia kills before acidosis does. With this patient's potassium at 4.8 mEq/L, insulin can be started immediately with potassium replacement running concurrently. If potassium were below 3.5 mEq/L, insulin would be withheld and potassium repleted (about 10 mEq/h) until it rises above that threshold. Aggressive isotonic fluid resuscitation corrects dehydration and improves renal perfusion. <div class="ec-src"><b>Source:</b> Umpierrez GE, et al. Hyperglycemic Crises in Adults With Diabetes: A Consensus Report (ADA/EASD/AACE/JBDS/DTS). Diabetes Care 2024;47(8):1257-1275; ADA Standards of Care 2026.</div></div></div> [[Try this question again->DKA management - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="DKA management. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Fluids alone do not stop ketogenesis.</div> Volume resuscitation is critical in DKA and modestly reduces glucose through dilution and improved renal clearance. However, without insulin, lipolysis and hepatic ketogenesis continue unchecked. Insulin is the only agent that directly suppresses the ketogenic pathway. <div class="ec-teach"><div class="th">What to do instead</div> Insulin is the only treatment that directly suppresses lipolysis and hepatic ketogenesis, the pathophysiologic engine of DKA. However, insulin cannot be given safely without addressing the potassium: insulin drives potassium intracellularly, and hypokalemia kills before acidosis does. With this patient's potassium at 4.8 mEq/L, insulin can be started immediately with potassium replacement running concurrently. If potassium were below 3.5 mEq/L, insulin would be withheld and potassium repleted (about 10 mEq/h) until it rises above that threshold. Aggressive isotonic fluid resuscitation corrects dehydration and improves renal perfusion. <div class="ec-src"><b>Source:</b> Umpierrez GE, et al. Hyperglycemic Crises in Adults With Diabetes: A Consensus Report (ADA/EASD/AACE/JBDS/DTS). Diabetes Care 2024;47(8):1257-1275; ADA Standards of Care 2026.</div></div></div> [[Try this question again->DKA management - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="DKA management. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Subcutaneous long-acting insulin is not the acute treatment.</div> The acute management of DKA requires a continuous intravenous insulin infusion for precise dose titration. Long-acting insulin is transitioned to once the anion gap closes and the patient can eat. <div class="ec-teach"><div class="th">What to do instead</div> Insulin is the only treatment that directly suppresses lipolysis and hepatic ketogenesis, the pathophysiologic engine of DKA. However, insulin cannot be given safely without addressing the potassium: insulin drives potassium intracellularly, and hypokalemia kills before acidosis does. With this patient's potassium at 4.8 mEq/L, insulin can be started immediately with potassium replacement running concurrently. If potassium were below 3.5 mEq/L, insulin would be withheld and potassium repleted (about 10 mEq/h) until it rises above that threshold. Aggressive isotonic fluid resuscitation corrects dehydration and improves renal perfusion. <div class="ec-src"><b>Source:</b> Umpierrez GE, et al. Hyperglycemic Crises in Adults With Diabetes: A Consensus Report (ADA/EASD/AACE/JBDS/DTS). Diabetes Care 2024;47(8):1257-1275; ADA Standards of Care 2026.</div></div></div> [[Try this question again->DKA management - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="DKA management. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Bicarbonate is not routinely indicated.</div> Sodium bicarbonate is considered only in severe acidosis with pH below 7.0. Routine use can worsen intracellular acidosis, cause hypokalemia, and delay ketone clearance. <div class="ec-teach"><div class="th">What to do instead</div> Insulin is the only treatment that directly suppresses lipolysis and hepatic ketogenesis, the pathophysiologic engine of DKA. However, insulin cannot be given safely without addressing the potassium: insulin drives potassium intracellularly, and hypokalemia kills before acidosis does. With this patient's potassium at 4.8 mEq/L, insulin can be started immediately with potassium replacement running concurrently. If potassium were below 3.5 mEq/L, insulin would be withheld and potassium repleted (about 10 mEq/h) until it rises above that threshold. Aggressive isotonic fluid resuscitation corrects dehydration and improves renal perfusion. <div class="ec-src"><b>Source:</b> Umpierrez GE, et al. Hyperglycemic Crises in Adults With Diabetes: A Consensus Report (ADA/EASD/AACE/JBDS/DTS). Diabetes Care 2024;47(8):1257-1275; ADA Standards of Care 2026.</div></div></div> [[Try this question again->DKA management - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 15:47</div> A 34-year-old woman with known primary adrenal insufficiency on maintenance hydrocortisone and fludrocortisone develops vomiting, severe weakness, and confusion after 2 days of gastroenteritis. Blood pressure is 78/46 mm Hg and pulse is 124/min. She has not been able to keep oral medications down. Serum sodium is 126 mEq/L, potassium 5.8 mEq/L, and glucose 52 mg/dL. <span class="ec-prompt">Which of the following is the most appropriate initial treatment?</span> [[Intravenous normal saline bolus alone without glucocorticoids->Adrenal crisis 2 - D1]] [[Intravenous stress-dose hydrocortisone->Adrenal crisis 2 - Correct]] [[Oral fludrocortisone alone->Adrenal crisis 2 - D3]] [[Oral levothyroxine alone->Adrenal crisis 2 - D2]] [[Oral prednisone 60 mg->Adrenal crisis 2 - D4]]

<span class="ec-case-marker" hidden data-entry="Adrenal crisis 2. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Intravenous stress-dose hydrocortisone.</div> Adrenal crisis is a life-threatening emergency requiring immediate parenteral glucocorticoid replacement. Hydrocortisone 100 mg IV bolus is given immediately, followed by 50 mg every 6–8 hours. At stress doses, hydrocortisone provides sufficient mineralocorticoid activity, so fludrocortisone is unnecessary acutely. Aggressive normal saline resuscitation with dextrose corrects the hypotension and hypoglycemia. The classic laboratory triad of hyponatremia, hyperkalemia, and hypoglycemia reflects combined glucocorticoid and mineralocorticoid deficiency. <div class="ec-src"><b>Source:</b> Bornstein SR, et al. Diagnosis and Treatment of Primary Adrenal Insufficiency: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2016;101(2):364-389.</div></div> [[Start another case->Hub]] [[Restart this case->Adrenal crisis 2 - Rx]] [[Next case →->Primary aldosteronism - Ix]]

<span class="ec-case-marker" hidden data-entry="Adrenal crisis 2. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Saline alone does not replace cortisol.</div> Normal saline corrects volume depletion but does not address the fundamental cortisol deficiency. Without exogenous glucocorticoid replacement, the hemodynamic instability and metabolic derangements of adrenal crisis will persist. <div class="ec-teach"><div class="th">What to do instead</div> Adrenal crisis is a life-threatening emergency requiring immediate parenteral glucocorticoid replacement. Hydrocortisone 100 mg IV bolus is given immediately, followed by 50 mg every 6–8 hours. At stress doses, hydrocortisone provides sufficient mineralocorticoid activity, so fludrocortisone is unnecessary acutely. Aggressive normal saline resuscitation with dextrose corrects the hypotension and hypoglycemia. The classic laboratory triad of hyponatremia, hyperkalemia, and hypoglycemia reflects combined glucocorticoid and mineralocorticoid deficiency. <div class="ec-src"><b>Source:</b> Bornstein SR, et al. Diagnosis and Treatment of Primary Adrenal Insufficiency: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2016;101(2):364-389.</div></div></div> [[Try this question again->Adrenal crisis 2 - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Adrenal crisis 2. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Levothyroxine does not treat adrenal crisis.</div> Giving thyroxine to a patient with unrecognized or untreated adrenal insufficiency can precipitate adrenal crisis by accelerating cortisol metabolism. <div class="ec-teach"><div class="th">What to do instead</div> Adrenal crisis is a life-threatening emergency requiring immediate parenteral glucocorticoid replacement. Hydrocortisone 100 mg IV bolus is given immediately, followed by 50 mg every 6–8 hours. At stress doses, hydrocortisone provides sufficient mineralocorticoid activity, so fludrocortisone is unnecessary acutely. Aggressive normal saline resuscitation with dextrose corrects the hypotension and hypoglycemia. The classic laboratory triad of hyponatremia, hyperkalemia, and hypoglycemia reflects combined glucocorticoid and mineralocorticoid deficiency. <div class="ec-src"><b>Source:</b> Bornstein SR, et al. Diagnosis and Treatment of Primary Adrenal Insufficiency: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2016;101(2):364-389.</div></div></div> [[Try this question again->Adrenal crisis 2 - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Adrenal crisis 2. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Oral fludrocortisone cannot be absorbed.</div> The patient is vomiting and cannot absorb oral medication. Stress-dose hydrocortisone provides adequate mineralocorticoid effect, making separate fludrocortisone unnecessary acutely. <div class="ec-teach"><div class="th">What to do instead</div> Adrenal crisis is a life-threatening emergency requiring immediate parenteral glucocorticoid replacement. Hydrocortisone 100 mg IV bolus is given immediately, followed by 50 mg every 6–8 hours. At stress doses, hydrocortisone provides sufficient mineralocorticoid activity, so fludrocortisone is unnecessary acutely. Aggressive normal saline resuscitation with dextrose corrects the hypotension and hypoglycemia. The classic laboratory triad of hyponatremia, hyperkalemia, and hypoglycemia reflects combined glucocorticoid and mineralocorticoid deficiency. <div class="ec-src"><b>Source:</b> Bornstein SR, et al. Diagnosis and Treatment of Primary Adrenal Insufficiency: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2016;101(2):364-389.</div></div></div> [[Try this question again->Adrenal crisis 2 - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Adrenal crisis 2. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Oral medication cannot be absorbed.</div> This patient is vomiting and cannot reliably absorb oral medication. Parenteral hydrocortisone is required, and oral prednisone at this dose lacks the mineralocorticoid activity that stress-dose hydrocortisone provides. <div class="ec-teach"><div class="th">What to do instead</div> Adrenal crisis is a life-threatening emergency requiring immediate parenteral glucocorticoid replacement. Hydrocortisone 100 mg IV bolus is given immediately, followed by 50 mg every 6–8 hours. At stress doses, hydrocortisone provides sufficient mineralocorticoid activity, so fludrocortisone is unnecessary acutely. Aggressive normal saline resuscitation with dextrose corrects the hypotension and hypoglycemia. The classic laboratory triad of hyponatremia, hyperkalemia, and hypoglycemia reflects combined glucocorticoid and mineralocorticoid deficiency. <div class="ec-src"><b>Source:</b> Bornstein SR, et al. Diagnosis and Treatment of Primary Adrenal Insufficiency: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2016;101(2):364-389.</div></div></div> [[Try this question again->Adrenal crisis 2 - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Obstetric clinic · 10:30</div> A 24-year-old woman at 18 weeks' gestation has a positive treponemal screen confirmed by positive RPR at 1:32. She has a painless genital ulcer consistent with a primary chancre. She has no known drug allergies. <span class="ec-prompt">Which of the following is the most appropriate treatment?</span> [[Doxycycline 100 mg twice daily for 14 days->Syphilis pregnancy - D1]] [[Intramuscular benzathine penicillin G, 2.4 million units->Syphilis pregnancy - Correct]] [[No treatment until after delivery->Syphilis pregnancy - D3]] [[Oral azithromycin 1 g single dose->Syphilis pregnancy - D4]] [[Oral ciprofloxacin for a 10-day treatment course->Syphilis pregnancy - D2]]

<span class="ec-case-marker" hidden data-entry="Syphilis pregnancy. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Intramuscular benzathine penicillin G, 2.4 million units</div> Parenteral penicillin G is the only treatment with adequate evidence for preventing congenital syphilis. For primary syphilis, a single dose of benzathine penicillin G 2.4 million units IM is standard. Penicillin-allergic pregnant patients should be desensitized and then treated with penicillin, there is no acceptable alternative regimen during pregnancy. The Jarisch-Herxheimer reaction may occur within 24 hours of treatment. <div class="ec-src"><b>Source:</b> Workowski KA, et al. Sexually Transmitted Infections Treatment Guidelines, 2021. MMWR Recomm Rep 2021;70(4):1-187.</div></div> [[Start another case->Hub]] [[Restart this case->Syphilis pregnancy - Rx]] [[Next case →->Pelvic inflammatory disease - Rx]]

<span class="ec-case-marker" hidden data-entry="Syphilis pregnancy. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Doxycycline is contraindicated in pregnancy.</div> Tetracyclines including doxycycline are contraindicated after the first trimester because of effects on fetal bone and tooth development. They are also not recommended for congenital syphilis prevention. <div class="ec-teach"><div class="th">What to do instead</div> Parenteral penicillin G is the only treatment with adequate evidence for preventing congenital syphilis. For primary syphilis, a single dose of benzathine penicillin G 2.4 million units IM is standard. Penicillin-allergic pregnant patients should be desensitized and then treated with penicillin, there is no acceptable alternative regimen during pregnancy. The Jarisch-Herxheimer reaction may occur within 24 hours of treatment. <div class="ec-src"><b>Source:</b> Workowski KA, et al. Sexually Transmitted Infections Treatment Guidelines, 2021. MMWR Recomm Rep 2021;70(4):1-187.</div></div></div> [[Try this question again->Syphilis pregnancy - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Syphilis pregnancy. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Ciprofloxacin does not treat syphilis.</div> Fluoroquinolones have no established efficacy against Treponema pallidum and are generally avoided in pregnancy. <div class="ec-teach"><div class="th">What to do instead</div> Parenteral penicillin G is the only treatment with adequate evidence for preventing congenital syphilis. For primary syphilis, a single dose of benzathine penicillin G 2.4 million units IM is standard. Penicillin-allergic pregnant patients should be desensitized and then treated with penicillin, there is no acceptable alternative regimen during pregnancy. The Jarisch-Herxheimer reaction may occur within 24 hours of treatment. <div class="ec-src"><b>Source:</b> Workowski KA, et al. Sexually Transmitted Infections Treatment Guidelines, 2021. MMWR Recomm Rep 2021;70(4):1-187.</div></div></div> [[Try this question again->Syphilis pregnancy - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Syphilis pregnancy. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Delay risks congenital syphilis.</div> Untreated maternal syphilis causes stillbirth, hydrops fetalis, and congenital syphilis. Treatment must begin as soon as the diagnosis is made, regardless of gestational age. <div class="ec-teach"><div class="th">What to do instead</div> Parenteral penicillin G is the only treatment with adequate evidence for preventing congenital syphilis. For primary syphilis, a single dose of benzathine penicillin G 2.4 million units IM is standard. Penicillin-allergic pregnant patients should be desensitized and then treated with penicillin, there is no acceptable alternative regimen during pregnancy. The Jarisch-Herxheimer reaction may occur within 24 hours of treatment. <div class="ec-src"><b>Source:</b> Workowski KA, et al. Sexually Transmitted Infections Treatment Guidelines, 2021. MMWR Recomm Rep 2021;70(4):1-187.</div></div></div> [[Try this question again->Syphilis pregnancy - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Syphilis pregnancy. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Azithromycin is unreliable for syphilis.</div> Macrolide resistance in T. pallidum has been documented globally, and azithromycin is not recommended as a reliable treatment for syphilis, especially in pregnancy where the stakes include congenital infection. <div class="ec-teach"><div class="th">What to do instead</div> Parenteral penicillin G is the only treatment with adequate evidence for preventing congenital syphilis. For primary syphilis, a single dose of benzathine penicillin G 2.4 million units IM is standard. Penicillin-allergic pregnant patients should be desensitized and then treated with penicillin, there is no acceptable alternative regimen during pregnancy. The Jarisch-Herxheimer reaction may occur within 24 hours of treatment. <div class="ec-src"><b>Source:</b> Workowski KA, et al. Sexually Transmitted Infections Treatment Guidelines, 2021. MMWR Recomm Rep 2021;70(4):1-187.</div></div></div> [[Try this question again->Syphilis pregnancy - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Sexual health clinic · 13:15</div> A 22-year-old man presents with dysuria and purulent urethral discharge for 3 days. Nucleic acid amplification testing confirms Neisseria gonorrhoeae. Chlamydia trachomatis testing is pending. <span class="ec-prompt">Which of the following is the most appropriate treatment?</span> [[Ceftriaxone 500 mg intramuscular plus oral doxycycline->Gonorrhea treatment - Correct]] [[Oral amoxicillin 500 mg three times daily->Gonorrhea treatment - D4]] [[Oral fluconazole 150 mg as a single dose->Gonorrhea treatment - D2]] [[Oral metronidazole for 7 days->Gonorrhea treatment - D1]] [[Oral rifampin for 10 days with test of cure->Gonorrhea treatment - D3]]

<span class="ec-case-marker" hidden data-entry="Gonorrhea treatment. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Ceftriaxone 500 mg intramuscular plus oral doxycycline</div> The 2021 CDC STI Treatment Guidelines recommend intramuscular ceftriaxone 500 mg as a single dose for uncomplicated gonorrhea (1 g if the patient weighs ≥150 kg). Because chlamydial coinfection is common and has not yet been excluded, concurrent treatment with doxycycline 100 mg twice daily for 7 days is indicated. If chlamydia testing returns negative, doxycycline can be discontinued. Dual therapy with azithromycin is no longer routinely recommended since the 2020 guideline update. <div class="ec-src"><b>Source:</b> Workowski KA, et al. Sexually Transmitted Infections Treatment Guidelines, 2021. MMWR Recomm Rep 2021;70(4):1-187.</div></div> [[Start another case->Hub]] [[Restart this case->Gonorrhea treatment - Rx]] [[Next case →->Syphilis pregnancy - Rx]]

<span class="ec-case-marker" hidden data-entry="Gonorrhea treatment. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Metronidazole treats anaerobes and Trichomonas.</div> Metronidazole is effective against anaerobic bacteria and Trichomonas vaginalis but has no activity against Neisseria gonorrhoeae. <div class="ec-teach"><div class="th">What to do instead</div> The 2021 CDC STI Treatment Guidelines recommend intramuscular ceftriaxone 500 mg as a single dose for uncomplicated gonorrhea (1 g if the patient weighs ≥150 kg). Because chlamydial coinfection is common and has not yet been excluded, concurrent treatment with doxycycline 100 mg twice daily for 7 days is indicated. If chlamydia testing returns negative, doxycycline can be discontinued. Dual therapy with azithromycin is no longer routinely recommended since the 2020 guideline update. <div class="ec-src"><b>Source:</b> Workowski KA, et al. Sexually Transmitted Infections Treatment Guidelines, 2021. MMWR Recomm Rep 2021;70(4):1-187.</div></div></div> [[Try this question again->Gonorrhea treatment - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Gonorrhea treatment. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Fluconazole is an antifungal.</div> Fluconazole treats Candida infections. It has no antibacterial activity against gonorrhea. <div class="ec-teach"><div class="th">What to do instead</div> The 2021 CDC STI Treatment Guidelines recommend intramuscular ceftriaxone 500 mg as a single dose for uncomplicated gonorrhea (1 g if the patient weighs ≥150 kg). Because chlamydial coinfection is common and has not yet been excluded, concurrent treatment with doxycycline 100 mg twice daily for 7 days is indicated. If chlamydia testing returns negative, doxycycline can be discontinued. Dual therapy with azithromycin is no longer routinely recommended since the 2020 guideline update. <div class="ec-src"><b>Source:</b> Workowski KA, et al. Sexually Transmitted Infections Treatment Guidelines, 2021. MMWR Recomm Rep 2021;70(4):1-187.</div></div></div> [[Try this question again->Gonorrhea treatment - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Gonorrhea treatment. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Rifampin does not treat gonorrhea.</div> Rifampin is used primarily for mycobacterial infections and as adjunctive therapy for certain staphylococcal infections. It is not part of gonorrhea treatment. <div class="ec-teach"><div class="th">What to do instead</div> The 2021 CDC STI Treatment Guidelines recommend intramuscular ceftriaxone 500 mg as a single dose for uncomplicated gonorrhea (1 g if the patient weighs ≥150 kg). Because chlamydial coinfection is common and has not yet been excluded, concurrent treatment with doxycycline 100 mg twice daily for 7 days is indicated. If chlamydia testing returns negative, doxycycline can be discontinued. Dual therapy with azithromycin is no longer routinely recommended since the 2020 guideline update. <div class="ec-src"><b>Source:</b> Workowski KA, et al. Sexually Transmitted Infections Treatment Guidelines, 2021. MMWR Recomm Rep 2021;70(4):1-187.</div></div></div> [[Try this question again->Gonorrhea treatment - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Gonorrhea treatment. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Amoxicillin is ineffective due to resistance.</div> Penicillin-class antibiotics are no longer effective against gonorrhea because of widespread beta-lactamase-producing and chromosomally mediated resistance in N. gonorrhoeae. <div class="ec-teach"><div class="th">What to do instead</div> The 2021 CDC STI Treatment Guidelines recommend intramuscular ceftriaxone 500 mg as a single dose for uncomplicated gonorrhea (1 g if the patient weighs ≥150 kg). Because chlamydial coinfection is common and has not yet been excluded, concurrent treatment with doxycycline 100 mg twice daily for 7 days is indicated. If chlamydia testing returns negative, doxycycline can be discontinued. Dual therapy with azithromycin is no longer routinely recommended since the 2020 guideline update. <div class="ec-src"><b>Source:</b> Workowski KA, et al. Sexually Transmitted Infections Treatment Guidelines, 2021. MMWR Recomm Rep 2021;70(4):1-187.</div></div></div> [[Try this question again->Gonorrhea treatment - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Psychiatric emergency · 22:10</div> A 27-year-old man with a known history of bipolar I disorder is brought in by his family after 5 days of decreased need for sleep, pressured speech, and impulsive spending. He has slept 2 hours per night for a week, has pressured speech, grandiose plans to start three businesses, and has spent $12,000 on credit cards in 4 days. Temperature is 37.2°C (99.0°F), blood pressure is 138/82 mm Hg, and pulse is 98/min. He is severely agitated but oriented. Urine drug screen is negative and there is no evidence of delirium. <span class="ec-prompt">Which of the following is the most appropriate pharmacologic treatment?</span> [[Amphetamine-based stimulant for mood elevation->Acute mania - D2]] [[Benzodiazepine monotherapy as the sole long-term treatment->Acute mania - D4]] [[Low-dose gabapentin for mood stabilization->Acute mania - D3]] [[Mood stabilizer or second-generation antipsychotic->Acute mania - Correct]] [[Selective serotonin reuptake inhibitor monotherapy->Acute mania - D1]]

<span class="ec-case-marker" hidden data-entry="Acute mania. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Mood stabilizer or second-generation antipsychotic</div> Acute mania requires an antimanic agent: lithium, valproate, or a second-generation antipsychotic (such as olanzapine, quetiapine, or aripiprazole) are first-line options. Benzodiazepines may be used adjunctively for acute agitation but are not definitive antimanic treatment. SSRI and stimulant monotherapy can destabilize mood and worsen mania. <div class="ec-src"><b>Source:</b> Yatham LN, et al. CANMAT and ISBD 2018 Guidelines for Management of Patients With Bipolar Disorder. Bipolar Disord 2018;20(2):97-170.</div></div> [[Start another case->Hub]] [[Restart this case->Acute mania - Rx]] [[Next case →->Anorexia nervosa - Opening]]

<span class="ec-case-marker" hidden data-entry="Acute mania. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ SSRIs can worsen mania.</div> Antidepressant monotherapy in bipolar disorder risks inducing or prolonging manic episodes and rapid cycling. Antidepressants should only be used, if at all, with concurrent antimanic coverage. <div class="ec-teach"><div class="th">What to do instead</div> Acute mania requires an antimanic agent: lithium, valproate, or a second-generation antipsychotic (such as olanzapine, quetiapine, or aripiprazole) are first-line options. Benzodiazepines may be used adjunctively for acute agitation but are not definitive antimanic treatment. SSRI and stimulant monotherapy can destabilize mood and worsen mania. <div class="ec-src"><b>Source:</b> Yatham LN, et al. CANMAT and ISBD 2018 Guidelines for Management of Patients With Bipolar Disorder. Bipolar Disord 2018;20(2):97-170.</div></div></div> [[Try this question again->Acute mania - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Acute mania. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Stimulants worsen mania.</div> Stimulants increase catecholamine activity and can exacerbate manic symptoms including agitation, grandiosity, and psychomotor activation. <div class="ec-teach"><div class="th">What to do instead</div> Acute mania requires an antimanic agent: lithium, valproate, or a second-generation antipsychotic (such as olanzapine, quetiapine, or aripiprazole) are first-line options. Benzodiazepines may be used adjunctively for acute agitation but are not definitive antimanic treatment. SSRI and stimulant monotherapy can destabilize mood and worsen mania. <div class="ec-src"><b>Source:</b> Yatham LN, et al. CANMAT and ISBD 2018 Guidelines for Management of Patients With Bipolar Disorder. Bipolar Disord 2018;20(2):97-170.</div></div></div> [[Try this question again->Acute mania - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Acute mania. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Gabapentin is not an effective antimanic agent.</div> Gabapentin lacks evidence for efficacy in acute mania. It is sometimes used for anxiety or pain but does not have antimanic properties. First-line options include lithium, valproate, and second-generation antipsychotics. <div class="ec-teach"><div class="th">What to do instead</div> Acute mania requires an antimanic agent: lithium, valproate, or a second-generation antipsychotic (such as olanzapine, quetiapine, or aripiprazole) are first-line options. Benzodiazepines may be used adjunctively for acute agitation but are not definitive antimanic treatment. SSRI and stimulant monotherapy can destabilize mood and worsen mania. <div class="ec-src"><b>Source:</b> Yatham LN, et al. CANMAT and ISBD 2018 Guidelines for Management of Patients With Bipolar Disorder. Bipolar Disord 2018;20(2):97-170.</div></div></div> [[Try this question again->Acute mania - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Acute mania. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Benzodiazepines are adjunctive only.</div> Benzodiazepines provide short-term sedation for acute agitation but do not treat the underlying manic episode. They are not appropriate as monotherapy for bipolar mania. <div class="ec-teach"><div class="th">What to do instead</div> Acute mania requires an antimanic agent: lithium, valproate, or a second-generation antipsychotic (such as olanzapine, quetiapine, or aripiprazole) are first-line options. Benzodiazepines may be used adjunctively for acute agitation but are not definitive antimanic treatment. SSRI and stimulant monotherapy can destabilize mood and worsen mania. <div class="ec-src"><b>Source:</b> Yatham LN, et al. CANMAT and ISBD 2018 Guidelines for Management of Patients With Bipolar Disorder. Bipolar Disord 2018;20(2):97-170.</div></div></div> [[Try this question again->Acute mania - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 04:55</div> A 41-year-old man with epilepsy has been seizing continuously for 12 minutes. Blood pressure is 162/94 mm Hg, pulse is 128/min, and oxygen saturation 88% on supplemental oxygen. He has received lorazepam 4 mg IV without termination of seizures. Glucose is 128 mg/dL. He remains in generalized tonic-clonic status. <span class="ec-prompt">Which of the following is the most appropriate next pharmacologic step?</span> [[Intravenous fosphenytoin, levetiracetam, or valproate->Refractory SE - Correct]] [[Intravenous haloperidol 5 mg->Refractory SE - D2]] [[Intravenous magnesium sulfate 2 g over 15 minutes->Refractory SE - D4]] [[Oral carbamazepine via nasogastric tube->Refractory SE - D1]] [[Repeat Intravenous lorazepam 4 mg->Refractory SE - D3]]

<span class="ec-case-marker" hidden data-entry="Refractory SE. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Intravenous fosphenytoin, levetiracetam, or valproate</div> Benzodiazepine-refractory convulsive status epilepticus requires urgent second-line IV therapy. Fosphenytoin, levetiracetam, and valproate are the established options, with the ESETT trial demonstrating similar efficacy among the three. The choice depends on patient factors: valproate is avoided in pregnancy and liver disease; fosphenytoin is avoided in cardiac conduction disease. If second-line therapy also fails, the patient has refractory status epilepticus requiring continuous IV anesthetic infusion and ICU admission. <div class="ec-src"><b>Source:</b> Kapur J, et al. Randomized Trial of Three Anticonvulsant Medications for Status Epilepticus (ESETT). N Engl J Med 2019;381(22):2103-2113.</div></div> [[Start another case->Hub]] [[Restart this case->Refractory SE - Rx]] [[Next case →->Febrile seizure - Dx]]

<span class="ec-case-marker" hidden data-entry="Refractory SE. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Oral medication cannot be given during active seizures.</div> A patient in generalized tonic-clonic status cannot swallow safely, and oral absorption is unreliable during status epilepticus anyway. <div class="ec-teach"><div class="th">What to do instead</div> Benzodiazepine-refractory convulsive status epilepticus requires urgent second-line IV therapy. Fosphenytoin, levetiracetam, and valproate are the established options, with the ESETT trial demonstrating similar efficacy among the three. The choice depends on patient factors: valproate is avoided in pregnancy and liver disease; fosphenytoin is avoided in cardiac conduction disease. If second-line therapy also fails, the patient has refractory status epilepticus requiring continuous IV anesthetic infusion and ICU admission. <div class="ec-src"><b>Source:</b> Kapur J, et al. Randomized Trial of Three Anticonvulsant Medications for Status Epilepticus (ESETT). N Engl J Med 2019;381(22):2103-2113.</div></div></div> [[Try this question again->Refractory SE - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Refractory SE. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Haloperidol does not terminate seizures.</div> Haloperidol is an antipsychotic used for agitation or delirium; it has no established antiseizure or anticonvulsant efficacy and does not address ongoing electrographic or convulsive seizure activity. Antipsychotics can also lower the seizure threshold. Guidelines mandate progressing to fosphenytoin, levetiracetam, or valproate. <div class="ec-teach"><div class="th">What to do instead</div> Benzodiazepine-refractory convulsive status epilepticus requires urgent second-line IV therapy. Fosphenytoin, levetiracetam, and valproate are the established options, with the ESETT trial demonstrating similar efficacy among the three. The choice depends on patient factors: valproate is avoided in pregnancy and liver disease; fosphenytoin is avoided in cardiac conduction disease. If second-line therapy also fails, the patient has refractory status epilepticus requiring continuous IV anesthetic infusion and ICU admission. <div class="ec-src"><b>Source:</b> Kapur J, et al. Randomized Trial of Three Anticonvulsant Medications for Status Epilepticus (ESETT). N Engl J Med 2019;381(22):2103-2113.</div></div></div> [[Try this question again->Refractory SE - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Refractory SE. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Repeating the failed first-line agent delays second-line therapy.</div> Lorazepam has already been given at an adequate dose without effect. Repeating a failed benzodiazepine delays the initiation of second-line therapy, during which seizure-related brain injury continues. Guidelines mandate progressing to fosphenytoin, levetiracetam, or valproate. <div class="ec-teach"><div class="th">What to do instead</div> Benzodiazepine-refractory convulsive status epilepticus requires urgent second-line IV therapy. Fosphenytoin, levetiracetam, and valproate are the established options, with the ESETT trial demonstrating similar efficacy among the three. The choice depends on patient factors: valproate is avoided in pregnancy and liver disease; fosphenytoin is avoided in cardiac conduction disease. If second-line therapy also fails, the patient has refractory status epilepticus requiring continuous IV anesthetic infusion and ICU admission. <div class="ec-src"><b>Source:</b> Kapur J, et al. Randomized Trial of Three Anticonvulsant Medications for Status Epilepticus (ESETT). N Engl J Med 2019;381(22):2103-2113.</div></div></div> [[Try this question again->Refractory SE - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Refractory SE. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Magnesium is not a standard second-line antiseizure agent.</div> IV magnesium is the treatment for eclamptic seizures and is used in torsades de pointes, but it is not a recommended second-line agent for convulsive status epilepticus. The ESETT trial validated fosphenytoin, levetiracetam, and valproate. <div class="ec-teach"><div class="th">What to do instead</div> Benzodiazepine-refractory convulsive status epilepticus requires urgent second-line IV therapy. Fosphenytoin, levetiracetam, and valproate are the established options, with the ESETT trial demonstrating similar efficacy among the three. The choice depends on patient factors: valproate is avoided in pregnancy and liver disease; fosphenytoin is avoided in cardiac conduction disease. If second-line therapy also fails, the patient has refractory status epilepticus requiring continuous IV anesthetic infusion and ICU admission. <div class="ec-src"><b>Source:</b> Kapur J, et al. Randomized Trial of Three Anticonvulsant Medications for Status Epilepticus (ESETT). N Engl J Med 2019;381(22):2103-2113.</div></div></div> [[Try this question again->Refractory SE - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 06:30</div> A 58-year-old man presents with acute severe pain, swelling, and erythema of the first metatarsophalangeal joint that began overnight. Temperature is 37.3°C (99.1°F), blood pressure 142/86 mm Hg, and pulse is 82/min. Arthrocentesis yields cloudy synovial fluid with needle-shaped, negatively birefringent crystals under polarized light. Gram stain is negative. Renal function is normal and he has no peptic ulcer disease. <span class="ec-prompt">Which of the following is the most appropriate treatment for this acute flare?</span> [[Empiric intravenous antibiotics->Acute gout - D3]] [[Febuxostat 80 mg daily for urate lowering->Acute gout - D5]] [[Initiation of allopurinol during the acute flare without anti-inflammatory coverage->Acute gout - D4]] [[NSAID, colchicine, or glucocorticoid->Acute gout - Correct]] [[Probenecid for uricosuric therapy->Acute gout - D2]]

<span class="ec-case-marker" hidden data-entry="Acute gout. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ NSAID, colchicine, or glucocorticoid.</div> Acute gout is treated with anti-inflammatory therapy to terminate the flare. NSAIDs (indomethacin, naproxen), colchicine (most effective within 36 hours of onset), and glucocorticoids (oral, IM, or intra-articular) are all first-line options. The choice depends on comorbidities: NSAIDs are avoided in CKD and peptic ulcer disease; colchicine requires dose adjustment in renal impairment. Urate-lowering therapy (allopurinol, febuxostat) is for chronic management and should not be initiated during an acute flare without concurrent anti-inflammatory prophylaxis, as sudden urate changes can prolong or worsen the attack. <div class="ec-src"><b>Source:</b> FitzGerald JD, et al. 2020 American College of Rheumatology Guideline for Management of Gout. Arthritis Care Res 2020;72(6):744-760.</div></div> [[Start another case->Hub]] [[Restart this case->Acute gout - Rx]] [[Next case →->XLA BTK - Mech]]

<span class="ec-case-marker" hidden data-entry="Acute gout. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Probenecid is for chronic management, not acute flares.</div> Probenecid enhances renal uric acid excretion for long-term urate lowering. It does not treat the acute inflammatory response of a gout flare and, like other urate-lowering agents, should not be started during an acute attack without anti-inflammatory coverage. <div class="ec-teach"><div class="th">What to do instead</div> Acute gout is treated with anti-inflammatory therapy to terminate the flare. NSAIDs (indomethacin, naproxen), colchicine (most effective within 36 hours of onset), and glucocorticoids (oral, IM, or intra-articular) are all first-line options. The choice depends on comorbidities: NSAIDs are avoided in CKD and peptic ulcer disease; colchicine requires dose adjustment in renal impairment. Urate-lowering therapy (allopurinol, febuxostat) is for chronic management and should not be initiated during an acute flare without concurrent anti-inflammatory prophylaxis, as sudden urate changes can prolong or worsen the attack. <div class="ec-src"><b>Source:</b> FitzGerald JD, et al. 2020 American College of Rheumatology Guideline for Management of Gout. Arthritis Care Res 2020;72(6):744-760.</div></div></div> [[Try this question again->Acute gout - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Acute gout. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ This is crystal arthritis, not septic arthritis.</div> The negatively birefringent crystals and negative Gram stain confirm gout. Antibiotics treat septic arthritis, which would show organisms on Gram stain or culture. <div class="ec-teach"><div class="th">What to do instead</div> Acute gout is treated with anti-inflammatory therapy to terminate the flare. NSAIDs (indomethacin, naproxen), colchicine (most effective within 36 hours of onset), and glucocorticoids (oral, IM, or intra-articular) are all first-line options. The choice depends on comorbidities: NSAIDs are avoided in CKD and peptic ulcer disease; colchicine requires dose adjustment in renal impairment. Urate-lowering therapy (allopurinol, febuxostat) is for chronic management and should not be initiated during an acute flare without concurrent anti-inflammatory prophylaxis, as sudden urate changes can prolong or worsen the attack. <div class="ec-src"><b>Source:</b> FitzGerald JD, et al. 2020 American College of Rheumatology Guideline for Management of Gout. Arthritis Care Res 2020;72(6):744-760.</div></div></div> [[Try this question again->Acute gout - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Acute gout. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Starting allopurinol during a flare can worsen it.</div> Initiating urate-lowering therapy during an acute flare without anti-inflammatory prophylaxis can destabilize urate crystals and prolong the attack. Start anti-inflammatory treatment first. <div class="ec-teach"><div class="th">What to do instead</div> Acute gout is treated with anti-inflammatory therapy to terminate the flare. NSAIDs (indomethacin, naproxen), colchicine (most effective within 36 hours of onset), and glucocorticoids (oral, IM, or intra-articular) are all first-line options. The choice depends on comorbidities: NSAIDs are avoided in CKD and peptic ulcer disease; colchicine requires dose adjustment in renal impairment. Urate-lowering therapy (allopurinol, febuxostat) is for chronic management and should not be initiated during an acute flare without concurrent anti-inflammatory prophylaxis, as sudden urate changes can prolong or worsen the attack. <div class="ec-src"><b>Source:</b> FitzGerald JD, et al. 2020 American College of Rheumatology Guideline for Management of Gout. Arthritis Care Res 2020;72(6):744-760.</div></div></div> [[Try this question again->Acute gout - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Primary care clinic · 14:00</div> A 32-year-old woman with heavy menstrual periods has had fatigue and exertional dyspnea for 3 months. Hemoglobin is 8.9 g/dL, mean corpuscular volume 68 fL, serum ferritin 6 ng/mL, and transferrin saturation 8%. Peripheral smear shows microcytic, hypochromic red cells. She is hemodynamically stable. <span class="ec-prompt">Which of the following is the most appropriate initial treatment?</span> [[Erythropoietin-stimulating agent as first line->Iron deficiency - D3]] [[Intramuscular vitamin vitamin B12 replacement therapy->Iron deficiency - D2]] [[Intravenous iron infusion as initial monotherapy->Iron deficiency - D4]] [[Oral iron with workup for the source of loss->Iron deficiency - Correct]] [[Packed red blood cell transfusion->Iron deficiency - D1]]

<span class="ec-case-marker" hidden data-entry="Iron deficiency. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Oral iron with workup for the source of loss</div> The classic laboratory profile, low ferritin, low transferrin saturation, microcytosis, and hypochromia, confirms iron deficiency anemia. Oral iron (ferrous sulfate, ferrous fumarate, or ferrous gluconate) is the standard initial treatment for stable patients who can tolerate it. Equally important is identifying and treating the source of iron loss: menorrhagia in this premenopausal woman is the likely cause, but occult GI bleeding must be considered if menstrual loss alone does not explain the severity. <div class="ec-src"><b>Source:</b> Camaschella C. Iron-Deficiency Anemia. N Engl J Med 2015;372(19):1832-1843; AGA Clinical Practice Guideline on the Management of Iron Deficiency Anemia.</div></div> [[Start another case->Hub]] [[Restart this case->Iron deficiency - Rx]] [[Next case →->RBC transfusion - Rx]]

<span class="ec-case-marker" hidden data-entry="Iron deficiency. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Transfusion is not indicated at this hemoglobin in a stable patient.</div> At hemoglobin 8.9 g/dL with hemodynamic stability and no acute bleeding, this patient is above the restrictive transfusion threshold of 7 g/dL. Oral iron supplementation is the appropriate initial treatment for stable iron deficiency anemia. <div class="ec-teach"><div class="th">What to do instead</div> The classic laboratory profile, low ferritin, low transferrin saturation, microcytosis, and hypochromia, confirms iron deficiency anemia. Oral iron (ferrous sulfate, ferrous fumarate, or ferrous gluconate) is the standard initial treatment for stable patients who can tolerate it. Equally important is identifying and treating the source of iron loss: menorrhagia in this premenopausal woman is the likely cause, but occult GI bleeding must be considered if menstrual loss alone does not explain the severity. <div class="ec-src"><b>Source:</b> Camaschella C. Iron-Deficiency Anemia. N Engl J Med 2015;372(19):1832-1843; AGA Clinical Practice Guideline on the Management of Iron Deficiency Anemia.</div></div></div> [[Try this question again->Iron deficiency - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Iron deficiency. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ B12 causes macrocytic anemia, not microcytic.</div> Vitamin B12 deficiency produces a macrocytic (high MCV) anemia, not the microcytic picture seen here. The low ferritin confirms iron deficiency. <div class="ec-teach"><div class="th">What to do instead</div> The classic laboratory profile, low ferritin, low transferrin saturation, microcytosis, and hypochromia, confirms iron deficiency anemia. Oral iron (ferrous sulfate, ferrous fumarate, or ferrous gluconate) is the standard initial treatment for stable patients who can tolerate it. Equally important is identifying and treating the source of iron loss: menorrhagia in this premenopausal woman is the likely cause, but occult GI bleeding must be considered if menstrual loss alone does not explain the severity. <div class="ec-src"><b>Source:</b> Camaschella C. Iron-Deficiency Anemia. N Engl J Med 2015;372(19):1832-1843; AGA Clinical Practice Guideline on the Management of Iron Deficiency Anemia.</div></div></div> [[Try this question again->Iron deficiency - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Iron deficiency. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ ESAs are not first-line for iron deficiency.</div> Erythropoietin-stimulating agents are used in anemia of chronic kidney disease or chemotherapy-induced anemia. They do not correct iron deficiency and are ineffective without adequate iron stores. <div class="ec-teach"><div class="th">What to do instead</div> The classic laboratory profile, low ferritin, low transferrin saturation, microcytosis, and hypochromia, confirms iron deficiency anemia. Oral iron (ferrous sulfate, ferrous fumarate, or ferrous gluconate) is the standard initial treatment for stable patients who can tolerate it. Equally important is identifying and treating the source of iron loss: menorrhagia in this premenopausal woman is the likely cause, but occult GI bleeding must be considered if menstrual loss alone does not explain the severity. <div class="ec-src"><b>Source:</b> Camaschella C. Iron-Deficiency Anemia. N Engl J Med 2015;372(19):1832-1843; AGA Clinical Practice Guideline on the Management of Iron Deficiency Anemia.</div></div></div> [[Try this question again->Iron deficiency - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Iron deficiency. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ IV iron is reserved for patients who cannot tolerate or absorb oral iron.</div> Intravenous iron is effective but is more expensive, requires clinical monitoring, and carries a small risk of infusion reactions. Oral iron is the standard initial treatment. IV iron is reserved for patients with oral intolerance, malabsorption, or ongoing losses exceeding oral replacement capacity. <div class="ec-teach"><div class="th">What to do instead</div> The classic laboratory profile, low ferritin, low transferrin saturation, microcytosis, and hypochromia, confirms iron deficiency anemia. Oral iron (ferrous sulfate, ferrous fumarate, or ferrous gluconate) is the standard initial treatment for stable patients who can tolerate it. Equally important is identifying and treating the source of iron loss: menorrhagia in this premenopausal woman is the likely cause, but occult GI bleeding must be considered if menstrual loss alone does not explain the severity. <div class="ec-src"><b>Source:</b> Camaschella C. Iron-Deficiency Anemia. N Engl J Med 2015;372(19):1832-1843; AGA Clinical Practice Guideline on the Management of Iron Deficiency Anemia.</div></div></div> [[Try this question again->Iron deficiency - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Primary care clinic · 11:22</div> A 20-year-old woman has asthma symptoms including wheezing and chest tightness several times per week and occasional nighttime awakenings. She currently uses an albuterol metered-dose inhaler as needed, with no controller therapy. Spirometry shows FEV1 82% predicted with positive bronchodilator reversibility. <span class="ec-prompt">Which of the following is the most appropriate treatment strategy?</span> [[A long-acting beta-agonist alone without inhaled corticosteroids->Asthma ICS - D4]] [[Continue short-acting beta-agonist alone as needed->Asthma ICS - D1]] [[Daily oral systemic corticosteroids indefinitely->Asthma ICS - D2]] [[Long-term prophylactic macrolide antibiotics->Asthma ICS - D3]] [[Low-dose ICS-formoterol as both maintenance and reliever->Asthma ICS - Correct]]

<span class="ec-case-marker" hidden data-entry="Asthma ICS. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Low-dose ICS-formoterol as both maintenance and reliever</div> The GINA strategy recommends against SABA-only treatment at any severity level because it addresses bronchospasm without treating the underlying inflammation, increasing the risk of severe exacerbations and death. For patients with symptoms more than twice per month, GINA recommends low-dose ICS-formoterol as both daily maintenance and as-needed reliever (the MART approach). This provides anti-inflammatory therapy with every dose of reliever, reducing exacerbation risk compared with the traditional paradigm of a separate SABA rescue inhaler. <div class="ec-src"><b>Source:</b> Global Initiative for Asthma (GINA). Global Strategy for Asthma Management and Prevention: 2025 GINA Report (updated November 2025). Global Initiative for Asthma.</div></div> [[Start another case->Hub]] [[Restart this case->Asthma ICS - Rx]] [[Next case →->Allergic asthma mechanism - Mech]]

<span class="ec-case-marker" hidden data-entry="Asthma ICS. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ SABA-only treatment is no longer recommended.</div> GINA no longer recommends SABA-alone treatment for any patient. Regular SABA use without ICS is associated with increased risk of severe exacerbations and near-fatal or fatal asthma. <div class="ec-teach"><div class="th">What to do instead</div> The GINA strategy recommends against SABA-only treatment at any severity level because it addresses bronchospasm without treating the underlying inflammation, increasing the risk of severe exacerbations and death. For patients with symptoms more than twice per month, GINA recommends low-dose ICS-formoterol as both daily maintenance and as-needed reliever (the MART approach). This provides anti-inflammatory therapy with every dose of reliever, reducing exacerbation risk compared with the traditional paradigm of a separate SABA rescue inhaler. <div class="ec-src"><b>Source:</b> Global Initiative for Asthma (GINA). Global Strategy for Asthma Management and Prevention: 2025 GINA Report (updated November 2025). Global Initiative for Asthma.</div></div></div> [[Try this question again->Asthma ICS - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Asthma ICS. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Chronic systemic steroids cause serious adverse effects.</div> Oral corticosteroids are reserved for severe exacerbations. Chronic use causes osteoporosis, adrenal suppression, diabetes, and immunosuppression. Inhaled corticosteroids deliver anti-inflammatory therapy to the airways with minimal systemic absorption. <div class="ec-teach"><div class="th">What to do instead</div> The GINA strategy recommends against SABA-only treatment at any severity level because it addresses bronchospasm without treating the underlying inflammation, increasing the risk of severe exacerbations and death. For patients with symptoms more than twice per month, GINA recommends low-dose ICS-formoterol as both daily maintenance and as-needed reliever (the MART approach). This provides anti-inflammatory therapy with every dose of reliever, reducing exacerbation risk compared with the traditional paradigm of a separate SABA rescue inhaler. <div class="ec-src"><b>Source:</b> Global Initiative for Asthma (GINA). Global Strategy for Asthma Management and Prevention: 2025 GINA Report (updated November 2025). Global Initiative for Asthma.</div></div></div> [[Try this question again->Asthma ICS - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Asthma ICS. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Antibiotics do not treat asthma.</div> Asthma is a chronic inflammatory airway disease, not an infection. Prophylactic antibiotics have no role and promote antimicrobial resistance. <div class="ec-teach"><div class="th">What to do instead</div> The GINA strategy recommends against SABA-only treatment at any severity level because it addresses bronchospasm without treating the underlying inflammation, increasing the risk of severe exacerbations and death. For patients with symptoms more than twice per month, GINA recommends low-dose ICS-formoterol as both daily maintenance and as-needed reliever (the MART approach). This provides anti-inflammatory therapy with every dose of reliever, reducing exacerbation risk compared with the traditional paradigm of a separate SABA rescue inhaler. <div class="ec-src"><b>Source:</b> Global Initiative for Asthma (GINA). Global Strategy for Asthma Management and Prevention: 2025 GINA Report (updated November 2025). Global Initiative for Asthma.</div></div></div> [[Try this question again->Asthma ICS - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Asthma ICS. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ LABA monotherapy without ICS is unsafe.</div> Long-acting beta-agonists used without an inhaled corticosteroid increase the risk of severe asthma exacerbations and asthma-related death. GINA and FDA labeling both contraindicate LABA monotherapy. LABAs should always be combined with ICS. <div class="ec-teach"><div class="th">What to do instead</div> The GINA strategy recommends against SABA-only treatment at any severity level because it addresses bronchospasm without treating the underlying inflammation, increasing the risk of severe exacerbations and death. For patients with symptoms more than twice per month, GINA recommends low-dose ICS-formoterol as both daily maintenance and as-needed reliever (the MART approach). This provides anti-inflammatory therapy with every dose of reliever, reducing exacerbation risk compared with the traditional paradigm of a separate SABA rescue inhaler. <div class="ec-src"><b>Source:</b> Global Initiative for Asthma (GINA). Global Strategy for Asthma Management and Prevention: 2025 GINA Report (updated November 2025). Global Initiative for Asthma.</div></div></div> [[Try this question again->Asthma ICS - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Obstetric clinic · 15:30</div> A 30-year-old woman at 29 weeks' gestation was diagnosed with gestational diabetes after a failed glucose tolerance test. Despite 2 weeks of medical nutrition therapy and regular physical activity, her fasting glucose remains 105–115 mg/dL and postprandial values frequently exceed 140 mg/dL at one hour. Blood pressure is 118/72 mm Hg. Fetal growth is appropriate for gestational age on recent ultrasound. <span class="ec-prompt">Which of the following is the most appropriate pharmacologic treatment?</span> [[A sulfonylurea such as glipizide->Gestational diabetes - D3]] [[Dietary management alone for an additional 4 weeks->Gestational diabetes - D2]] [[Insulin->Gestational diabetes - Correct]] [[Oral glyburide as the preferred first-line agent->Gestational diabetes - D4]] [[Oral metformin->Gestational diabetes - D1]]

<span class="ec-case-marker" hidden data-entry="Gestational diabetes. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Insulin.</div> Insulin is the preferred pharmacologic treatment for gestational diabetes when medical nutrition therapy fails to achieve glycemic targets. It does not cross the placenta and allows precise dose titration. While metformin and glyburide are used in some settings, insulin remains the ACOG first-line recommendation because of its established safety profile and the uncertainty about long-term offspring effects of oral agents. <div class="ec-src"><b>Source:</b> ACOG Practice Bulletin No. 190: Gestational Diabetes Mellitus. Obstet Gynecol 2018;131(2):e49-e64; ADA Standards of Care 2026.</div></div> [[Start another case->Hub]] [[Restart this case->Gestational diabetes - Rx]] [[Next case →->Thyroid storm - Dx]]

<span class="ec-case-marker" hidden data-entry="Gestational diabetes. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Metformin is an alternative but not preferred.</div> Metformin crosses the placenta and its long-term effects on offspring are not fully established. While it is used in practice, ACOG considers insulin the preferred first-line pharmacologic agent for gestational diabetes because of its established safety profile and precise dose titration. <div class="ec-teach"><div class="th">What to do instead</div> Insulin is the preferred pharmacologic treatment for gestational diabetes when medical nutrition therapy fails to achieve glycemic targets. It does not cross the placenta and allows precise dose titration. While metformin and glyburide are used in some settings, insulin remains the ACOG first-line recommendation because of its established safety profile and the uncertainty about long-term offspring effects of oral agents. <div class="ec-src"><b>Source:</b> ACOG Practice Bulletin No. 190: Gestational Diabetes Mellitus. Obstet Gynecol 2018;131(2):e49-e64; ADA Standards of Care 2026.</div></div></div> [[Try this question again->Gestational diabetes - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Gestational diabetes. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Further diet trial delays glycemic control.</div> 2 weeks of adequate dietary therapy have already failed to achieve glycemic targets. Prolonging diet alone while fasting glucose exceeds 105 mg/dL and postprandial values exceed 140 mg/dL exposes the fetus to continued hyperglycemia, increasing the risk of macrosomia and birth injury. <div class="ec-teach"><div class="th">What to do instead</div> Insulin is the preferred pharmacologic treatment for gestational diabetes when medical nutrition therapy fails to achieve glycemic targets. It does not cross the placenta and allows precise dose titration. While metformin and glyburide are used in some settings, insulin remains the ACOG first-line recommendation because of its established safety profile and the uncertainty about long-term offspring effects of oral agents. <div class="ec-src"><b>Source:</b> ACOG Practice Bulletin No. 190: Gestational Diabetes Mellitus. Obstet Gynecol 2018;131(2):e49-e64; ADA Standards of Care 2026.</div></div></div> [[Try this question again->Gestational diabetes - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Gestational diabetes. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Sulfonylureas are not preferred in pregnancy.</div> Sulfonylureas cross the placenta and can cause neonatal hypoglycemia. They are generally less favored than insulin for gestational diabetes. Glyburide, once considered an alternative, has fallen out of favor due to higher rates of neonatal hypoglycemia and macrosomia compared with insulin. <div class="ec-teach"><div class="th">What to do instead</div> Insulin is the preferred pharmacologic treatment for gestational diabetes when medical nutrition therapy fails to achieve glycemic targets. It does not cross the placenta and allows precise dose titration. While metformin and glyburide are used in some settings, insulin remains the ACOG first-line recommendation because of its established safety profile and the uncertainty about long-term offspring effects of oral agents. <div class="ec-src"><b>Source:</b> ACOG Practice Bulletin No. 190: Gestational Diabetes Mellitus. Obstet Gynecol 2018;131(2):e49-e64; ADA Standards of Care 2026.</div></div></div> [[Try this question again->Gestational diabetes - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Gestational diabetes. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Glyburide is no longer preferred.</div> While glyburide crosses the placenta less than other sulfonylureas, recent data show higher rates of neonatal hypoglycemia and macrosomia compared with insulin. ACOG considers insulin the preferred agent, with metformin as an alternative. <div class="ec-teach"><div class="th">What to do instead</div> Insulin is the preferred pharmacologic treatment for gestational diabetes when medical nutrition therapy fails to achieve glycemic targets. It does not cross the placenta and allows precise dose titration. While metformin and glyburide are used in some settings, insulin remains the ACOG first-line recommendation because of its established safety profile and the uncertainty about long-term offspring effects of oral agents. <div class="ec-src"><b>Source:</b> ACOG Practice Bulletin No. 190: Gestational Diabetes Mellitus. Obstet Gynecol 2018;131(2):e49-e64; ADA Standards of Care 2026.</div></div></div> [[Try this question again->Gestational diabetes - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 20:30</div> A 67-year-old man with stage 4 CKD and missed dialysis sessions has had generalized weakness for 2 days. Blood pressure is 152/88 mm Hg and pulse is 54/min. Serum potassium is 7.1 mEq/L. ECG shows peaked T waves, prolonged PR interval, and QRS widening to 140 ms. <span class="ec-prompt">Which of the following is the most appropriate immediate treatment?</span> [[Furosemide alone->Hyperkalemia - D2]] [[Inhaled albuterol nebulization as the sole initial therapy->Hyperkalemia - D4]] [[Intravenous calcium gluconate->Hyperkalemia - Correct]] [[Intravenous regular insulin with dextrose as the first intervention->Hyperkalemia - D3]] [[Oral sodium polystyrene sulfonate alone->Hyperkalemia - D1]]

<span class="ec-case-marker" hidden data-entry="Hyperkalemia. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Intravenous calcium gluconate.</div> With ECG changes indicating myocardial toxicity, the immediate priority is cardioprotection. IV calcium stabilizes the cardiac membrane within minutes by restoring the threshold potential, reducing the risk of arrhythmia and cardiac arrest. It does not lower the serum potassium level. After calcium, potassium-shifting agents (insulin with glucose, inhaled albuterol, and potentially sodium bicarbonate) are administered to move potassium intracellularly, followed by potassium-removal strategies (dialysis, loop diuretics, or potassium binders). <div class="ec-src"><b>Source:</b> Palmer BF, Clegg DJ. Diagnosis and Treatment of Hyperkalemia. Cleve Clin J Med 2017;84(12):934-942; KDIGO Clinical Practice Guideline for Acute Kidney Injury.</div></div> [[Start another case->Hub]] [[Restart this case->Hyperkalemia - Rx]] [[Next case →->Contraction alkalosis - Mech]]

<span class="ec-case-marker" hidden data-entry="Hyperkalemia. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Polystyrene sulfonate is too slow.</div> Oral potassium binders take hours to reduce serum potassium. With ECG changes indicating imminent arrhythmia risk, the first priority is cardiac membrane stabilization with calcium. <div class="ec-teach"><div class="th">What to do instead</div> With ECG changes indicating myocardial toxicity, the immediate priority is cardioprotection. IV calcium stabilizes the cardiac membrane within minutes by restoring the threshold potential, reducing the risk of arrhythmia and cardiac arrest. It does not lower the serum potassium level. After calcium, potassium-shifting agents (insulin with glucose, inhaled albuterol, and potentially sodium bicarbonate) are administered to move potassium intracellularly, followed by potassium-removal strategies (dialysis, loop diuretics, or potassium binders). <div class="ec-src"><b>Source:</b> Palmer BF, Clegg DJ. Diagnosis and Treatment of Hyperkalemia. Cleve Clin J Med 2017;84(12):934-942; KDIGO Clinical Practice Guideline for Acute Kidney Injury.</div></div></div> [[Try this question again->Hyperkalemia - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Hyperkalemia. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Furosemide alone is insufficient and too slow.</div> Loop diuretics promote renal potassium excretion but take 30–60 minutes to act, and this patient with stage 4 CKD has limited renal response. The cardiac membrane needs immediate protection. <div class="ec-teach"><div class="th">What to do instead</div> With ECG changes indicating myocardial toxicity, the immediate priority is cardioprotection. IV calcium stabilizes the cardiac membrane within minutes by restoring the threshold potential, reducing the risk of arrhythmia and cardiac arrest. It does not lower the serum potassium level. After calcium, potassium-shifting agents (insulin with glucose, inhaled albuterol, and potentially sodium bicarbonate) are administered to move potassium intracellularly, followed by potassium-removal strategies (dialysis, loop diuretics, or potassium binders). <div class="ec-src"><b>Source:</b> Palmer BF, Clegg DJ. Diagnosis and Treatment of Hyperkalemia. Cleve Clin J Med 2017;84(12):934-942; KDIGO Clinical Practice Guideline for Acute Kidney Injury.</div></div></div> [[Try this question again->Hyperkalemia - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Hyperkalemia. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Insulin shifts potassium but does not stabilize the membrane.</div> Insulin with dextrose effectively shifts potassium intracellularly within 15–30 minutes. However, when ECG changes are present, peaked T waves, QRS widening, cardiac membrane stabilization with IV calcium must come first. Calcium works within minutes to prevent arrhythmia while potassium-shifting agents are being prepared. <div class="ec-teach"><div class="th">What to do instead</div> With ECG changes indicating myocardial toxicity, the immediate priority is cardioprotection. IV calcium stabilizes the cardiac membrane within minutes by restoring the threshold potential, reducing the risk of arrhythmia and cardiac arrest. It does not lower the serum potassium level. After calcium, potassium-shifting agents (insulin with glucose, inhaled albuterol, and potentially sodium bicarbonate) are administered to move potassium intracellularly, followed by potassium-removal strategies (dialysis, loop diuretics, or potassium binders). <div class="ec-src"><b>Source:</b> Palmer BF, Clegg DJ. Diagnosis and Treatment of Hyperkalemia. Cleve Clin J Med 2017;84(12):934-942; KDIGO Clinical Practice Guideline for Acute Kidney Injury.</div></div></div> [[Try this question again->Hyperkalemia - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Hyperkalemia. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Albuterol alone is insufficient with ECG changes.</div> Nebulized albuterol promotes intracellular potassium shift and is a useful adjunct. However, with QRS widening and severe hyperkalemia, calcium for membrane stabilization must precede all potassium-shifting agents. Albuterol alone does not address the immediate arrhythmia risk. <div class="ec-teach"><div class="th">What to do instead</div> With ECG changes indicating myocardial toxicity, the immediate priority is cardioprotection. IV calcium stabilizes the cardiac membrane within minutes by restoring the threshold potential, reducing the risk of arrhythmia and cardiac arrest. It does not lower the serum potassium level. After calcium, potassium-shifting agents (insulin with glucose, inhaled albuterol, and potentially sodium bicarbonate) are administered to move potassium intracellularly, followed by potassium-removal strategies (dialysis, loop diuretics, or potassium binders). <div class="ec-src"><b>Source:</b> Palmer BF, Clegg DJ. Diagnosis and Treatment of Hyperkalemia. Cleve Clin J Med 2017;84(12):934-942; KDIGO Clinical Practice Guideline for Acute Kidney Injury.</div></div></div> [[Try this question again->Hyperkalemia - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Cardiology clinic · 10:00</div> A 72-year-old man with nonvalvular atrial fibrillation is being evaluated for stroke prevention. His CHA2DS2-VASc score is 4. He has no mechanical heart valve, no moderate-to-severe rheumatic mitral stenosis, and no severe renal impairment. He has a history of peptic ulcer disease that was treated and healed 2 years ago. <span class="ec-prompt">Which of the following is the most appropriate anticoagulation strategy?</span> [[Aspirin alone->AF anticoagulation - D1]] [[Direct oral anticoagulant->AF anticoagulation - Correct]] [[Dual antiplatelet therapy with aspirin and clopidogrel->AF anticoagulation - D2]] [[Rate control with diltiazem alone without anticoagulation->AF anticoagulation - D3]] [[Warfarin with INR goal 2.0 to 3.0->AF anticoagulation - D4]]

<span class="ec-case-marker" hidden data-entry="AF anticoagulation. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Direct oral anticoagulant.</div> The 2023 ACC/AHA/ACCP/HRS AF guideline recommends DOACs over warfarin for eligible patients with nonvalvular AF. DOACs (apixaban, rivaroxaban, edoxaban, dabigatran) have a more favorable risk-benefit profile, with lower rates of intracranial hemorrhage and no requirement for routine INR monitoring. Warfarin remains appropriate for patients with mechanical heart valves or moderate-to-severe rheumatic mitral stenosis. Among the DOACs, apixaban had the lowest major bleeding rate in its pivotal trial, which may be relevant given this patient's ulcer history. <div class="ec-src"><b>Source:</b> Joglar JA, et al. 2023 ACC/AHA/ACCP/HRS Guideline for Diagnosis and Management of Atrial Fibrillation. Circulation 2024;149(1):e1-e156.</div></div> [[Start another case->Hub]] [[Restart this case->AF anticoagulation - Rx]] [[Next case →->SVT - Dx]]

<span class="ec-case-marker" hidden data-entry="AF anticoagulation. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Aspirin alone is insufficient.</div> Aspirin provides inadequate stroke prevention compared with anticoagulation in patients with a CHA2DS2-VASc score ≥2. Current guidelines do not recommend aspirin alone for AF stroke prevention. <div class="ec-teach"><div class="th">What to do instead</div> The 2023 ACC/AHA/ACCP/HRS AF guideline recommends DOACs over warfarin for eligible patients with nonvalvular AF. DOACs (apixaban, rivaroxaban, edoxaban, dabigatran) have a more favorable risk-benefit profile, with lower rates of intracranial hemorrhage and no requirement for routine INR monitoring. Warfarin remains appropriate for patients with mechanical heart valves or moderate-to-severe rheumatic mitral stenosis. Among the DOACs, apixaban had the lowest major bleeding rate in its pivotal trial, which may be relevant given this patient's ulcer history. <div class="ec-src"><b>Source:</b> Joglar JA, et al. 2023 ACC/AHA/ACCP/HRS Guideline for Diagnosis and Management of Atrial Fibrillation. Circulation 2024;149(1):e1-e156.</div></div></div> [[Try this question again->AF anticoagulation - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="AF anticoagulation. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Warfarin is acceptable but no longer preferred.</div> Warfarin was the standard for decades but DOACs have demonstrated a more favorable risk-benefit profile in nonvalvular AF: lower intracranial hemorrhage rates, no routine INR monitoring, and fewer drug-food interactions. Current guidelines recommend DOACs over warfarin for eligible patients. Warfarin remains appropriate for mechanical valves or moderate-to-severe rheumatic mitral stenosis. <div class="ec-teach"><div class="th">What to do instead</div> The 2023 ACC/AHA/ACCP/HRS AF guideline recommends DOACs over warfarin for eligible patients with nonvalvular AF. DOACs (apixaban, rivaroxaban, edoxaban, dabigatran) have a more favorable risk-benefit profile, with lower rates of intracranial hemorrhage and no requirement for routine INR monitoring. Warfarin remains appropriate for patients with mechanical heart valves or moderate-to-severe rheumatic mitral stenosis. Among the DOACs, apixaban had the lowest major bleeding rate in its pivotal trial, which may be relevant given this patient's ulcer history. <div class="ec-src"><b>Source:</b> Joglar JA, et al. 2023 ACC/AHA/ACCP/HRS Guideline for Diagnosis and Management of Atrial Fibrillation. Circulation 2024;149(1):e1-e156.</div></div></div> [[Try this question again->AF anticoagulation - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="AF anticoagulation. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Rate control does not prevent stroke.</div> Controlling the ventricular rate improves symptoms but does not reduce the thromboembolic risk of atrial fibrillation. With a CHA2DS2-VASc score of 4, the annual stroke risk is approximately 4% and requires anticoagulation regardless of rate or rhythm strategy. <div class="ec-teach"><div class="th">What to do instead</div> The 2023 ACC/AHA/ACCP/HRS AF guideline recommends DOACs over warfarin for eligible patients with nonvalvular AF. DOACs (apixaban, rivaroxaban, edoxaban, dabigatran) have a more favorable risk-benefit profile, with lower rates of intracranial hemorrhage and no requirement for routine INR monitoring. Warfarin remains appropriate for patients with mechanical heart valves or moderate-to-severe rheumatic mitral stenosis. Among the DOACs, apixaban had the lowest major bleeding rate in its pivotal trial, which may be relevant given this patient's ulcer history. <div class="ec-src"><b>Source:</b> Joglar JA, et al. 2023 ACC/AHA/ACCP/HRS Guideline for Diagnosis and Management of Atrial Fibrillation. Circulation 2024;149(1):e1-e156.</div></div></div> [[Try this question again->AF anticoagulation - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Medical floor · 08:45</div> A 66-year-old hospitalized man develops watery diarrhea 6 days into a course of piperacillin-tazobactam for complicated pneumonia. Temperature is 38.1°C (100.6°F), blood pressure 128/76 mm Hg, and pulse is 86/min. He has 8–10 watery stools per day. Stool PCR confirms Clostridioides difficile toxin. He has no hypotension, ileus, leukocytosis above 15,000, or other markers of fulminant disease. This is his first episode. <span class="ec-prompt">Which of the following is the most appropriate antibiotic treatment?</span> [[Loperamide for symptomatic diarrhea control->C difficile - D1]] [[Oral ciprofloxacin for a 10-day treatment course->C difficile - D2]] [[Oral fidaxomicin->C difficile - Correct]] [[Oral metronidazole for a 10-day course->C difficile - D3]] [[Oral vancomycin 125 mg four times daily for 10 days->C difficile - D4]]

<span class="ec-case-marker" hidden data-entry="C difficile. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Oral fidaxomicin.</div> The 2021 IDSA/SHEA focused update recommends fidaxomicin over a standard course of oral vancomycin for an initial non-fulminant CDI episode when feasible, because fidaxomicin is associated with a significantly lower recurrence rate. Oral vancomycin remains an acceptable alternative. Metronidazole is no longer recommended as initial therapy due to inferior cure rates. The offending antibiotic should be discontinued or narrowed whenever possible. <div class="ec-src"><b>Source:</b> Johnson S, et al. Clinical Practice Guideline by the IDSA and SHEA: 2021 Focused Update on Management of Clostridioides difficile Infection in Adults. Clin Infect Dis 2021;73(5):e1029-e1044.</div></div> [[Start another case->Hub]] [[Restart this case->C difficile - Rx]] [[Next case →->Pancreatitis - Ix]]

<span class="ec-case-marker" hidden data-entry="C difficile. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Loperamide is harmful in CDI.</div> Antimotility agents like loperamide are generally avoided in active CDI: they can mask clinical progression and are associated with toxic megacolon and worse outcomes when used without concurrent effective anti-C. difficile therapy. <div class="ec-teach"><div class="th">What to do instead</div> The 2021 IDSA/SHEA focused update recommends fidaxomicin over a standard course of oral vancomycin for an initial non-fulminant CDI episode when feasible, because fidaxomicin is associated with a significantly lower recurrence rate. Oral vancomycin remains an acceptable alternative. Metronidazole is no longer recommended as initial therapy due to inferior cure rates. The offending antibiotic should be discontinued or narrowed whenever possible. <div class="ec-src"><b>Source:</b> Johnson S, et al. Clinical Practice Guideline by the IDSA and SHEA: 2021 Focused Update on Management of Clostridioides difficile Infection in Adults. Clin Infect Dis 2021;73(5):e1029-e1044.</div></div></div> [[Try this question again->C difficile - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="C difficile. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Fluoroquinolones are a CDI risk factor.</div> Fluoroquinolones disrupt the gut microbiome and are among the antibiotics most strongly associated with causing C. difficile infection. They do not treat it. <div class="ec-teach"><div class="th">What to do instead</div> The 2021 IDSA/SHEA focused update recommends fidaxomicin over a standard course of oral vancomycin for an initial non-fulminant CDI episode when feasible, because fidaxomicin is associated with a significantly lower recurrence rate. Oral vancomycin remains an acceptable alternative. Metronidazole is no longer recommended as initial therapy due to inferior cure rates. The offending antibiotic should be discontinued or narrowed whenever possible. <div class="ec-src"><b>Source:</b> Johnson S, et al. Clinical Practice Guideline by the IDSA and SHEA: 2021 Focused Update on Management of Clostridioides difficile Infection in Adults. Clin Infect Dis 2021;73(5):e1029-e1044.</div></div></div> [[Try this question again->C difficile - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="C difficile. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Metronidazole is no longer preferred.</div> Oral metronidazole has inferior cure rates compared with vancomycin and fidaxomicin and is no longer recommended as first-line therapy for CDI by IDSA/SHEA. <div class="ec-teach"><div class="th">What to do instead</div> The 2021 IDSA/SHEA focused update recommends fidaxomicin over a standard course of oral vancomycin for an initial non-fulminant CDI episode when feasible, because fidaxomicin is associated with a significantly lower recurrence rate. Oral vancomycin remains an acceptable alternative. Metronidazole is no longer recommended as initial therapy due to inferior cure rates. The offending antibiotic should be discontinued or narrowed whenever possible. <div class="ec-src"><b>Source:</b> Johnson S, et al. Clinical Practice Guideline by the IDSA and SHEA: 2021 Focused Update on Management of Clostridioides difficile Infection in Adults. Clin Infect Dis 2021;73(5):e1029-e1044.</div></div></div> [[Try this question again->C difficile - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="C difficile. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Oral vancomycin is acceptable but has a higher recurrence rate.</div> Oral vancomycin is effective for initial CDI and remains an option. However, the 2021 IDSA/SHEA focused update conditionally recommends fidaxomicin over vancomycin for an initial non-fulminant episode because fidaxomicin is associated with significantly lower recurrence rates (approximately 13% vs 27%). <div class="ec-teach"><div class="th">What to do instead</div> The 2021 IDSA/SHEA focused update recommends fidaxomicin over a standard course of oral vancomycin for an initial non-fulminant CDI episode when feasible, because fidaxomicin is associated with a significantly lower recurrence rate. Oral vancomycin remains an acceptable alternative. Metronidazole is no longer recommended as initial therapy due to inferior cure rates. The offending antibiotic should be discontinued or narrowed whenever possible. <div class="ec-src"><b>Source:</b> Johnson S, et al. Clinical Practice Guideline by the IDSA and SHEA: 2021 Focused Update on Management of Clostridioides difficile Infection in Adults. Clin Infect Dis 2021;73(5):e1029-e1044.</div></div></div> [[Try this question again->C difficile - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Neurology clinic · 09:30</div> A 69-year-old man has had progressive bradykinesia, asymmetric resting tremor of the right hand, cogwheel rigidity, and a shuffling gait for 18 months, now interfering substantially with his daily activities. His symptoms have worsened over 18 months. Blood pressure is 134/78 mm Hg supine and 118/70 mm Hg standing. Neurologic examination confirms asymmetric resting tremor, lead-pipe rigidity with cogwheeling, and reduced arm swing on the right. <span class="ec-prompt">Which of the following is the most appropriate initial pharmacotherapy?</span> [[Amantadine for symptomatic benefit->Parkinson treatment - D3]] [[Benztropine for anticholinergic symptom relief->Parkinson treatment - D4]] [[Levodopa/carbidopa->Parkinson treatment - Correct]] [[Pramipexole as a dopamine agonist->Parkinson treatment - D1]] [[Rasagiline as an monoamine oxidase B inhibitor->Parkinson treatment - D2]]

<span class="ec-case-marker" hidden data-entry="Parkinson treatment. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Levodopa/carbidopa.</div> Levodopa remains the most effective symptomatic treatment for Parkinson disease motor symptoms. It is converted to dopamine in the brain, replacing the deficient neurotransmitter. Carbidopa inhibits peripheral decarboxylation, reducing nausea and increasing CNS bioavailability. While dopamine agonists (pramipexole, ropinirole) and MAO-B inhibitors (rasagiline, selegiline) are alternatives for early or mild disease, none match the motor benefit of levodopa. Long-term levodopa use is associated with motor fluctuations and dyskinesias, but delaying treatment does not prevent these complications. <div class="ec-src"><b>Source:</b> Fox SH, et al. International Parkinson and Movement Disorder Society Evidence-Based Medicine Review: Update on Treatments for Motor Symptoms. Mov Disord 2018;33(8):1248-1266.</div></div> [[Start another case->Hub]] [[Restart this case->Parkinson treatment - Rx]] [[Next case →->Parkinson basal ganglia - Mech]]

<span class="ec-case-marker" hidden data-entry="Parkinson treatment. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Dopamine agonists provide less motor benefit than levodopa.</div> Pramipexole is a dopamine agonist used in early Parkinson disease, especially in younger patients where minimizing levodopa exposure may delay motor fluctuations. However, it provides less motor improvement than levodopa and carries risks of impulse control disorders, somnolence, and hallucinations. For a patient with substantial functional impairment, levodopa is preferred. <div class="ec-teach"><div class="th">What to do instead</div> Levodopa remains the most effective symptomatic treatment for Parkinson disease motor symptoms. It is converted to dopamine in the brain, replacing the deficient neurotransmitter. Carbidopa inhibits peripheral decarboxylation, reducing nausea and increasing CNS bioavailability. While dopamine agonists (pramipexole, ropinirole) and MAO-B inhibitors (rasagiline, selegiline) are alternatives for early or mild disease, none match the motor benefit of levodopa. Long-term levodopa use is associated with motor fluctuations and dyskinesias, but delaying treatment does not prevent these complications. <div class="ec-src"><b>Source:</b> Fox SH, et al. International Parkinson and Movement Disorder Society Evidence-Based Medicine Review: Update on Treatments for Motor Symptoms. Mov Disord 2018;33(8):1248-1266.</div></div></div> [[Try this question again->Parkinson treatment - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Parkinson treatment. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ MAO-B inhibitors provide modest symptomatic benefit.</div> Rasagiline inhibits monoamine oxidase B, increasing synaptic dopamine availability. It provides mild symptomatic improvement and may be used as initial monotherapy in very mild disease. For this patient with significant daily activity interference, levodopa provides superior motor benefit. <div class="ec-teach"><div class="th">What to do instead</div> Levodopa remains the most effective symptomatic treatment for Parkinson disease motor symptoms. It is converted to dopamine in the brain, replacing the deficient neurotransmitter. Carbidopa inhibits peripheral decarboxylation, reducing nausea and increasing CNS bioavailability. While dopamine agonists (pramipexole, ropinirole) and MAO-B inhibitors (rasagiline, selegiline) are alternatives for early or mild disease, none match the motor benefit of levodopa. Long-term levodopa use is associated with motor fluctuations and dyskinesias, but delaying treatment does not prevent these complications. <div class="ec-src"><b>Source:</b> Fox SH, et al. International Parkinson and Movement Disorder Society Evidence-Based Medicine Review: Update on Treatments for Motor Symptoms. Mov Disord 2018;33(8):1248-1266.</div></div></div> [[Try this question again->Parkinson treatment - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Parkinson treatment. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Amantadine is not first-line for motor symptoms.</div> Amantadine is primarily used to manage levodopa-induced dyskinesias in advanced Parkinson disease. Its antiparkinsonian effect as monotherapy is modest and insufficient for a patient with substantial bradykinesia, rigidity, and gait impairment. <div class="ec-teach"><div class="th">What to do instead</div> Levodopa remains the most effective symptomatic treatment for Parkinson disease motor symptoms. It is converted to dopamine in the brain, replacing the deficient neurotransmitter. Carbidopa inhibits peripheral decarboxylation, reducing nausea and increasing CNS bioavailability. While dopamine agonists (pramipexole, ropinirole) and MAO-B inhibitors (rasagiline, selegiline) are alternatives for early or mild disease, none match the motor benefit of levodopa. Long-term levodopa use is associated with motor fluctuations and dyskinesias, but delaying treatment does not prevent these complications. <div class="ec-src"><b>Source:</b> Fox SH, et al. International Parkinson and Movement Disorder Society Evidence-Based Medicine Review: Update on Treatments for Motor Symptoms. Mov Disord 2018;33(8):1248-1266.</div></div></div> [[Try this question again->Parkinson treatment - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Parkinson treatment. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Anticholinergics are not preferred in elderly patients.</div> Benztropine may help tremor-predominant disease in younger patients but causes significant cognitive and anticholinergic side effects (confusion, constipation, urinary retention) that are poorly tolerated in older adults. It is not recommended as initial therapy, particularly in a 69-year-old patient. <div class="ec-teach"><div class="th">What to do instead</div> Levodopa remains the most effective symptomatic treatment for Parkinson disease motor symptoms. It is converted to dopamine in the brain, replacing the deficient neurotransmitter. Carbidopa inhibits peripheral decarboxylation, reducing nausea and increasing CNS bioavailability. While dopamine agonists (pramipexole, ropinirole) and MAO-B inhibitors (rasagiline, selegiline) are alternatives for early or mild disease, none match the motor benefit of levodopa. Long-term levodopa use is associated with motor fluctuations and dyskinesias, but delaying treatment does not prevent these complications. <div class="ec-src"><b>Source:</b> Fox SH, et al. International Parkinson and Movement Disorder Society Evidence-Based Medicine Review: Update on Treatments for Motor Symptoms. Mov Disord 2018;33(8):1248-1266.</div></div></div> [[Try this question again->Parkinson treatment - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Medical floor · 03:20</div> A 59-year-old man with known cirrhosis and portal hypertension is brought in with progressive confusion over 2 days. Temperature is 37.4°C (99.3°F), blood pressure is 108/64 mm Hg, and pulse is 92/min. He has asterixis and is disoriented to time and place. Fingerstick glucose is 98 mg/dL. CT head is unremarkable. Ammonia level is elevated. There is no focal neurologic deficit. <span class="ec-prompt">Which of the following is the most appropriate initial treatment?</span> [[Lactulose->Hepatic encephalopathy - Correct]] [[Loperamide for symptomatic diarrhea control->Hepatic encephalopathy - D1]] [[Propranolol for portal pressure reduction->Hepatic encephalopathy - D2]] [[Protein restriction to less than 0.5 g/kg daily->Hepatic encephalopathy - D3]] [[Rifaximin alone without lactulose->Hepatic encephalopathy - D4]]

<span class="ec-case-marker" hidden data-entry="Hepatic encephalopathy. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Lactulose.</div> Lactulose is an osmotic laxative that acidifies the colonic lumen, converting ammonia (NH3) to ammonium (NH4⁺), which cannot be absorbed. It reduces both serum ammonia and clinical encephalopathy. Rifaximin is added for secondary prophylaxis after a second episode. Precipitating factors, infection, GI bleeding, constipation, hypokalemia, excessive dietary protein, sedatives, must be identified and corrected simultaneously. <div class="ec-src"><b>Source:</b> Vilstrup H, et al. Hepatic Encephalopathy in Chronic Liver Disease: AASLD/EASL Practice Guideline. Hepatology 2014;60(2):715-735.</div></div> [[Start another case->Hub]] [[Restart this case->Hepatic encephalopathy - Rx]] [[Next case →->SBP - Ix]]

<span class="ec-case-marker" hidden data-entry="Hepatic encephalopathy. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Loperamide worsens encephalopathy.</div> Loperamide slows gut transit and increases ammonia absorption. The treatment requires increased colonic clearance, the opposite of what antimotility agents do. <div class="ec-teach"><div class="th">What to do instead</div> Lactulose is an osmotic laxative that acidifies the colonic lumen, converting ammonia (NH3) to ammonium (NH4⁺), which cannot be absorbed. It reduces both serum ammonia and clinical encephalopathy. Rifaximin is added for secondary prophylaxis after a second episode. Precipitating factors, infection, GI bleeding, constipation, hypokalemia, excessive dietary protein, sedatives, must be identified and corrected simultaneously. <div class="ec-src"><b>Source:</b> Vilstrup H, et al. Hepatic Encephalopathy in Chronic Liver Disease: AASLD/EASL Practice Guideline. Hepatology 2014;60(2):715-735.</div></div></div> [[Try this question again->Hepatic encephalopathy - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Hepatic encephalopathy. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Propranolol prevents variceal bleeding.</div> Non-selective beta-blockers reduce portal pressure for variceal prophylaxis but do not treat hepatic encephalopathy. <div class="ec-teach"><div class="th">What to do instead</div> Lactulose is an osmotic laxative that acidifies the colonic lumen, converting ammonia (NH3) to ammonium (NH4⁺), which cannot be absorbed. It reduces both serum ammonia and clinical encephalopathy. Rifaximin is added for secondary prophylaxis after a second episode. Precipitating factors, infection, GI bleeding, constipation, hypokalemia, excessive dietary protein, sedatives, must be identified and corrected simultaneously. <div class="ec-src"><b>Source:</b> Vilstrup H, et al. Hepatic Encephalopathy in Chronic Liver Disease: AASLD/EASL Practice Guideline. Hepatology 2014;60(2):715-735.</div></div></div> [[Try this question again->Hepatic encephalopathy - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Hepatic encephalopathy. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Severe protein restriction is no longer recommended.</div> Older practice restricted dietary protein in hepatic encephalopathy, but current guidelines recommend maintaining adequate protein intake (1.2–1.5 g/kg/day) because protein restriction worsens sarcopenia without improving encephalopathy outcomes. <div class="ec-teach"><div class="th">What to do instead</div> Lactulose is an osmotic laxative that acidifies the colonic lumen, converting ammonia (NH3) to ammonium (NH4⁺), which cannot be absorbed. It reduces both serum ammonia and clinical encephalopathy. Rifaximin is added for secondary prophylaxis after a second episode. Precipitating factors, infection, GI bleeding, constipation, hypokalemia, excessive dietary protein, sedatives, must be identified and corrected simultaneously. <div class="ec-src"><b>Source:</b> Vilstrup H, et al. Hepatic Encephalopathy in Chronic Liver Disease: AASLD/EASL Practice Guideline. Hepatology 2014;60(2):715-735.</div></div></div> [[Try this question again->Hepatic encephalopathy - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Hepatic encephalopathy. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Rifaximin is for secondary prophylaxis, not initial treatment.</div> Rifaximin is a gut-selective antibiotic added after a second episode of hepatic encephalopathy for secondary prophylaxis. For the initial episode, lactulose is the first-line agent. Rifaximin is used in addition to lactulose, not instead of it. <div class="ec-teach"><div class="th">What to do instead</div> Lactulose is an osmotic laxative that acidifies the colonic lumen, converting ammonia (NH3) to ammonium (NH4⁺), which cannot be absorbed. It reduces both serum ammonia and clinical encephalopathy. Rifaximin is added for secondary prophylaxis after a second episode. Precipitating factors, infection, GI bleeding, constipation, hypokalemia, excessive dietary protein, sedatives, must be identified and corrected simultaneously. <div class="ec-src"><b>Source:</b> Vilstrup H, et al. Hepatic Encephalopathy in Chronic Liver Disease: AASLD/EASL Practice Guideline. Hepatology 2014;60(2):715-735.</div></div></div> [[Try this question again->Hepatic encephalopathy - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Pediatric ward · 16:00</div> A 3-year-old boy has had fever for 6 days with bilateral non-exudative conjunctival injection, cracked erythematous lips, a polymorphous truncal rash, and bilateral swelling of the hands and feet. Temperature is 39.6°C (103.3°F), blood pressure is 88/52 mm Hg, and pulse is 142/min. C-reactive protein is 112 mg/L. Echocardiography today is normal. <span class="ec-prompt">Which of the following is the most appropriate initial treatment?</span> [[High-dose aspirin alone without immunoglobulin->Kawasaki treatment - D1]] [[Intravenous immunoglobulin 2 g/kg plus aspirin->Kawasaki treatment - Correct]] [[Intravenous methylprednisolone alone as initial therapy->Kawasaki treatment - D4]] [[No treatment until coronary abnormalities appear->Kawasaki treatment - D3]] [[Penicillin alone->Kawasaki treatment - D2]]

<span class="ec-case-marker" hidden data-entry="Kawasaki treatment. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Intravenous immunoglobulin 2 g/kg plus aspirin</div> IVIG given within 10 days of fever onset reduces the incidence of coronary artery aneurysms from approximately 25% to under 5%. A single 2 g/kg infusion is superior to divided doses. Aspirin is given concurrently for its anti-inflammatory and later antiplatelet effect. A normal echocardiogram does not exclude the diagnosis and must not delay treatment, coronary changes may develop later. <div class="ec-src"><b>Source:</b> Jone P-N, et al. Update on Diagnosis and Management of Kawasaki Disease: AHA Scientific Statement. Circulation 2024;150(23):e481-e500.</div></div> [[Start another case->Hub]] [[Restart this case->Kawasaki treatment - Rx]] [[Next case →->Febrile infant - Ix]]

<span class="ec-case-marker" hidden data-entry="Kawasaki treatment. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Aspirin alone does not prevent coronary aneurysms.</div> Aspirin is part of the treatment regimen but alone does not reduce the incidence of coronary artery aneurysms to the same degree as IVIG. The landmark studies demonstrated that IVIG plus aspirin is superior to aspirin alone. <div class="ec-teach"><div class="th">What to do instead</div> IVIG given within 10 days of fever onset reduces the incidence of coronary artery aneurysms from approximately 25% to under 5%. A single 2 g/kg infusion is superior to divided doses. Aspirin is given concurrently for its anti-inflammatory and later antiplatelet effect. A normal echocardiogram does not exclude the diagnosis and must not delay treatment, coronary changes may develop later. <div class="ec-src"><b>Source:</b> Jone P-N, et al. Update on Diagnosis and Management of Kawasaki Disease: AHA Scientific Statement. Circulation 2024;150(23):e481-e500.</div></div></div> [[Try this question again->Kawasaki treatment - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Kawasaki treatment. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Penicillin alone is insufficient.</div> Kawasaki disease is not a bacterial infection. While it enters the differential with scarlet fever, the full clinical picture with conjunctival and extremity involvement points to Kawasaki disease, which requires IVIG. <div class="ec-teach"><div class="th">What to do instead</div> IVIG given within 10 days of fever onset reduces the incidence of coronary artery aneurysms from approximately 25% to under 5%. A single 2 g/kg infusion is superior to divided doses. Aspirin is given concurrently for its anti-inflammatory and later antiplatelet effect. A normal echocardiogram does not exclude the diagnosis and must not delay treatment, coronary changes may develop later. <div class="ec-src"><b>Source:</b> Jone P-N, et al. Update on Diagnosis and Management of Kawasaki Disease: AHA Scientific Statement. Circulation 2024;150(23):e481-e500.</div></div></div> [[Try this question again->Kawasaki treatment - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Kawasaki treatment. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Waiting for coronary changes is too late.</div> The purpose of IVIG is to prevent coronary aneurysms. Waiting for coronary changes to appear before treating dramatically increases the risk of permanent coronary damage. <div class="ec-teach"><div class="th">What to do instead</div> IVIG given within 10 days of fever onset reduces the incidence of coronary artery aneurysms from approximately 25% to under 5%. A single 2 g/kg infusion is superior to divided doses. Aspirin is given concurrently for its anti-inflammatory and later antiplatelet effect. A normal echocardiogram does not exclude the diagnosis and must not delay treatment, coronary changes may develop later. <div class="ec-src"><b>Source:</b> Jone P-N, et al. Update on Diagnosis and Management of Kawasaki Disease: AHA Scientific Statement. Circulation 2024;150(23):e481-e500.</div></div></div> [[Try this question again->Kawasaki treatment - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Kawasaki treatment. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Corticosteroids alone are not first-line.</div> IV corticosteroids may be used as adjunctive or rescue therapy in IVIG-resistant Kawasaki disease, but they are not recommended as initial monotherapy. IVIG remains the cornerstone of initial treatment. <div class="ec-teach"><div class="th">What to do instead</div> IVIG given within 10 days of fever onset reduces the incidence of coronary artery aneurysms from approximately 25% to under 5%. A single 2 g/kg infusion is superior to divided doses. Aspirin is given concurrently for its anti-inflammatory and later antiplatelet effect. A normal echocardiogram does not exclude the diagnosis and must not delay treatment, coronary changes may develop later. <div class="ec-src"><b>Source:</b> Jone P-N, et al. Update on Diagnosis and Management of Kawasaki Disease: AHA Scientific Statement. Circulation 2024;150(23):e481-e500.</div></div></div> [[Try this question again->Kawasaki treatment - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Oncology ward · 11:30</div> A 61-year-old man with newly diagnosed Burkitt lymphoma has bulky disease with extensive lymphadenopathy and an lactate dehydrogenase of 1,850 U/L. Temperature is 37.2°C (99.0°F), blood pressure is 128/74 mm Hg, and pulse is 84/min. Baseline uric acid is 9.2 mg/dL, creatinine is 1.1 mg/dL, and potassium is 4.6 mEq/L. Intensive chemotherapy is planned. <span class="ec-prompt">Which of the following prophylactic strategies is most appropriate before initiating chemotherapy?</span> [[Aggressive Intravenous hydration, rasburicase, and close laboratory monitoring->TLS prophylaxis - Correct]] [[Delay all laboratory monitoring until 48 hours after chemotherapy->TLS prophylaxis - D3]] [[Restrict intravenous fluids to minimize edema->TLS prophylaxis - D1]] [[Routine calcium supplementation->TLS prophylaxis - D4]] [[Routine potassium supplementation->TLS prophylaxis - D2]]

<span class="ec-case-marker" hidden data-entry="TLS prophylaxis. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Aggressive Intravenous hydration, rasburicase, and close laboratory monitoring</div> Burkitt lymphoma with bulky disease and elevated LDH places this patient in the highest risk category for tumor lysis syndrome. Aggressive IV hydration (2.5–3 L/m2/day) maintains renal perfusion and uric acid clearance. Rasburicase (recombinant urate oxidase) rapidly reduces uric acid and is preferred over allopurinol in high-risk patients because it acts within hours. Laboratory monitoring (potassium, phosphorus, calcium, uric acid, creatinine) should begin before chemotherapy and continue every 6–8 hours for 48–72 hours. Allopurinol prevents new uric acid formation but does not break down existing uric acid. <div class="ec-src"><b>Source:</b> Coiffier B, et al. Guidelines for the Management of Pediatric and Adult Tumor Lysis Syndrome. J Clin Oncol 2008;26(16):2767-2778; Cairo MS, et al. Tumor Lysis Syndrome: New Therapeutic Strategies and Classification. Br J Haematol 2004;127(1):3-11.</div></div> [[Start another case->Hub]] [[Restart this case->TLS prophylaxis - Rx]] [[Next case →->Neutropenic fever - Dx]]

<span class="ec-case-marker" hidden data-entry="TLS prophylaxis. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Fluid restriction worsens TLS.</div> Aggressive hydration is the cornerstone of TLS prevention. It maintains renal blood flow, promotes uric acid excretion, and prevents crystal deposition. Restricting fluids directly increases the risk of TLS-related acute kidney injury. <div class="ec-teach"><div class="th">What to do instead</div> Burkitt lymphoma with bulky disease and elevated LDH places this patient in the highest risk category for tumor lysis syndrome. Aggressive IV hydration (2.5–3 L/m2/day) maintains renal perfusion and uric acid clearance. Rasburicase (recombinant urate oxidase) rapidly reduces uric acid and is preferred over allopurinol in high-risk patients because it acts within hours. Laboratory monitoring (potassium, phosphorus, calcium, uric acid, creatinine) should begin before chemotherapy and continue every 6–8 hours for 48–72 hours. Allopurinol prevents new uric acid formation but does not break down existing uric acid. <div class="ec-src"><b>Source:</b> Coiffier B, et al. Guidelines for the Management of Pediatric and Adult Tumor Lysis Syndrome. J Clin Oncol 2008;26(16):2767-2778; Cairo MS, et al. Tumor Lysis Syndrome: New Therapeutic Strategies and Classification. Br J Haematol 2004;127(1):3-11.</div></div></div> [[Try this question again->TLS prophylaxis - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="TLS prophylaxis. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Potassium supplementation is dangerous.</div> TLS releases massive amounts of intracellular potassium. Supplementation would worsen hyperkalemia, which can cause fatal cardiac arrhythmias. <div class="ec-teach"><div class="th">What to do instead</div> Burkitt lymphoma with bulky disease and elevated LDH places this patient in the highest risk category for tumor lysis syndrome. Aggressive IV hydration (2.5–3 L/m2/day) maintains renal perfusion and uric acid clearance. Rasburicase (recombinant urate oxidase) rapidly reduces uric acid and is preferred over allopurinol in high-risk patients because it acts within hours. Laboratory monitoring (potassium, phosphorus, calcium, uric acid, creatinine) should begin before chemotherapy and continue every 6–8 hours for 48–72 hours. Allopurinol prevents new uric acid formation but does not break down existing uric acid. <div class="ec-src"><b>Source:</b> Coiffier B, et al. Guidelines for the Management of Pediatric and Adult Tumor Lysis Syndrome. J Clin Oncol 2008;26(16):2767-2778; Cairo MS, et al. Tumor Lysis Syndrome: New Therapeutic Strategies and Classification. Br J Haematol 2004;127(1):3-11.</div></div></div> [[Try this question again->TLS prophylaxis - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="TLS prophylaxis. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Delayed monitoring misses the critical window.</div> TLS can develop within hours of chemotherapy initiation. Monitoring must begin before treatment and continue frequently. A 48-hour delay risks missing life-threatening electrolyte derangements. <div class="ec-teach"><div class="th">What to do instead</div> Burkitt lymphoma with bulky disease and elevated LDH places this patient in the highest risk category for tumor lysis syndrome. Aggressive IV hydration (2.5–3 L/m2/day) maintains renal perfusion and uric acid clearance. Rasburicase (recombinant urate oxidase) rapidly reduces uric acid and is preferred over allopurinol in high-risk patients because it acts within hours. Laboratory monitoring (potassium, phosphorus, calcium, uric acid, creatinine) should begin before chemotherapy and continue every 6–8 hours for 48–72 hours. Allopurinol prevents new uric acid formation but does not break down existing uric acid. <div class="ec-src"><b>Source:</b> Coiffier B, et al. Guidelines for the Management of Pediatric and Adult Tumor Lysis Syndrome. J Clin Oncol 2008;26(16):2767-2778; Cairo MS, et al. Tumor Lysis Syndrome: New Therapeutic Strategies and Classification. Br J Haematol 2004;127(1):3-11.</div></div></div> [[Try this question again->TLS prophylaxis - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="TLS prophylaxis. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Calcium supplementation is generally avoided.</div> Hyperphosphatemia in TLS causes calcium-phosphate precipitation and secondary hypocalcemia. Routine calcium supplementation can worsen calcium-phosphate deposition in tissues and kidneys unless symptomatic hypocalcemia is life-threatening. <div class="ec-teach"><div class="th">What to do instead</div> Burkitt lymphoma with bulky disease and elevated LDH places this patient in the highest risk category for tumor lysis syndrome. Aggressive IV hydration (2.5–3 L/m2/day) maintains renal perfusion and uric acid clearance. Rasburicase (recombinant urate oxidase) rapidly reduces uric acid and is preferred over allopurinol in high-risk patients because it acts within hours. Laboratory monitoring (potassium, phosphorus, calcium, uric acid, creatinine) should begin before chemotherapy and continue every 6–8 hours for 48–72 hours. Allopurinol prevents new uric acid formation but does not break down existing uric acid. <div class="ec-src"><b>Source:</b> Coiffier B, et al. Guidelines for the Management of Pediatric and Adult Tumor Lysis Syndrome. J Clin Oncol 2008;26(16):2767-2778; Cairo MS, et al. Tumor Lysis Syndrome: New Therapeutic Strategies and Classification. Br J Haematol 2004;127(1):3-11.</div></div></div> [[Try this question again->TLS prophylaxis - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Quality committee · 12:00</div> A hospital identifies 14 anticoagulation dosing errors over 6 months, including three that reached patients. A multidisciplinary team is assembled to reduce these errors. They want a systematic improvement method. <span class="ec-prompt">Which of the following approaches best represents a quality improvement framework?</span> [[Conduct a single satisfaction survey and consider the problem resolved->QI PDSA - D4]] [[Implement a targeted change, measure its effect, and modify iteratively->QI PDSA - Correct]] [[Punish the clinicians involved without collecting further data->QI PDSA - D1]] [[Replace all anticoagulants with a single formulary agent->QI PDSA - D2]] [[Wait for another serious event before justifying action->QI PDSA - D3]]

<span class="ec-case-marker" hidden data-entry="QI PDSA. Opening"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Implement a targeted change, measure its effect, and modify iteratively</div> The PDSA cycle is the iterative improvement method recommended by the Institute for Healthcare Improvement. The team identifies a specific aim, designs a small test of change (Plan), implements it (Do), analyzes the results (Study), and refines the intervention (Act). Multiple rapid PDSA cycles progressively reduce errors. This is fundamentally different from blame-based or one-time approaches, which do not produce sustained improvement. <div class="ec-src"><b>Source:</b> Institute for Healthcare Improvement. The Breakthrough Series: IHI's Collaborative Model for Achieving Breakthrough Improvement. IHI Innovation Series White Paper.</div></div> [[Start another case->Hub]] [[Restart this case->QI PDSA - Opening]] [[Next case →->Just culture after error - QI]]

<span class="ec-case-marker" hidden data-entry="QI PDSA. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Blame does not produce system improvement.</div> Punishing individuals without understanding the system creates a culture of fear, drives error reporting underground, and leaves the underlying process unchanged. <div class="ec-teach"><div class="th">What to do instead</div> The PDSA cycle is the iterative improvement method recommended by the Institute for Healthcare Improvement. The team identifies a specific aim, designs a small test of change (Plan), implements it (Do), analyzes the results (Study), and refines the intervention (Act). Multiple rapid PDSA cycles progressively reduce errors. This is fundamentally different from blame-based or one-time approaches, which do not produce sustained improvement. <div class="ec-src"><b>Source:</b> Institute for Healthcare Improvement. The Breakthrough Series: IHI's Collaborative Model for Achieving Breakthrough Improvement. IHI Innovation Series White Paper.</div></div></div> [[Try this question again->QI PDSA - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="QI PDSA. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Formulary restriction does not address the dosing process.</div> Replacing anticoagulants does not fix the dosing calculation, verification, or administration process that generated the errors. <div class="ec-teach"><div class="th">What to do instead</div> The PDSA cycle is the iterative improvement method recommended by the Institute for Healthcare Improvement. The team identifies a specific aim, designs a small test of change (Plan), implements it (Do), analyzes the results (Study), and refines the intervention (Act). Multiple rapid PDSA cycles progressively reduce errors. This is fundamentally different from blame-based or one-time approaches, which do not produce sustained improvement. <div class="ec-src"><b>Source:</b> Institute for Healthcare Improvement. The Breakthrough Series: IHI's Collaborative Model for Achieving Breakthrough Improvement. IHI Innovation Series White Paper.</div></div></div> [[Try this question again->QI PDSA - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="QI PDSA. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Reactive approaches miss preventable harm.</div> Waiting for a serious event before acting ignores the near-misses and minor events that signal system vulnerability. Proactive improvement prevents harm. <div class="ec-teach"><div class="th">What to do instead</div> The PDSA cycle is the iterative improvement method recommended by the Institute for Healthcare Improvement. The team identifies a specific aim, designs a small test of change (Plan), implements it (Do), analyzes the results (Study), and refines the intervention (Act). Multiple rapid PDSA cycles progressively reduce errors. This is fundamentally different from blame-based or one-time approaches, which do not produce sustained improvement. <div class="ec-src"><b>Source:</b> Institute for Healthcare Improvement. The Breakthrough Series: IHI's Collaborative Model for Achieving Breakthrough Improvement. IHI Innovation Series White Paper.</div></div></div> [[Try this question again->QI PDSA - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="QI PDSA. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ A single survey is not iterative improvement.</div> One survey provides a snapshot but does not constitute a quality improvement cycle. Sustainable improvement requires iterative testing and measurement. <div class="ec-teach"><div class="th">What to do instead</div> The PDSA cycle is the iterative improvement method recommended by the Institute for Healthcare Improvement. The team identifies a specific aim, designs a small test of change (Plan), implements it (Do), analyzes the results (Study), and refines the intervention (Act). Multiple rapid PDSA cycles progressively reduce errors. This is fundamentally different from blame-based or one-time approaches, which do not produce sustained improvement. <div class="ec-src"><b>Source:</b> Institute for Healthcare Improvement. The Breakthrough Series: IHI's Collaborative Model for Achieving Breakthrough Improvement. IHI Innovation Series White Paper.</div></div></div> [[Try this question again->QI PDSA - Opening]] [[Start another case->Hub]]

<div class="ec-scene">Quality committee · 14:00</div> A hospital has a 30-day heart failure readmission rate significantly above the national benchmark. Case review of 40 readmissions reveals that the most common modifiable factor is medication discrepancies at the time of discharge, patients leave without correct doses of their guideline-directed therapies or with duplicated medications from the pre-admission regimen. Interviews with patients reveal that many did not understand which medications had been changed during hospitalization. <span class="ec-prompt">Which of the following is the most appropriate intervention to reduce readmissions?</span> [[Eliminating same-day discharge planning->Med reconciliation - D3]] [[Extended hospitalization until all lab values normalize->Med reconciliation - D1]] [[Intensive patient education alone without medication review->Med reconciliation - D2]] [[Structured medication reconciliation across transitions of care->Med reconciliation - Correct]] [[Transferring all heart failure patients to cardiac rehabilitation directly->Med reconciliation - D4]]

<span class="ec-case-marker" hidden data-entry="Med reconciliation. Opening"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Structured medication reconciliation across transitions of care</div> Medication reconciliation is the systematic process of comparing a patient's current medication regimen against orders at every transition of care, admission, transfer, and discharge. When done properly, it catches omissions, duplications, and dose errors that are the leading modifiable cause of post-discharge adverse events in heart failure. Reconciliation should include a patient-facing medication review before discharge. <div class="ec-src"><b>Source:</b> AHRQ. Medication Reconciliation. Patient Safety Primer. Agency for Healthcare Research and Quality.</div></div> [[Start another case->Hub]] [[Restart this case->Med reconciliation - Opening]] [[Next case →->Surgical safety - Opening]]

<span class="ec-case-marker" hidden data-entry="Med reconciliation. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Extended hospitalization does not fix medication errors.</div> Longer stays increase cost and nosocomial risk without addressing the root cause, inaccurate medication lists at discharge. The identified problem is at the transition, not during hospitalization. <div class="ec-teach"><div class="th">What to do instead</div> Medication reconciliation is the systematic process of comparing a patient's current medication regimen against orders at every transition of care, admission, transfer, and discharge. When done properly, it catches omissions, duplications, and dose errors that are the leading modifiable cause of post-discharge adverse events in heart failure. Reconciliation should include a patient-facing medication review before discharge. <div class="ec-src"><b>Source:</b> AHRQ. Medication Reconciliation. Patient Safety Primer. Agency for Healthcare Research and Quality.</div></div></div> [[Try this question again->Med reconciliation - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Med reconciliation. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Education alone does not catch discrepancies.</div> Patient education is important but does not systematically identify missing or duplicated medications. Structured reconciliation by a pharmacist or provider compares the pre-admission regimen against discharge orders, which education alone cannot accomplish. <div class="ec-teach"><div class="th">What to do instead</div> Medication reconciliation is the systematic process of comparing a patient's current medication regimen against orders at every transition of care, admission, transfer, and discharge. When done properly, it catches omissions, duplications, and dose errors that are the leading modifiable cause of post-discharge adverse events in heart failure. Reconciliation should include a patient-facing medication review before discharge. <div class="ec-src"><b>Source:</b> AHRQ. Medication Reconciliation. Patient Safety Primer. Agency for Healthcare Research and Quality.</div></div></div> [[Try this question again->Med reconciliation - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Med reconciliation. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Same-day planning does not cause medication errors.</div> The timing of discharge planning is not the identified problem. The problem is that the medication list itself is inaccurate at the time of discharge. <div class="ec-teach"><div class="th">What to do instead</div> Medication reconciliation is the systematic process of comparing a patient's current medication regimen against orders at every transition of care, admission, transfer, and discharge. When done properly, it catches omissions, duplications, and dose errors that are the leading modifiable cause of post-discharge adverse events in heart failure. Reconciliation should include a patient-facing medication review before discharge. <div class="ec-src"><b>Source:</b> AHRQ. Medication Reconciliation. Patient Safety Primer. Agency for Healthcare Research and Quality.</div></div></div> [[Try this question again->Med reconciliation - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Med reconciliation. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Cardiac rehabilitation does not address medication discrepancies.</div> Cardiac rehabilitation improves exercise capacity and quality of life but does not systematically review or correct medication errors at discharge. <div class="ec-teach"><div class="th">What to do instead</div> Medication reconciliation is the systematic process of comparing a patient's current medication regimen against orders at every transition of care, admission, transfer, and discharge. When done properly, it catches omissions, duplications, and dose errors that are the leading modifiable cause of post-discharge adverse events in heart failure. Reconciliation should include a patient-facing medication review before discharge. <div class="ec-src"><b>Source:</b> AHRQ. Medication Reconciliation. Patient Safety Primer. Agency for Healthcare Research and Quality.</div></div></div> [[Try this question again->Med reconciliation - Opening]] [[Start another case->Hub]]

<div class="ec-scene">Primary care practice meeting · 08:00</div> A primary-care clinic has an adolescent human papillomavirus vaccination completion rate of 38%, well below the national target of 80%. A chart review of 200 eligible patients reveals that clinicians frequently do not check vaccination status during visits, and eligible patients leave without being offered the vaccine. The clinic has posted educational materials in waiting areas, but staff report they do not have time to manually check immunization records before each visit. <span class="ec-prompt">Which of the following is the most appropriate intervention to improve vaccination rates?</span> [[Annual educational newsletter to families about HPV vaccination->Vaccination QI - D1]] [[Extend clinic visit intervals to reduce workload->Vaccination QI - D4]] [[Point-of-care electronic reminders for due vaccines->Vaccination QI - Correct]] [[Reduce clinic visit frequency to lower exposure risk->Vaccination QI - D2]] [[Require families to track immunization records independently->Vaccination QI - D3]]

<span class="ec-case-marker" hidden data-entry="Vaccination QI. Opening"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Point-of-care electronic reminders for due vaccines</div> The CDC Community Preventive Services Task Force recommends client reminder/recall systems and provider reminder systems as evidence-based interventions to improve vaccination rates. Electronic alerts integrated into the EHR flag eligible patients at the point of care, directly addressing the identified failure, clinicians not checking status. Standing orders that allow nurses to administer vaccines without individual physician orders further reduce missed opportunities. <div class="ec-src"><b>Source:</b> Community Preventive Services Task Force. Vaccination Programs: Client Reminder and Recall Systems. www.thecommunityguide.org; CDC Immunization Strategies.</div></div> [[Start another case->Hub]] [[Restart this case->Vaccination QI - Opening]] [[Next case →->QI PDSA - Opening]]

<span class="ec-case-marker" hidden data-entry="Vaccination QI. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Education alone has limited impact on vaccination rates.</div> While educational materials raise awareness, passive educational interventions without systems-level changes have consistently shown modest impact on vaccination rates. The identified problem is that clinicians do not check status, education does not solve a workflow gap. <div class="ec-teach"><div class="th">What to do instead</div> The CDC Community Preventive Services Task Force recommends client reminder/recall systems and provider reminder systems as evidence-based interventions to improve vaccination rates. Electronic alerts integrated into the EHR flag eligible patients at the point of care, directly addressing the identified failure, clinicians not checking status. Standing orders that allow nurses to administer vaccines without individual physician orders further reduce missed opportunities. <div class="ec-src"><b>Source:</b> Community Preventive Services Task Force. Vaccination Programs: Client Reminder and Recall Systems. www.thecommunityguide.org; CDC Immunization Strategies.</div></div></div> [[Try this question again->Vaccination QI - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Vaccination QI. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Fewer visits means fewer vaccination opportunities.</div> Each clinic visit is a potential vaccination opportunity. Reducing visits reduces the chances to catch up on missing vaccines. <div class="ec-teach"><div class="th">What to do instead</div> The CDC Community Preventive Services Task Force recommends client reminder/recall systems and provider reminder systems as evidence-based interventions to improve vaccination rates. Electronic alerts integrated into the EHR flag eligible patients at the point of care, directly addressing the identified failure, clinicians not checking status. Standing orders that allow nurses to administer vaccines without individual physician orders further reduce missed opportunities. <div class="ec-src"><b>Source:</b> Community Preventive Services Task Force. Vaccination Programs: Client Reminder and Recall Systems. www.thecommunityguide.org; CDC Immunization Strategies.</div></div></div> [[Try this question again->Vaccination QI - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Vaccination QI. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Family-dependent tracking is unreliable.</div> Expecting families to independently track complex multi-dose vaccine schedules is less reliable than provider-initiated, system-integrated reminders. The audit showed the failure is at the provider level, not the family level. <div class="ec-teach"><div class="th">What to do instead</div> The CDC Community Preventive Services Task Force recommends client reminder/recall systems and provider reminder systems as evidence-based interventions to improve vaccination rates. Electronic alerts integrated into the EHR flag eligible patients at the point of care, directly addressing the identified failure, clinicians not checking status. Standing orders that allow nurses to administer vaccines without individual physician orders further reduce missed opportunities. <div class="ec-src"><b>Source:</b> Community Preventive Services Task Force. Vaccination Programs: Client Reminder and Recall Systems. www.thecommunityguide.org; CDC Immunization Strategies.</div></div></div> [[Try this question again->Vaccination QI - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Vaccination QI. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Fewer visits reduce vaccination opportunities.</div> Reducing visit frequency means fewer chances to identify and administer missing vaccines. Every clinical encounter is a potential vaccination opportunity. <div class="ec-teach"><div class="th">What to do instead</div> The CDC Community Preventive Services Task Force recommends client reminder/recall systems and provider reminder systems as evidence-based interventions to improve vaccination rates. Electronic alerts integrated into the EHR flag eligible patients at the point of care, directly addressing the identified failure, clinicians not checking status. Standing orders that allow nurses to administer vaccines without individual physician orders further reduce missed opportunities. <div class="ec-src"><b>Source:</b> Community Preventive Services Task Force. Vaccination Programs: Client Reminder and Recall Systems. www.thecommunityguide.org; CDC Immunization Strategies.</div></div></div> [[Try this question again->Vaccination QI - Opening]] [[Start another case->Hub]]

<div class="ec-scene">Surgical quality meeting · 13:00</div> A hospital's surgical-site infection rate for colorectal surgery is 8.2%, above the national benchmark of 4%. An audit of 60 cases identifies that prophylactic antibiotics are administered at inconsistent times, sometimes more than 90 minutes before incision, sometimes after incision, and occasionally missed entirely. <span class="ec-prompt">Which of the following is the most appropriate quality improvement intervention?</span> [[Continue prophylactic antibiotics for 7 days->SSI prevention - D2]] [[External surgical attending physician review of each case->SSI prevention - D3]] [[Standardized antibiotic timing with audit->SSI prevention - Correct]] [[Stop measuring surgical infection rates->SSI prevention - D4]] [[Withdraw all prophylactic antibiotics->SSI prevention - D1]]

<span class="ec-case-marker" hidden data-entry="SSI prevention. Opening"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Standardized antibiotic timing with audit</div> Prophylactic antibiotics should be administered within 60 minutes before surgical incision (120 minutes for vancomycin and fluoroquinolones). A standardized protocol with a checklist-driven administration time, combined with ongoing audit and real-time feedback to the surgical team, directly addresses inconsistent timing. This is the principle behind the Surgical Care Improvement Project (SCIP) measures and the WHO Surgical Safety Checklist. <div class="ec-src"><b>Source:</b> Berríos-Torres SI, et al. CDC Guideline for the Prevention of Surgical Site Infection, 2017. JAMA Surg 2017;152(8):784-791.</div></div> [[Start another case->Hub]] [[Restart this case->SSI prevention - Opening]] [[Next case →->Hand hygiene - Opening]]

<span class="ec-case-marker" hidden data-entry="SSI prevention. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Stopping prophylaxis increases infections.</div> Perioperative antibiotic prophylaxis is one of the most evidence-based interventions in surgery. Eliminating it would dramatically increase SSI rates. <div class="ec-teach"><div class="th">What to do instead</div> Prophylactic antibiotics should be administered within 60 minutes before surgical incision (120 minutes for vancomycin and fluoroquinolones). A standardized protocol with a checklist-driven administration time, combined with ongoing audit and real-time feedback to the surgical team, directly addresses inconsistent timing. This is the principle behind the Surgical Care Improvement Project (SCIP) measures and the WHO Surgical Safety Checklist. <div class="ec-src"><b>Source:</b> Berríos-Torres SI, et al. CDC Guideline for the Prevention of Surgical Site Infection, 2017. JAMA Surg 2017;152(8):784-791.</div></div></div> [[Try this question again->SSI prevention - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="SSI prevention. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Extends exposure without correcting the underlying process.</div> Extending prophylaxis to a full 7-day course does not correct the identified failure, inconsistent perioperative dosing, and provides no additional protection against surgical-site infection beyond the standard single perioperative dose (given within 60 minutes of incision and discontinued within 24 hours of surgery). Prolonging antibiotic exposure instead increases the risk of Clostridioides difficile infection and antimicrobial resistance without lowering the SSI rate. <div class="ec-teach"><div class="th">What to do instead</div> Prophylactic antibiotics should be administered within 60 minutes before surgical incision (120 minutes for vancomycin and fluoroquinolones). A standardized protocol with a checklist-driven administration time, combined with ongoing audit and real-time feedback to the surgical team, directly addresses inconsistent timing. This is the principle behind the Surgical Care Improvement Project (SCIP) measures and the WHO Surgical Safety Checklist. <div class="ec-src"><b>Source:</b> Berríos-Torres SI, et al. CDC Guideline for the Prevention of Surgical Site Infection, 2017. JAMA Surg 2017;152(8):784-791.</div></div></div> [[Try this question again->SSI prevention - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="SSI prevention. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Routine external attending physician review of every case is resource-intensive and does not address the identified root cause, inconsistent antibiotic timing. A standardized protocol directly targets the process failure. <div class="ec-teach"><div class="th">What to do instead</div> Prophylactic antibiotics should be administered within 60 minutes before surgical incision (120 minutes for vancomycin and fluoroquinolones). A standardized protocol with a checklist-driven administration time, combined with ongoing audit and real-time feedback to the surgical team, directly addresses inconsistent timing. This is the principle behind the Surgical Care Improvement Project (SCIP) measures and the WHO Surgical Safety Checklist. <div class="ec-src"><b>Source:</b> Berríos-Torres SI, et al. CDC Guideline for the Prevention of Surgical Site Infection, 2017. JAMA Surg 2017;152(8):784-791.</div></div></div> [[Try this question again->SSI prevention - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="SSI prevention. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Stopping measurement prevents improvement.</div> One cannot improve what one does not measure. Surveillance is essential for identifying problems and evaluating interventions. <div class="ec-teach"><div class="th">What to do instead</div> Prophylactic antibiotics should be administered within 60 minutes before surgical incision (120 minutes for vancomycin and fluoroquinolones). A standardized protocol with a checklist-driven administration time, combined with ongoing audit and real-time feedback to the surgical team, directly addresses inconsistent timing. This is the principle behind the Surgical Care Improvement Project (SCIP) measures and the WHO Surgical Safety Checklist. <div class="ec-src"><b>Source:</b> Berríos-Torres SI, et al. CDC Guideline for the Prevention of Surgical Site Infection, 2017. JAMA Surg 2017;152(8):784-791.</div></div></div> [[Try this question again->SSI prevention - Opening]] [[Start another case->Hub]]

<div class="ec-scene">Morbidity and mortality conference · 07:30</div> A 62-year-old physician has had three cases in the past year in which pulmonary embolism was initially missed. In each case, she anchored on the patient's known anxiety disorder, attributing dyspnea and tachycardia to panic attacks without adequately considering alternative diagnoses. Two patients experienced delayed treatment, and one required ICU admission. <span class="ec-prompt">Which of the following interventions best targets the cognitive mechanism producing these errors?</span> [[A diagnostic time-out requiring alternative diagnoses->Diagnostic error - Correct]] [[Assign a dedicated diagnostic specialist to review all emergency department cases->Diagnostic error - D3]] [[Increase clinical experience requirements before independent practice->Diagnostic error - D4]] [[Order every available laboratory test on every dyspneic patient->Diagnostic error - D1]] [[Require CT pulmonary angiography for every patient with dyspnea->Diagnostic error - D2]]

<span class="ec-case-marker" hidden data-entry="Diagnostic error. Opening"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ A diagnostic time-out requiring alternative diagnoses</div> Anchoring bias occurs when the clinician locks onto an initial diagnosis (anxiety) and fails to adequately consider alternatives. A diagnostic time-out, a deliberate pause requiring the clinician to ask "what else could this be?" and explicitly consider at least two alternative diagnoses, directly interrupts this cognitive shortcut. This is a form of cognitive debiasing recommended by the AHRQ and the National Academies' Improving Diagnosis in Health Care report. <div class="ec-src"><b>Source:</b> National Academies of Sciences, Engineering, and Medicine. Improving Diagnosis in Health Care. Washington, DC: The National Academies Press; 2015; AHRQ PSNet Diagnostic Errors.</div></div> [[Start another case->Hub]] [[Restart this case->Diagnostic error - Opening]] [[Next case →->Med reconciliation - Opening]]

<span class="ec-case-marker" hidden data-entry="Diagnostic error. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Overtesting is not the solution.</div> Ordering every test is expensive, produces false positives, and does not address the underlying cognitive error. The physician needs to think differently, not test indiscriminately. <div class="ec-teach"><div class="th">What to do instead</div> Anchoring bias occurs when the clinician locks onto an initial diagnosis (anxiety) and fails to adequately consider alternatives. A diagnostic time-out, a deliberate pause requiring the clinician to ask "what else could this be?" and explicitly consider at least two alternative diagnoses, directly interrupts this cognitive shortcut. This is a form of cognitive debiasing recommended by the AHRQ and the National Academies' Improving Diagnosis in Health Care report. <div class="ec-src"><b>Source:</b> National Academies of Sciences, Engineering, and Medicine. Improving Diagnosis in Health Care. Washington, DC: The National Academies Press; 2015; AHRQ PSNet Diagnostic Errors.</div></div></div> [[Try this question again->Diagnostic error - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Diagnostic error. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Universal CTPA for dyspnea is not feasible.</div> Ordering CT pulmonary angiography on every dyspneic patient would expose many patients to unnecessary radiation, contrast, and incidental findings. The problem is cognitive, not technological, the physician needs to broaden the differential, not scan indiscriminately. <div class="ec-teach"><div class="th">What to do instead</div> Anchoring bias occurs when the clinician locks onto an initial diagnosis (anxiety) and fails to adequately consider alternatives. A diagnostic time-out, a deliberate pause requiring the clinician to ask "what else could this be?" and explicitly consider at least two alternative diagnoses, directly interrupts this cognitive shortcut. This is a form of cognitive debiasing recommended by the AHRQ and the National Academies' Improving Diagnosis in Health Care report. <div class="ec-src"><b>Source:</b> National Academies of Sciences, Engineering, and Medicine. Improving Diagnosis in Health Care. Washington, DC: The National Academies Press; 2015; AHRQ PSNet Diagnostic Errors.</div></div></div> [[Try this question again->Diagnostic error - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Diagnostic error. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Specialist review is not scalable.</div> A dedicated diagnostic specialist cannot review every case in a busy ED. The solution must be embedded in the clinician's own reasoning process through structured cognitive debiasing techniques. <div class="ec-teach"><div class="th">What to do instead</div> Anchoring bias occurs when the clinician locks onto an initial diagnosis (anxiety) and fails to adequately consider alternatives. A diagnostic time-out, a deliberate pause requiring the clinician to ask "what else could this be?" and explicitly consider at least two alternative diagnoses, directly interrupts this cognitive shortcut. This is a form of cognitive debiasing recommended by the AHRQ and the National Academies' Improving Diagnosis in Health Care report. <div class="ec-src"><b>Source:</b> National Academies of Sciences, Engineering, and Medicine. Improving Diagnosis in Health Care. Washington, DC: The National Academies Press; 2015; AHRQ PSNet Diagnostic Errors.</div></div></div> [[Try this question again->Diagnostic error - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Diagnostic error. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Experience alone does not prevent anchoring.</div> Anchoring bias affects experienced clinicians as well as novices, in fact, experienced clinicians may anchor more strongly on pattern recognition. The intervention must target the cognitive process, not the experience level. <div class="ec-teach"><div class="th">What to do instead</div> Anchoring bias occurs when the clinician locks onto an initial diagnosis (anxiety) and fails to adequately consider alternatives. A diagnostic time-out, a deliberate pause requiring the clinician to ask "what else could this be?" and explicitly consider at least two alternative diagnoses, directly interrupts this cognitive shortcut. This is a form of cognitive debiasing recommended by the AHRQ and the National Academies' Improving Diagnosis in Health Care report. <div class="ec-src"><b>Source:</b> National Academies of Sciences, Engineering, and Medicine. Improving Diagnosis in Health Care. Washington, DC: The National Academies Press; 2015; AHRQ PSNet Diagnostic Errors.</div></div></div> [[Try this question again->Diagnostic error - Opening]] [[Start another case->Hub]]

<div class="ec-scene">Infection control meeting · 09:00</div> A hospital's hand-hygiene compliance rate is 42% despite annual educational lectures and poster campaigns. Healthcare-associated infection rates remain elevated above the national benchmark. Direct observation audits reveal that compliance is lowest during high-acuity periods and between patients in shared rooms. <span class="ec-prompt">Which of the following is the most appropriate improvement strategy?</span> [[Annual educational lecture without direct observation or feedback->Hand hygiene - D2]] [[Discontinue compliance monitoring and reporting->Hand hygiene - D4]] [[Monthly hand-hygiene compliance reports without point-of-care access->Hand hygiene - D3]] [[Remove alcohol-based hand rub dispensers from clinical areas->Hand hygiene - D1]] [[System change, real-time monitoring, feedback, reminders, and safety culture->Hand hygiene - Correct]]

<span class="ec-case-marker" hidden data-entry="Hand hygiene. Opening"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ System change, real-time monitoring, feedback, reminders, and safety culture</div> The WHO "5 Moments for Hand Hygiene" multimodal strategy has five components: (1) system change (accessible alcohol-based hand rub at point of care), (2) training and education, (3) observation and feedback, (4) workplace reminders, and (5) institutional safety climate. Education alone has consistently failed to produce sustained improvement. The most effective programs make hand hygiene easy, visible, measured, and culturally expected. <div class="ec-src"><b>Source:</b> World Health Organization. WHO Guidelines on Hand Hygiene in Health Care. Geneva: WHO; 2009.</div></div> [[Start another case->Hub]] [[Restart this case->Hand hygiene - Opening]] [[Next case →->Vaccination QI - Opening]]

<span class="ec-case-marker" hidden data-entry="Hand hygiene. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Removing hand rub makes compliance impossible.</div> Point-of-care alcohol-based hand rub is the foundation of hand-hygiene improvement. Removing it eliminates the most convenient and effective system for hand decontamination. <div class="ec-teach"><div class="th">What to do instead</div> The WHO "5 Moments for Hand Hygiene" multimodal strategy has five components: (1) system change (accessible alcohol-based hand rub at point of care), (2) training and education, (3) observation and feedback, (4) workplace reminders, and (5) institutional safety climate. Education alone has consistently failed to produce sustained improvement. The most effective programs make hand hygiene easy, visible, measured, and culturally expected. <div class="ec-src"><b>Source:</b> World Health Organization. WHO Guidelines on Hand Hygiene in Health Care. Geneva: WHO; 2009.</div></div></div> [[Try this question again->Hand hygiene - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Hand hygiene. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Annual lectures alone do not change bedside behavior.</div> A once-yearly didactic lecture, without direct observation or individualized feedback, is exactly the intervention this hospital already has in place, and compliance is stuck at 42% despite it. Passive education is only one of the WHO's five multimodal components; without observation, real-time feedback, reminders, system change, and a safety culture behind it, lecture-based training does not produce durable improvement in hand-hygiene compliance. <div class="ec-teach"><div class="th">What to do instead</div> The WHO "5 Moments for Hand Hygiene" multimodal strategy has five components: (1) system change (accessible alcohol-based hand rub at point of care), (2) training and education, (3) observation and feedback, (4) workplace reminders, and (5) institutional safety climate. Education alone has consistently failed to produce sustained improvement. The most effective programs make hand hygiene easy, visible, measured, and culturally expected. <div class="ec-src"><b>Source:</b> World Health Organization. WHO Guidelines on Hand Hygiene in Health Care. Geneva: WHO; 2009.</div></div></div> [[Try this question again->Hand hygiene - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Hand hygiene. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Reports alone do not change behavior at the bedside.</div> Monthly aggregate reports are too delayed and impersonal to drive real-time behavior change. Effective programs use direct observation with immediate individual feedback, not periodic summary statistics alone. <div class="ec-teach"><div class="th">What to do instead</div> The WHO "5 Moments for Hand Hygiene" multimodal strategy has five components: (1) system change (accessible alcohol-based hand rub at point of care), (2) training and education, (3) observation and feedback, (4) workplace reminders, and (5) institutional safety climate. Education alone has consistently failed to produce sustained improvement. The most effective programs make hand hygiene easy, visible, measured, and culturally expected. <div class="ec-src"><b>Source:</b> World Health Organization. WHO Guidelines on Hand Hygiene in Health Care. Geneva: WHO; 2009.</div></div></div> [[Try this question again->Hand hygiene - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Hand hygiene. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Measurement drives improvement.</div> One cannot improve compliance one does not measure. Real-time monitoring with feedback is a core component of effective programs. <div class="ec-teach"><div class="th">What to do instead</div> The WHO "5 Moments for Hand Hygiene" multimodal strategy has five components: (1) system change (accessible alcohol-based hand rub at point of care), (2) training and education, (3) observation and feedback, (4) workplace reminders, and (5) institutional safety climate. Education alone has consistently failed to produce sustained improvement. The most effective programs make hand hygiene easy, visible, measured, and culturally expected. <div class="ec-src"><b>Source:</b> World Health Organization. WHO Guidelines on Hand Hygiene in Health Care. Geneva: WHO; 2009.</div></div></div> [[Try this question again->Hand hygiene - Opening]] [[Start another case->Hub]]

<div class="ec-scene">Inpatient psychiatry · 10:00</div> A 24-year-old man hospitalized for a severe depressive episode with suicidal ideation has improved on medication and therapy. Discharge is planned for tomorrow. He lives alone and has limited social support. Research shows the first 30 days after psychiatric discharge carry the highest suicide risk. <span class="ec-prompt">Which of the following is the most appropriate intervention to reduce post-discharge risk?</span> [[Discharge with crisis hotline information and a safety leaflet->Psych transition - D3]] [[Follow-up within 7 days with a safety plan->Psych transition - Correct]] [[Schedule outpatient follow-up within 30 days without interim contact->Psych transition - D2]] [[Taper and discontinue medications over the first post-discharge week->Psych transition - D1]] [[Tell the patient to return only if symptoms become severe->Psych transition - D4]]

<span class="ec-case-marker" hidden data-entry="Psych transition. Opening"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Follow-up within 7 days with a safety plan</div> The post-discharge period is the highest-risk window for completed suicide. Evidence-based transition interventions include scheduling outpatient follow-up within 7 days (a HEDIS quality measure), completing a structured safety plan (not a "no-suicide contract"), ensuring medication continuity, confirming means restriction (especially firearms), and making a caring contact (phone call or message) within 48–72 hours of discharge. Each element independently reduces risk. <div class="ec-src"><b>Source:</b> Chung DT, et al. Suicide Rates After Discharge From Psychiatric Facilities: A Systematic Review and Meta-analysis. JAMA Psychiatry 2017;74(7):694-702; HEDIS Follow-Up After Hospitalization for Mental Illness Measure.</div></div> [[Start another case->Hub]] [[Restart this case->Psych transition - Opening]] [[Next case →->Panic disorder - Dx]]

<span class="ec-case-marker" hidden data-entry="Psych transition. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Tapering medications immediately post-discharge destabilizes recovery.</div> The first week after psychiatric discharge is the highest-risk period. Abrupt changes to a regimen that produced improvement risk relapse and worsening suicidality. Medication changes should be made by the outpatient provider, not automatically at discharge. <div class="ec-teach"><div class="th">What to do instead</div> The post-discharge period is the highest-risk window for completed suicide. Evidence-based transition interventions include scheduling outpatient follow-up within 7 days (a HEDIS quality measure), completing a structured safety plan (not a "no-suicide contract"), ensuring medication continuity, confirming means restriction (especially firearms), and making a caring contact (phone call or message) within 48–72 hours of discharge. Each element independently reduces risk. <div class="ec-src"><b>Source:</b> Chung DT, et al. Suicide Rates After Discharge From Psychiatric Facilities: A Systematic Review and Meta-analysis. JAMA Psychiatry 2017;74(7):694-702; HEDIS Follow-Up After Hospitalization for Mental Illness Measure.</div></div></div> [[Try this question again->Psych transition - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Psych transition. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Thirty-day follow-up is too late.</div> The highest suicide risk is in the first 7–14 days after discharge. HEDIS quality measures require follow-up within 7 days of psychiatric hospitalization. A 30-day window misses the critical transition period. <div class="ec-teach"><div class="th">What to do instead</div> The post-discharge period is the highest-risk window for completed suicide. Evidence-based transition interventions include scheduling outpatient follow-up within 7 days (a HEDIS quality measure), completing a structured safety plan (not a "no-suicide contract"), ensuring medication continuity, confirming means restriction (especially firearms), and making a caring contact (phone call or message) within 48–72 hours of discharge. Each element independently reduces risk. <div class="ec-src"><b>Source:</b> Chung DT, et al. Suicide Rates After Discharge From Psychiatric Facilities: A Systematic Review and Meta-analysis. JAMA Psychiatry 2017;74(7):694-702; HEDIS Follow-Up After Hospitalization for Mental Illness Measure.</div></div></div> [[Try this question again->Psych transition - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Psych transition. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Hotline information alone is passive.</div> Providing a crisis hotline number without scheduled follow-up, a safety plan, or active outreach places the entire burden on the patient during their most vulnerable period. Active system-initiated contact is needed. <div class="ec-teach"><div class="th">What to do instead</div> The post-discharge period is the highest-risk window for completed suicide. Evidence-based transition interventions include scheduling outpatient follow-up within 7 days (a HEDIS quality measure), completing a structured safety plan (not a "no-suicide contract"), ensuring medication continuity, confirming means restriction (especially firearms), and making a caring contact (phone call or message) within 48–72 hours of discharge. Each element independently reduces risk. <div class="ec-src"><b>Source:</b> Chung DT, et al. Suicide Rates After Discharge From Psychiatric Facilities: A Systematic Review and Meta-analysis. JAMA Psychiatry 2017;74(7):694-702; HEDIS Follow-Up After Hospitalization for Mental Illness Measure.</div></div></div> [[Try this question again->Psych transition - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Psych transition. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ This places the entire burden on the patient.</div> Patients in crisis may not accurately assess their own severity. The system must initiate follow-up rather than relying on patient self-referral during a vulnerable period. <div class="ec-teach"><div class="th">What to do instead</div> The post-discharge period is the highest-risk window for completed suicide. Evidence-based transition interventions include scheduling outpatient follow-up within 7 days (a HEDIS quality measure), completing a structured safety plan (not a "no-suicide contract"), ensuring medication continuity, confirming means restriction (especially firearms), and making a caring contact (phone call or message) within 48–72 hours of discharge. Each element independently reduces risk. <div class="ec-src"><b>Source:</b> Chung DT, et al. Suicide Rates After Discharge From Psychiatric Facilities: A Systematic Review and Meta-analysis. JAMA Psychiatry 2017;74(7):694-702; HEDIS Follow-Up After Hospitalization for Mental Illness Measure.</div></div></div> [[Try this question again->Psych transition - Opening]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 16:27</div> A 65-year-old man with metastatic prostate cancer develops progressive bilateral lower extremity weakness over 48 hours with a sensory level at T8 and new urinary retention. Temperature is 37.0°C (98.6°F), blood pressure is 142/86 mm Hg, and pulse is 88/min. MRI of the spine shows an epidural mass compressing the thoracic spinal cord at T7-T9. <span class="ec-prompt">Which of the following is the most appropriate initial treatment?</span> [[Intravenous dexamethasone and urgent radiation oncology consult->Cord compression - Correct]] [[Lumbar puncture for cerebrospinal fluid cytology before treatment->Cord compression - D3]] [[Oral ibuprofen 400 mg three times daily->Cord compression - D2]] [[Outpatient physical therapy referral->Cord compression - D4]] [[Repeat MRI with contrast in 4 weeks->Cord compression - D1]]

<span class="ec-case-marker" hidden data-entry="Cord compression. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Intravenous dexamethasone and urgent radiation oncology consult</div> Malignant spinal cord compression is an oncologic emergency. IV dexamethasone reduces cord edema and preserves neurologic function while definitive treatment, radiation therapy, surgical decompression, or both, is organized. Ambulatory status at the time of treatment initiation is the strongest predictor of functional outcome. Delay of even hours can result in permanent paraplegia. <div class="ec-src"><b>Source:</b> Loblaw DA, et al. Systematic Review of the Diagnosis and Management of Malignant Extradural Spinal Cord Compression. J Clin Oncol 2005;23(9):2028-2037.</div></div> [[Start another case->Hub]] [[Restart this case->Cord compression - Rx]] [[Next case →->Breast cancer prognosis - Dx]]

<span class="ec-case-marker" hidden data-entry="Cord compression. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ One-month delay risks permanent paralysis.</div> Spinal cord compression progresses rapidly. Delay allows irreversible damage to the cord, converting recoverable weakness to permanent paraplegia. <div class="ec-teach"><div class="th">What to do instead</div> Malignant spinal cord compression is an oncologic emergency. IV dexamethasone reduces cord edema and preserves neurologic function while definitive treatment, radiation therapy, surgical decompression, or both, is organized. Ambulatory status at the time of treatment initiation is the strongest predictor of functional outcome. Delay of even hours can result in permanent paraplegia. <div class="ec-src"><b>Source:</b> Loblaw DA, et al. Systematic Review of the Diagnosis and Management of Malignant Extradural Spinal Cord Compression. J Clin Oncol 2005;23(9):2028-2037.</div></div></div> [[Try this question again->Cord compression - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Cord compression. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ NSAIDs do not address the cord compression.</div> NSAIDs may provide analgesia but do not reduce the epidural mass or cord edema. High-dose corticosteroids are needed. <div class="ec-teach"><div class="th">What to do instead</div> Malignant spinal cord compression is an oncologic emergency. IV dexamethasone reduces cord edema and preserves neurologic function while definitive treatment, radiation therapy, surgical decompression, or both, is organized. Ambulatory status at the time of treatment initiation is the strongest predictor of functional outcome. Delay of even hours can result in permanent paraplegia. <div class="ec-src"><b>Source:</b> Loblaw DA, et al. Systematic Review of the Diagnosis and Management of Malignant Extradural Spinal Cord Compression. J Clin Oncol 2005;23(9):2028-2037.</div></div></div> [[Try this question again->Cord compression - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Cord compression. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Lumbar puncture is contraindicated.</div> With a compressive epidural mass, lumbar puncture risks neurologic deterioration from pressure changes. MRI has already identified the lesion. <div class="ec-teach"><div class="th">What to do instead</div> Malignant spinal cord compression is an oncologic emergency. IV dexamethasone reduces cord edema and preserves neurologic function while definitive treatment, radiation therapy, surgical decompression, or both, is organized. Ambulatory status at the time of treatment initiation is the strongest predictor of functional outcome. Delay of even hours can result in permanent paraplegia. <div class="ec-src"><b>Source:</b> Loblaw DA, et al. Systematic Review of the Diagnosis and Management of Malignant Extradural Spinal Cord Compression. J Clin Oncol 2005;23(9):2028-2037.</div></div></div> [[Try this question again->Cord compression - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Cord compression. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Physical therapy alone does not treat the compression.</div> Rehabilitation is important during recovery, but without urgent treatment of the compression, the neurologic deficit will progress to irreversibility. <div class="ec-teach"><div class="th">What to do instead</div> Malignant spinal cord compression is an oncologic emergency. IV dexamethasone reduces cord edema and preserves neurologic function while definitive treatment, radiation therapy, surgical decompression, or both, is organized. Ambulatory status at the time of treatment initiation is the strongest predictor of functional outcome. Delay of even hours can result in permanent paraplegia. <div class="ec-src"><b>Source:</b> Loblaw DA, et al. Systematic Review of the Diagnosis and Management of Malignant Extradural Spinal Cord Compression. J Clin Oncol 2005;23(9):2028-2037.</div></div></div> [[Try this question again->Cord compression - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Cardiology clinic · 11:30</div> A 76-year-old man has had exertional syncope and progressive dyspnea on exertion for 3 months. Echocardiography shows a heavily calcified aortic valve with a mean gradient of 48 mm Hg, valve area of 0.7 cm2, and preserved LVEF. He has no other significant comorbidities. <span class="ec-prompt">Which of the following is the most appropriate management?</span> [[Cardiac catheterization for stent placement->Aortic stenosis - D3]] [[Lifelong beta-blocker monotherapy->Aortic stenosis - D4]] [[Referral for aortic valve replacement->Aortic stenosis - Correct]] [[Start vasodilator therapy with hydralazine->Aortic stenosis - D2]] [[Watchful waiting with annual echocardiography->Aortic stenosis - D1]]

<span class="ec-case-marker" hidden data-entry="Aortic stenosis. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Referral for aortic valve replacement.</div> Symptomatic severe aortic stenosis (valve area <1.0 cm2 with syncope, heart failure, or angina) has a dismal natural history, average survival is 2–3 years without intervention. Aortic valve replacement (surgical AVR or transcatheter TAVR) is the only treatment that alters the disease course. No medical therapy substitutes for mechanical relief of the obstruction. This patient with syncope and a valve area of 0.7 cm2 has a class I indication. <div class="ec-src"><b>Source:</b> Otto CM, et al. 2020 ACC/AHA Guideline for the Management of Patients With Valvular Heart Disease. Circulation 2021;143(5):e72-e227.</div></div> [[Start another case->Hub]] [[Restart this case->Aortic stenosis - Rx]] [[Next case →->HCM - Rx]]

<span class="ec-case-marker" hidden data-entry="Aortic stenosis. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Watchful waiting is for asymptomatic patients.</div> Once symptoms develop in severe aortic stenosis, survival drops precipitously. Continued observation risks sudden cardiac death or progressive heart failure. <div class="ec-teach"><div class="th">What to do instead</div> Symptomatic severe aortic stenosis (valve area <1.0 cm2 with syncope, heart failure, or angina) has a dismal natural history, average survival is 2–3 years without intervention. Aortic valve replacement (surgical AVR or transcatheter TAVR) is the only treatment that alters the disease course. No medical therapy substitutes for mechanical relief of the obstruction. This patient with syncope and a valve area of 0.7 cm2 has a class I indication. <div class="ec-src"><b>Source:</b> Otto CM, et al. 2020 ACC/AHA Guideline for the Management of Patients With Valvular Heart Disease. Circulation 2021;143(5):e72-e227.</div></div></div> [[Try this question again->Aortic stenosis - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Aortic stenosis. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Vasodilators are dangerous in severe AS.</div> Vasodilators can cause catastrophic hypotension in the setting of a fixed obstruction. The stenotic valve cannot increase output to compensate for reduced afterload. <div class="ec-teach"><div class="th">What to do instead</div> Symptomatic severe aortic stenosis (valve area <1.0 cm2 with syncope, heart failure, or angina) has a dismal natural history, average survival is 2–3 years without intervention. Aortic valve replacement (surgical AVR or transcatheter TAVR) is the only treatment that alters the disease course. No medical therapy substitutes for mechanical relief of the obstruction. This patient with syncope and a valve area of 0.7 cm2 has a class I indication. <div class="ec-src"><b>Source:</b> Otto CM, et al. 2020 ACC/AHA Guideline for the Management of Patients With Valvular Heart Disease. Circulation 2021;143(5):e72-e227.</div></div></div> [[Try this question again->Aortic stenosis - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Aortic stenosis. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Coronary stenting does not treat aortic stenosis.</div> The obstruction is at the valve, not in the coronary arteries. While coronary artery disease should be assessed before valve surgery, stenting does not address the valvular pathology. <div class="ec-teach"><div class="th">What to do instead</div> Symptomatic severe aortic stenosis (valve area <1.0 cm2 with syncope, heart failure, or angina) has a dismal natural history, average survival is 2–3 years without intervention. Aortic valve replacement (surgical AVR or transcatheter TAVR) is the only treatment that alters the disease course. No medical therapy substitutes for mechanical relief of the obstruction. This patient with syncope and a valve area of 0.7 cm2 has a class I indication. <div class="ec-src"><b>Source:</b> Otto CM, et al. 2020 ACC/AHA Guideline for the Management of Patients With Valvular Heart Disease. Circulation 2021;143(5):e72-e227.</div></div></div> [[Try this question again->Aortic stenosis - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Aortic stenosis. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Beta-blockers do not replace valve intervention.</div> No medical therapy improves survival in symptomatic severe aortic stenosis. Beta-blockers may be used cautiously for rate control but do not address the underlying mechanical obstruction. <div class="ec-teach"><div class="th">What to do instead</div> Symptomatic severe aortic stenosis (valve area <1.0 cm2 with syncope, heart failure, or angina) has a dismal natural history, average survival is 2–3 years without intervention. Aortic valve replacement (surgical AVR or transcatheter TAVR) is the only treatment that alters the disease course. No medical therapy substitutes for mechanical relief of the obstruction. This patient with syncope and a valve area of 0.7 cm2 has a class I indication. <div class="ec-src"><b>Source:</b> Otto CM, et al. 2020 ACC/AHA Guideline for the Management of Patients With Valvular Heart Disease. Circulation 2021;143(5):e72-e227.</div></div></div> [[Try this question again->Aortic stenosis - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Wound care clinic · 14:00</div> A 62-year-old man with poorly controlled type 2 diabetes has had a neuropathic ulcer on the plantar surface of his right foot for 4 months. It has been present for 6 weeks and is not improving with home wound care. There are no signs of osteomyelitis or systemic infection. Ankle-brachial index is 0.9. <span class="ec-prompt">Which of the following is the most appropriate treatment to promote healing?</span> [[Hyperbaric oxygen therapy as the primary intervention->Diabetic foot - D1]] [[Immediate below-knee amputation of the affected limb->Diabetic foot - D2]] [[Offloading with a total contact cast or equivalent device->Diabetic foot - Correct]] [[Oral prednisone 40 mg daily for 6 weeks->Diabetic foot - D3]] [[Tight elastic compression stockings on both legs->Diabetic foot - D4]]

<span class="ec-case-marker" hidden data-entry="Diabetic foot. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Offloading with a total contact cast or equivalent device</div> Repetitive mechanical pressure on the insensate neuropathic foot is the primary obstacle to healing. Total contact casting or irremovable offloading devices redistribute plantar pressure and are the evidence-based standard for healing neuropathic plantar ulcers. Additional pillars include glycemic optimization, appropriate wound care, infection management when present, and vascular assessment. Without offloading, wound care alone is insufficient. <div class="ec-src"><b>Source:</b> Bus SA, et al. IWGDF Guidelines on Offloading Foot Ulcers. Diabetes Metab Res Rev 2020;36 Suppl 1:e3274; ADA Standards of Care 2026.</div></div> [[Start another case->Hub]] [[Restart this case->Diabetic foot - Rx]] [[Next case →->Diabetic retinopathy - Opening]]

<span class="ec-case-marker" hidden data-entry="Diabetic foot. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Hyperbaric oxygen is adjunctive, not primary.</div> Hyperbaric oxygen may be considered for refractory wounds, but the evidence does not support it as primary therapy. Offloading is the cornerstone. <div class="ec-teach"><div class="th">What to do instead</div> Repetitive mechanical pressure on the insensate neuropathic foot is the primary obstacle to healing. Total contact casting or irremovable offloading devices redistribute plantar pressure and are the evidence-based standard for healing neuropathic plantar ulcers. Additional pillars include glycemic optimization, appropriate wound care, infection management when present, and vascular assessment. Without offloading, wound care alone is insufficient. <div class="ec-src"><b>Source:</b> Bus SA, et al. IWGDF Guidelines on Offloading Foot Ulcers. Diabetes Metab Res Rev 2020;36 Suppl 1:e3274; ADA Standards of Care 2026.</div></div></div> [[Try this question again->Diabetic foot - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Diabetic foot. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Amputation is not indicated.</div> This is a non-infected neuropathic ulcer with adequate perfusion. Amputation is reserved for limb-threatening infection, gangrene, or non-reconstructable vascular disease. <div class="ec-teach"><div class="th">What to do instead</div> Repetitive mechanical pressure on the insensate neuropathic foot is the primary obstacle to healing. Total contact casting or irremovable offloading devices redistribute plantar pressure and are the evidence-based standard for healing neuropathic plantar ulcers. Additional pillars include glycemic optimization, appropriate wound care, infection management when present, and vascular assessment. Without offloading, wound care alone is insufficient. <div class="ec-src"><b>Source:</b> Bus SA, et al. IWGDF Guidelines on Offloading Foot Ulcers. Diabetes Metab Res Rev 2020;36 Suppl 1:e3274; ADA Standards of Care 2026.</div></div></div> [[Try this question again->Diabetic foot - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Diabetic foot. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Corticosteroids impair wound healing.</div> Systemic corticosteroids worsen hyperglycemia, impair the immune response, and inhibit wound healing. <div class="ec-teach"><div class="th">What to do instead</div> Repetitive mechanical pressure on the insensate neuropathic foot is the primary obstacle to healing. Total contact casting or irremovable offloading devices redistribute plantar pressure and are the evidence-based standard for healing neuropathic plantar ulcers. Additional pillars include glycemic optimization, appropriate wound care, infection management when present, and vascular assessment. Without offloading, wound care alone is insufficient. <div class="ec-src"><b>Source:</b> Bus SA, et al. IWGDF Guidelines on Offloading Foot Ulcers. Diabetes Metab Res Rev 2020;36 Suppl 1:e3274; ADA Standards of Care 2026.</div></div></div> [[Try this question again->Diabetic foot - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Diabetic foot. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Compression stockings worsen neuropathic ulcers.</div> Compression therapy is used for venous ulcers, not neuropathic plantar ulcers. It does not address the mechanical pressure problem and could impair arterial flow. <div class="ec-teach"><div class="th">What to do instead</div> Repetitive mechanical pressure on the insensate neuropathic foot is the primary obstacle to healing. Total contact casting or irremovable offloading devices redistribute plantar pressure and are the evidence-based standard for healing neuropathic plantar ulcers. Additional pillars include glycemic optimization, appropriate wound care, infection management when present, and vascular assessment. Without offloading, wound care alone is insufficient. <div class="ec-src"><b>Source:</b> Bus SA, et al. IWGDF Guidelines on Offloading Foot Ulcers. Diabetes Metab Res Rev 2020;36 Suppl 1:e3274; ADA Standards of Care 2026.</div></div></div> [[Try this question again->Diabetic foot - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Labor and delivery unit · 20:00</div> A 31-year-old woman at 37 weeks' gestation presents with blood pressure 168/112 mm Hg confirmed on two readings 15 minutes apart, a severe headache unresponsive to acetaminophen, visual disturbances, and epigastric pain. Platelet count is 92,000/mm3, AST is 188 U/L, and creatinine is 1.2 mg/dL. Fetal heart tracing is category I. <span class="ec-prompt">Which of the following is the most appropriate management?</span> [[Discharge home with oral antihypertensives and weekly follow-up->Severe preeclampsia - D1]] [[Expectant management with close monitoring until 40 weeks->Severe preeclampsia - D2]] [[Immediate high-dose aspirin for platelet aggregation inhibition->Severe preeclampsia - D3]] [[Magnesium sulfate, acute blood pressure management, and delivery->Severe preeclampsia - Correct]] [[Strict bed rest alone without antihypertensive medication->Severe preeclampsia - D4]]

<span class="ec-case-marker" hidden data-entry="Severe preeclampsia. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Magnesium sulfate, acute blood pressure management, and delivery</div> Preeclampsia with severe features at ≥37 weeks is an indication for delivery after maternal stabilization. Magnesium sulfate is administered for seizure prophylaxis (the Magpie Trial demonstrated a 58% reduction in eclampsia). Acute severe hypertension (≥160/110) requires IV labetalol, IV hydralazine, or oral immediate-release nifedipine. The definitive treatment is delivery of the placenta; at 37 weeks, there is no benefit to expectant management. <div class="ec-src"><b>Source:</b> ACOG Practice Bulletin No. 222: Gestational Hypertension and Preeclampsia. Obstet Gynecol 2020;135(6):e237-e260; Magpie Trial Collaborative Group. Do Women With Pre-eclampsia, and Their Babies, Benefit From Magnesium Sulphate? Lancet 2002;359(9321):1877-1890.</div></div> [[Start another case->Hub]] [[Restart this case->Severe preeclampsia - Rx]] [[Next case →->Preeclampsia expectant - Prog]]

<span class="ec-case-marker" hidden data-entry="Severe preeclampsia. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Discharge is dangerous with severe features.</div> This patient has multiple indicators of end-organ damage: thrombocytopenia, elevated liver enzymes, renal impairment, headache, and visual changes. She requires immediate inpatient management and delivery. <div class="ec-teach"><div class="th">What to do instead</div> Preeclampsia with severe features at ≥37 weeks is an indication for delivery after maternal stabilization. Magnesium sulfate is administered for seizure prophylaxis (the Magpie Trial demonstrated a 58% reduction in eclampsia). Acute severe hypertension (≥160/110) requires IV labetalol, IV hydralazine, or oral immediate-release nifedipine. The definitive treatment is delivery of the placenta; at 37 weeks, there is no benefit to expectant management. <div class="ec-src"><b>Source:</b> ACOG Practice Bulletin No. 222: Gestational Hypertension and Preeclampsia. Obstet Gynecol 2020;135(6):e237-e260; Magpie Trial Collaborative Group. Do Women With Pre-eclampsia, and Their Babies, Benefit From Magnesium Sulphate? Lancet 2002;359(9321):1877-1890.</div></div></div> [[Try this question again->Severe preeclampsia - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Severe preeclampsia. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Expectant management is not appropriate at term.</div> At 37 weeks with severe features, the risks of continuing the pregnancy substantially outweigh the benefits. Delivery is indicated. <div class="ec-teach"><div class="th">What to do instead</div> Preeclampsia with severe features at ≥37 weeks is an indication for delivery after maternal stabilization. Magnesium sulfate is administered for seizure prophylaxis (the Magpie Trial demonstrated a 58% reduction in eclampsia). Acute severe hypertension (≥160/110) requires IV labetalol, IV hydralazine, or oral immediate-release nifedipine. The definitive treatment is delivery of the placenta; at 37 weeks, there is no benefit to expectant management. <div class="ec-src"><b>Source:</b> ACOG Practice Bulletin No. 222: Gestational Hypertension and Preeclampsia. Obstet Gynecol 2020;135(6):e237-e260; Magpie Trial Collaborative Group. Do Women With Pre-eclampsia, and Their Babies, Benefit From Magnesium Sulphate? Lancet 2002;359(9321):1877-1890.</div></div></div> [[Try this question again->Severe preeclampsia - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Severe preeclampsia. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ High-dose aspirin does not treat acute preeclampsia.</div> Low-dose aspirin is used for preeclampsia prevention in high-risk patients starting in the first trimester. It has no role in acute management of severe preeclampsia at term. <div class="ec-teach"><div class="th">What to do instead</div> Preeclampsia with severe features at ≥37 weeks is an indication for delivery after maternal stabilization. Magnesium sulfate is administered for seizure prophylaxis (the Magpie Trial demonstrated a 58% reduction in eclampsia). Acute severe hypertension (≥160/110) requires IV labetalol, IV hydralazine, or oral immediate-release nifedipine. The definitive treatment is delivery of the placenta; at 37 weeks, there is no benefit to expectant management. <div class="ec-src"><b>Source:</b> ACOG Practice Bulletin No. 222: Gestational Hypertension and Preeclampsia. Obstet Gynecol 2020;135(6):e237-e260; Magpie Trial Collaborative Group. Do Women With Pre-eclampsia, and Their Babies, Benefit From Magnesium Sulphate? Lancet 2002;359(9321):1877-1890.</div></div></div> [[Try this question again->Severe preeclampsia - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Severe preeclampsia. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Bed rest alone is insufficient.</div> Bed rest does not prevent seizures, control severe hypertension, or address the end-organ damage. Active pharmacologic management and delivery are required. <div class="ec-teach"><div class="th">What to do instead</div> Preeclampsia with severe features at ≥37 weeks is an indication for delivery after maternal stabilization. Magnesium sulfate is administered for seizure prophylaxis (the Magpie Trial demonstrated a 58% reduction in eclampsia). Acute severe hypertension (≥160/110) requires IV labetalol, IV hydralazine, or oral immediate-release nifedipine. The definitive treatment is delivery of the placenta; at 37 weeks, there is no benefit to expectant management. <div class="ec-src"><b>Source:</b> ACOG Practice Bulletin No. 222: Gestational Hypertension and Preeclampsia. Obstet Gynecol 2020;135(6):e237-e260; Magpie Trial Collaborative Group. Do Women With Pre-eclampsia, and Their Babies, Benefit From Magnesium Sulphate? Lancet 2002;359(9321):1877-1890.</div></div></div> [[Try this question again->Severe preeclampsia - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Primary care clinic · 09:45</div> A 48-year-old man with type 2 diabetes diagnosed 2 years ago has never had a dilated eye examination. His hemoglobin A1c is 8.2% and he is on metformin alone. <span class="ec-prompt">Which of the following is the most appropriate screening recommendation?</span> [[After 10 years of diabetes only->Diabetic retinopathy - D2]] [[At the time of diabetes diagnosis or shortly thereafter->Diabetic retinopathy - Correct]] [[Only after the patient is transitioned to insulin therapy->Diabetic retinopathy - D4]] [[Only after visual symptoms develop->Diabetic retinopathy - D1]] [[Only if the patient requests it->Diabetic retinopathy - D3]]

<span class="ec-case-marker" hidden data-entry="Diabetic retinopathy. Opening"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ At the time of diabetes diagnosis or shortly thereafter</div> The ADA recommends an initial dilated eye examination at the time of type 2 diabetes diagnosis, because retinopathy may already be present, unlike type 1, where the onset of disease is usually clear. Screening should be repeated at least annually (more frequently if retinopathy is detected). Diabetic retinopathy is the leading cause of new blindness in working-age adults, and early detection allows timely laser photocoagulation or anti-VEGF therapy that prevents vision loss. <div class="ec-src"><b>Source:</b> ADA Standards of Care in Diabetes-2026. Diabetes Care 2026;49(Suppl 1); Solomon SD, et al. Diabetic Retinopathy: A Position Statement by the American Diabetes Association. Diabetes Care 2017;40(3):412-418.</div></div> [[Start another case->Hub]] [[Restart this case->Diabetic retinopathy - Opening]] [[Next case →->Gestational diabetes - Rx]]

<span class="ec-case-marker" hidden data-entry="Diabetic retinopathy. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Symptoms appear late.</div> Diabetic retinopathy is asymptomatic until it reaches an advanced stage. By the time visual symptoms develop, irreversible damage may have occurred. Screening identifies treatable disease before symptoms appear. <div class="ec-teach"><div class="th">What to do instead</div> The ADA recommends an initial dilated eye examination at the time of type 2 diabetes diagnosis, because retinopathy may already be present, unlike type 1, where the onset of disease is usually clear. Screening should be repeated at least annually (more frequently if retinopathy is detected). Diabetic retinopathy is the leading cause of new blindness in working-age adults, and early detection allows timely laser photocoagulation or anti-VEGF therapy that prevents vision loss. <div class="ec-src"><b>Source:</b> ADA Standards of Care in Diabetes-2026. Diabetes Care 2026;49(Suppl 1); Solomon SD, et al. Diabetic Retinopathy: A Position Statement by the American Diabetes Association. Diabetes Care 2017;40(3):412-418.</div></div></div> [[Try this question again->Diabetic retinopathy - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Diabetic retinopathy. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Retinopathy can be present at diagnosis in type 2.</div> Unlike type 1, type 2 diabetes may have been present for years before clinical diagnosis. Waiting 10 years misses the window for early treatment. <div class="ec-teach"><div class="th">What to do instead</div> The ADA recommends an initial dilated eye examination at the time of type 2 diabetes diagnosis, because retinopathy may already be present, unlike type 1, where the onset of disease is usually clear. Screening should be repeated at least annually (more frequently if retinopathy is detected). Diabetic retinopathy is the leading cause of new blindness in working-age adults, and early detection allows timely laser photocoagulation or anti-VEGF therapy that prevents vision loss. <div class="ec-src"><b>Source:</b> ADA Standards of Care in Diabetes-2026. Diabetes Care 2026;49(Suppl 1); Solomon SD, et al. Diabetic Retinopathy: A Position Statement by the American Diabetes Association. Diabetes Care 2017;40(3):412-418.</div></div></div> [[Try this question again->Diabetic retinopathy - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Diabetic retinopathy. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Screening should be physician-initiated.</div> Relying on patient request results in missed screening. Evidence-based guidelines recommend systematic screening as part of diabetes care. <div class="ec-teach"><div class="th">What to do instead</div> The ADA recommends an initial dilated eye examination at the time of type 2 diabetes diagnosis, because retinopathy may already be present, unlike type 1, where the onset of disease is usually clear. Screening should be repeated at least annually (more frequently if retinopathy is detected). Diabetic retinopathy is the leading cause of new blindness in working-age adults, and early detection allows timely laser photocoagulation or anti-VEGF therapy that prevents vision loss. <div class="ec-src"><b>Source:</b> ADA Standards of Care in Diabetes-2026. Diabetes Care 2026;49(Suppl 1); Solomon SD, et al. Diabetic Retinopathy: A Position Statement by the American Diabetes Association. Diabetes Care 2017;40(3):412-418.</div></div></div> [[Try this question again->Diabetic retinopathy - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Diabetic retinopathy. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Insulin use does not determine screening timing.</div> Retinopathy risk is related to glycemic exposure over time, not the specific treatment regimen. Screening is recommended for all patients with diabetes regardless of therapy. <div class="ec-teach"><div class="th">What to do instead</div> The ADA recommends an initial dilated eye examination at the time of type 2 diabetes diagnosis, because retinopathy may already be present, unlike type 1, where the onset of disease is usually clear. Screening should be repeated at least annually (more frequently if retinopathy is detected). Diabetic retinopathy is the leading cause of new blindness in working-age adults, and early detection allows timely laser photocoagulation or anti-VEGF therapy that prevents vision loss. <div class="ec-src"><b>Source:</b> ADA Standards of Care in Diabetes-2026. Diabetes Care 2026;49(Suppl 1); Solomon SD, et al. Diabetic Retinopathy: A Position Statement by the American Diabetes Association. Diabetes Care 2017;40(3):412-418.</div></div></div> [[Try this question again->Diabetic retinopathy - Opening]] [[Start another case->Hub]]

<div class="ec-scene">Preventive medicine clinic · 10:30</div> A 28-year-old woman with no significant medical history asks about cervical cancer screening. She has been sexually active since age 18. She has had no prior Pap tests. <span class="ec-prompt">Which of the following is the most appropriate screening strategy?</span> [[Annual Pap test starting at age 18->Cervical screening - D1]] [[Cervical cytology alone every 3 years at ages 21 to 29->Cervical screening - Correct]] [[No screening necessary until age 40->Cervical screening - D2]] [[Primary HPV DNA testing alone beginning at age 25->Cervical screening - D3]] [[Screening only after symptoms develop->Cervical screening - D4]]

<span class="ec-case-marker" hidden data-entry="Cervical screening. Opening"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Cervical cytology alone every 3 years at ages 21 to 29</div> USPSTF and ACOG (2026) recommend initiating cervical cancer screening at age 21 regardless of sexual debut. For women aged 21–29, screening is with cervical cytology (Pap test) alone every 3 years. Starting at age 30, primary hrHPV testing every 5 years is preferred, with co-testing every 5 years or cytology alone every 3 years as acceptable alternatives. Screening before age 21 is not recommended because of the high rate of transient HPV infections and spontaneous regression in adolescents. The ACS 2020 update recommends starting at age 25 with primary HPV testing, an alternative framework, but this question follows the USPSTF/ACOG standard. <div class="ec-src"><b>Source:</b> USPSTF Cervical Cancer Screening Recommendation Statement 2018; ACOG Committee Statement, Screening for Cervical Cancer, Obstet Gynecol 2026 (aligned with WPSI 2026 update); ACS 2020 (Fontham et al.) offers an alternative age-25/HPV-first framework.</div></div> [[Start another case->Hub]] [[Restart this case->Cervical screening - Opening]] [[Next case →->Adolescent well visit - Opening]]

<span class="ec-case-marker" hidden data-entry="Cervical screening. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Annual screening is no longer recommended.</div> Every-3-year screening is adequate because cervical cancer develops slowly through well-characterized precursor stages. Annual screening leads to overdiagnosis and unnecessary procedures. <div class="ec-teach"><div class="th">What to do instead</div> USPSTF and ACOG (2026) recommend initiating cervical cancer screening at age 21 regardless of sexual debut. For women aged 21–29, screening is with cervical cytology (Pap test) alone every 3 years. Starting at age 30, primary hrHPV testing every 5 years is preferred, with co-testing every 5 years or cytology alone every 3 years as acceptable alternatives. Screening before age 21 is not recommended because of the high rate of transient HPV infections and spontaneous regression in adolescents. The ACS 2020 update recommends starting at age 25 with primary HPV testing, an alternative framework, but this question follows the USPSTF/ACOG standard. <div class="ec-src"><b>Source:</b> USPSTF Cervical Cancer Screening Recommendation Statement 2018; ACOG Committee Statement, Screening for Cervical Cancer, Obstet Gynecol 2026 (aligned with WPSI 2026 update); ACS 2020 (Fontham et al.) offers an alternative age-25/HPV-first framework.</div></div></div> [[Try this question again->Cervical screening - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Cervical screening. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Screening begins at age 21.</div> Delaying screening until age 40 misses the opportunity to detect and treat high-grade precancerous lesions during the peak incidence years. <div class="ec-teach"><div class="th">What to do instead</div> USPSTF and ACOG (2026) recommend initiating cervical cancer screening at age 21 regardless of sexual debut. For women aged 21–29, screening is with cervical cytology (Pap test) alone every 3 years. Starting at age 30, primary hrHPV testing every 5 years is preferred, with co-testing every 5 years or cytology alone every 3 years as acceptable alternatives. Screening before age 21 is not recommended because of the high rate of transient HPV infections and spontaneous regression in adolescents. The ACS 2020 update recommends starting at age 25 with primary HPV testing, an alternative framework, but this question follows the USPSTF/ACOG standard. <div class="ec-src"><b>Source:</b> USPSTF Cervical Cancer Screening Recommendation Statement 2018; ACOG Committee Statement, Screening for Cervical Cancer, Obstet Gynecol 2026 (aligned with WPSI 2026 update); ACS 2020 (Fontham et al.) offers an alternative age-25/HPV-first framework.</div></div></div> [[Try this question again->Cervical screening - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Cervical screening. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ HPV-only testing is for age 30 and above.</div> Primary HPV testing alone is an option beginning at age 30, but for women 21–29, cervical cytology is the recommended screening method. <div class="ec-teach"><div class="th">What to do instead</div> USPSTF and ACOG (2026) recommend initiating cervical cancer screening at age 21 regardless of sexual debut. For women aged 21–29, screening is with cervical cytology (Pap test) alone every 3 years. Starting at age 30, primary hrHPV testing every 5 years is preferred, with co-testing every 5 years or cytology alone every 3 years as acceptable alternatives. Screening before age 21 is not recommended because of the high rate of transient HPV infections and spontaneous regression in adolescents. The ACS 2020 update recommends starting at age 25 with primary HPV testing, an alternative framework, but this question follows the USPSTF/ACOG standard. <div class="ec-src"><b>Source:</b> USPSTF Cervical Cancer Screening Recommendation Statement 2018; ACOG Committee Statement, Screening for Cervical Cancer, Obstet Gynecol 2026 (aligned with WPSI 2026 update); ACS 2020 (Fontham et al.) offers an alternative age-25/HPV-first framework.</div></div></div> [[Try this question again->Cervical screening - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Cervical screening. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Screening prevents cancer, not just detects it.</div> The purpose of screening is to identify precancerous lesions before they progress to invasive cancer. Waiting for symptoms means the cancer has already developed. <div class="ec-teach"><div class="th">What to do instead</div> USPSTF and ACOG (2026) recommend initiating cervical cancer screening at age 21 regardless of sexual debut. For women aged 21–29, screening is with cervical cytology (Pap test) alone every 3 years. Starting at age 30, primary hrHPV testing every 5 years is preferred, with co-testing every 5 years or cytology alone every 3 years as acceptable alternatives. Screening before age 21 is not recommended because of the high rate of transient HPV infections and spontaneous regression in adolescents. The ACS 2020 update recommends starting at age 25 with primary HPV testing, an alternative framework, but this question follows the USPSTF/ACOG standard. <div class="ec-src"><b>Source:</b> USPSTF Cervical Cancer Screening Recommendation Statement 2018; ACOG Committee Statement, Screening for Cervical Cancer, Obstet Gynecol 2026 (aligned with WPSI 2026 update); ACS 2020 (Fontham et al.) offers an alternative age-25/HPV-first framework.</div></div></div> [[Try this question again->Cervical screening - Opening]] [[Start another case->Hub]]

<div class="ec-scene">Pediatric Emergency Department · 03:45</div> A 21-day-old full-term infant is brought in with a rectal temperature of 38.4°C that began 4 hours ago. The infant was born without complications and has been feeding well until today. Examination shows the infant appears slightly irritable but has no focal findings. The parents report no sick contacts. <span class="ec-prompt">Which of the following is the most appropriate evaluation?</span> [[Acetaminophen alone with outpatient follow-up in 48 hours->Febrile infant - D2]] [[Chest radiograph without blood or urine cultures->Febrile infant - D3]] [[Full sepsis workup, empiric Intravenous antibiotics, and admission->Febrile infant - Correct]] [[Observation without laboratory evaluation or treatment->Febrile infant - D4]] [[Reassurance and discharge with oral amoxicillin->Febrile infant - D1]]

<span class="ec-case-marker" hidden data-entry="Febrile infant. Ix"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Full sepsis workup, empiric Intravenous antibiotics, and admission</div> Infants ≤28 days with fever ≥38°C are at high risk for serious bacterial infection, including bacteremia, urinary tract infection, and meningitis. Clinical appearance is unreliable for excluding serious infection at this age. Guidelines recommend a full sepsis evaluation: blood culture, complete blood count, urinalysis with culture, and lumbar puncture for CSF analysis and culture. Empiric parenteral antibiotics (typically ampicillin plus gentamicin or a third-generation cephalosporin) are started pending culture results, and the infant is admitted. <div class="ec-src"><b>Source:</b> Pantell RH, et al. Evaluation and Management of Well-Appearing Febrile Infants 8 to 60 Days Old. Pediatrics 2021;148(2):e2021052228.</div></div> [[Start another case->Hub]] [[Restart this case->Febrile infant - Ix]] [[Next case →->Partner notification - Ethics]]

<span class="ec-case-marker" hidden data-entry="Febrile infant. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Oral antibiotics and discharge are insufficient.</div> A 21-day-old infant with fever cannot be safely managed as an outpatient. The risk of meningitis, bacteremia, and rapid deterioration requires inpatient monitoring and IV antibiotics. <div class="ec-teach"><div class="th">What to do instead</div> Infants ≤28 days with fever ≥38°C are at high risk for serious bacterial infection, including bacteremia, urinary tract infection, and meningitis. Clinical appearance is unreliable for excluding serious infection at this age. Guidelines recommend a full sepsis evaluation: blood culture, complete blood count, urinalysis with culture, and lumbar puncture for CSF analysis and culture. Empiric parenteral antibiotics (typically ampicillin plus gentamicin or a third-generation cephalosporin) are started pending culture results, and the infant is admitted. <div class="ec-src"><b>Source:</b> Pantell RH, et al. Evaluation and Management of Well-Appearing Febrile Infants 8 to 60 Days Old. Pediatrics 2021;148(2):e2021052228.</div></div></div> [[Try this question again->Febrile infant - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Febrile infant. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Antipyretics do not treat infection.</div> Acetaminophen may reduce fever but does not address the underlying cause. A 48-hour delay in a neonate with potential sepsis or meningitis can be fatal. <div class="ec-teach"><div class="th">What to do instead</div> Infants ≤28 days with fever ≥38°C are at high risk for serious bacterial infection, including bacteremia, urinary tract infection, and meningitis. Clinical appearance is unreliable for excluding serious infection at this age. Guidelines recommend a full sepsis evaluation: blood culture, complete blood count, urinalysis with culture, and lumbar puncture for CSF analysis and culture. Empiric parenteral antibiotics (typically ampicillin plus gentamicin or a third-generation cephalosporin) are started pending culture results, and the infant is admitted. <div class="ec-src"><b>Source:</b> Pantell RH, et al. Evaluation and Management of Well-Appearing Febrile Infants 8 to 60 Days Old. Pediatrics 2021;148(2):e2021052228.</div></div></div> [[Try this question again->Febrile infant - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Febrile infant. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Chest X-ray alone is inadequate.</div> Pneumonia is only one possible source. The evaluation must include blood, urine, and CSF to exclude bacteremia and meningitis. <div class="ec-teach"><div class="th">What to do instead</div> Infants ≤28 days with fever ≥38°C are at high risk for serious bacterial infection, including bacteremia, urinary tract infection, and meningitis. Clinical appearance is unreliable for excluding serious infection at this age. Guidelines recommend a full sepsis evaluation: blood culture, complete blood count, urinalysis with culture, and lumbar puncture for CSF analysis and culture. Empiric parenteral antibiotics (typically ampicillin plus gentamicin or a third-generation cephalosporin) are started pending culture results, and the infant is admitted. <div class="ec-src"><b>Source:</b> Pantell RH, et al. Evaluation and Management of Well-Appearing Febrile Infants 8 to 60 Days Old. Pediatrics 2021;148(2):e2021052228.</div></div></div> [[Try this question again->Febrile infant - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Febrile infant. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Observation without labs misses infections.</div> Clinical appearance alone cannot reliably exclude serious bacterial infection in neonates. Laboratory evaluation is essential. <div class="ec-teach"><div class="th">What to do instead</div> Infants ≤28 days with fever ≥38°C are at high risk for serious bacterial infection, including bacteremia, urinary tract infection, and meningitis. Clinical appearance is unreliable for excluding serious infection at this age. Guidelines recommend a full sepsis evaluation: blood culture, complete blood count, urinalysis with culture, and lumbar puncture for CSF analysis and culture. Empiric parenteral antibiotics (typically ampicillin plus gentamicin or a third-generation cephalosporin) are started pending culture results, and the infant is admitted. <div class="ec-src"><b>Source:</b> Pantell RH, et al. Evaluation and Management of Well-Appearing Febrile Infants 8 to 60 Days Old. Pediatrics 2021;148(2):e2021052228.</div></div></div> [[Try this question again->Febrile infant - Ix]] [[Start another case->Hub]]

<div class="ec-scene">Newborn nursery · 08:00</div> A full-term, otherwise healthy 3-day-old infant appears visibly jaundiced. Temperature is 37.0°C (98.6°F), pulse is 148/min, and respirations are 42/min. Total serum bilirubin is 19.8 mg/dL, which plots above the phototherapy treatment threshold on the AAP's hour- and gestational-age-specific treatment-threshold graph for this age (a separate tool from the Bhutani nomogram, which is used for predischarge risk prediction, not for the phototherapy treatment decision). The direct bilirubin is 0.4 mg/dL. The infant is breastfeeding well and has no signs of hemolysis. <span class="ec-prompt">Which of the following is the most appropriate next step?</span> [[Discontinue breastfeeding permanently->Neonatal jaundice - D2]] [[Immediate exchange transfusion->Neonatal jaundice - D1]] [[Intensive phototherapy->Neonatal jaundice - Correct]] [[Observe without treatment for 72 hours->Neonatal jaundice - D3]] [[Phenobarbital->Neonatal jaundice - D4]]

<span class="ec-case-marker" hidden data-entry="Neonatal jaundice. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Intensive phototherapy.</div> When the total serum bilirubin exceeds the phototherapy threshold on the gestational-age- and hour-specific nomogram, intensive phototherapy is the first-line treatment. Phototherapy converts bilirubin into water-soluble photoisomers that can be excreted without hepatic conjugation. Exchange transfusion is reserved for bilirubin levels approaching or exceeding the exchange threshold, or when phototherapy fails. Breastfeeding should be continued, supplementation may be offered to improve hydration and enteral output, but permanent discontinuation is not recommended. <div class="ec-src"><b>Source:</b> AAP Subcommittee on Hyperbilirubinemia. Management of Hyperbilirubinemia in the Newborn Infant 35 or More Weeks of Gestation: Clinical Practice Guideline Revision. Pediatrics 2022;150(3):e2022058859.</div></div> [[Start another case->Hub]] [[Restart this case->Neonatal jaundice - Rx]] [[Next case →->Emergency care of a minor - Ethics]]

<span class="ec-case-marker" hidden data-entry="Neonatal jaundice. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Exchange transfusion is for higher levels.</div> Exchange transfusion is reserved for bilirubin approaching or exceeding the exchange transfusion threshold (typically 25–30 mg/dL for term infants without risk factors), or when intensive phototherapy fails to produce an adequate rate of decline. <div class="ec-teach"><div class="th">What to do instead</div> When the total serum bilirubin exceeds the phototherapy threshold on the gestational-age- and hour-specific nomogram, intensive phototherapy is the first-line treatment. Phototherapy converts bilirubin into water-soluble photoisomers that can be excreted without hepatic conjugation. Exchange transfusion is reserved for bilirubin levels approaching or exceeding the exchange threshold, or when phototherapy fails. Breastfeeding should be continued, supplementation may be offered to improve hydration and enteral output, but permanent discontinuation is not recommended. <div class="ec-src"><b>Source:</b> AAP Subcommittee on Hyperbilirubinemia. Management of Hyperbilirubinemia in the Newborn Infant 35 or More Weeks of Gestation: Clinical Practice Guideline Revision. Pediatrics 2022;150(3):e2022058859.</div></div></div> [[Try this question again->Neonatal jaundice - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Neonatal jaundice. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Breastfeeding should continue.</div> Breast-milk jaundice is benign and self-limited. Discontinuing breastfeeding permanently deprives the infant of the established benefits of human milk and is not recommended. <div class="ec-teach"><div class="th">What to do instead</div> When the total serum bilirubin exceeds the phototherapy threshold on the gestational-age- and hour-specific nomogram, intensive phototherapy is the first-line treatment. Phototherapy converts bilirubin into water-soluble photoisomers that can be excreted without hepatic conjugation. Exchange transfusion is reserved for bilirubin levels approaching or exceeding the exchange threshold, or when phototherapy fails. Breastfeeding should be continued, supplementation may be offered to improve hydration and enteral output, but permanent discontinuation is not recommended. <div class="ec-src"><b>Source:</b> AAP Subcommittee on Hyperbilirubinemia. Management of Hyperbilirubinemia in the Newborn Infant 35 or More Weeks of Gestation: Clinical Practice Guideline Revision. Pediatrics 2022;150(3):e2022058859.</div></div></div> [[Try this question again->Neonatal jaundice - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Neonatal jaundice. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Observation risks kernicterus.</div> At 19.8 mg/dL, which is above the phototherapy threshold, untreated hyperbilirubinemia can progress to bilirubin encephalopathy (kernicterus), causing permanent neurologic damage. <div class="ec-teach"><div class="th">What to do instead</div> When the total serum bilirubin exceeds the phototherapy threshold on the gestational-age- and hour-specific nomogram, intensive phototherapy is the first-line treatment. Phototherapy converts bilirubin into water-soluble photoisomers that can be excreted without hepatic conjugation. Exchange transfusion is reserved for bilirubin levels approaching or exceeding the exchange threshold, or when phototherapy fails. Breastfeeding should be continued, supplementation may be offered to improve hydration and enteral output, but permanent discontinuation is not recommended. <div class="ec-src"><b>Source:</b> AAP Subcommittee on Hyperbilirubinemia. Management of Hyperbilirubinemia in the Newborn Infant 35 or More Weeks of Gestation: Clinical Practice Guideline Revision. Pediatrics 2022;150(3):e2022058859.</div></div></div> [[Try this question again->Neonatal jaundice - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Neonatal jaundice. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Phenobarbital is not standard treatment.</div> While phenobarbital can induce hepatic glucuronidation enzymes, it is not first-line therapy for neonatal jaundice. Phototherapy is more effective and has a more favorable risk profile in neonates. <div class="ec-teach"><div class="th">What to do instead</div> When the total serum bilirubin exceeds the phototherapy threshold on the gestational-age- and hour-specific nomogram, intensive phototherapy is the first-line treatment. Phototherapy converts bilirubin into water-soluble photoisomers that can be excreted without hepatic conjugation. Exchange transfusion is reserved for bilirubin levels approaching or exceeding the exchange threshold, or when phototherapy fails. Breastfeeding should be continued, supplementation may be offered to improve hydration and enteral output, but permanent discontinuation is not recommended. <div class="ec-src"><b>Source:</b> AAP Subcommittee on Hyperbilirubinemia. Management of Hyperbilirubinemia in the Newborn Infant 35 or More Weeks of Gestation: Clinical Practice Guideline Revision. Pediatrics 2022;150(3):e2022058859.</div></div></div> [[Try this question again->Neonatal jaundice - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Pediatric clinic · 15:00</div> An 8-month-old girl presents with 2 days of fever, fussiness, and pulling at her right ear. Otoscopic examination shows a bulging, erythematous, and opacified right tympanic membrane. She has no drug allergies and has not had otitis media before. <span class="ec-prompt">Which of the following is the most appropriate treatment?</span> [[Immediate myringotomy->Otitis media - D2]] [[Oral amoxicillin->Otitis media - Correct]] [[Oral decongestants alone->Otitis media - D3]] [[Topical otic fluoroquinolone drops only->Otitis media - D1]] [[Watchful waiting for 72 hours without antibiotics->Otitis media - D4]]

<span class="ec-case-marker" hidden data-entry="Otitis media. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Oral amoxicillin.</div> AAP guidelines recommend immediate antibiotic therapy for acute otitis media in children under 2 years of age with bilateral disease or otorrhea, and for any child with severe symptoms. An 8-month-old with a bulging TM and fever warrants treatment. High-dose amoxicillin (80–90 mg/kg/day) is the first-line agent because of its activity against the most common pathogens (Streptococcus pneumoniae, non-typeable Haemophilus influenzae, and Moraxella catarrhalis). <div class="ec-src"><b>Source:</b> Lieberthal AS, et al. The Diagnosis and Management of Acute Otitis Media. Pediatrics 2013;131(3):e964-e999; AAP Clinical Practice Guideline.</div></div> [[Start another case->Hub]] [[Restart this case->Otitis media - Rx]] [[Next case →->Peritonsillar abscess - Rx]]

<span class="ec-case-marker" hidden data-entry="Otitis media. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Topical drops are for external otitis.</div> Otic drops alone do not penetrate the middle ear space. They are used for otitis externa or when tympanostomy tubes are in place. Systemic antibiotics are needed for AOM. <div class="ec-teach"><div class="th">What to do instead</div> AAP guidelines recommend immediate antibiotic therapy for acute otitis media in children under 2 years of age with bilateral disease or otorrhea, and for any child with severe symptoms. An 8-month-old with a bulging TM and fever warrants treatment. High-dose amoxicillin (80–90 mg/kg/day) is the first-line agent because of its activity against the most common pathogens (Streptococcus pneumoniae, non-typeable Haemophilus influenzae, and Moraxella catarrhalis). <div class="ec-src"><b>Source:</b> Lieberthal AS, et al. The Diagnosis and Management of Acute Otitis Media. Pediatrics 2013;131(3):e964-e999; AAP Clinical Practice Guideline.</div></div></div> [[Try this question again->Otitis media - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Otitis media. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Myringotomy is not first-line.</div> Myringotomy is reserved for recurrent or refractory cases, or for diagnostic aspiration. First-line management of uncomplicated AOM is oral antibiotics. <div class="ec-teach"><div class="th">What to do instead</div> AAP guidelines recommend immediate antibiotic therapy for acute otitis media in children under 2 years of age with bilateral disease or otorrhea, and for any child with severe symptoms. An 8-month-old with a bulging TM and fever warrants treatment. High-dose amoxicillin (80–90 mg/kg/day) is the first-line agent because of its activity against the most common pathogens (Streptococcus pneumoniae, non-typeable Haemophilus influenzae, and Moraxella catarrhalis). <div class="ec-src"><b>Source:</b> Lieberthal AS, et al. The Diagnosis and Management of Acute Otitis Media. Pediatrics 2013;131(3):e964-e999; AAP Clinical Practice Guideline.</div></div></div> [[Try this question again->Otitis media - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Otitis media. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Decongestants do not treat AOM.</div> Decongestants and antihistamines have not been shown to improve outcomes in acute otitis media and are not recommended. <div class="ec-teach"><div class="th">What to do instead</div> AAP guidelines recommend immediate antibiotic therapy for acute otitis media in children under 2 years of age with bilateral disease or otorrhea, and for any child with severe symptoms. An 8-month-old with a bulging TM and fever warrants treatment. High-dose amoxicillin (80–90 mg/kg/day) is the first-line agent because of its activity against the most common pathogens (Streptococcus pneumoniae, non-typeable Haemophilus influenzae, and Moraxella catarrhalis). <div class="ec-src"><b>Source:</b> Lieberthal AS, et al. The Diagnosis and Management of Acute Otitis Media. Pediatrics 2013;131(3):e964-e999; AAP Clinical Practice Guideline.</div></div></div> [[Try this question again->Otitis media - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Otitis media. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Watchful waiting may be inappropriate at this age.</div> While observation is an option for children ≥6 months with mild unilateral AOM without otorrhea, this infant has clear bulging and fever, and many guidelines favor treatment in children under 2. <div class="ec-teach"><div class="th">What to do instead</div> AAP guidelines recommend immediate antibiotic therapy for acute otitis media in children under 2 years of age with bilateral disease or otorrhea, and for any child with severe symptoms. An 8-month-old with a bulging TM and fever warrants treatment. High-dose amoxicillin (80–90 mg/kg/day) is the first-line agent because of its activity against the most common pathogens (Streptococcus pneumoniae, non-typeable Haemophilus influenzae, and Moraxella catarrhalis). <div class="ec-src"><b>Source:</b> Lieberthal AS, et al. The Diagnosis and Management of Acute Otitis Media. Pediatrics 2013;131(3):e964-e999; AAP Clinical Practice Guideline.</div></div></div> [[Try this question again->Otitis media - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Pediatric Emergency Department · 18:30</div> An 18-month-old boy with a URI and a temperature of 39.4°C had a generalized tonic-clonic seizure lasting 2 minutes that self-resolved. He is now alert, playful, and neurologically normal. He has no history of seizures and has met all developmental milestones. There is no neck stiffness or bulging fontanelle. <span class="ec-prompt">Which of the following is the most likely diagnosis?</span> [[Bacterial meningitis->Febrile seizure - D1]] [[Brain tumor->Febrile seizure - D4]] [[Epilepsy requiring long-term antiseizure medication->Febrile seizure - D2]] [[Non-accidental trauma->Febrile seizure - D3]] [[Simple febrile seizure->Febrile seizure - Correct]]

<span class="ec-case-marker" hidden data-entry="Febrile seizure. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Simple febrile seizure.</div> A simple febrile seizure is a generalized seizure lasting <15 minutes, occurring once in 24 hours, in a neurologically normal child aged 6 months to 5 years with fever. It is the most common seizure type in childhood, affecting 2–5% of children. Simple febrile seizures do not increase the risk of epilepsy above the baseline population risk and do not cause brain damage. Management is parental reassurance, antipyretics for comfort, and identification of the fever source. Continuous antiseizure medication is not indicated. <div class="ec-src"><b>Source:</b> Subcommittee on Febrile Seizures, AAP. Neurodiagnostic Evaluation of the Child With a Simple Febrile Seizure. Pediatrics 2011;127(2):389-394 (evaluation); AAP. Clinical Practice Guideline for the Long-term Management of the Child With Simple Febrile Seizures. Pediatrics 2008;121(6):1281-1286 (management, anticonvulsant therapy not recommended).</div></div> [[Start another case->Hub]] [[Restart this case->Febrile seizure - Dx]] [[Next case →->Guillain-Barre - Dx]]

<span class="ec-case-marker" hidden data-entry="Febrile seizure. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Meningitis is unlikely with a normal exam.</div> This child is alert, playful, and has no meningeal signs. A well-appearing child with a brief generalized seizure during a febrile illness is most consistent with a simple febrile seizure. <div class="ec-teach"><div class="th">What to do instead</div> A simple febrile seizure is a generalized seizure lasting <15 minutes, occurring once in 24 hours, in a neurologically normal child aged 6 months to 5 years with fever. It is the most common seizure type in childhood, affecting 2–5% of children. Simple febrile seizures do not increase the risk of epilepsy above the baseline population risk and do not cause brain damage. Management is parental reassurance, antipyretics for comfort, and identification of the fever source. Continuous antiseizure medication is not indicated. <div class="ec-src"><b>Source:</b> Subcommittee on Febrile Seizures, AAP. Neurodiagnostic Evaluation of the Child With a Simple Febrile Seizure. Pediatrics 2011;127(2):389-394 (evaluation); AAP. Clinical Practice Guideline for the Long-term Management of the Child With Simple Febrile Seizures. Pediatrics 2008;121(6):1281-1286 (management, anticonvulsant therapy not recommended).</div></div></div> [[Try this question again->Febrile seizure - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Febrile seizure. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ This does not meet criteria for epilepsy.</div> A single febrile seizure is not epilepsy. Epilepsy requires recurrent unprovoked seizures. Simple febrile seizures do not require long-term antiseizure medication. <div class="ec-teach"><div class="th">What to do instead</div> A simple febrile seizure is a generalized seizure lasting <15 minutes, occurring once in 24 hours, in a neurologically normal child aged 6 months to 5 years with fever. It is the most common seizure type in childhood, affecting 2–5% of children. Simple febrile seizures do not increase the risk of epilepsy above the baseline population risk and do not cause brain damage. Management is parental reassurance, antipyretics for comfort, and identification of the fever source. Continuous antiseizure medication is not indicated. <div class="ec-src"><b>Source:</b> Subcommittee on Febrile Seizures, AAP. Neurodiagnostic Evaluation of the Child With a Simple Febrile Seizure. Pediatrics 2011;127(2):389-394 (evaluation); AAP. Clinical Practice Guideline for the Long-term Management of the Child With Simple Febrile Seizures. Pediatrics 2008;121(6):1281-1286 (management, anticonvulsant therapy not recommended).</div></div></div> [[Try this question again->Febrile seizure - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Febrile seizure. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ There is no evidence of trauma.</div> The seizure occurred in the context of a febrile illness with a normal neurologic examination. Non-accidental trauma would typically present with additional concerning findings. <div class="ec-teach"><div class="th">What to do instead</div> A simple febrile seizure is a generalized seizure lasting <15 minutes, occurring once in 24 hours, in a neurologically normal child aged 6 months to 5 years with fever. It is the most common seizure type in childhood, affecting 2–5% of children. Simple febrile seizures do not increase the risk of epilepsy above the baseline population risk and do not cause brain damage. Management is parental reassurance, antipyretics for comfort, and identification of the fever source. Continuous antiseizure medication is not indicated. <div class="ec-src"><b>Source:</b> Subcommittee on Febrile Seizures, AAP. Neurodiagnostic Evaluation of the Child With a Simple Febrile Seizure. Pediatrics 2011;127(2):389-394 (evaluation); AAP. Clinical Practice Guideline for the Long-term Management of the Child With Simple Febrile Seizures. Pediatrics 2008;121(6):1281-1286 (management, anticonvulsant therapy not recommended).</div></div></div> [[Try this question again->Febrile seizure - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Febrile seizure. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ A brain tumor would cause focal findings.</div> Brain tumors typically present with focal neurologic deficits, progressive symptoms, or complex seizures. A brief generalized seizure with fever and normal recovery is not concerning for intracranial pathology. <div class="ec-teach"><div class="th">What to do instead</div> A simple febrile seizure is a generalized seizure lasting <15 minutes, occurring once in 24 hours, in a neurologically normal child aged 6 months to 5 years with fever. It is the most common seizure type in childhood, affecting 2–5% of children. Simple febrile seizures do not increase the risk of epilepsy above the baseline population risk and do not cause brain damage. Management is parental reassurance, antipyretics for comfort, and identification of the fever source. Continuous antiseizure medication is not indicated. <div class="ec-src"><b>Source:</b> Subcommittee on Febrile Seizures, AAP. Neurodiagnostic Evaluation of the Child With a Simple Febrile Seizure. Pediatrics 2011;127(2):389-394 (evaluation); AAP. Clinical Practice Guideline for the Long-term Management of the Child With Simple Febrile Seizures. Pediatrics 2008;121(6):1281-1286 (management, anticonvulsant therapy not recommended).</div></div></div> [[Try this question again->Febrile seizure - Dx]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 22:15</div> A 27-year-old woman with 7 weeks of amenorrhea presents with sudden-onset left lower quadrant pain and vaginal spotting. She has a history of pelvic inflammatory disease. Temperature is 37.0°C (98.6°F), blood pressure is 118/74 mm Hg, and pulse is 92/min. Urine pregnancy test is positive. Transvaginal ultrasound shows no intrauterine gestational sac and a thickened endometrium. Quantitative β-hCG is 2,800 mIU/mL. <span class="ec-prompt">Which of the following is the most likely diagnosis?</span> [[Complete hydatidiform mole->Ectopic pregnancy 2 - D3]] [[Early intrauterine pregnancy too small to visualize->Ectopic pregnancy 2 - D1]] [[Ectopic pregnancy->Ectopic pregnancy 2 - Correct]] [[Endometrial cancer->Ectopic pregnancy 2 - D4]] [[Placenta previa->Ectopic pregnancy 2 - D2]]

<span class="ec-case-marker" hidden data-entry="Ectopic pregnancy 2. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Ectopic pregnancy.</div> A positive pregnancy test with no intrauterine pregnancy on transvaginal ultrasound at a β-hCG level above the discriminatory zone (typically 1,500–3,000 mIU/mL) strongly suggests ectopic pregnancy. Risk factors include prior PID, tubal surgery, and prior ectopic. This patient's β-hCG of 2,800 is above the discriminatory zone, and the absence of an intrauterine sac makes an early viable intrauterine pregnancy unlikely. Management depends on clinical stability, β-hCG trends, and imaging: options range from methotrexate for unruptured ectopic to surgical intervention for ruptured or unstable cases. <div class="ec-src"><b>Source:</b> ACOG Practice Bulletin No. 193: Tubal Ectopic Pregnancy. Obstet Gynecol 2018;131(3):e91-e103.</div></div> [[Start another case->Hub]] [[Restart this case->Ectopic pregnancy 2 - Dx]] [[Next case →->Eclampsia - Dx]]

<span class="ec-case-marker" hidden data-entry="Ectopic pregnancy 2. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ An IUP is unlikely above the discriminatory zone.</div> At a β-hCG of 2,800 mIU/mL, above the discriminatory zone, a normal intrauterine pregnancy should be visible on transvaginal ultrasound. The absence of an intrauterine gestational sac at this level makes ectopic pregnancy the primary concern, not an early IUP. <div class="ec-teach"><div class="th">What to do instead</div> A positive pregnancy test with no intrauterine pregnancy on transvaginal ultrasound at a β-hCG level above the discriminatory zone (typically 1,500–3,000 mIU/mL) strongly suggests ectopic pregnancy. Risk factors include prior PID, tubal surgery, and prior ectopic. This patient's β-hCG of 2,800 is above the discriminatory zone, and the absence of an intrauterine sac makes an early viable intrauterine pregnancy unlikely. Management depends on clinical stability, β-hCG trends, and imaging: options range from methotrexate for unruptured ectopic to surgical intervention for ruptured or unstable cases. <div class="ec-src"><b>Source:</b> ACOG Practice Bulletin No. 193: Tubal Ectopic Pregnancy. Obstet Gynecol 2018;131(3):e91-e103.</div></div></div> [[Try this question again->Ectopic pregnancy 2 - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Ectopic pregnancy 2. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Placenta previa requires an intrauterine pregnancy.</div> Placenta previa is abnormal placental location over the cervical os in an established intrauterine pregnancy. There is no intrauterine pregnancy here. <div class="ec-teach"><div class="th">What to do instead</div> A positive pregnancy test with no intrauterine pregnancy on transvaginal ultrasound at a β-hCG level above the discriminatory zone (typically 1,500–3,000 mIU/mL) strongly suggests ectopic pregnancy. Risk factors include prior PID, tubal surgery, and prior ectopic. This patient's β-hCG of 2,800 is above the discriminatory zone, and the absence of an intrauterine sac makes an early viable intrauterine pregnancy unlikely. Management depends on clinical stability, β-hCG trends, and imaging: options range from methotrexate for unruptured ectopic to surgical intervention for ruptured or unstable cases. <div class="ec-src"><b>Source:</b> ACOG Practice Bulletin No. 193: Tubal Ectopic Pregnancy. Obstet Gynecol 2018;131(3):e91-e103.</div></div></div> [[Try this question again->Ectopic pregnancy 2 - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Ectopic pregnancy 2. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ A molar pregnancy would show a uterine mass.</div> Complete moles typically produce very high β-hCG levels and a characteristic "snowstorm" uterine appearance on ultrasound. This ultrasound shows an empty uterus. <div class="ec-teach"><div class="th">What to do instead</div> A positive pregnancy test with no intrauterine pregnancy on transvaginal ultrasound at a β-hCG level above the discriminatory zone (typically 1,500–3,000 mIU/mL) strongly suggests ectopic pregnancy. Risk factors include prior PID, tubal surgery, and prior ectopic. This patient's β-hCG of 2,800 is above the discriminatory zone, and the absence of an intrauterine sac makes an early viable intrauterine pregnancy unlikely. Management depends on clinical stability, β-hCG trends, and imaging: options range from methotrexate for unruptured ectopic to surgical intervention for ruptured or unstable cases. <div class="ec-src"><b>Source:</b> ACOG Practice Bulletin No. 193: Tubal Ectopic Pregnancy. Obstet Gynecol 2018;131(3):e91-e103.</div></div></div> [[Try this question again->Ectopic pregnancy 2 - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Ectopic pregnancy 2. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Endometrial cancer does not cause a positive pregnancy test.</div> Endometrial cancer would not produce β-hCG (except for rare trophoblastic differentiation) and typically presents with postmenopausal bleeding. <div class="ec-teach"><div class="th">What to do instead</div> A positive pregnancy test with no intrauterine pregnancy on transvaginal ultrasound at a β-hCG level above the discriminatory zone (typically 1,500–3,000 mIU/mL) strongly suggests ectopic pregnancy. Risk factors include prior PID, tubal surgery, and prior ectopic. This patient's β-hCG of 2,800 is above the discriminatory zone, and the absence of an intrauterine sac makes an early viable intrauterine pregnancy unlikely. Management depends on clinical stability, β-hCG trends, and imaging: options range from methotrexate for unruptured ectopic to surgical intervention for ruptured or unstable cases. <div class="ec-src"><b>Source:</b> ACOG Practice Bulletin No. 193: Tubal Ectopic Pregnancy. Obstet Gynecol 2018;131(3):e91-e103.</div></div></div> [[Try this question again->Ectopic pregnancy 2 - Dx]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 13:40</div> A 25-year-old woman presents with her fourth episode in 2 months of sudden-onset palpitations, chest tightness, dyspnea, trembling, and a feeling she is going to die. Episodes peak within 10 minutes and resolve within 30. Between episodes, she avoids shopping malls where two attacks have occurred. Temperature is 36.8°C (98.2°F), blood pressure is 124/78 mm Hg, and pulse is 76/min. ECG, troponin, TSH, and urine drug screen are all normal. Physical examination is unremarkable. <span class="ec-prompt">Which of the following is the most likely diagnosis?</span> [[Acute coronary syndrome->Panic disorder - D1]] [[Generalized anxiety disorder->Panic disorder - D4]] [[Hyperthyroidism->Panic disorder - D3]] [[Panic disorder->Panic disorder - Correct]] [[Pheochromocytoma->Panic disorder - D2]]

<span class="ec-case-marker" hidden data-entry="Panic disorder. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Panic disorder.</div> Recurrent unexpected panic attacks, discrete episodes of intense fear with cardiorespiratory and autonomic symptoms peaking within minutes, followed by persistent concern about additional attacks and maladaptive behavioral change (avoidance of malls) fulfill DSM-5-TR criteria for panic disorder. A thorough medical workup excluding cardiac, thyroid, and substance-related causes is essential before making the diagnosis. First-line treatment includes CBT and/or an SSRI. <div class="ec-src"><b>Source:</b> American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 5th Edition, Text Revision (DSM-5-TR). Washington, DC: APA; 2022.</div></div> [[Start another case->Hub]] [[Restart this case->Panic disorder - Dx]] [[Next case →->Acute mania - Rx]]

<span class="ec-case-marker" hidden data-entry="Panic disorder. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Cardiac evaluation is normal.</div> Normal ECG, troponin, and examination effectively exclude acute coronary syndrome. ACS typically presents with exertional or prolonged chest pain, not brief recurrent episodes with a normal workup. <div class="ec-teach"><div class="th">What to do instead</div> Recurrent unexpected panic attacks, discrete episodes of intense fear with cardiorespiratory and autonomic symptoms peaking within minutes, followed by persistent concern about additional attacks and maladaptive behavioral change (avoidance of malls) fulfill DSM-5-TR criteria for panic disorder. A thorough medical workup excluding cardiac, thyroid, and substance-related causes is essential before making the diagnosis. First-line treatment includes CBT and/or an SSRI. <div class="ec-src"><b>Source:</b> American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 5th Edition, Text Revision (DSM-5-TR). Washington, DC: APA; 2022.</div></div></div> [[Try this question again->Panic disorder - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Panic disorder. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Pheochromocytoma causes hypertension.</div> Pheochromocytoma can mimic panic attacks but typically causes sustained or paroxysmal hypertension and elevated metanephrines. The normal workup argues against it, though plasma metanephrines could be checked if clinical suspicion remains. <div class="ec-teach"><div class="th">What to do instead</div> Recurrent unexpected panic attacks, discrete episodes of intense fear with cardiorespiratory and autonomic symptoms peaking within minutes, followed by persistent concern about additional attacks and maladaptive behavioral change (avoidance of malls) fulfill DSM-5-TR criteria for panic disorder. A thorough medical workup excluding cardiac, thyroid, and substance-related causes is essential before making the diagnosis. First-line treatment includes CBT and/or an SSRI. <div class="ec-src"><b>Source:</b> American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 5th Edition, Text Revision (DSM-5-TR). Washington, DC: APA; 2022.</div></div></div> [[Try this question again->Panic disorder - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Panic disorder. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ TSH is normal.</div> Hyperthyroidism can cause anxiety and palpitations but would show suppressed TSH and is usually accompanied by weight loss, tremor, and heat intolerance. <div class="ec-teach"><div class="th">What to do instead</div> Recurrent unexpected panic attacks, discrete episodes of intense fear with cardiorespiratory and autonomic symptoms peaking within minutes, followed by persistent concern about additional attacks and maladaptive behavioral change (avoidance of malls) fulfill DSM-5-TR criteria for panic disorder. A thorough medical workup excluding cardiac, thyroid, and substance-related causes is essential before making the diagnosis. First-line treatment includes CBT and/or an SSRI. <div class="ec-src"><b>Source:</b> American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 5th Edition, Text Revision (DSM-5-TR). Washington, DC: APA; 2022.</div></div></div> [[Try this question again->Panic disorder - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Panic disorder. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ GAD has a different pattern.</div> Generalized anxiety disorder involves chronic, pervasive worry about multiple domains without the discrete, sudden-onset panic attacks that characterize panic disorder. <div class="ec-teach"><div class="th">What to do instead</div> Recurrent unexpected panic attacks, discrete episodes of intense fear with cardiorespiratory and autonomic symptoms peaking within minutes, followed by persistent concern about additional attacks and maladaptive behavioral change (avoidance of malls) fulfill DSM-5-TR criteria for panic disorder. A thorough medical workup excluding cardiac, thyroid, and substance-related causes is essential before making the diagnosis. First-line treatment includes CBT and/or an SSRI. <div class="ec-src"><b>Source:</b> American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 5th Edition, Text Revision (DSM-5-TR). Washington, DC: APA; 2022.</div></div></div> [[Try this question again->Panic disorder - Dx]] [[Start another case->Hub]]

<div class="ec-scene">Infectious disease consult · 11:00</div> A 58-year-old man with a mechanical aortic valve presents with 3 weeks of fevers and malaise. Temperature is 38.8°C (101.8°F), blood pressure 118/72 mm Hg, and pulse is 96/min. Four of four blood cultures grow methicillin-sensitive Staphylococcus aureus. Transesophageal echocardiography shows a 14-mm vegetation on the prosthetic valve with moderate paravalvular regurgitation. He is hemodynamically stable. <span class="ec-prompt">Which of the following is the most appropriate management?</span> [[Intensification of anticoagulation alone without antibiotics->Infective endocarditis - D4]] [[Intravenous antibiotics with early surgical consultation->Infective endocarditis - Correct]] [[Observation with serial blood cultures and no antibiotics->Infective endocarditis - D2]] [[Oral antibiotics alone for a 14-day outpatient course->Infective endocarditis - D1]] [[Watchful waiting with serial echocardiography every 2 weeks->Infective endocarditis - D3]]

<span class="ec-case-marker" hidden data-entry="Infective endocarditis. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Intravenous antibiotics with early surgical consultation</div> Prosthetic-valve endocarditis caused by S. aureus with a large vegetation (≥10 mm) and paravalvular complications meets guideline criteria for early surgery. IV bactericidal antibiotics (nafcillin or oxacillin for MSSA, plus rifampin and gentamicin per ESC/AHA guidance) are initiated immediately. Surgical indications include prosthetic valve involvement with S. aureus, paravalvular extension, large vegetations with embolic risk, and hemodynamic compromise. Even in stable patients, early surgery reduces mortality compared with antibiotic therapy alone when these features are present. <div class="ec-src"><b>Source:</b> Delgado V, et al. 2023 ESC Guidelines for the Management of Endocarditis. Eur Heart J 2023;44(39):3948-4042.</div></div> [[Start another case->Hub]] [[Restart this case->Infective endocarditis - Rx]] [[Next case →->Viridans endocarditis - Micro]]

<span class="ec-case-marker" hidden data-entry="Infective endocarditis. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Oral antibiotics are insufficient.</div> Endocarditis requires prolonged IV bactericidal therapy, typically 6 weeks for prosthetic-valve infection. Oral therapy alone provides inadequate serum bactericidal activity for a deep-seated intravascular infection. <div class="ec-teach"><div class="th">What to do instead</div> Prosthetic-valve endocarditis caused by S. aureus with a large vegetation (≥10 mm) and paravalvular complications meets guideline criteria for early surgery. IV bactericidal antibiotics (nafcillin or oxacillin for MSSA, plus rifampin and gentamicin per ESC/AHA guidance) are initiated immediately. Surgical indications include prosthetic valve involvement with S. aureus, paravalvular extension, large vegetations with embolic risk, and hemodynamic compromise. Even in stable patients, early surgery reduces mortality compared with antibiotic therapy alone when these features are present. <div class="ec-src"><b>Source:</b> Delgado V, et al. 2023 ESC Guidelines for the Management of Endocarditis. Eur Heart J 2023;44(39):3948-4042.</div></div></div> [[Try this question again->Infective endocarditis - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Infective endocarditis. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Untreated endocarditis is fatal.</div> S. aureus prosthetic-valve endocarditis has extremely high mortality without treatment. Observation is not an option. <div class="ec-teach"><div class="th">What to do instead</div> Prosthetic-valve endocarditis caused by S. aureus with a large vegetation (≥10 mm) and paravalvular complications meets guideline criteria for early surgery. IV bactericidal antibiotics (nafcillin or oxacillin for MSSA, plus rifampin and gentamicin per ESC/AHA guidance) are initiated immediately. Surgical indications include prosthetic valve involvement with S. aureus, paravalvular extension, large vegetations with embolic risk, and hemodynamic compromise. Even in stable patients, early surgery reduces mortality compared with antibiotic therapy alone when these features are present. <div class="ec-src"><b>Source:</b> Delgado V, et al. 2023 ESC Guidelines for the Management of Endocarditis. Eur Heart J 2023;44(39):3948-4042.</div></div></div> [[Try this question again->Infective endocarditis - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Infective endocarditis. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Watchful waiting risks catastrophic embolization.</div> A 14-mm vegetation with S. aureus on a prosthetic valve carries extremely high embolic and mortality risk. Serial echocardiography without surgical consultation allows the vegetation to grow and embolize. Early surgical evaluation is indicated by current guidelines. <div class="ec-teach"><div class="th">What to do instead</div> Prosthetic-valve endocarditis caused by S. aureus with a large vegetation (≥10 mm) and paravalvular complications meets guideline criteria for early surgery. IV bactericidal antibiotics (nafcillin or oxacillin for MSSA, plus rifampin and gentamicin per ESC/AHA guidance) are initiated immediately. Surgical indications include prosthetic valve involvement with S. aureus, paravalvular extension, large vegetations with embolic risk, and hemodynamic compromise. Even in stable patients, early surgery reduces mortality compared with antibiotic therapy alone when these features are present. <div class="ec-src"><b>Source:</b> Delgado V, et al. 2023 ESC Guidelines for the Management of Endocarditis. Eur Heart J 2023;44(39):3948-4042.</div></div></div> [[Try this question again->Infective endocarditis - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Infective endocarditis. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Anticoagulation alone does not treat infection.</div> While mechanical valve patients require anticoagulation, it does not treat the underlying infection or prevent vegetation growth. Management of anticoagulation during active endocarditis is complex and requires multidisciplinary input. <div class="ec-teach"><div class="th">What to do instead</div> Prosthetic-valve endocarditis caused by S. aureus with a large vegetation (≥10 mm) and paravalvular complications meets guideline criteria for early surgery. IV bactericidal antibiotics (nafcillin or oxacillin for MSSA, plus rifampin and gentamicin per ESC/AHA guidance) are initiated immediately. Surgical indications include prosthetic valve involvement with S. aureus, paravalvular extension, large vegetations with embolic risk, and hemodynamic compromise. Even in stable patients, early surgery reduces mortality compared with antibiotic therapy alone when these features are present. <div class="ec-src"><b>Source:</b> Delgado V, et al. 2023 ESC Guidelines for the Management of Endocarditis. Eur Heart J 2023;44(39):3948-4042.</div></div></div> [[Try this question again->Infective endocarditis - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Pediatric hematology clinic · 14:30</div> A 9-year-old boy has had intermittent jaundice for several years, with mild splenomegaly, a hemoglobin of 10.2 g/dL, and reticulocytosis. His mother has a similar history. Peripheral smear shows spherocytes. Direct antiglobulin test is negative. <span class="ec-prompt">Which of the following tests best confirms the suspected diagnosis?</span> [[Bone marrow aspiration with cytogenetic analysis->Hereditary spherocytosis - D3]] [[Eosin-5-maleimide binding test or osmotic fragility test->Hereditary spherocytosis - Correct]] [[Hemoglobin electrophoresis for variant hemoglobins->Hereditary spherocytosis - D1]] [[Serum iron, TIBC, and ferritin panel->Hereditary spherocytosis - D2]] [[Serum vitamin vitamin B12 and methylmalonic acid levels->Hereditary spherocytosis - D4]]

<span class="ec-case-marker" hidden data-entry="Hereditary spherocytosis. Ix"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Eosin-5-maleimide binding test or osmotic fragility test</div> Hereditary spherocytosis is confirmed by demonstrating reduced red cell membrane protein (band 3, spectrin) with the eosin-5-maleimide (EMA) flow cytometry binding test, which has largely replaced the traditional osmotic fragility test due to superior sensitivity and specificity. The negative DAT excludes autoimmune hemolytic anemia, which also produces spherocytes. Family history of similar episodes supports an inherited membrane defect. <div class="ec-src"><b>Source:</b> Bolton-Maggs PHB, et al. Guidelines for the Diagnosis and Management of Hereditary Spherocytosis-2011 Update. Br J Haematol 2012;156(1):37-49.</div></div> [[Start another case->Hub]] [[Restart this case->Hereditary spherocytosis - Ix]] [[Next case →->HbS polymerization - Mech]]

<span class="ec-case-marker" hidden data-entry="Hereditary spherocytosis. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Electrophoresis detects hemoglobinopathies.</div> Hemoglobin electrophoresis identifies sickle cell disease and thalassemias. It does not detect red cell membrane defects. <div class="ec-teach"><div class="th">What to do instead</div> Hereditary spherocytosis is confirmed by demonstrating reduced red cell membrane protein (band 3, spectrin) with the eosin-5-maleimide (EMA) flow cytometry binding test, which has largely replaced the traditional osmotic fragility test due to superior sensitivity and specificity. The negative DAT excludes autoimmune hemolytic anemia, which also produces spherocytes. Family history of similar episodes supports an inherited membrane defect. <div class="ec-src"><b>Source:</b> Bolton-Maggs PHB, et al. Guidelines for the Diagnosis and Management of Hereditary Spherocytosis-2011 Update. Br J Haematol 2012;156(1):37-49.</div></div></div> [[Try this question again->Hereditary spherocytosis - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Hereditary spherocytosis. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Iron studies are for iron deficiency.</div> This is a hemolytic anemia with reticulocytosis, not iron deficiency. Iron stores are typically normal or elevated in chronic hemolysis. <div class="ec-teach"><div class="th">What to do instead</div> Hereditary spherocytosis is confirmed by demonstrating reduced red cell membrane protein (band 3, spectrin) with the eosin-5-maleimide (EMA) flow cytometry binding test, which has largely replaced the traditional osmotic fragility test due to superior sensitivity and specificity. The negative DAT excludes autoimmune hemolytic anemia, which also produces spherocytes. Family history of similar episodes supports an inherited membrane defect. <div class="ec-src"><b>Source:</b> Bolton-Maggs PHB, et al. Guidelines for the Diagnosis and Management of Hereditary Spherocytosis-2011 Update. Br J Haematol 2012;156(1):37-49.</div></div></div> [[Try this question again->Hereditary spherocytosis - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Hereditary spherocytosis. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Bone marrow biopsy is not needed.</div> The diagnosis can be made with peripheral blood testing. Bone marrow biopsy is unnecessary and overly invasive for hereditary spherocytosis. <div class="ec-teach"><div class="th">What to do instead</div> Hereditary spherocytosis is confirmed by demonstrating reduced red cell membrane protein (band 3, spectrin) with the eosin-5-maleimide (EMA) flow cytometry binding test, which has largely replaced the traditional osmotic fragility test due to superior sensitivity and specificity. The negative DAT excludes autoimmune hemolytic anemia, which also produces spherocytes. Family history of similar episodes supports an inherited membrane defect. <div class="ec-src"><b>Source:</b> Bolton-Maggs PHB, et al. Guidelines for the Diagnosis and Management of Hereditary Spherocytosis-2011 Update. Br J Haematol 2012;156(1):37-49.</div></div></div> [[Try this question again->Hereditary spherocytosis - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Hereditary spherocytosis. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ B12 deficiency causes macrocytic anemia.</div> Vitamin B12 deficiency produces large oval macrocytes and hypersegmented neutrophils, not spherocytes. <div class="ec-teach"><div class="th">What to do instead</div> Hereditary spherocytosis is confirmed by demonstrating reduced red cell membrane protein (band 3, spectrin) with the eosin-5-maleimide (EMA) flow cytometry binding test, which has largely replaced the traditional osmotic fragility test due to superior sensitivity and specificity. The negative DAT excludes autoimmune hemolytic anemia, which also produces spherocytes. Family history of similar episodes supports an inherited membrane defect. <div class="ec-src"><b>Source:</b> Bolton-Maggs PHB, et al. Guidelines for the Diagnosis and Management of Hereditary Spherocytosis-2011 Update. Br J Haematol 2012;156(1):37-49.</div></div></div> [[Try this question again->Hereditary spherocytosis - Ix]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 17:00</div> A 73-year-old woman has had a new severe temporal headache and jaw claudication for 2 weeks, with tenderness over both temporal arteries. Temperature is 37.6°C (99.7°F), blood pressure is 156/84 mm Hg, and pulse is 86/min. ESR is 94 mm/h and C-reactive protein is 78 mg/L. She has had two episodes of transient monocular visual loss over the past 48 hours. <span class="ec-prompt">Which of the following is the most appropriate initial treatment?</span> [[High-dose glucocorticoid therapy->Giant cell arteritis - Correct]] [[Intravenous pulse cyclophosphamide for immunosuppression->Giant cell arteritis - D3]] [[Oral prednisone 10 mg daily as initial dose->Giant cell arteritis - D4]] [[Tocilizumab alone as initial treatment->Giant cell arteritis - D2]] [[Wait for temporal artery biopsy results before treating->Giant cell arteritis - D1]]

<span class="ec-case-marker" hidden data-entry="Giant cell arteritis. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ High-dose glucocorticoid therapy.</div> Suspected GCA with visual symptoms is an emergency. IV methylprednisolone (1 g daily for 3 days) followed by oral prednisone 1 mg/kg/day is recommended when visual loss has occurred or is threatened. Glucocorticoids must not be delayed for biopsy, temporal artery biopsy remains diagnostic for at least 2 weeks after initiating steroids. Permanent bilateral blindness from anterior ischemic optic neuropathy occurs in 15–20% of untreated patients with visual symptoms. Tocilizumab is used as a steroid-sparing agent for maintenance. <div class="ec-src"><b>Source:</b> Maz M, et al. 2021 ACR/Vasculitis Foundation Guideline for the Management of Giant Cell Arteritis and Takayasu Arteritis. Arthritis Rheumatol 2021;73(8):1349-1365.</div></div> [[Start another case->Hub]] [[Restart this case->Giant cell arteritis - Rx]] [[Next case →->Acute gout - Rx]]

<span class="ec-case-marker" hidden data-entry="Giant cell arteritis. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Waiting risks permanent blindness.</div> Temporal artery biopsy can be performed within 2 weeks of starting steroids without affecting diagnostic yield. The visual symptoms mandate immediate treatment. <div class="ec-teach"><div class="th">What to do instead</div> Suspected GCA with visual symptoms is an emergency. IV methylprednisolone (1 g daily for 3 days) followed by oral prednisone 1 mg/kg/day is recommended when visual loss has occurred or is threatened. Glucocorticoids must not be delayed for biopsy, temporal artery biopsy remains diagnostic for at least 2 weeks after initiating steroids. Permanent bilateral blindness from anterior ischemic optic neuropathy occurs in 15–20% of untreated patients with visual symptoms. Tocilizumab is used as a steroid-sparing agent for maintenance. <div class="ec-src"><b>Source:</b> Maz M, et al. 2021 ACR/Vasculitis Foundation Guideline for the Management of Giant Cell Arteritis and Takayasu Arteritis. Arthritis Rheumatol 2021;73(8):1349-1365.</div></div></div> [[Try this question again->Giant cell arteritis - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Giant cell arteritis. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Tocilizumab is steroid-sparing, not a replacement.</div> Tocilizumab is FDA-approved for GCA and reduces the cumulative steroid dose during maintenance. However, in acute GCA with threatened vision, high-dose glucocorticoids must be initiated immediately. Tocilizumab is added as a steroid-sparing strategy, not used alone as initial therapy. <div class="ec-teach"><div class="th">What to do instead</div> Suspected GCA with visual symptoms is an emergency. IV methylprednisolone (1 g daily for 3 days) followed by oral prednisone 1 mg/kg/day is recommended when visual loss has occurred or is threatened. Glucocorticoids must not be delayed for biopsy, temporal artery biopsy remains diagnostic for at least 2 weeks after initiating steroids. Permanent bilateral blindness from anterior ischemic optic neuropathy occurs in 15–20% of untreated patients with visual symptoms. Tocilizumab is used as a steroid-sparing agent for maintenance. <div class="ec-src"><b>Source:</b> Maz M, et al. 2021 ACR/Vasculitis Foundation Guideline for the Management of Giant Cell Arteritis and Takayasu Arteritis. Arthritis Rheumatol 2021;73(8):1349-1365.</div></div></div> [[Try this question again->Giant cell arteritis - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Giant cell arteritis. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Cyclophosphamide is not used for GCA.</div> Cyclophosphamide is used in ANCA-associated vasculitis, not giant cell arteritis. GCA responds to high-dose glucocorticoids. Tocilizumab is the evidence-based steroid-sparing agent for GCA, not cyclophosphamide. <div class="ec-teach"><div class="th">What to do instead</div> Suspected GCA with visual symptoms is an emergency. IV methylprednisolone (1 g daily for 3 days) followed by oral prednisone 1 mg/kg/day is recommended when visual loss has occurred or is threatened. Glucocorticoids must not be delayed for biopsy, temporal artery biopsy remains diagnostic for at least 2 weeks after initiating steroids. Permanent bilateral blindness from anterior ischemic optic neuropathy occurs in 15–20% of untreated patients with visual symptoms. Tocilizumab is used as a steroid-sparing agent for maintenance. <div class="ec-src"><b>Source:</b> Maz M, et al. 2021 ACR/Vasculitis Foundation Guideline for the Management of Giant Cell Arteritis and Takayasu Arteritis. Arthritis Rheumatol 2021;73(8):1349-1365.</div></div></div> [[Try this question again->Giant cell arteritis - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Giant cell arteritis. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Low-dose prednisone is insufficient for visual symptoms.</div> When visual loss or threatened vision is present, GCA requires IV pulse methylprednisolone (1 g daily for 3 days) followed by high-dose oral prednisone (1 mg/kg/day). Starting at 10 mg daily risks permanent blindness from inadequate inflammation suppression. <div class="ec-teach"><div class="th">What to do instead</div> Suspected GCA with visual symptoms is an emergency. IV methylprednisolone (1 g daily for 3 days) followed by oral prednisone 1 mg/kg/day is recommended when visual loss has occurred or is threatened. Glucocorticoids must not be delayed for biopsy, temporal artery biopsy remains diagnostic for at least 2 weeks after initiating steroids. Permanent bilateral blindness from anterior ischemic optic neuropathy occurs in 15–20% of untreated patients with visual symptoms. Tocilizumab is used as a steroid-sparing agent for maintenance. <div class="ec-src"><b>Source:</b> Maz M, et al. 2021 ACR/Vasculitis Foundation Guideline for the Management of Giant Cell Arteritis and Takayasu Arteritis. Arthritis Rheumatol 2021;73(8):1349-1365.</div></div></div> [[Try this question again->Giant cell arteritis - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Internal medicine clinic · 10:00</div> A 45-year-old man presents with progressive bilateral lower extremity edema and foamy urine over 4 weeks. Serum albumin is 2.1 g/dL. Urinalysis shows 4+ protein; 24-hour urine protein is 8.2 g. Serum cholesterol is 340 mg/dL. Serum creatinine is 0.9 mg/dL. <span class="ec-prompt">Which of the following best describes this clinical syndrome?</span> [[Acute interstitial nephritis->Nephrotic syndrome - D2]] [[Diabetic nephropathy without nephrotic-range proteinuria->Nephrotic syndrome - D4]] [[Nephritic syndrome->Nephrotic syndrome - D1]] [[Nephrotic syndrome->Nephrotic syndrome - Correct]] [[Urinary tract infection->Nephrotic syndrome - D3]]

<span class="ec-case-marker" hidden data-entry="Nephrotic syndrome. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Nephrotic syndrome.</div> The classic nephrotic syndrome pentad is: (1) massive proteinuria (>3.5 g/day), (2) hypoalbuminemia, (3) peripheral edema, (4) hyperlipidemia, and (5) lipiduria. This patient demonstrates all five features. Common causes in adults include membranous nephropathy, focal segmental glomerulosclerosis, minimal change disease, and diabetic nephropathy. Renal biopsy is typically indicated in adults to determine the underlying cause and guide treatment. <div class="ec-src"><b>Source:</b> Kodner C. Diagnosis and Management of Nephrotic Syndrome in Adults. Am Fam Physician 2016;93(6):479-485; KDIGO Glomerulonephritis Guidelines.</div></div> [[Start another case->Hub]] [[Restart this case->Nephrotic syndrome - Dx]] [[Next case →->Glomerular hematuria - Ix]]

<span class="ec-case-marker" hidden data-entry="Nephrotic syndrome. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Nephritic syndrome has different features.</div> Nephritic syndrome is characterized by hematuria (often with RBC casts), mild-to-moderate proteinuria, hypertension, and reduced GFR. This patient has massive proteinuria without hematuria, which is nephrotic. <div class="ec-teach"><div class="th">What to do instead</div> The classic nephrotic syndrome pentad is: (1) massive proteinuria (>3.5 g/day), (2) hypoalbuminemia, (3) peripheral edema, (4) hyperlipidemia, and (5) lipiduria. This patient demonstrates all five features. Common causes in adults include membranous nephropathy, focal segmental glomerulosclerosis, minimal change disease, and diabetic nephropathy. Renal biopsy is typically indicated in adults to determine the underlying cause and guide treatment. <div class="ec-src"><b>Source:</b> Kodner C. Diagnosis and Management of Nephrotic Syndrome in Adults. Am Fam Physician 2016;93(6):479-485; KDIGO Glomerulonephritis Guidelines.</div></div></div> [[Try this question again->Nephrotic syndrome - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Nephrotic syndrome. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ AIN presents differently.</div> Acute interstitial nephritis typically presents with rising creatinine, eosinophilia, and sometimes a drug exposure history. Massive proteinuria is not characteristic. <div class="ec-teach"><div class="th">What to do instead</div> The classic nephrotic syndrome pentad is: (1) massive proteinuria (>3.5 g/day), (2) hypoalbuminemia, (3) peripheral edema, (4) hyperlipidemia, and (5) lipiduria. This patient demonstrates all five features. Common causes in adults include membranous nephropathy, focal segmental glomerulosclerosis, minimal change disease, and diabetic nephropathy. Renal biopsy is typically indicated in adults to determine the underlying cause and guide treatment. <div class="ec-src"><b>Source:</b> Kodner C. Diagnosis and Management of Nephrotic Syndrome in Adults. Am Fam Physician 2016;93(6):479-485; KDIGO Glomerulonephritis Guidelines.</div></div></div> [[Try this question again->Nephrotic syndrome - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Nephrotic syndrome. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ UTI does not cause massive proteinuria.</div> Urinary tract infections cause dysuria, frequency, and pyuria, not 8 g/day proteinuria with hypoalbuminemia and edema. <div class="ec-teach"><div class="th">What to do instead</div> The classic nephrotic syndrome pentad is: (1) massive proteinuria (>3.5 g/day), (2) hypoalbuminemia, (3) peripheral edema, (4) hyperlipidemia, and (5) lipiduria. This patient demonstrates all five features. Common causes in adults include membranous nephropathy, focal segmental glomerulosclerosis, minimal change disease, and diabetic nephropathy. Renal biopsy is typically indicated in adults to determine the underlying cause and guide treatment. <div class="ec-src"><b>Source:</b> Kodner C. Diagnosis and Management of Nephrotic Syndrome in Adults. Am Fam Physician 2016;93(6):479-485; KDIGO Glomerulonephritis Guidelines.</div></div></div> [[Try this question again->Nephrotic syndrome - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Nephrotic syndrome. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ The proteinuria exceeds what diabetic nephropathy typically presents without additional features.</div> While diabetic nephropathy can cause nephrotic syndrome, this patient has no stated history of diabetes, and the full nephrotic syndrome pentad, proteinuria >3.5 g/day, hypoalbuminemia, edema, hyperlipidemia, is better classified as nephrotic syndrome requiring evaluation for underlying glomerular disease. <div class="ec-teach"><div class="th">What to do instead</div> The classic nephrotic syndrome pentad is: (1) massive proteinuria (>3.5 g/day), (2) hypoalbuminemia, (3) peripheral edema, (4) hyperlipidemia, and (5) lipiduria. This patient demonstrates all five features. Common causes in adults include membranous nephropathy, focal segmental glomerulosclerosis, minimal change disease, and diabetic nephropathy. Renal biopsy is typically indicated in adults to determine the underlying cause and guide treatment. <div class="ec-src"><b>Source:</b> Kodner C. Diagnosis and Management of Nephrotic Syndrome in Adults. Am Fam Physician 2016;93(6):479-485; KDIGO Glomerulonephritis Guidelines.</div></div></div> [[Try this question again->Nephrotic syndrome - Dx]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 01:22</div> A 19-year-old man presents with 18 hours of abdominal pain that began periumbilically and migrated to the right lower quadrant. He has anorexia, nausea, and low-grade fever. Temperature is 37.9°C (100.2°F), blood pressure 122/76 mm Hg, and pulse is 94/min. Examination shows focal tenderness at McBurney's point with guarding. WBC is 14,200/mm3. CT abdomen shows a dilated appendix with periappendiceal fat stranding and no perforation. <span class="ec-prompt">Which of the following is the most appropriate management?</span> [[Intravenous antibiotics alone without surgery->Acute appendicitis - D2]] [[Laparoscopic appendectomy within 24 hours->Acute appendicitis - Correct]] [[Observation with serial abdominal examinations for 1 week->Acute appendicitis - D3]] [[Oral antibiotics and outpatient follow-up->Acute appendicitis - D1]] [[Percutaneous CT-guided drainage->Acute appendicitis - D4]]

<span class="ec-case-marker" hidden data-entry="Acute appendicitis. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Laparoscopic appendectomy within 24 hours</div> Acute uncomplicated appendicitis in a young adult with CT confirmation is a surgical indication. Laparoscopic appendectomy remains the standard of care and is associated with low complication rates, rapid recovery, and definitive treatment. While recent trials have explored antibiotic-first strategies for uncomplicated appendicitis, appendectomy remains the guideline-recommended definitive treatment, particularly given the 25–40% recurrence rate with antibiotic-only management. <div class="ec-src"><b>Source:</b> Di Saverio S, et al. Diagnosis and Treatment of Acute Appendicitis: 2020 Update of the WSES Jerusalem Guidelines. World J Emerg Surg 2020;15(1):27.</div></div> [[Start another case->Hub]] [[Restart this case->Acute appendicitis - Rx]] [[Next case →->Ulcerative colitis - Rx]]

<span class="ec-case-marker" hidden data-entry="Acute appendicitis. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Antibiotics alone have a 25–40% recurrence rate.</div> The CODA trial and others have shown that antibiotic treatment of uncomplicated appendicitis is feasible but carries a substantial recurrence risk. Appendectomy remains the guideline-recommended definitive treatment, particularly in a young, healthy patient with a clear CT diagnosis. <div class="ec-teach"><div class="th">What to do instead</div> Acute uncomplicated appendicitis in a young adult with CT confirmation is a surgical indication. Laparoscopic appendectomy remains the standard of care and is associated with low complication rates, rapid recovery, and definitive treatment. While recent trials have explored antibiotic-first strategies for uncomplicated appendicitis, appendectomy remains the guideline-recommended definitive treatment, particularly given the 25–40% recurrence rate with antibiotic-only management. <div class="ec-src"><b>Source:</b> Di Saverio S, et al. Diagnosis and Treatment of Acute Appendicitis: 2020 Update of the WSES Jerusalem Guidelines. World J Emerg Surg 2020;15(1):27.</div></div></div> [[Try this question again->Acute appendicitis - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Acute appendicitis. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Prolonged observation risks complications.</div> A week of observation for confirmed appendicitis risks progression to perforation, abscess, and peritonitis. <div class="ec-teach"><div class="th">What to do instead</div> Acute uncomplicated appendicitis in a young adult with CT confirmation is a surgical indication. Laparoscopic appendectomy remains the standard of care and is associated with low complication rates, rapid recovery, and definitive treatment. While recent trials have explored antibiotic-first strategies for uncomplicated appendicitis, appendectomy remains the guideline-recommended definitive treatment, particularly given the 25–40% recurrence rate with antibiotic-only management. <div class="ec-src"><b>Source:</b> Di Saverio S, et al. Diagnosis and Treatment of Acute Appendicitis: 2020 Update of the WSES Jerusalem Guidelines. World J Emerg Surg 2020;15(1):27.</div></div></div> [[Try this question again->Acute appendicitis - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Acute appendicitis. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Percutaneous drainage is for complicated appendicitis.</div> CT-guided drainage is used for appendiceal abscess in patients who are poor surgical candidates or as a temporizing measure. In uncomplicated appendicitis confirmed by CT, appendectomy is the definitive treatment. <div class="ec-teach"><div class="th">What to do instead</div> Acute uncomplicated appendicitis in a young adult with CT confirmation is a surgical indication. Laparoscopic appendectomy remains the standard of care and is associated with low complication rates, rapid recovery, and definitive treatment. While recent trials have explored antibiotic-first strategies for uncomplicated appendicitis, appendectomy remains the guideline-recommended definitive treatment, particularly given the 25–40% recurrence rate with antibiotic-only management. <div class="ec-src"><b>Source:</b> Di Saverio S, et al. Diagnosis and Treatment of Acute Appendicitis: 2020 Update of the WSES Jerusalem Guidelines. World J Emerg Surg 2020;15(1):27.</div></div></div> [[Try this question again->Acute appendicitis - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Ent clinic · 14:45</div> A 46-year-old woman has recurrent episodes of severe rotatory vertigo lasting 2–4 hours, accompanied by unilateral tinnitus and a sensation of aural fullness in the left ear. Audiometry during an episode shows low-frequency sensorineural hearing loss in the left ear. Between episodes she has mild residual hearing loss. <span class="ec-prompt">Which of the following is the most likely diagnosis?</span> [[Benign paroxysmal positional vertigo->Meniere disease - D1]] [[Ménière disease->Meniere disease - Correct]] [[Otitis externa->Meniere disease - D3]] [[Vestibular neuritis->Meniere disease - D2]] [[Vestibular schwannoma->Meniere disease - D4]]

<span class="ec-case-marker" hidden data-entry="Meniere disease. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Ménière disease.</div> The combination of episodic vertigo lasting 20 minutes to 12 hours, fluctuating low-frequency sensorineural hearing loss, tinnitus, and aural fullness, all localized to one ear, defines Ménière disease. The pathophysiology involves endolymphatic hydrops. Acute attacks are managed with vestibular suppressants and antiemetics. Long-term management includes dietary sodium restriction, diuretics, and intratympanic therapies for refractory cases. <div class="ec-src"><b>Source:</b> Basura GJ, et al. Clinical Practice Guideline: Ménière Disease. Otolaryngol Head Neck Surg 2020;162(2 Suppl):S1-S55.</div></div> [[Start another case->Hub]] [[Restart this case->Meniere disease - Dx]] [[Next case →->Post-arrest neuroprognostication - Prog]]

<span class="ec-case-marker" hidden data-entry="Meniere disease. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ BPPV has a different pattern.</div> BPPV causes brief episodes (<1 minute) of positional vertigo triggered by head movement, without hearing loss or tinnitus. This patient's episodes last hours. <div class="ec-teach"><div class="th">What to do instead</div> The combination of episodic vertigo lasting 20 minutes to 12 hours, fluctuating low-frequency sensorineural hearing loss, tinnitus, and aural fullness, all localized to one ear, defines Ménière disease. The pathophysiology involves endolymphatic hydrops. Acute attacks are managed with vestibular suppressants and antiemetics. Long-term management includes dietary sodium restriction, diuretics, and intratympanic therapies for refractory cases. <div class="ec-src"><b>Source:</b> Basura GJ, et al. Clinical Practice Guideline: Ménière Disease. Otolaryngol Head Neck Surg 2020;162(2 Suppl):S1-S55.</div></div></div> [[Try this question again->Meniere disease - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Meniere disease. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Vestibular neuritis is a single prolonged episode.</div> Vestibular neuritis causes a single severe episode of vertigo lasting days, without hearing loss. It does not recur in the episodic pattern described here. <div class="ec-teach"><div class="th">What to do instead</div> The combination of episodic vertigo lasting 20 minutes to 12 hours, fluctuating low-frequency sensorineural hearing loss, tinnitus, and aural fullness, all localized to one ear, defines Ménière disease. The pathophysiology involves endolymphatic hydrops. Acute attacks are managed with vestibular suppressants and antiemetics. Long-term management includes dietary sodium restriction, diuretics, and intratympanic therapies for refractory cases. <div class="ec-src"><b>Source:</b> Basura GJ, et al. Clinical Practice Guideline: Ménière Disease. Otolaryngol Head Neck Surg 2020;162(2 Suppl):S1-S55.</div></div></div> [[Try this question again->Meniere disease - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Meniere disease. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Otitis externa does not cause vertigo.</div> Otitis externa causes ear canal pain and discharge but does not cause vertigo, sensorineural hearing loss, or tinnitus. <div class="ec-teach"><div class="th">What to do instead</div> The combination of episodic vertigo lasting 20 minutes to 12 hours, fluctuating low-frequency sensorineural hearing loss, tinnitus, and aural fullness, all localized to one ear, defines Ménière disease. The pathophysiology involves endolymphatic hydrops. Acute attacks are managed with vestibular suppressants and antiemetics. Long-term management includes dietary sodium restriction, diuretics, and intratympanic therapies for refractory cases. <div class="ec-src"><b>Source:</b> Basura GJ, et al. Clinical Practice Guideline: Ménière Disease. Otolaryngol Head Neck Surg 2020;162(2 Suppl):S1-S55.</div></div></div> [[Try this question again->Meniere disease - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Meniere disease. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Schwannoma causes progressive unilateral hearing loss.</div> Vestibular schwannoma (acoustic neuroma) typically presents with slowly progressive unilateral sensorineural hearing loss and tinnitus, but not episodic vertigo. MRI should be considered to exclude this diagnosis. <div class="ec-teach"><div class="th">What to do instead</div> The combination of episodic vertigo lasting 20 minutes to 12 hours, fluctuating low-frequency sensorineural hearing loss, tinnitus, and aural fullness, all localized to one ear, defines Ménière disease. The pathophysiology involves endolymphatic hydrops. Acute attacks are managed with vestibular suppressants and antiemetics. Long-term management includes dietary sodium restriction, diuretics, and intratympanic therapies for refractory cases. <div class="ec-src"><b>Source:</b> Basura GJ, et al. Clinical Practice Guideline: Ménière Disease. Otolaryngol Head Neck Surg 2020;162(2 Suppl):S1-S55.</div></div></div> [[Try this question again->Meniere disease - Dx]] [[Start another case->Hub]]

<div class="ec-scene">Labor and delivery unit · 23:30</div> A 35-year-old woman at 36 weeks' gestation with a history of chronic hypertension develops sudden severe abdominal pain and dark vaginal bleeding. Her uterus is firm, tender, and contracted. Fetal heart rate tracing shows recurrent late decelerations. Blood pressure is 162/104 mm Hg. <span class="ec-prompt">Which of the following is the most likely diagnosis?</span> [[Cervical insufficiency->Placental abruption - D2]] [[Ectopic pregnancy->Placental abruption - D4]] [[Placenta previa->Placental abruption - D3]] [[Placental abruption->Placental abruption - Correct]] [[Vasa previa->Placental abruption - D1]]

<span class="ec-case-marker" hidden data-entry="Placental abruption. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Placental abruption.</div> Sudden painful vaginal bleeding with a rigid, tender uterus and fetal heart rate abnormalities in the third trimester is the classic presentation of placental abruption. Chronic hypertension is the strongest risk factor. The clinical triad, painful bleeding, uterine hypertonicity, and fetal distress, distinguishes abruption from placenta previa, which classically causes painless bright-red bleeding with a soft, nontender uterus. <div class="ec-src"><b>Source:</b> Oyelese Y, Ananth CV. Placental Abruption. Obstet Gynecol 2006;108(4):1005-1016.</div></div> [[Start another case->Hub]] [[Restart this case->Placental abruption - Dx]] [[Next case →->Postpartum hemorrhage - Opening]]

<span class="ec-case-marker" hidden data-entry="Placental abruption. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Vasa previa causes painless bleeding at membrane rupture.</div> Vasa previa presents with painless bleeding at the time of membrane rupture, with rapid fetal heart rate deterioration due to fetal blood loss. The uterus is not rigid or tender. <div class="ec-teach"><div class="th">What to do instead</div> Sudden painful vaginal bleeding with a rigid, tender uterus and fetal heart rate abnormalities in the third trimester is the classic presentation of placental abruption. Chronic hypertension is the strongest risk factor. The clinical triad, painful bleeding, uterine hypertonicity, and fetal distress, distinguishes abruption from placenta previa, which classically causes painless bright-red bleeding with a soft, nontender uterus. <div class="ec-src"><b>Source:</b> Oyelese Y, Ananth CV. Placental Abruption. Obstet Gynecol 2006;108(4):1005-1016.</div></div></div> [[Try this question again->Placental abruption - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Placental abruption. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Cervical insufficiency presents in the second trimester.</div> Cervical insufficiency causes painless cervical dilation typically in the second trimester. It does not present with a rigid uterus and severe pain at 36 weeks. <div class="ec-teach"><div class="th">What to do instead</div> Sudden painful vaginal bleeding with a rigid, tender uterus and fetal heart rate abnormalities in the third trimester is the classic presentation of placental abruption. Chronic hypertension is the strongest risk factor. The clinical triad, painful bleeding, uterine hypertonicity, and fetal distress, distinguishes abruption from placenta previa, which classically causes painless bright-red bleeding with a soft, nontender uterus. <div class="ec-src"><b>Source:</b> Oyelese Y, Ananth CV. Placental Abruption. Obstet Gynecol 2006;108(4):1005-1016.</div></div></div> [[Try this question again->Placental abruption - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Placental abruption. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Placenta previa causes painless bleeding.</div> The classic distinction: placenta previa produces painless bright-red bleeding with a soft uterus, while abruption produces painful dark bleeding with a rigid tender uterus. <div class="ec-teach"><div class="th">What to do instead</div> Sudden painful vaginal bleeding with a rigid, tender uterus and fetal heart rate abnormalities in the third trimester is the classic presentation of placental abruption. Chronic hypertension is the strongest risk factor. The clinical triad, painful bleeding, uterine hypertonicity, and fetal distress, distinguishes abruption from placenta previa, which classically causes painless bright-red bleeding with a soft, nontender uterus. <div class="ec-src"><b>Source:</b> Oyelese Y, Ananth CV. Placental Abruption. Obstet Gynecol 2006;108(4):1005-1016.</div></div></div> [[Try this question again->Placental abruption - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Placental abruption. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Ectopic pregnancy does not occur at 36 weeks.</div> Ectopic pregnancy presents in the first trimester. At 36 weeks, the pregnancy is well-established in the uterus. <div class="ec-teach"><div class="th">What to do instead</div> Sudden painful vaginal bleeding with a rigid, tender uterus and fetal heart rate abnormalities in the third trimester is the classic presentation of placental abruption. Chronic hypertension is the strongest risk factor. The clinical triad, painful bleeding, uterine hypertonicity, and fetal distress, distinguishes abruption from placenta previa, which classically causes painless bright-red bleeding with a soft, nontender uterus. <div class="ec-src"><b>Source:</b> Oyelese Y, Ananth CV. Placental Abruption. Obstet Gynecol 2006;108(4):1005-1016.</div></div></div> [[Try this question again->Placental abruption - Dx]] [[Start another case->Hub]]

<div class="ec-scene">Sports medicine clinic · 09:00</div> A 19-year-old college basketball player had exertional presyncope during a game 2 hours ago. His father died suddenly at age 42. Examination shows a grade 3/6 systolic murmur at the left sternal border that becomes louder when he stands up from a squat and softer when he squats down. Echocardiography shows asymmetric septal hypertrophy of 22 mm with systolic anterior motion of the mitral valve. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Activity restriction, beta blocker, risk stratification->HCM - Correct]] [[Clearance for continued competitive athletics participation->HCM - D1]] [[Nifedipine for afterload reduction and symptom control->HCM - D2]] [[Reassurance with no further cardiac evaluation needed->HCM - D4]] [[Referral for aortic valve replacement surgery->HCM - D3]]

<span class="ec-case-marker" hidden data-entry="HCM. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Activity restriction, beta blocker, risk stratification</div> This patient has obstructive HCM confirmed by echocardiography. The dynamic murmur that increases with reduced preload (standing) and decreases with increased preload (squatting) is highly characteristic of HCM. Management includes: (1) beta-blocker therapy to reduce the outflow gradient and symptoms, (2) formal SCD risk stratification using factors including family history of sudden death, unexplained (exertional) syncope, maximal wall thickness, and exercise testing to determine whether an implantable cardioverter-defibrillator is indicated, and (3) holding him from competitive play until that risk stratification and a shared decision-making conversation with his care team have taken place. The 2024 AHA/ACC/AMSSM/HRS/PACES/SCMR guideline explicitly moved away from automatically disqualifying athletes with HCM from competitive sports; it now recommends individualized shared decision-making informed by the athlete's specific risk profile, not blanket restriction. <div class="ec-src"><b>Source:</b> Ommen SR, et al. 2024 AHA/ACC/AMSSM/HRS/PACES/SCMR Guideline for the Management of Hypertrophic Cardiomyopathy. Circulation 2024;149(23):e1239-e1311.</div></div> [[Start another case->Hub]] [[Restart this case->HCM - Rx]] [[Next case →->Cardiac tamponade - Dx]]

<span class="ec-case-marker" hidden data-entry="HCM. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not before risk stratification.</div> HCM is the leading cause of sudden cardiac death in young athletes, and this patient has high-risk features (exertional presyncope, a first-degree relative who died suddenly at age 42). Clearing him for unrestricted competitive play right now, before beta-blocker therapy and formal SCD risk stratification, skips the steps that determine whether, and how, he can safely return to play. This does not mean sports are automatically forbidden either: per the 2024 multisociety guideline, return-to-play is decided through individualized shared decision-making after that risk assessment, not blanket restriction and not immediate clearance. <div class="ec-teach"><div class="th">What to do instead</div> This patient has obstructive HCM confirmed by echocardiography. The dynamic murmur that increases with reduced preload (standing) and decreases with increased preload (squatting) is highly characteristic of HCM. Management includes: (1) beta-blocker therapy to reduce the outflow gradient and symptoms, (2) formal SCD risk stratification using factors including family history of sudden death, unexplained (exertional) syncope, maximal wall thickness, and exercise testing to determine whether an implantable cardioverter-defibrillator is indicated, and (3) holding him from competitive play until that risk stratification and a shared decision-making conversation with his care team have taken place. The 2024 AHA/ACC/AMSSM/HRS/PACES/SCMR guideline explicitly moved away from automatically disqualifying athletes with HCM from competitive sports; it now recommends individualized shared decision-making informed by the athlete's specific risk profile, not blanket restriction. <div class="ec-src"><b>Source:</b> Ommen SR, et al. 2024 AHA/ACC/AMSSM/HRS/PACES/SCMR Guideline for the Management of Hypertrophic Cardiomyopathy. Circulation 2024;149(23):e1239-e1311.</div></div></div> [[Try this question again->HCM - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="HCM. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Vasodilators are harmful.</div> Vasodilators reduce afterload and worsen the dynamic LVOT obstruction by decreasing the ventricular cavity size. They are contraindicated in obstructive HCM. <div class="ec-teach"><div class="th">What to do instead</div> This patient has obstructive HCM confirmed by echocardiography. The dynamic murmur that increases with reduced preload (standing) and decreases with increased preload (squatting) is highly characteristic of HCM. Management includes: (1) beta-blocker therapy to reduce the outflow gradient and symptoms, (2) formal SCD risk stratification using factors including family history of sudden death, unexplained (exertional) syncope, maximal wall thickness, and exercise testing to determine whether an implantable cardioverter-defibrillator is indicated, and (3) holding him from competitive play until that risk stratification and a shared decision-making conversation with his care team have taken place. The 2024 AHA/ACC/AMSSM/HRS/PACES/SCMR guideline explicitly moved away from automatically disqualifying athletes with HCM from competitive sports; it now recommends individualized shared decision-making informed by the athlete's specific risk profile, not blanket restriction. <div class="ec-src"><b>Source:</b> Ommen SR, et al. 2024 AHA/ACC/AMSSM/HRS/PACES/SCMR Guideline for the Management of Hypertrophic Cardiomyopathy. Circulation 2024;149(23):e1239-e1311.</div></div></div> [[Try this question again->HCM - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="HCM. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ The aortic valve is not the problem.</div> The pathology is in the interventricular septum and mitral valve, not the aortic valve. Surgical myectomy (not valve replacement) is considered for refractory symptomatic obstruction. <div class="ec-teach"><div class="th">What to do instead</div> This patient has obstructive HCM confirmed by echocardiography. The dynamic murmur that increases with reduced preload (standing) and decreases with increased preload (squatting) is highly characteristic of HCM. Management includes: (1) beta-blocker therapy to reduce the outflow gradient and symptoms, (2) formal SCD risk stratification using factors including family history of sudden death, unexplained (exertional) syncope, maximal wall thickness, and exercise testing to determine whether an implantable cardioverter-defibrillator is indicated, and (3) holding him from competitive play until that risk stratification and a shared decision-making conversation with his care team have taken place. The 2024 AHA/ACC/AMSSM/HRS/PACES/SCMR guideline explicitly moved away from automatically disqualifying athletes with HCM from competitive sports; it now recommends individualized shared decision-making informed by the athlete's specific risk profile, not blanket restriction. <div class="ec-src"><b>Source:</b> Ommen SR, et al. 2024 AHA/ACC/AMSSM/HRS/PACES/SCMR Guideline for the Management of Hypertrophic Cardiomyopathy. Circulation 2024;149(23):e1239-e1311.</div></div></div> [[Try this question again->HCM - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="HCM. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ This requires urgent evaluation.</div> A young athlete with syncope, family history of sudden death, and confirmed HCM requires immediate beta-blocker therapy and comprehensive SCD risk stratification, not reassurance without further cardiac evaluation. <div class="ec-teach"><div class="th">What to do instead</div> This patient has obstructive HCM confirmed by echocardiography. The dynamic murmur that increases with reduced preload (standing) and decreases with increased preload (squatting) is highly characteristic of HCM. Management includes: (1) beta-blocker therapy to reduce the outflow gradient and symptoms, (2) formal SCD risk stratification using factors including family history of sudden death, unexplained (exertional) syncope, maximal wall thickness, and exercise testing to determine whether an implantable cardioverter-defibrillator is indicated, and (3) holding him from competitive play until that risk stratification and a shared decision-making conversation with his care team have taken place. The 2024 AHA/ACC/AMSSM/HRS/PACES/SCMR guideline explicitly moved away from automatically disqualifying athletes with HCM from competitive sports; it now recommends individualized shared decision-making informed by the athlete's specific risk profile, not blanket restriction. <div class="ec-src"><b>Source:</b> Ommen SR, et al. 2024 AHA/ACC/AMSSM/HRS/PACES/SCMR Guideline for the Management of Hypertrophic Cardiomyopathy. Circulation 2024;149(23):e1239-e1311.</div></div></div> [[Try this question again->HCM - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Gastroenterology clinic · 13:00</div> A 26-year-old man has recurrent bloody diarrhea, urgency, and tenesmus for 8 weeks. Colonoscopy shows continuous mucosal inflammation extending from the rectum to the splenic flexure with friability and loss of vascular pattern. Biopsies confirm chronic active colitis with crypt abscesses and no granulomas. Stool studies for infection are negative. <span class="ec-prompt">Which of the following is the most appropriate initial treatment for moderate ulcerative colitis?</span> [[Immediate colectomy->Ulcerative colitis - D1]] [[Observation without treatment->Ulcerative colitis - D4]] [[Oral budesonide alone without 5-ASA therapy->Ulcerative colitis - D2]] [[Oral loperamide as definitive therapy->Ulcerative colitis - D3]] [[Oral mesalamine plus topical mesalamine->Ulcerative colitis - Correct]]

<span class="ec-case-marker" hidden data-entry="Ulcerative colitis. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Oral mesalamine plus topical mesalamine</div> Moderate ulcerative colitis extending to the splenic flexure is best treated with combined oral and topical (rectal) mesalamine, which is superior to either formulation alone for induction of remission. If mesalamine is insufficient, oral corticosteroids (budesonide MMX or prednisone) are used for induction, followed by thiopurines or biologics for maintenance. Continuous mucosal inflammation starting at the rectum with no skip lesions and no granulomas distinguishes UC from Crohn disease. <div class="ec-src"><b>Source:</b> Rubin DT, et al. ACG Clinical Guideline: Ulcerative Colitis in Adults. Am J Gastroenterol 2019;114(3):384-413.</div></div> [[Start another case->Hub]] [[Restart this case->Ulcerative colitis - Rx]] [[Next case →->Celiac disease - Dx]]

<span class="ec-case-marker" hidden data-entry="Ulcerative colitis. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Colectomy is for refractory or fulminant disease.</div> Surgery is reserved for patients who fail medical therapy, develop dysplasia or cancer, or present with fulminant colitis or toxic megacolon. Medical therapy is always attempted first. <div class="ec-teach"><div class="th">What to do instead</div> Moderate ulcerative colitis extending to the splenic flexure is best treated with combined oral and topical (rectal) mesalamine, which is superior to either formulation alone for induction of remission. If mesalamine is insufficient, oral corticosteroids (budesonide MMX or prednisone) are used for induction, followed by thiopurines or biologics for maintenance. Continuous mucosal inflammation starting at the rectum with no skip lesions and no granulomas distinguishes UC from Crohn disease. <div class="ec-src"><b>Source:</b> Rubin DT, et al. ACG Clinical Guideline: Ulcerative Colitis in Adults. Am J Gastroenterol 2019;114(3):384-413.</div></div></div> [[Try this question again->Ulcerative colitis - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Ulcerative colitis. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Budesonide is for induction, not as solo first-line for moderate UC.</div> Budesonide MMX may be used for mild-to-moderate UC induction but is not as effective as combined oral and topical mesalamine for left-sided UC. Corticosteroids should not be used for maintenance, mesalamine is the first-line maintenance agent. <div class="ec-teach"><div class="th">What to do instead</div> Moderate ulcerative colitis extending to the splenic flexure is best treated with combined oral and topical (rectal) mesalamine, which is superior to either formulation alone for induction of remission. If mesalamine is insufficient, oral corticosteroids (budesonide MMX or prednisone) are used for induction, followed by thiopurines or biologics for maintenance. Continuous mucosal inflammation starting at the rectum with no skip lesions and no granulomas distinguishes UC from Crohn disease. <div class="ec-src"><b>Source:</b> Rubin DT, et al. ACG Clinical Guideline: Ulcerative Colitis in Adults. Am J Gastroenterol 2019;114(3):384-413.</div></div></div> [[Try this question again->Ulcerative colitis - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Ulcerative colitis. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Loperamide masks symptoms without treating inflammation.</div> Antimotility agents can be dangerous in active UC. The underlying mucosal inflammation must be treated, not masked. <div class="ec-teach"><div class="th">What to do instead</div> Moderate ulcerative colitis extending to the splenic flexure is best treated with combined oral and topical (rectal) mesalamine, which is superior to either formulation alone for induction of remission. If mesalamine is insufficient, oral corticosteroids (budesonide MMX or prednisone) are used for induction, followed by thiopurines or biologics for maintenance. Continuous mucosal inflammation starting at the rectum with no skip lesions and no granulomas distinguishes UC from Crohn disease. <div class="ec-src"><b>Source:</b> Rubin DT, et al. ACG Clinical Guideline: Ulcerative Colitis in Adults. Am J Gastroenterol 2019;114(3):384-413.</div></div></div> [[Try this question again->Ulcerative colitis - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Ulcerative colitis. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Active UC requires treatment.</div> Untreated moderate ulcerative colitis progresses, causes anemia and malnutrition, and increases the long-term risk of colorectal cancer. <div class="ec-teach"><div class="th">What to do instead</div> Moderate ulcerative colitis extending to the splenic flexure is best treated with combined oral and topical (rectal) mesalamine, which is superior to either formulation alone for induction of remission. If mesalamine is insufficient, oral corticosteroids (budesonide MMX or prednisone) are used for induction, followed by thiopurines or biologics for maintenance. Continuous mucosal inflammation starting at the rectum with no skip lesions and no granulomas distinguishes UC from Crohn disease. <div class="ec-src"><b>Source:</b> Rubin DT, et al. ACG Clinical Guideline: Ulcerative Colitis in Adults. Am J Gastroenterol 2019;114(3):384-413.</div></div></div> [[Try this question again->Ulcerative colitis - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Sleep medicine clinic · 10:30</div> A 49-year-old man with BMI 34 has had loud nightly snoring for 2 years, with witnessed apneic episodes reported by his wife, morning headaches, and excessive daytime sleepiness. His Epworth Sleepiness Scale score is 16. Blood pressure is 148/94 mm Hg. <span class="ec-prompt">Which of the following is the most appropriate diagnostic study?</span> [[Empiric CPAP trial without diagnostic testing->Sleep apnea - D4]] [[Lateral cephalometric radiography->Sleep apnea - D1]] [[Nocturnal pulse oximetry alone->Sleep apnea - D2]] [[Overnight polysomnography->Sleep apnea - Correct]] [[Serum TSH and morning cortisol->Sleep apnea - D3]]

<span class="ec-case-marker" hidden data-entry="Sleep apnea. Ix"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Overnight polysomnography.</div> In-laboratory polysomnography is the reference standard for diagnosing obstructive sleep apnea. It quantifies the apnea-hypopnea index (AHI), determines sleep architecture, and identifies oxygen desaturation patterns. Home sleep apnea testing is an acceptable alternative for patients with high pretest probability and no significant comorbidities. Treatment with CPAP reduces daytime sleepiness, improves quality of life, and lowers blood pressure. OSA is independently associated with resistant hypertension, atrial fibrillation, and cardiovascular mortality. <div class="ec-src"><b>Source:</b> Kapur VK, et al. Clinical Practice Guideline for Diagnostic Testing for Adult Obstructive Sleep Apnea: AASM. J Clin Sleep Med 2017;13(3):479-504.</div></div> [[Start another case->Hub]] [[Restart this case->Sleep apnea - Ix]] [[Next case →->IPF FVC decline - Prog]]

<span class="ec-case-marker" hidden data-entry="Sleep apnea. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Cephalometric imaging assesses anatomy, not sleep events.</div> Lateral cephalometry evaluates upper airway anatomy and is sometimes used in surgical planning for OSA but does not diagnose or quantify sleep-disordered breathing. <div class="ec-teach"><div class="th">What to do instead</div> In-laboratory polysomnography is the reference standard for diagnosing obstructive sleep apnea. It quantifies the apnea-hypopnea index (AHI), determines sleep architecture, and identifies oxygen desaturation patterns. Home sleep apnea testing is an acceptable alternative for patients with high pretest probability and no significant comorbidities. Treatment with CPAP reduces daytime sleepiness, improves quality of life, and lowers blood pressure. OSA is independently associated with resistant hypertension, atrial fibrillation, and cardiovascular mortality. <div class="ec-src"><b>Source:</b> Kapur VK, et al. Clinical Practice Guideline for Diagnostic Testing for Adult Obstructive Sleep Apnea: AASM. J Clin Sleep Med 2017;13(3):479-504.</div></div></div> [[Try this question again->Sleep apnea - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Sleep apnea. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Pulse oximetry alone has insufficient sensitivity.</div> Nocturnal pulse oximetry detects desaturations but cannot quantify apneas, hypopneas, arousals, or sleep staging. It misses obstructive events that do not cause significant desaturation and has unacceptable false-negative rates for OSA diagnosis. <div class="ec-teach"><div class="th">What to do instead</div> In-laboratory polysomnography is the reference standard for diagnosing obstructive sleep apnea. It quantifies the apnea-hypopnea index (AHI), determines sleep architecture, and identifies oxygen desaturation patterns. Home sleep apnea testing is an acceptable alternative for patients with high pretest probability and no significant comorbidities. Treatment with CPAP reduces daytime sleepiness, improves quality of life, and lowers blood pressure. OSA is independently associated with resistant hypertension, atrial fibrillation, and cardiovascular mortality. <div class="ec-src"><b>Source:</b> Kapur VK, et al. Clinical Practice Guideline for Diagnostic Testing for Adult Obstructive Sleep Apnea: AASM. J Clin Sleep Med 2017;13(3):479-504.</div></div></div> [[Try this question again->Sleep apnea - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Sleep apnea. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Endocrine testing does not diagnose OSA.</div> TSH should be checked to exclude hypothyroidism as a contributor, but it does not diagnose or quantify obstructive sleep apnea. The diagnostic study must directly measure respiratory events during sleep. <div class="ec-teach"><div class="th">What to do instead</div> In-laboratory polysomnography is the reference standard for diagnosing obstructive sleep apnea. It quantifies the apnea-hypopnea index (AHI), determines sleep architecture, and identifies oxygen desaturation patterns. Home sleep apnea testing is an acceptable alternative for patients with high pretest probability and no significant comorbidities. Treatment with CPAP reduces daytime sleepiness, improves quality of life, and lowers blood pressure. OSA is independently associated with resistant hypertension, atrial fibrillation, and cardiovascular mortality. <div class="ec-src"><b>Source:</b> Kapur VK, et al. Clinical Practice Guideline for Diagnostic Testing for Adult Obstructive Sleep Apnea: AASM. J Clin Sleep Med 2017;13(3):479-504.</div></div></div> [[Try this question again->Sleep apnea - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Sleep apnea. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Empiric CPAP without diagnosis is inappropriate.</div> Starting CPAP without objective diagnosis misses the opportunity to determine OSA severity, identify central apneas that require different treatment, and document the diagnosis for insurance authorization and long-term management. <div class="ec-teach"><div class="th">What to do instead</div> In-laboratory polysomnography is the reference standard for diagnosing obstructive sleep apnea. It quantifies the apnea-hypopnea index (AHI), determines sleep architecture, and identifies oxygen desaturation patterns. Home sleep apnea testing is an acceptable alternative for patients with high pretest probability and no significant comorbidities. Treatment with CPAP reduces daytime sleepiness, improves quality of life, and lowers blood pressure. OSA is independently associated with resistant hypertension, atrial fibrillation, and cardiovascular mortality. <div class="ec-src"><b>Source:</b> Kapur VK, et al. Clinical Practice Guideline for Diagnostic Testing for Adult Obstructive Sleep Apnea: AASM. J Clin Sleep Med 2017;13(3):479-504.</div></div></div> [[Try this question again->Sleep apnea - Ix]] [[Start another case->Hub]]

<div class="ec-scene">Endocrinology clinic · 11:00</div> A 43-year-old woman has resistant hypertension despite three antihypertensive agents and spontaneous hypokalemia (serum potassium 3.1 mEq/L on two occasions, off diuretics). Blood pressure is 168/102 mm Hg. Screening shows plasma aldosterone 28 ng/dL with suppressed renin (aldosterone-to-renin ratio 45). She is a surgical candidate and wishes to pursue potential cure. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Adrenal CT followed by adrenal vein sampling->Primary aldosteronism - Correct]] [[Immediate bilateral adrenalectomy without further workup->Primary aldosteronism - D1]] [[Loop diuretic monotherapy with no additional investigation->Primary aldosteronism - D2]] [[No additional workup based on the screening result alone->Primary aldosteronism - D3]] [[Overnight dexamethasone suppression test for cortisol excess->Primary aldosteronism - D4]]

<span class="ec-case-marker" hidden data-entry="Primary aldosteronism. Ix"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Adrenal CT followed by adrenal vein sampling</div> Under the 2025 Endocrine Society guideline, the biochemical triad of suppressed renin, elevated aldosterone, and elevated ARR, particularly in the presence of spontaneous hypokalemia, establishes primary aldosteronism without mandatory suppression testing. Confirmatory testing is now reserved for intermediate-probability cases when surgery is being considered. In a surgical candidate pursuing potential cure, the next step is lateralization: adrenal CT identifies gross anatomy, and adrenal vein sampling (AVS) determines whether aldosterone excess is unilateral (adenoma, curable by adrenalectomy) or bilateral (hyperplasia, managed medically with a mineralocorticoid receptor antagonist). AVS is essential because CT cannot reliably distinguish functioning adenomas from non-functioning incidentalomas. <div class="ec-src"><b>Source:</b> Adler GK, Stowasser M, Correa RR, et al. Primary Aldosteronism: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2025;110(9):2453-2495.</div></div> [[Start another case->Hub]] [[Restart this case->Primary aldosteronism - Ix]] [[Next case →->Vitamin D deficiency - Opening]]

<span class="ec-case-marker" hidden data-entry="Primary aldosteronism. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Bilateral adrenalectomy would cause permanent adrenal insufficiency. The entire point of adrenal vein sampling is to determine whether disease is unilateral (curable by unilateral adrenalectomy) or bilateral (managed medically). <div class="ec-teach"><div class="th">What to do instead</div> Under the 2025 Endocrine Society guideline, the biochemical triad of suppressed renin, elevated aldosterone, and elevated ARR, particularly in the presence of spontaneous hypokalemia, establishes primary aldosteronism without mandatory suppression testing. Confirmatory testing is now reserved for intermediate-probability cases when surgery is being considered. In a surgical candidate pursuing potential cure, the next step is lateralization: adrenal CT identifies gross anatomy, and adrenal vein sampling (AVS) determines whether aldosterone excess is unilateral (adenoma, curable by adrenalectomy) or bilateral (hyperplasia, managed medically with a mineralocorticoid receptor antagonist). AVS is essential because CT cannot reliably distinguish functioning adenomas from non-functioning incidentalomas. <div class="ec-src"><b>Source:</b> Adler GK, Stowasser M, Correa RR, et al. Primary Aldosteronism: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2025;110(9):2453-2495.</div></div></div> [[Try this question again->Primary aldosteronism - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Primary aldosteronism. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Loop diuretics do not treat the cause.</div> Loop diuretics do not block aldosterone and do not address the autonomous aldosterone secretion driving the hypertension and hypokalemia. Mineralocorticoid receptor antagonists (spironolactone, eplerenone) are the targeted medical therapy for patients who are not surgical candidates or who have bilateral disease on AVS. <div class="ec-teach"><div class="th">What to do instead</div> Under the 2025 Endocrine Society guideline, the biochemical triad of suppressed renin, elevated aldosterone, and elevated ARR, particularly in the presence of spontaneous hypokalemia, establishes primary aldosteronism without mandatory suppression testing. Confirmatory testing is now reserved for intermediate-probability cases when surgery is being considered. In a surgical candidate pursuing potential cure, the next step is lateralization: adrenal CT identifies gross anatomy, and adrenal vein sampling (AVS) determines whether aldosterone excess is unilateral (adenoma, curable by adrenalectomy) or bilateral (hyperplasia, managed medically with a mineralocorticoid receptor antagonist). AVS is essential because CT cannot reliably distinguish functioning adenomas from non-functioning incidentalomas. <div class="ec-src"><b>Source:</b> Adler GK, Stowasser M, Correa RR, et al. Primary Aldosteronism: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2025;110(9):2453-2495.</div></div></div> [[Try this question again->Primary aldosteronism - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Primary aldosteronism. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Diagnosis without lateralization is insufficient.</div> The 2025 Endocrine Society criteria establish the biochemical diagnosis of primary aldosteronism in this patient, but a surgical candidate pursuing potential cure still requires lateralization with adrenal CT and adrenal vein sampling before treatment planning. Doing nothing leaves her with uncontrolled hypertension, hypokalemia, and the excess cardiovascular risk that primary aldosteronism carries independent of blood pressure. <div class="ec-teach"><div class="th">What to do instead</div> Under the 2025 Endocrine Society guideline, the biochemical triad of suppressed renin, elevated aldosterone, and elevated ARR, particularly in the presence of spontaneous hypokalemia, establishes primary aldosteronism without mandatory suppression testing. Confirmatory testing is now reserved for intermediate-probability cases when surgery is being considered. In a surgical candidate pursuing potential cure, the next step is lateralization: adrenal CT identifies gross anatomy, and adrenal vein sampling (AVS) determines whether aldosterone excess is unilateral (adenoma, curable by adrenalectomy) or bilateral (hyperplasia, managed medically with a mineralocorticoid receptor antagonist). AVS is essential because CT cannot reliably distinguish functioning adenomas from non-functioning incidentalomas. <div class="ec-src"><b>Source:</b> Adler GK, Stowasser M, Correa RR, et al. Primary Aldosteronism: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2025;110(9):2453-2495.</div></div></div> [[Try this question again->Primary aldosteronism - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Primary aldosteronism. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Dexamethasone suppression tests for Cushing syndrome.</div> The overnight dexamethasone suppression test evaluates cortisol excess, not primary aldosteronism. Different hormonal axis, different disease. <div class="ec-teach"><div class="th">What to do instead</div> Under the 2025 Endocrine Society guideline, the biochemical triad of suppressed renin, elevated aldosterone, and elevated ARR, particularly in the presence of spontaneous hypokalemia, establishes primary aldosteronism without mandatory suppression testing. Confirmatory testing is now reserved for intermediate-probability cases when surgery is being considered. In a surgical candidate pursuing potential cure, the next step is lateralization: adrenal CT identifies gross anatomy, and adrenal vein sampling (AVS) determines whether aldosterone excess is unilateral (adenoma, curable by adrenalectomy) or bilateral (hyperplasia, managed medically with a mineralocorticoid receptor antagonist). AVS is essential because CT cannot reliably distinguish functioning adenomas from non-functioning incidentalomas. <div class="ec-src"><b>Source:</b> Adler GK, Stowasser M, Correa RR, et al. Primary Aldosteronism: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2025;110(9):2453-2495.</div></div></div> [[Try this question again->Primary aldosteronism - Ix]] [[Start another case->Hub]]

<div class="ec-scene">Student health center · 15:00</div> A 17-year-old student has fever, profound fatigue, sore throat, and posterior cervical lymphadenopathy for 10 days. Temperature is 38.4°C (101.1°F), blood pressure is 112/68 mm Hg, and pulse is 84/min. Rapid strep test is negative. CBC shows lymphocyte-predominant leukocytosis with 18% atypical lymphocytes. Heterophile antibody test (Monospot) is positive. His spleen is palpably enlarged. <span class="ec-prompt">Which of the following is the most appropriate management recommendation?</span> [[Amoxicillin 500 mg three times daily for pharyngitis->Mononucleosis - D1]] [[Avoidance of contact sports until splenomegaly resolves->Mononucleosis - Correct]] [[Immediate return to contact sports and full activity->Mononucleosis - D2]] [[Oral acyclovir 800 mg five times daily for 7 days->Mononucleosis - D4]] [[Systemic corticosteroid therapy->Mononucleosis - D3]]

<span class="ec-case-marker" hidden data-entry="Mononucleosis. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Avoidance of contact sports until splenomegaly resolves</div> Splenic rupture is the most feared complication of infectious mononucleosis and the leading cause of mono-related death. Patients with splenomegaly should avoid contact sports and strenuous activity for at least 3–4 weeks or until imaging confirms splenic size normalization. Management is otherwise supportive: rest, hydration, and analgesics. Amoxicillin and ampicillin must be avoided because they cause a characteristic morbilliform rash in 70–80% of EBV-infected patients. <div class="ec-src"><b>Source:</b> Womack J, Jimenez M. Common Questions About Infectious Mononucleosis. Am Fam Physician 2015;91(6):372-376; CDC Epstein-Barr Virus Guidance.</div></div> [[Start another case->Hub]] [[Restart this case->Mononucleosis - Rx]] [[Next case →->Toxoplasma AIDS - Dx]]

<span class="ec-case-marker" hidden data-entry="Mononucleosis. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Amoxicillin causes a rash in EBV.</div> Aminopenicillins (amoxicillin, ampicillin) trigger a generalized maculopapular rash in the majority of patients with acute EBV infection. This is not a true penicillin allergy but a specific drug-virus interaction. <div class="ec-teach"><div class="th">What to do instead</div> Splenic rupture is the most feared complication of infectious mononucleosis and the leading cause of mono-related death. Patients with splenomegaly should avoid contact sports and strenuous activity for at least 3–4 weeks or until imaging confirms splenic size normalization. Management is otherwise supportive: rest, hydration, and analgesics. Amoxicillin and ampicillin must be avoided because they cause a characteristic morbilliform rash in 70–80% of EBV-infected patients. <div class="ec-src"><b>Source:</b> Womack J, Jimenez M. Common Questions About Infectious Mononucleosis. Am Fam Physician 2015;91(6):372-376; CDC Epstein-Barr Virus Guidance.</div></div></div> [[Try this question again->Mononucleosis - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Mononucleosis. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The spleen is enlarged and friable during acute mononucleosis. A direct blow or sudden deceleration can cause splenic rupture, which is life-threatening. <div class="ec-teach"><div class="th">What to do instead</div> Splenic rupture is the most feared complication of infectious mononucleosis and the leading cause of mono-related death. Patients with splenomegaly should avoid contact sports and strenuous activity for at least 3–4 weeks or until imaging confirms splenic size normalization. Management is otherwise supportive: rest, hydration, and analgesics. Amoxicillin and ampicillin must be avoided because they cause a characteristic morbilliform rash in 70–80% of EBV-infected patients. <div class="ec-src"><b>Source:</b> Womack J, Jimenez M. Common Questions About Infectious Mononucleosis. Am Fam Physician 2015;91(6):372-376; CDC Epstein-Barr Virus Guidance.</div></div></div> [[Try this question again->Mononucleosis - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Mononucleosis. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Routine steroids are not recommended.</div> Corticosteroids are reserved for specific complications such as airway compromise from tonsillar enlargement, hemolytic anemia, or severe thrombocytopenia. They are not indicated for routine mono. <div class="ec-teach"><div class="th">What to do instead</div> Splenic rupture is the most feared complication of infectious mononucleosis and the leading cause of mono-related death. Patients with splenomegaly should avoid contact sports and strenuous activity for at least 3–4 weeks or until imaging confirms splenic size normalization. Management is otherwise supportive: rest, hydration, and analgesics. Amoxicillin and ampicillin must be avoided because they cause a characteristic morbilliform rash in 70–80% of EBV-infected patients. <div class="ec-src"><b>Source:</b> Womack J, Jimenez M. Common Questions About Infectious Mononucleosis. Am Fam Physician 2015;91(6):372-376; CDC Epstein-Barr Virus Guidance.</div></div></div> [[Try this question again->Mononucleosis - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Mononucleosis. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Acyclovir is ineffective for EBV.</div> Although EBV is a herpesvirus, acyclovir has not been shown to improve clinical outcomes in infectious mononucleosis. <div class="ec-teach"><div class="th">What to do instead</div> Splenic rupture is the most feared complication of infectious mononucleosis and the leading cause of mono-related death. Patients with splenomegaly should avoid contact sports and strenuous activity for at least 3–4 weeks or until imaging confirms splenic size normalization. Management is otherwise supportive: rest, hydration, and analgesics. Amoxicillin and ampicillin must be avoided because they cause a characteristic morbilliform rash in 70–80% of EBV-infected patients. <div class="ec-src"><b>Source:</b> Womack J, Jimenez M. Common Questions About Infectious Mononucleosis. Am Fam Physician 2015;91(6):372-376; CDC Epstein-Barr Virus Guidance.</div></div></div> [[Try this question again->Mononucleosis - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 07:15</div> A 64-year-old man develops sudden dyspnea and pleuritic chest pain 4 days after major abdominal surgery. He is tachycardic at 128/min and hypoxemic on supplemental oxygen. CT pulmonary angiography demonstrates a large saddle pulmonary embolus. Despite oxygen and a 1-liter fluid bolus, his blood pressure remains 78/46 mm Hg with signs of right ventricular strain on bedside echocardiography. <span class="ec-prompt">Which of the following interventions is most appropriate?</span> [[Elective outpatient anticoagulation->Unstable PE - D4]] [[Inferior vena cava filter placement as sole therapy->Unstable PE - D3]] [[Observation with repeat CT in 24 hours->Unstable PE - D2]] [[Systemic thrombolysis->Unstable PE - Correct]] [[Therapeutic-dose anticoagulation alone without reperfusion->Unstable PE - D1]]

<span class="ec-case-marker" hidden data-entry="Unstable PE. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Systemic thrombolysis.</div> Massive (high-risk) pulmonary embolism is defined by sustained hemodynamic instability, systolic BP <90 mm Hg or requiring vasopressors, with evidence of RV dysfunction. In this setting, systemic thrombolysis (alteplase) is the guideline-recommended reperfusion strategy when there is no absolute contraindication. Surgical embolectomy or catheter-directed therapy are alternatives when thrombolysis is contraindicated or fails. The recent surgery increases bleeding risk but is a relative, not absolute, contraindication when the PE is immediately life-threatening. <div class="ec-src"><b>Source:</b> Konstantinides SV, et al. 2019 ESC Guidelines for the Diagnosis and Management of Acute Pulmonary Embolism. Eur Heart J 2020;41(4):543-603.</div></div> [[Start another case->Hub]] [[Restart this case->Unstable PE - Rx]] [[Next case →->CAP CURB-65 - Dx]]

<span class="ec-case-marker" hidden data-entry="Unstable PE. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Anticoagulation alone is insufficient for massive PE with shock.</div> Therapeutic anticoagulation is standard for hemodynamically stable PE but does not provide acute clot lysis. In massive PE with hemodynamic instability, systemic thrombolysis or catheter-directed therapy is needed to rapidly restore pulmonary blood flow. <div class="ec-teach"><div class="th">What to do instead</div> Massive (high-risk) pulmonary embolism is defined by sustained hemodynamic instability, systolic BP <90 mm Hg or requiring vasopressors, with evidence of RV dysfunction. In this setting, systemic thrombolysis (alteplase) is the guideline-recommended reperfusion strategy when there is no absolute contraindication. Surgical embolectomy or catheter-directed therapy are alternatives when thrombolysis is contraindicated or fails. The recent surgery increases bleeding risk but is a relative, not absolute, contraindication when the PE is immediately life-threatening. <div class="ec-src"><b>Source:</b> Konstantinides SV, et al. 2019 ESC Guidelines for the Diagnosis and Management of Acute Pulmonary Embolism. Eur Heart J 2020;41(4):543-603.</div></div></div> [[Try this question again->Unstable PE - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Unstable PE. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Observation risks cardiac arrest.</div> This patient has obstructive shock from massive PE. Observation without reperfusion therapy allows progressive RV failure and cardiac arrest. <div class="ec-teach"><div class="th">What to do instead</div> Massive (high-risk) pulmonary embolism is defined by sustained hemodynamic instability, systolic BP <90 mm Hg or requiring vasopressors, with evidence of RV dysfunction. In this setting, systemic thrombolysis (alteplase) is the guideline-recommended reperfusion strategy when there is no absolute contraindication. Surgical embolectomy or catheter-directed therapy are alternatives when thrombolysis is contraindicated or fails. The recent surgery increases bleeding risk but is a relative, not absolute, contraindication when the PE is immediately life-threatening. <div class="ec-src"><b>Source:</b> Konstantinides SV, et al. 2019 ESC Guidelines for the Diagnosis and Management of Acute Pulmonary Embolism. Eur Heart J 2020;41(4):543-603.</div></div></div> [[Try this question again->Unstable PE - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Unstable PE. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ IVC filter does not treat existing PE.</div> An IVC filter prevents new emboli from reaching the lungs but does nothing to the clot already causing obstructive shock. It is a prophylactic device, not a treatment for acute hemodynamically significant PE. <div class="ec-teach"><div class="th">What to do instead</div> Massive (high-risk) pulmonary embolism is defined by sustained hemodynamic instability, systolic BP <90 mm Hg or requiring vasopressors, with evidence of RV dysfunction. In this setting, systemic thrombolysis (alteplase) is the guideline-recommended reperfusion strategy when there is no absolute contraindication. Surgical embolectomy or catheter-directed therapy are alternatives when thrombolysis is contraindicated or fails. The recent surgery increases bleeding risk but is a relative, not absolute, contraindication when the PE is immediately life-threatening. <div class="ec-src"><b>Source:</b> Konstantinides SV, et al. 2019 ESC Guidelines for the Diagnosis and Management of Acute Pulmonary Embolism. Eur Heart J 2020;41(4):543-603.</div></div></div> [[Try this question again->Unstable PE - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Unstable PE. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Outpatient anticoagulation is for stable PE.</div> Outpatient anticoagulation is appropriate for low-risk PE. A hemodynamically unstable patient with massive PE requires immediate inpatient reperfusion therapy. <div class="ec-teach"><div class="th">What to do instead</div> Massive (high-risk) pulmonary embolism is defined by sustained hemodynamic instability, systolic BP <90 mm Hg or requiring vasopressors, with evidence of RV dysfunction. In this setting, systemic thrombolysis (alteplase) is the guideline-recommended reperfusion strategy when there is no absolute contraindication. Surgical embolectomy or catheter-directed therapy are alternatives when thrombolysis is contraindicated or fails. The recent surgery increases bleeding risk but is a relative, not absolute, contraindication when the PE is immediately life-threatening. <div class="ec-src"><b>Source:</b> Konstantinides SV, et al. 2019 ESC Guidelines for the Diagnosis and Management of Acute Pulmonary Embolism. Eur Heart J 2020;41(4):543-603.</div></div></div> [[Try this question again->Unstable PE - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 19:00</div> A 31-year-old woman with no known liver disease develops jaundice, nausea, and confusion over 5 days after a febrile illness. Temperature is 37.8°C (100.0°F), blood pressure is 98/62 mm Hg, and pulse is 108/min. AST is 3,200 U/L and ALT is 2,800 U/L. INR is 2.8. She is becoming increasingly disoriented. <span class="ec-prompt">Which of the following findings most strongly indicates acute liver failure requiring urgent transplant-center evaluation?</span> [[Elevated aminotransferases with preserved synthetic function->Acute liver failure - D2]] [[Encephalopathy with coagulopathy without preexisting cirrhosis->Acute liver failure - Correct]] [[Hepatomegaly on physical examination->Acute liver failure - D3]] [[Jaundice with normal mental status and normal coagulation->Acute liver failure - D4]] [[Mild isolated elevation of alkaline phosphatase alone->Acute liver failure - D1]]

<span class="ec-case-marker" hidden data-entry="Acute liver failure. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Encephalopathy with coagulopathy without preexisting cirrhosis.</div> Acute liver failure is defined as hepatic injury with coagulopathy (INR ≥1.5) and hepatic encephalopathy in a patient without prior chronic liver disease, developing within 26 weeks of symptom onset. This patient has all three elements. Transfer to a transplant center is urgent because deterioration can be rapid and unpredictable, cerebral edema, infection, and multi-organ failure develop quickly. The most common cause in the US is acetaminophen toxicity; other causes include viral hepatitis, autoimmune hepatitis, Wilson disease, and drug-induced liver injury. <div class="ec-src"><b>Source:</b> Lee WM, et al. Acute Liver Failure: Summary of a Workshop. Hepatology 2008;47(4):1401-1415; AASLD Position Paper on Acute Liver Failure.</div></div> [[Start another case->Hub]] [[Restart this case->Acute liver failure - Dx]] [[Next case →->Hepatic encephalopathy - Rx]]

<span class="ec-case-marker" hidden data-entry="Acute liver failure. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Isolated ALP elevation suggests cholestasis.</div> A mild isolated alkaline phosphatase elevation suggests cholestatic disease, not the hepatocellular injury pattern with massive transaminase elevation seen here. <div class="ec-teach"><div class="th">What to do instead</div> Acute liver failure is defined as hepatic injury with coagulopathy (INR ≥1.5) and hepatic encephalopathy in a patient without prior chronic liver disease, developing within 26 weeks of symptom onset. This patient has all three elements. Transfer to a transplant center is urgent because deterioration can be rapid and unpredictable, cerebral edema, infection, and multi-organ failure develop quickly. The most common cause in the US is acetaminophen toxicity; other causes include viral hepatitis, autoimmune hepatitis, Wilson disease, and drug-induced liver injury. <div class="ec-src"><b>Source:</b> Lee WM, et al. Acute Liver Failure: Summary of a Workshop. Hepatology 2008;47(4):1401-1415; AASLD Position Paper on Acute Liver Failure.</div></div></div> [[Try this question again->Acute liver failure - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Acute liver failure. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Preserved synthetic function rules out liver failure.</div> Elevated aminotransferases alone reflect hepatocellular injury but not necessarily failure. Liver failure is defined by the combination of synthetic dysfunction (coagulopathy) and encephalopathy. If INR and mental status are normal, the patient has hepatitis, not liver failure. <div class="ec-teach"><div class="th">What to do instead</div> Acute liver failure is defined as hepatic injury with coagulopathy (INR ≥1.5) and hepatic encephalopathy in a patient without prior chronic liver disease, developing within 26 weeks of symptom onset. This patient has all three elements. Transfer to a transplant center is urgent because deterioration can be rapid and unpredictable, cerebral edema, infection, and multi-organ failure develop quickly. The most common cause in the US is acetaminophen toxicity; other causes include viral hepatitis, autoimmune hepatitis, Wilson disease, and drug-induced liver injury. <div class="ec-src"><b>Source:</b> Lee WM, et al. Acute Liver Failure: Summary of a Workshop. Hepatology 2008;47(4):1401-1415; AASLD Position Paper on Acute Liver Failure.</div></div></div> [[Try this question again->Acute liver failure - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Acute liver failure. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Hepatomegaly alone does not define ALF.</div> Hepatomegaly may reflect inflammation, congestion, or infiltration but does not by itself indicate loss of hepatic synthetic function or the development of encephalopathy. <div class="ec-teach"><div class="th">What to do instead</div> Acute liver failure is defined as hepatic injury with coagulopathy (INR ≥1.5) and hepatic encephalopathy in a patient without prior chronic liver disease, developing within 26 weeks of symptom onset. This patient has all three elements. Transfer to a transplant center is urgent because deterioration can be rapid and unpredictable, cerebral edema, infection, and multi-organ failure develop quickly. The most common cause in the US is acetaminophen toxicity; other causes include viral hepatitis, autoimmune hepatitis, Wilson disease, and drug-induced liver injury. <div class="ec-src"><b>Source:</b> Lee WM, et al. Acute Liver Failure: Summary of a Workshop. Hepatology 2008;47(4):1401-1415; AASLD Position Paper on Acute Liver Failure.</div></div></div> [[Try this question again->Acute liver failure - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Acute liver failure. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Normal coagulation and mental status mean the liver is still functioning.</div> Jaundice indicates bilirubin metabolism impairment but liver failure requires coagulopathy and encephalopathy. This patient has hepatic injury but not failure, a critical distinction for transplant-center referral. <div class="ec-teach"><div class="th">What to do instead</div> Acute liver failure is defined as hepatic injury with coagulopathy (INR ≥1.5) and hepatic encephalopathy in a patient without prior chronic liver disease, developing within 26 weeks of symptom onset. This patient has all three elements. Transfer to a transplant center is urgent because deterioration can be rapid and unpredictable, cerebral edema, infection, and multi-organ failure develop quickly. The most common cause in the US is acetaminophen toxicity; other causes include viral hepatitis, autoimmune hepatitis, Wilson disease, and drug-induced liver injury. <div class="ec-src"><b>Source:</b> Lee WM, et al. Acute Liver Failure: Summary of a Workshop. Hepatology 2008;47(4):1401-1415; AASLD Position Paper on Acute Liver Failure.</div></div></div> [[Try this question again->Acute liver failure - Dx]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 12:30</div> A 69-year-old man with severe COPD has had worsening dyspnea and increased purulent sputum production for 3 days. Blood pressure is 148/88 mm Hg, pulse is 104/min, and respirations are 28/min. Despite initial nebulized bronchodilators and systemic corticosteroids, he remains severely dyspneic. Arterial blood gas analysis shows pH 7.25, PaCO2 68 mm Hg, PaO2 52 mm Hg. He is awake, following commands, and able to protect his airway. <span class="ec-prompt">Which of the following interventions is most appropriate?</span> [[High-flow nasal cannula oxygen at 60 L/min->COPD ventilation - D2]] [[Immediate endotracheal intubation as the first intervention->COPD ventilation - D1]] [[Immediate lung transplant evaluation without acute stabilization->COPD ventilation - D4]] [[Intravenous aminophylline infusion->COPD ventilation - D3]] [[Noninvasive positive-pressure ventilation->COPD ventilation - Correct]]

<span class="ec-case-marker" hidden data-entry="COPD ventilation. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Noninvasive positive-pressure ventilation.</div> Acute hypercapnic respiratory failure with acidosis (pH <7.35, PaCO2 >45) during a COPD exacerbation is the strongest indication for NIV (BiPAP). In patients who can protect their airway and have no contraindications, NIV reduces intubation rates, ICU length of stay, and mortality compared with invasive mechanical ventilation. It works by reducing the work of breathing and improving alveolar ventilation. If NIV fails (worsening pH, rising PaCO2, declining consciousness), intubation should not be delayed. <div class="ec-src"><b>Source:</b> Rochwerg B, et al. Official ERS/ATS Clinical Practice Guidelines: Noninvasive Ventilation for Acute Respiratory Failure. Eur Respir J 2017;50(2):1602426; GOLD 2026 Report.</div></div> [[Start another case->Hub]] [[Restart this case->COPD ventilation - Rx]] [[Next case →->DLCO in emphysema - Ix]]

<span class="ec-case-marker" hidden data-entry="COPD ventilation. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Intubation is not the first step in an awake, cooperative patient.</div> This patient can protect his airway, follow commands, and cooperate with treatment, making him an ideal candidate for noninvasive ventilation. Intubation carries risks of ventilator-associated pneumonia and prolonged ICU stay. NIV should be tried first, with intubation reserved for NIV failure. <div class="ec-teach"><div class="th">What to do instead</div> Acute hypercapnic respiratory failure with acidosis (pH <7.35, PaCO2 >45) during a COPD exacerbation is the strongest indication for NIV (BiPAP). In patients who can protect their airway and have no contraindications, NIV reduces intubation rates, ICU length of stay, and mortality compared with invasive mechanical ventilation. It works by reducing the work of breathing and improving alveolar ventilation. If NIV fails (worsening pH, rising PaCO2, declining consciousness), intubation should not be delayed. <div class="ec-src"><b>Source:</b> Rochwerg B, et al. Official ERS/ATS Clinical Practice Guidelines: Noninvasive Ventilation for Acute Respiratory Failure. Eur Respir J 2017;50(2):1602426; GOLD 2026 Report.</div></div></div> [[Try this question again->COPD ventilation - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="COPD ventilation. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> HFNC delivers heated, humidified oxygen and generates modest positive end-expiratory pressure but does not provide the inspiratory pressure support needed to reduce work of breathing and correct hypercapnia in acute COPD exacerbation. <div class="ec-teach"><div class="th">What to do instead</div> Acute hypercapnic respiratory failure with acidosis (pH <7.35, PaCO2 >45) during a COPD exacerbation is the strongest indication for NIV (BiPAP). In patients who can protect their airway and have no contraindications, NIV reduces intubation rates, ICU length of stay, and mortality compared with invasive mechanical ventilation. It works by reducing the work of breathing and improving alveolar ventilation. If NIV fails (worsening pH, rising PaCO2, declining consciousness), intubation should not be delayed. <div class="ec-src"><b>Source:</b> Rochwerg B, et al. Official ERS/ATS Clinical Practice Guidelines: Noninvasive Ventilation for Acute Respiratory Failure. Eur Respir J 2017;50(2):1602426; GOLD 2026 Report.</div></div></div> [[Try this question again->COPD ventilation - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="COPD ventilation. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Aminophylline has a narrow therapeutic index and limited benefit.</div> Methylxanthines like aminophylline are no longer recommended in acute COPD exacerbations due to limited efficacy, narrow therapeutic window, and significant toxicity risk (arrhythmias, seizures). NIV addresses the immediate ventilatory failure. <div class="ec-teach"><div class="th">What to do instead</div> Acute hypercapnic respiratory failure with acidosis (pH <7.35, PaCO2 >45) during a COPD exacerbation is the strongest indication for NIV (BiPAP). In patients who can protect their airway and have no contraindications, NIV reduces intubation rates, ICU length of stay, and mortality compared with invasive mechanical ventilation. It works by reducing the work of breathing and improving alveolar ventilation. If NIV fails (worsening pH, rising PaCO2, declining consciousness), intubation should not be delayed. <div class="ec-src"><b>Source:</b> Rochwerg B, et al. Official ERS/ATS Clinical Practice Guidelines: Noninvasive Ventilation for Acute Respiratory Failure. Eur Respir J 2017;50(2):1602426; GOLD 2026 Report.</div></div></div> [[Try this question again->COPD ventilation - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="COPD ventilation. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Transplant evaluation is premature without acute stabilization.</div> The immediate priority is treating the acute respiratory failure. Lung transplant is a long-term consideration for end-stage COPD, not an acute intervention. <div class="ec-teach"><div class="th">What to do instead</div> Acute hypercapnic respiratory failure with acidosis (pH <7.35, PaCO2 >45) during a COPD exacerbation is the strongest indication for NIV (BiPAP). In patients who can protect their airway and have no contraindications, NIV reduces intubation rates, ICU length of stay, and mortality compared with invasive mechanical ventilation. It works by reducing the work of breathing and improving alveolar ventilation. If NIV fails (worsening pH, rising PaCO2, declining consciousness), intubation should not be delayed. <div class="ec-src"><b>Source:</b> Rochwerg B, et al. Official ERS/ATS Clinical Practice Guidelines: Noninvasive Ventilation for Acute Respiratory Failure. Eur Respir J 2017;50(2):1602426; GOLD 2026 Report.</div></div></div> [[Try this question again->COPD ventilation - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Breast cancer tumor board · 08:30</div> A 52-year-old woman has a newly diagnosed 2.3-cm invasive ductal carcinoma. Blood pressure is 124/78 mm Hg and pulse is 74/min. Immunohistochemistry shows ER-negative, PR-negative, and HER2-negative. Ki-67 is 75%. She has no family history of BRCA mutations. There is no palpable axillary lymphadenopathy. <span class="ec-prompt">Which of the following terms best describes this tumor?</span> [[Ductal carcinoma in situ - noninvasive and low risk->Triple negative breast - D4]] [[HER2-enriched - eligible for trastuzumab->Triple negative breast - D2]] [[Hormone-receptor-positive - excellent endocrine response->Triple negative breast - D3]] [[Luminal A - the most indolent subtype->Triple negative breast - D1]] [[Triple-negative - aggressive subtype lacking targeted therapy->Triple negative breast - Correct]]

<span class="ec-case-marker" hidden data-entry="Triple negative breast. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Triple-negative, aggressive subtype lacking targeted therapy</div> The absence of ER, PR, and HER2 expression defines triple-negative breast cancer (TNBC), which represents approximately 15% of breast cancers. TNBC is associated with higher proliferation rates, earlier recurrence, and a worse overall prognosis compared with hormone-receptor-positive subtypes. Because it lacks the three major therapeutic targets, TNBC does not respond to endocrine therapy or HER2-directed agents. Treatment relies on chemotherapy, and increasingly on immune checkpoint inhibitors (pembrolizumab) in appropriate candidates. BRCA testing is recommended because TNBC is enriched for BRCA1 mutations. <div class="ec-src"><b>Source:</b> Bianchini G, et al. Triple-Negative Breast Cancer: Challenges and Opportunities of a Heterogeneous Disease. Nat Rev Clin Oncol 2016;13(11):674-690; NCCN Breast Cancer Guidelines.</div></div> [[Start another case->Hub]] [[Restart this case->Triple negative breast - Dx]] [[Next case →->Heparin-induced thrombocytopenia mechanism - Mech]]

<span class="ec-case-marker" hidden data-entry="Triple negative breast. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Luminal A is ER/PR-positive, HER2-negative.</div> Luminal A tumors are hormone-receptor-positive with low proliferation and have the best prognosis. This tumor is ER/PR-negative with high Ki-67. <div class="ec-teach"><div class="th">What to do instead</div> The absence of ER, PR, and HER2 expression defines triple-negative breast cancer (TNBC), which represents approximately 15% of breast cancers. TNBC is associated with higher proliferation rates, earlier recurrence, and a worse overall prognosis compared with hormone-receptor-positive subtypes. Because it lacks the three major therapeutic targets, TNBC does not respond to endocrine therapy or HER2-directed agents. Treatment relies on chemotherapy, and increasingly on immune checkpoint inhibitors (pembrolizumab) in appropriate candidates. BRCA testing is recommended because TNBC is enriched for BRCA1 mutations. <div class="ec-src"><b>Source:</b> Bianchini G, et al. Triple-Negative Breast Cancer: Challenges and Opportunities of a Heterogeneous Disease. Nat Rev Clin Oncol 2016;13(11):674-690; NCCN Breast Cancer Guidelines.</div></div></div> [[Try this question again->Triple negative breast - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Triple negative breast. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ HER2-enriched requires HER2 overexpression.</div> HER2-enriched tumors are HER2-positive by IHC or FISH. This tumor is HER2-negative and therefore not eligible for HER2-targeted therapies like trastuzumab. <div class="ec-teach"><div class="th">What to do instead</div> The absence of ER, PR, and HER2 expression defines triple-negative breast cancer (TNBC), which represents approximately 15% of breast cancers. TNBC is associated with higher proliferation rates, earlier recurrence, and a worse overall prognosis compared with hormone-receptor-positive subtypes. Because it lacks the three major therapeutic targets, TNBC does not respond to endocrine therapy or HER2-directed agents. Treatment relies on chemotherapy, and increasingly on immune checkpoint inhibitors (pembrolizumab) in appropriate candidates. BRCA testing is recommended because TNBC is enriched for BRCA1 mutations. <div class="ec-src"><b>Source:</b> Bianchini G, et al. Triple-Negative Breast Cancer: Challenges and Opportunities of a Heterogeneous Disease. Nat Rev Clin Oncol 2016;13(11):674-690; NCCN Breast Cancer Guidelines.</div></div></div> [[Try this question again->Triple negative breast - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Triple negative breast. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ This tumor is hormone-receptor-negative.</div> ER-negative and PR-negative means endocrine therapy (tamoxifen, aromatase inhibitors) will have no effect. <div class="ec-teach"><div class="th">What to do instead</div> The absence of ER, PR, and HER2 expression defines triple-negative breast cancer (TNBC), which represents approximately 15% of breast cancers. TNBC is associated with higher proliferation rates, earlier recurrence, and a worse overall prognosis compared with hormone-receptor-positive subtypes. Because it lacks the three major therapeutic targets, TNBC does not respond to endocrine therapy or HER2-directed agents. Treatment relies on chemotherapy, and increasingly on immune checkpoint inhibitors (pembrolizumab) in appropriate candidates. BRCA testing is recommended because TNBC is enriched for BRCA1 mutations. <div class="ec-src"><b>Source:</b> Bianchini G, et al. Triple-Negative Breast Cancer: Challenges and Opportunities of a Heterogeneous Disease. Nat Rev Clin Oncol 2016;13(11):674-690; NCCN Breast Cancer Guidelines.</div></div></div> [[Try this question again->Triple negative breast - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Triple negative breast. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ This is invasive, not in situ.</div> The pathology explicitly describes invasive ductal carcinoma. DCIS is a noninvasive precursor lesion; this has already invaded. <div class="ec-teach"><div class="th">What to do instead</div> The absence of ER, PR, and HER2 expression defines triple-negative breast cancer (TNBC), which represents approximately 15% of breast cancers. TNBC is associated with higher proliferation rates, earlier recurrence, and a worse overall prognosis compared with hormone-receptor-positive subtypes. Because it lacks the three major therapeutic targets, TNBC does not respond to endocrine therapy or HER2-directed agents. Treatment relies on chemotherapy, and increasingly on immune checkpoint inhibitors (pembrolizumab) in appropriate candidates. BRCA testing is recommended because TNBC is enriched for BRCA1 mutations. <div class="ec-src"><b>Source:</b> Bianchini G, et al. Triple-Negative Breast Cancer: Challenges and Opportunities of a Heterogeneous Disease. Nat Rev Clin Oncol 2016;13(11):674-690; NCCN Breast Cancer Guidelines.</div></div></div> [[Try this question again->Triple negative breast - Dx]] [[Start another case->Hub]]

<div class="ec-scene">Pediatric oncology clinic · 10:00</div> A 16-year-old adolescent boy is diagnosed with B-cell acute lymphoblastic leukemia. His presenting white blood cell count is 180,000/mm3. He is being risk-stratified for treatment assignment. <span class="ec-prompt">Which of the following features most strongly places him in a higher-risk category?</span> [[Absence of fever at the time of initial diagnosis->ALL high risk - D1]] [[Age 10 years or older with a presenting WBC above 50,000/mm3->ALL high risk - Correct]] [[Male sex as an isolated prognostic variable->ALL high risk - D2]] [[Mild fatigue without other constitutional symptoms->ALL high risk - D3]] [[Normal platelet count on the initial CBC->ALL high risk - D4]]

<span class="ec-case-marker" hidden data-entry="ALL high risk. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Age 10 years or older with a presenting WBC above 50,000/mm3</div> The NCI risk classification for B-cell ALL uses age and presenting WBC as the initial stratifying variables. Standard risk is defined as age 1–9.99 years and WBC <50,000/mm3. High risk is age under 1 year or 10 years and older, or a presenting WBC of 50,000/mm3 or greater. This patient is 16 with a WBC of 180,000/mm3, so he meets both criteria independently. Adolescent-age ALL has a higher incidence of adverse cytogenetic features (Ph-like ALL, iAMP21) and historically worse outcomes, though adolescent-and-young-adult (AYA) protocols have narrowed the gap. MRD response after induction then further refines the risk assignment. <div class="ec-src"><b>Source:</b> Hunger SP, Mullighan CG. Acute Lymphoblastic Leukemia in Children. N Engl J Med 2015;373(16):1541-1552; NCI/COG Risk Stratification Criteria.</div></div> [[Start another case->Hub]] [[Restart this case->ALL high risk - Dx]] [[Next case →->ALL prognosis - Dx]]

<span class="ec-case-marker" hidden data-entry="ALL high risk. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Fever at presentation does not determine risk.</div> The presence or absence of fever at diagnosis is not a prognostic factor in the NCI/COG risk-stratification system for ALL. <div class="ec-teach"><div class="th">What to do instead</div> The NCI risk classification for B-cell ALL uses age and presenting WBC as the initial stratifying variables. Standard risk is defined as age 1–9.99 years and WBC <50,000/mm3. This patient's age of 16 and WBC of 180,000/mm3 both independently confer high risk. Adolescent-age ALL has a higher incidence of adverse cytogenetic features (Ph-like ALL, iAMP21) and historically worse outcomes, though adolescent-and-young-adult (AYA) protocols have narrowed the gap. MRD response after induction then further refines the risk assignment. <div class="ec-src"><b>Source:</b> Hunger SP, Mullighan CG. Acute Lymphoblastic Leukemia in Children. N Engl J Med 2015;373(16):1541-1552; NCI/COG Risk Stratification Criteria.</div></div></div> [[Try this question again->ALL high risk - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="ALL high risk. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Male sex alone is not the primary risk factor.</div> While male sex has historically been associated with slightly worse outcomes (partly due to the need for testicular irradiation in CNS protocols), it is not the dominant factor here. <div class="ec-teach"><div class="th">What to do instead</div> The NCI risk classification for B-cell ALL uses age and presenting WBC as the initial stratifying variables. Standard risk is defined as age 1–9.99 years and WBC <50,000/mm3. This patient's age of 16 and WBC of 180,000/mm3 both independently confer high risk. Adolescent-age ALL has a higher incidence of adverse cytogenetic features (Ph-like ALL, iAMP21) and historically worse outcomes, though adolescent-and-young-adult (AYA) protocols have narrowed the gap. MRD response after induction then further refines the risk assignment. <div class="ec-src"><b>Source:</b> Hunger SP, Mullighan CG. Acute Lymphoblastic Leukemia in Children. N Engl J Med 2015;373(16):1541-1552; NCI/COG Risk Stratification Criteria.</div></div></div> [[Try this question again->ALL high risk - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="ALL high risk. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Fatigue is a nonspecific symptom.</div> Fatigue at presentation does not factor into ALL risk stratification. <div class="ec-teach"><div class="th">What to do instead</div> The NCI risk classification for B-cell ALL uses age and presenting WBC as the initial stratifying variables. Standard risk is defined as age 1–9.99 years and WBC <50,000/mm3. This patient's age of 16 and WBC of 180,000/mm3 both independently confer high risk. Adolescent-age ALL has a higher incidence of adverse cytogenetic features (Ph-like ALL, iAMP21) and historically worse outcomes, though adolescent-and-young-adult (AYA) protocols have narrowed the gap. MRD response after induction then further refines the risk assignment. <div class="ec-src"><b>Source:</b> Hunger SP, Mullighan CG. Acute Lymphoblastic Leukemia in Children. N Engl J Med 2015;373(16):1541-1552; NCI/COG Risk Stratification Criteria.</div></div></div> [[Try this question again->ALL high risk - Dx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="ALL high risk. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Platelet count is not a risk-stratification variable.</div> Platelet count at diagnosis reflects marrow involvement but is not used in the standard NCI risk classification. <div class="ec-teach"><div class="th">What to do instead</div> The NCI risk classification for B-cell ALL uses age and presenting WBC as the initial stratifying variables. Standard risk is defined as age 1–9.99 years and WBC <50,000/mm3. This patient's age of 16 and WBC of 180,000/mm3 both independently confer high risk. Adolescent-age ALL has a higher incidence of adverse cytogenetic features (Ph-like ALL, iAMP21) and historically worse outcomes, though adolescent-and-young-adult (AYA) protocols have narrowed the gap. MRD response after induction then further refines the risk assignment. <div class="ec-src"><b>Source:</b> Hunger SP, Mullighan CG. Acute Lymphoblastic Leukemia in Children. N Engl J Med 2015;373(16):1541-1552; NCI/COG Risk Stratification Criteria.</div></div></div> [[Try this question again->ALL high risk - Dx]] [[Start another case->Hub]]

<div class="ec-scene">Medical floor · 06:30</div> A 66-year-old man is hospitalized for community-acquired pneumonia. Temperature is 38.2°C (100.8°F), blood pressure is 128/76 mm Hg, and pulse is 82/min. He is hemodynamically stable with no active bleeding, no acute coronary syndrome, and no symptoms attributable to anemia. His hemoglobin is 6.8 g/dL. <span class="ec-prompt">Which of the following is the most appropriate management?</span> [[Give fresh frozen plasma->RBC transfusion - D2]] [[Give intravenous iron as the sole immediate treatment->RBC transfusion - D4]] [[Give platelets->RBC transfusion - D1]] [[Start erythropoietin immediately->RBC transfusion - D3]] [[Transfuse packed red blood cells->RBC transfusion - Correct]]

<span class="ec-case-marker" hidden data-entry="RBC transfusion. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Transfuse packed red blood cells.</div> For most hemodynamically stable hospitalized adults without specific indications for a higher threshold, the 2023 AABB International Guidelines recommend a restrictive transfusion strategy with a trigger of approximately 7 g/dL. This patient's hemoglobin of 6.8 g/dL is below that threshold, making transfusion appropriate. A restrictive strategy (transfusing one unit at a time and reassessing) is preferred over a liberal strategy because it reduces transfusion-related complications without increasing mortality or morbidity in this population. Patients with acute coronary syndrome may benefit from a higher threshold of 8 g/dL. <div class="ec-src"><b>Source:</b> Carson JL, et al. Red Blood Cell Transfusion: 2023 AABB International Guidelines. JAMA 2023;330(19):1892-1902.</div></div> [[Start another case->Hub]] [[Restart this case->RBC transfusion - Rx]] [[Next case →->Hereditary spherocytosis - Ix]]

<span class="ec-case-marker" hidden data-entry="RBC transfusion. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Platelets treat thrombocytopenia.</div> Platelets are indicated for severe thrombocytopenia with bleeding or before procedures. They do not treat anemia. <div class="ec-teach"><div class="th">What to do instead</div> For most hemodynamically stable hospitalized adults without specific indications for a higher threshold, the 2023 AABB International Guidelines recommend a restrictive transfusion strategy with a trigger of approximately 7 g/dL. This patient's hemoglobin of 6.8 g/dL is below that threshold, making transfusion appropriate. A restrictive strategy (transfusing one unit at a time and reassessing) is preferred over a liberal strategy because it reduces transfusion-related complications without increasing mortality or morbidity in this population. Patients with acute coronary syndrome may benefit from a higher threshold of 8 g/dL. <div class="ec-src"><b>Source:</b> Carson JL, et al. Red Blood Cell Transfusion: 2023 AABB International Guidelines. JAMA 2023;330(19):1892-1902.</div></div></div> [[Try this question again->RBC transfusion - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="RBC transfusion. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ FFP treats coagulopathy.</div> Fresh frozen plasma replaces clotting factors in patients with coagulopathy. It does not treat anemia or increase hemoglobin. <div class="ec-teach"><div class="th">What to do instead</div> For most hemodynamically stable hospitalized adults without specific indications for a higher threshold, the 2023 AABB International Guidelines recommend a restrictive transfusion strategy with a trigger of approximately 7 g/dL. This patient's hemoglobin of 6.8 g/dL is below that threshold, making transfusion appropriate. A restrictive strategy (transfusing one unit at a time and reassessing) is preferred over a liberal strategy because it reduces transfusion-related complications without increasing mortality or morbidity in this population. Patients with acute coronary syndrome may benefit from a higher threshold of 8 g/dL. <div class="ec-src"><b>Source:</b> Carson JL, et al. Red Blood Cell Transfusion: 2023 AABB International Guidelines. JAMA 2023;330(19):1892-1902.</div></div></div> [[Try this question again->RBC transfusion - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="RBC transfusion. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Erythropoietin takes weeks to work.</div> ESAs stimulate red cell production over weeks. They are not appropriate for acute management of significant anemia below the transfusion threshold. <div class="ec-teach"><div class="th">What to do instead</div> For most hemodynamically stable hospitalized adults without specific indications for a higher threshold, the 2023 AABB International Guidelines recommend a restrictive transfusion strategy with a trigger of approximately 7 g/dL. This patient's hemoglobin of 6.8 g/dL is below that threshold, making transfusion appropriate. A restrictive strategy (transfusing one unit at a time and reassessing) is preferred over a liberal strategy because it reduces transfusion-related complications without increasing mortality or morbidity in this population. Patients with acute coronary syndrome may benefit from a higher threshold of 8 g/dL. <div class="ec-src"><b>Source:</b> Carson JL, et al. Red Blood Cell Transfusion: 2023 AABB International Guidelines. JAMA 2023;330(19):1892-1902.</div></div></div> [[Try this question again->RBC transfusion - Rx]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="RBC transfusion. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ IV iron alone is too slow.</div> IV iron replaces iron stores and is appropriate for iron deficiency, but it takes days to weeks to raise hemoglobin. At 6.8 g/dL, which is below the transfusion threshold, transfusion is the immediate intervention. <div class="ec-teach"><div class="th">What to do instead</div> For most hemodynamically stable hospitalized adults without specific indications for a higher threshold, the 2023 AABB International Guidelines recommend a restrictive transfusion strategy with a trigger of approximately 7 g/dL. This patient's hemoglobin of 6.8 g/dL is below that threshold, making transfusion appropriate. A restrictive strategy (transfusing one unit at a time and reassessing) is preferred over a liberal strategy because it reduces transfusion-related complications without increasing mortality or morbidity in this population. Patients with acute coronary syndrome may benefit from a higher threshold of 8 g/dL. <div class="ec-src"><b>Source:</b> Carson JL, et al. Red Blood Cell Transfusion: 2023 AABB International Guidelines. JAMA 2023;330(19):1892-1902.</div></div></div> [[Try this question again->RBC transfusion - Rx]] [[Start another case->Hub]]

<div class="ec-scene">Cardiology clinic · 09:20</div> A 68-year-old man had an anterior myocardial infarction 8 months ago. He now has progressive exertional dyspnea. Temperature is 36.8°C (98.2°F), blood pressure is 118/74 mm Hg, pulse is 92/min, and respirations are 20/min. Echocardiography shows an ejection fraction of 30% and a dilated left ventricle. <span class="ec-prompt">Which of the following processes most directly contributes to the ventricular dilation?</span> [[Compensatory increase in myocardial contractility->Post-MI remodeling - E]] [[Concentric hypertrophy from pressure overload->Post-MI remodeling - A]] [[Eccentric remodeling from chronic wall stress->Post-MI remodeling - Correct]] [[Increased vagal tone reducing contractility->Post-MI remodeling - C]] [[Progressive reduction in end-diastolic volume->Post-MI remodeling - D]]

<span class="ec-case-marker" hidden data-entry="Post-MI remodeling. Mech"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Eccentric remodeling from chronic wall stress.</div> Loss of functioning myocardium after infarction increases wall stress (Laplace's law), triggering eccentric hypertrophy, sarcomere addition in series that produces chamber dilation. Concentric hypertrophy (sarcomeres in parallel) is the response to pressure overload, not volume overload. <div class="ec-src"><b>Source:</b> Sutton MG, Sharpe N. Circulation 2000;101(25):2981-2988.</div></div> [[Start another case->Hub]] [[Restart this case->Post-MI remodeling - Mech]] [[Next case →->Post-MI sudden death risk - Prog]]

<span class="ec-case-marker" hidden data-entry="Post-MI remodeling. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is Eccentric remodeling from chronic wall stress. Loss of functioning myocardium after infarction increases wall stress (Laplace's law), triggering eccentric hypertrophy, sarcomere addition in series that produces chamber dilation. Concentric hypertrophy (sarcomeres in parallel) is the response to pressure overload, not volume overload. <div class="ec-src"><b>Source:</b> Sutton MG, Sharpe N. Circulation 2000;101(25):2981-2988.</div></div> [[Try this question again->Post-MI remodeling - Mech]] [[Start another case->Hub]]

<div class="ec-scene">Cardiology clinic · 14:10</div> A 61-year-old man has had exertional chest pressure for 3 months that resolves within several minutes of rest. He has no known coronary disease. Temperature is 36.7°C (98.1°F), blood pressure is 138/82 mm Hg, pulse is 74/min, and respirations are 16/min. ECG shows normal sinus rhythm without ST-T abnormalities. He can exercise on a treadmill without limitation. <span class="ec-prompt">Which of the following tests is most appropriate to evaluate for inducible myocardial ischemia?</span> [[24-hour Holter monitoring->Exercise stress test - A]] [[Exercise treadmill ECG stress test->Exercise stress test - Correct]] [[High-sensitivity D-dimer assay->Exercise stress test - D]] [[Invasive electrophysiologic study->Exercise stress test - E]] [[Resting transthoracic echocardiography->Exercise stress test - B]]

<span class="ec-case-marker" hidden data-entry="Exercise stress test. Ix"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Exercise treadmill ECG stress test.</div> In a patient with suspected stable ischemic heart disease who can exercise and has an interpretable baseline ECG, exercise treadmill testing is the initial study of choice (ACC/AHA). Holter monitors arrhythmia burden, not inducible ischemia. Resting echo cannot provoke ischemia. D-dimer evaluates for thromboembolism. <div class="ec-src"><b>Source:</b> Gulati M, et al. 2021 AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR Guideline for the Evaluation and Diagnosis of Chest Pain. Circulation 2021;144(22):e368-e454.</div></div> [[Start another case->Hub]] [[Restart this case->Exercise stress test - Ix]] [[Next case →->Aortic dissection - Dx]]

<span class="ec-case-marker" hidden data-entry="Exercise stress test. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is Exercise treadmill ECG stress test. In a patient with suspected stable ischemic heart disease who can exercise and has an interpretable baseline ECG, exercise treadmill testing is the initial study of choice (ACC/AHA). Holter monitors arrhythmia burden, not inducible ischemia. Resting echo cannot provoke ischemia. D-dimer evaluates for thromboembolism. <div class="ec-src"><b>Source:</b> Gulati M, et al. 2021 AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR Guideline for the Evaluation and Diagnosis of Chest Pain. Circulation 2021;144(22):e368-e454.</div></div> [[Try this question again->Exercise stress test - Ix]] [[Start another case->Hub]]

<div class="ec-scene">Heart failure clinic · 11:35</div> A 74-year-old man with heart failure with reduced ejection fraction has an ejection fraction of 25%. Despite guideline-directed medical therapy, he has dyspnea with minimal activity and has been hospitalized twice in the past 6 months. Pulse is 96/min and blood pressure is 82/58 mm Hg. <span class="ec-prompt">Which of the following findings most directly indicates inadequate cardiac output?</span> [[Bilateral lower-extremity edema->HFrEF cardiac output - D]] [[First-degree atrioventricular block->HFrEF cardiac output - E]] [[Mild tricuspid regurgitation on echocardiography->HFrEF cardiac output - A]] [[Persistent resting hypotension->HFrEF cardiac output - Correct]] [[Sinus tachycardia at rest->HFrEF cardiac output - C]]

<span class="ec-case-marker" hidden data-entry="HFrEF cardiac output. Prog"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Persistent resting hypotension.</div> Persistent hypotension in advanced HFrEF directly reflects inadequate cardiac output, the heart cannot generate sufficient stroke volume to maintain perfusion pressure. Tachycardia is a compensatory response, not a direct indicator of low output. Edema reflects venous congestion (preload), not forward output. Mild TR and first-degree AV block are structural/conduction findings without direct output implications. <div class="ec-src"><b>Source:</b> Heidenreich PA, et al. Circulation 2022;145(18):e895-e1032.</div></div> [[Start another case->Hub]] [[Restart this case->HFrEF cardiac output - Prog]] [[Next case →->Post-MI remodeling - Mech]]

<span class="ec-case-marker" hidden data-entry="HFrEF cardiac output. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is Persistent resting hypotension. Persistent hypotension in advanced HFrEF directly reflects inadequate cardiac output, the heart cannot generate sufficient stroke volume to maintain perfusion pressure. Tachycardia is a compensatory response, not a direct indicator of low output. Edema reflects venous congestion (preload), not forward output. Mild TR and first-degree AV block are structural/conduction findings without direct output implications. <div class="ec-src"><b>Source:</b> Heidenreich PA, et al. Circulation 2022;145(18):e895-e1032.</div></div> [[Try this question again->HFrEF cardiac output - Prog]] [[Start another case->Hub]]

<div class="ec-scene">Allergy clinic · 10:15</div> A 22-year-old woman develops wheezing, chest tightness, and dyspnea within minutes of entering a house containing cats. Temperature is 37.0°C (98.6°F), blood pressure is 122/78 mm Hg, pulse is 104/min, respirations are 24/min, and oxygen saturation is 94% on room air. <span class="ec-prompt">Which of the following processes most directly causes the acute airway narrowing?</span> [[CD8+ T-cell lysis of bronchial epithelium->Allergic asthma mechanism - B]] [[Complement-mediated smooth muscle necrosis->Allergic asthma mechanism - E]] [[IgE cross-linking on mast cells with mediator release->Allergic asthma mechanism - Correct]] [[IgG-mediated alveolar wall destruction->Allergic asthma mechanism - A]] [[Immune-complex deposition in small airways->Allergic asthma mechanism - C]]

<span class="ec-case-marker" hidden data-entry="Allergic asthma mechanism. Mech"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ IgE cross-linking on mast cells with mediator release.</div> Acute allergic asthma is a type I hypersensitivity reaction: allergen cross-links IgE on mast cells, releasing histamine and leukotrienes that cause bronchoconstriction, mucosal edema, and mucus secretion. Type II (IgG-mediated), type III (immune-complex), and type IV (T-cell-mediated) reactions cause different patterns of tissue injury. <div class="ec-src"><b>Source:</b> Abbas AK, et al. Basic Immunology. 7th ed. Elsevier; 2024.</div></div> [[Start another case->Hub]] [[Restart this case->Allergic asthma mechanism - Mech]] [[Next case →->Methacholine challenge - Dx]]

<span class="ec-case-marker" hidden data-entry="Allergic asthma mechanism. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is IgE cross-linking on mast cells with mediator release. Acute allergic asthma is a type I hypersensitivity reaction: allergen cross-links IgE on mast cells, releasing histamine and leukotrienes that cause bronchoconstriction, mucosal edema, and mucus secretion. Type II (IgG-mediated), type III (immune-complex), and type IV (T-cell-mediated) reactions cause different patterns of tissue injury. <div class="ec-src"><b>Source:</b> Abbas AK, et al. Basic Immunology. 7th ed. Elsevier; 2024.</div></div> [[Try this question again->Allergic asthma mechanism - Mech]] [[Start another case->Hub]]

<div class="ec-scene">Pulmonary function laboratory · 08:45</div> A 67-year-old man with a 45-pack-year smoking history has had progressive exertional dyspnea for 2 years. Spirometry demonstrates an FEV1/FVC ratio of 0.55. Chest CT shows upper-lobe-predominant areas of parenchymal destruction. <span class="ec-prompt">Which of the following additional pulmonary function findings is most consistent with this presentation?</span> [[Decreased diffusing capacity for carbon monoxide->DLCO in emphysema - Correct]] [[Decreased residual volume->DLCO in emphysema - D]] [[Decreased total lung capacity->DLCO in emphysema - C]] [[Increased diffusing capacity for carbon monoxide->DLCO in emphysema - A]] [[Increased ratio of forced expiratory volume in 1 second to forced vital capacity after bronchodilator->DLCO in emphysema - E]]

<span class="ec-case-marker" hidden data-entry="DLCO in emphysema. Ix"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Decreased diffusing capacity for carbon monoxide.</div> Emphysema destroys alveolar walls, reducing the surface area available for gas exchange and lowering DLCO. Total lung capacity and residual volume are typically increased due to air trapping and loss of elastic recoil. The FEV1/FVC ratio remains low even after bronchodilator in established emphysema. <div class="ec-src"><b>Source:</b> GOLD 2024 Report.</div></div> [[Start another case->Hub]] [[Restart this case->DLCO in emphysema - Ix]] [[Next case →->Sleep apnea - Ix]]

<span class="ec-case-marker" hidden data-entry="DLCO in emphysema. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is Decreased diffusing capacity for carbon monoxide. Emphysema destroys alveolar walls, reducing the surface area available for gas exchange and lowering DLCO. Total lung capacity and residual volume are typically increased due to air trapping and loss of elastic recoil. The FEV1/FVC ratio remains low even after bronchodilator in established emphysema. <div class="ec-src"><b>Source:</b> GOLD 2024 Report.</div></div> [[Try this question again->DLCO in emphysema - Ix]] [[Start another case->Hub]]

<div class="ec-scene">Interstitial lung disease clinic · 13:40</div> A 71-year-old man with idiopathic pulmonary fibrosis undergoes serial pulmonary function testing. Over the past 12 months, his forced vital capacity has declined from 78% to 61% of predicted. His diffusing capacity has also fallen. <span class="ec-prompt">Which of the following interpretation of these findings is most appropriate?</span> [[The decline confirms the presence of concurrent pulmonary hypertension->IPF FVC decline - C]] [[The decline is consistent with steroid-responsive airway inflammation->IPF FVC decline - A]] [[The decline suggests clinically significant disease progression->IPF FVC decline - Correct]] [[The decline supports a diagnosis of primary airway obstruction->IPF FVC decline - D]] [[The decline warrants a trial of inhaled bronchodilators before further workup->IPF FVC decline - E]]

<span class="ec-case-marker" hidden data-entry="IPF FVC decline. Prog"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ The decline suggests clinically significant disease progression.</div> A forced vital capacity decline of ≥10% absolute over 6 to 12 months is an established marker of disease progression in IPF and is associated with increased mortality. IPF does not respond to corticosteroids (PANTHER-IPF trial showed harm from prednisone/azathioprine/NAC). Bronchodilators do not reverse fibrotic restriction. PFTs alone cannot diagnose pulmonary hypertension. <div class="ec-src"><b>Source:</b> du Bois RM, et al. Am J Respir Crit Care Med 2011;184(12):1382-1389.</div></div> [[Start another case->Hub]] [[Restart this case->IPF FVC decline - Prog]] [[Next case →->SSc-ILD mortality - Prog]]

<span class="ec-case-marker" hidden data-entry="IPF FVC decline. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is The decline suggests clinically significant disease progression. A forced vital capacity decline of ≥10% absolute over 6 to 12 months is an established marker of disease progression in IPF and is associated with increased mortality. IPF does not respond to corticosteroids (PANTHER-IPF trial showed harm from prednisone/azathioprine/NAC). Bronchodilators do not reverse fibrotic restriction. PFTs alone cannot diagnose pulmonary hypertension. <div class="ec-src"><b>Source:</b> du Bois RM, et al. Am J Respir Crit Care Med 2011;184(12):1382-1389.</div></div> [[Try this question again->IPF FVC decline - Prog]] [[Start another case->Hub]]

<div class="ec-scene">Pulmonary clinic · 15:05</div> A 28-year-old woman has episodes of cough, wheezing, and chest tightness that occur several times per month and occasionally wake her at night. Between episodes, she is asymptomatic. Spirometry performed during an asymptomatic interval is normal. Methacholine challenge testing causes a 23% decrease in FEV1. <span class="ec-prompt">Which of the following is the most likely diagnosis?</span> [[Chronic obstructive pulmonary disease->Methacholine challenge - A]] [[Early idiopathic pulmonary fibrosis->Methacholine challenge - D]] [[Idiopathic bronchiectasis->Methacholine challenge - B]] [[Intermittent bronchial asthma->Methacholine challenge - Correct]] [[Paradoxical vocal fold motion disorder->Methacholine challenge - E]]

<span class="ec-case-marker" hidden data-entry="Methacholine challenge. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Intermittent bronchial asthma.</div> Episodic wheezing, cough, and chest tightness with normal baseline spirometry and a positive methacholine challenge (≥20% FEV1 decline) is diagnostic of asthma with bronchial hyperresponsiveness. COPD causes persistent airflow limitation. Pulmonary fibrosis shows restriction, not obstruction. PVFM can mimic asthma but does not produce a positive methacholine test. <div class="ec-src"><b>Source:</b> Crapo RO, et al. Am J Respir Crit Care Med 2000;161(1):309-329.</div></div> [[Start another case->Hub]] [[Restart this case->Methacholine challenge - Dx]] [[Next case →->Anaphylaxis - Ix]]

<span class="ec-case-marker" hidden data-entry="Methacholine challenge. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is Intermittent bronchial asthma. Episodic wheezing, cough, and chest tightness with normal baseline spirometry and a positive methacholine challenge (≥20% FEV1 decline) is diagnostic of asthma with bronchial hyperresponsiveness. COPD causes persistent airflow limitation. Pulmonary fibrosis shows restriction, not obstruction. PVFM can mimic asthma but does not produce a positive methacholine test. <div class="ec-src"><b>Source:</b> Crapo RO, et al. Am J Respir Crit Care Med 2000;161(1):309-329.</div></div> [[Try this question again->Methacholine challenge - Dx]] [[Start another case->Hub]]

<div class="ec-scene">Medical ward · 06:37</div> A 48-year-old man has had persistent vomiting for 3 days and has developed a metabolic alkalosis. Temperature is 37.0°C (98.6°F), blood pressure is 98/64 mm Hg, and pulse is 108/min with orthostatic changes. Serum chloride is 88 mEq/L, urine chloride is 8 mEq/L, and he has signs of extracellular volume depletion. <span class="ec-prompt">Which of the following renal processes most directly maintains his alkalosis?</span> [[Enhanced distal chloride reabsorption->Contraction alkalosis - D]] [[Increased distal bicarbonate secretion->Contraction alkalosis - A]] [[Increased proximal bicarbonate reabsorption->Contraction alkalosis - Correct]] [[Inhibition of angiotensin II production->Contraction alkalosis - E]] [[Suppression of aldosterone release->Contraction alkalosis - B]]

<span class="ec-case-marker" hidden data-entry="Contraction alkalosis. Mech"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Increased proximal bicarbonate reabsorption.</div> Volume contraction activates the renin-angiotensin-aldosterone system, increasing proximal tubular sodium and bicarbonate reabsorption. This mechanism perpetuates the alkalosis, the kidney "chooses" volume over acid-base balance. Low urine chloride (<20 mEq/L) confirms a chloride-responsive (volume-depleted) alkalosis. <div class="ec-src"><b>Source:</b> Luke RG, Galla JH. J Am Soc Nephrol 2012;23(2):204-207.</div></div> [[Start another case->Hub]] [[Restart this case->Contraction alkalosis - Mech]] [[Next case →->PTH phosphaturia - Mech]]

<span class="ec-case-marker" hidden data-entry="Contraction alkalosis. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is Increased proximal bicarbonate reabsorption. Volume contraction activates the renin-angiotensin-aldosterone system, increasing proximal tubular sodium and bicarbonate reabsorption. This mechanism perpetuates the alkalosis, the kidney "chooses" volume over acid-base balance. Low urine chloride (<20 mEq/L) confirms a chloride-responsive (volume-depleted) alkalosis. <div class="ec-src"><b>Source:</b> Luke RG, Galla JH. J Am Soc Nephrol 2012;23(2):204-207.</div></div> [[Try this question again->Contraction alkalosis - Mech]] [[Start another case->Hub]]

<div class="ec-scene">Nephrology clinic · 10:50</div> A 52-year-old woman with diabetic kidney disease has an eGFR of 48 mL/min/1.73 m2. Over 18 months, her urine albumin-to-creatinine ratio increases from 180 to 920 mg/g despite stable blood pressure and serum creatinine. <span class="ec-prompt">Which of the following findings most strongly predicts progression to kidney failure?</span> [[Declining serum bicarbonate level->Albuminuria progression - B]] [[Increasing serum phosphorus concentration->Albuminuria progression - D]] [[Progressive increase in albuminuria->Albuminuria progression - Correct]] [[Rising parathyroid hormone level->Albuminuria progression - E]] [[Rising serum uric acid concentration->Albuminuria progression - A]]

<span class="ec-case-marker" hidden data-entry="Albuminuria progression. Prog"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Progressive increase in albuminuria.</div> Rising albuminuria independently predicts CKD progression and reflects worsening glomerular injury (KDIGO risk classification). While declining bicarbonate, rising phosphorus, and rising PTH occur in advancing CKD, they are consequences of falling GFR rather than independent predictors of progression. Uric acid is a weaker and more contested predictor than albuminuria. <div class="ec-src"><b>Source:</b> KDIGO 2024 CKD Guideline.</div></div> [[Start another case->Hub]] [[Restart this case->Albuminuria progression - Prog]] [[Next case →->Testicular torsion - Ix]]

<span class="ec-case-marker" hidden data-entry="Albuminuria progression. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is Progressive increase in albuminuria. Rising albuminuria independently predicts CKD progression and reflects worsening glomerular injury (KDIGO risk classification). While declining bicarbonate, rising phosphorus, and rising PTH occur in advancing CKD, they are consequences of falling GFR rather than independent predictors of progression. Uric acid is a weaker and more contested predictor than albuminuria. <div class="ec-src"><b>Source:</b> KDIGO 2024 CKD Guideline.</div></div> [[Try this question again->Albuminuria progression - Prog]] [[Start another case->Hub]]

<div class="ec-scene">Nephrology clinic · 09:05</div> A 35-year-old man has had periorbital edema and dark urine for 5 days. Urinalysis shows 3+ blood. Microscopy demonstrates dysmorphic red blood cells and red blood cell casts. <span class="ec-prompt">Which of the following anatomic structures is the most likely source of the hematuria?</span> [[Cortical collecting duct->Glomerular hematuria - D]] [[Glomerular capillary tuft->Glomerular hematuria - Correct]] [[Proximal convoluted tubule->Glomerular hematuria - A]] [[Thin descending limb of Henle->Glomerular hematuria - B]] [[Transitional epithelium of the renal pelvis->Glomerular hematuria - E]]

<span class="ec-case-marker" hidden data-entry="Glomerular hematuria. Ix"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Glomerular capillary tuft.</div> Dysmorphic RBCs form as they squeeze through a damaged glomerular basement membrane, and RBC casts form as cells become trapped in Tamm-Horsfall protein in the tubule. Together they localize the bleeding to the glomerulus. Lower urinary tract bleeding produces isomorphic (normal-shaped) RBCs without casts. <div class="ec-src"><b>Source:</b> Fogazzi GB, et al. Comprehensive Clinical Nephrology. 7th ed. 2024.</div></div> [[Start another case->Hub]] [[Restart this case->Glomerular hematuria - Ix]] [[Next case →->Poststreptococcal GN - Dx]]

<span class="ec-case-marker" hidden data-entry="Glomerular hematuria. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is Glomerular capillary tuft. Dysmorphic RBCs form as they squeeze through a damaged glomerular basement membrane, and RBC casts form as cells become trapped in Tamm-Horsfall protein in the tubule. Together they localize the bleeding to the glomerulus. Lower urinary tract bleeding produces isomorphic (normal-shaped) RBCs without casts. <div class="ec-src"><b>Source:</b> Fogazzi GB, et al. Comprehensive Clinical Nephrology. 7th ed. 2024.</div></div> [[Try this question again->Glomerular hematuria - Ix]] [[Start another case->Hub]]

<div class="ec-scene">Pediatric clinic · 16:20</div> A 12-year-old boy develops periorbital edema and cola-colored urine 2 weeks after an episode of impetigo. Temperature is 37.4°C (99.3°F), blood pressure is 142/92 mm Hg, and pulse is 88/min. Urinalysis shows 3+ blood and 2+ protein with red blood cell casts. Serum C3 is decreased and C4 is normal. <span class="ec-prompt">Which of the following is the most likely diagnosis?</span> [[Anti-glomerular basement membrane disease->Poststreptococcal GN - E]] [[Hereditary nephritis (Alport syndrome)->Poststreptococcal GN - D]] [[IgA nephropathy->Poststreptococcal GN - A]] [[Minimal change disease->Poststreptococcal GN - C]] [[Postinfectious glomerulonephritis->Poststreptococcal GN - Correct]]

<span class="ec-case-marker" hidden data-entry="Poststreptococcal GN. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Postinfectious glomerulonephritis.</div> A nephritic presentation 1–3 weeks after a streptococcal skin infection with low C3, normal C4, and an active sediment is classic for postinfectious (poststreptococcal) glomerulonephritis. IgA nephropathy typically presents within days of a URI (synpharyngitic). Minimal change disease presents with nephrotic syndrome. Alport is hereditary with hearing loss. Anti-GBM disease is rare in children. <div class="ec-src"><b>Source:</b> Rodriguez-Iturbe B. J Am Soc Nephrol 2008;19(10):1855-1864.</div></div> [[Start another case->Hub]] [[Restart this case->Poststreptococcal GN - Dx]] [[Next case →->Lupus nephritis - Mech]]

<span class="ec-case-marker" hidden data-entry="Poststreptococcal GN. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is Postinfectious glomerulonephritis. A nephritic presentation 1–3 weeks after a streptococcal skin infection with low C3, normal C4, and an active sediment is classic for postinfectious (poststreptococcal) glomerulonephritis. IgA nephropathy typically presents within days of a URI (synpharyngitic). Minimal change disease presents with nephrotic syndrome. Alport is hereditary with hearing loss. Anti-GBM disease is rare in children. <div class="ec-src"><b>Source:</b> Rodriguez-Iturbe B. J Am Soc Nephrol 2008;19(10):1855-1864.</div></div> [[Try this question again->Poststreptococcal GN - Dx]] [[Start another case->Hub]]

<div class="ec-scene">Gastroenterology clinic · 11:10</div> A 49-year-old man with chronic alcohol-associated pancreatitis has had weight loss and bulky, foul-smelling, oily stools for 6 months. Serum albumin is 3.1 g/dL. <span class="ec-prompt">Which of the following abnormalities most directly causes his steatorrhea?</span> [[Accelerated colonic transit reducing water absorption->Pancreatic insufficiency - D]] [[Excessive gastric acid inactivating digestive enzymes->Pancreatic insufficiency - C]] [[Impaired hepatic bile acid conjugation->Pancreatic insufficiency - A]] [[Insufficient pancreatic lipase secretion->Pancreatic insufficiency - Correct]] [[Reduced intestinal brush-border disaccharidase activity->Pancreatic insufficiency - E]]

<span class="ec-case-marker" hidden data-entry="Pancreatic insufficiency. Mech"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Insufficient pancreatic lipase secretion.</div> Exocrine pancreatic insufficiency from chronic pancreatitis results in inadequate pancreatic lipase reaching the duodenum, causing fat maldigestion and steatorrhea. Clinical steatorrhea typically appears when lipase output falls below 10% of normal. Bile acid deficiency can cause fat malabsorption but is not the primary defect in chronic pancreatitis. <div class="ec-src"><b>Source:</b> Dominguez-Munoz JE. J Gastroenterol Hepatol 2011;26(S2):12-16.</div></div> [[Start another case->Hub]] [[Restart this case->Pancreatic insufficiency - Mech]] [[Next case →->Cholangitis - Ix]]

<span class="ec-case-marker" hidden data-entry="Pancreatic insufficiency. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is Insufficient pancreatic lipase secretion. Exocrine pancreatic insufficiency from chronic pancreatitis results in inadequate pancreatic lipase reaching the duodenum, causing fat maldigestion and steatorrhea. Clinical steatorrhea typically appears when lipase output falls below 10% of normal. Bile acid deficiency can cause fat malabsorption but is not the primary defect in chronic pancreatitis. <div class="ec-src"><b>Source:</b> Dominguez-Munoz JE. J Gastroenterol Hepatol 2011;26(S2):12-16.</div></div> [[Try this question again->Pancreatic insufficiency - Mech]] [[Start another case->Hub]]

<div class="ec-scene">Hepatology clinic · 14:35</div> A 58-year-old man with alcohol-associated cirrhosis is hospitalized with a first episode of spontaneous bacterial peritonitis. Ascitic fluid culture grows Escherichia coli. He responds to antibiotic therapy and his ascites resolves with diuretics. <span class="ec-prompt">Which of the following best describes his risk of recurrent spontaneous bacterial peritonitis after discharge?</span> [[Recurrence is prevented by proton-pump inhibitor therapy alone->SBP recurrence - C]] [[Recurrence risk is eliminated by paracentesis at regular intervals->SBP recurrence - D]] [[Recurrence risk is negligible and no prophylaxis is indicated->SBP recurrence - A]] [[The one-year recurrence rate is approximately 15% without prophylaxis->SBP recurrence - E]] [[The one-year recurrence rate is approximately 70% without prophylaxis->SBP recurrence - Correct]]

<span class="ec-case-marker" hidden data-entry="SBP recurrence. Prog"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ The one-year recurrence rate is approximately 70% without prophylaxis.</div> After a first episode of SBP, the one-year recurrence rate is approximately 70% without secondary prophylaxis (Ginès et al., Hepatology 1990). AASLD practice guidance recommends long-term secondary prophylaxis; U.S. options are ciprofloxacin 500 mg PO daily or trimethoprim-sulfamethoxazole double-strength daily (norfloxacin was withdrawn from the U.S. market in 2015 and remains guideline-listed where available internationally). PPIs do not prevent SBP and may increase risk (Bajaj, Am J Gastroenterol 2009). <div class="ec-src"><b>Source:</b> Gines P, et al. Hepatology 1990;12(4):716-724.</div></div> [[Start another case->Hub]] [[Restart this case->SBP recurrence - Prog]] [[Next case →->MELD score - Dx]]

<span class="ec-case-marker" hidden data-entry="SBP recurrence. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is The one-year recurrence rate is approximately 70% without prophylaxis. After a first episode of SBP, the one-year recurrence rate is approximately 70% without secondary prophylaxis (Ginès et al., Hepatology 1990). AASLD practice guidance recommends long-term secondary prophylaxis; U.S. options are ciprofloxacin 500 mg PO daily or trimethoprim-sulfamethoxazole double-strength daily (norfloxacin was withdrawn from the U.S. market in 2015 and remains guideline-listed where available internationally). PPIs do not prevent SBP and may increase risk (Bajaj, Am J Gastroenterol 2009). <div class="ec-src"><b>Source:</b> Gines P, et al. Hepatology 1990;12(4):716-724.</div></div> [[Try this question again->SBP recurrence - Prog]] [[Start another case->Hub]]

<div class="ec-scene">Gastroenterology clinic · 08:55</div> A 57-year-old man has progressive dysphagia to solids for 6 months that now includes liquids. He has lost 4 kg. Temperature is 36.6°C (97.9°F), blood pressure is 132/80 mm Hg, and pulse is 78/min. Upper endoscopy shows no obstructing lesion and normal-appearing mucosa. <span class="ec-prompt">Which of the following studies is most appropriate next?</span> [[4-hour gastric emptying scintigraphy->Esophageal manometry - D]] [[Abdominal CT without intravenous contrast->Esophageal manometry - E]] [[Colonoscopy with random biopsies->Esophageal manometry - A]] [[Esophageal high-resolution manometry->Esophageal manometry - Correct]] [[Hepatobiliary iminodiacetic acid scan->Esophageal manometry - C]]

<span class="ec-case-marker" hidden data-entry="Esophageal manometry. Ix"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Esophageal high-resolution manometry.</div> When endoscopy excludes mechanical obstruction, progressive dysphagia to both solids and liquids suggests an esophageal motility disorder such as achalasia. High-resolution manometry is the reference standard for diagnosing esophageal motility disorders. Gastric emptying studies evaluate gastroparesis, not esophageal dysphagia. <div class="ec-src"><b>Source:</b> Kahrilas PJ, et al. Neurogastroenterol Motil 2021;33(1):e14058.</div></div> [[Start another case->Hub]] [[Restart this case->Esophageal manometry - Ix]] [[Next case →->Acute liver failure - Dx]]

<span class="ec-case-marker" hidden data-entry="Esophageal manometry. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is Esophageal high-resolution manometry. When endoscopy excludes mechanical obstruction, progressive dysphagia to both solids and liquids suggests an esophageal motility disorder such as achalasia. High-resolution manometry is the reference standard for diagnosing esophageal motility disorders. Gastric emptying studies evaluate gastroparesis, not esophageal dysphagia. <div class="ec-src"><b>Source:</b> Kahrilas PJ, et al. Neurogastroenterol Motil 2021;33(1):e14058.</div></div> [[Try this question again->Esophageal manometry - Ix]] [[Start another case->Hub]]

<div class="ec-scene">Primary care clinic · 10:25</div> A 32-year-old woman has 6 months of intermittent diarrhea, bloating, and a 5-kg weight loss. She has an itchy, grouped vesicular rash on her elbows and knees. Laboratory studies show hemoglobin 10.8 g/dL, mean corpuscular volume 74 fL, and iron studies consistent with iron deficiency. Tissue transglutaminase IgA antibody is strongly positive. <span class="ec-prompt">Which of the following is the most likely diagnosis?</span> [[Celiac disease->Celiac disease - Correct]] [[Chronic pancreatitis->Celiac disease - E]] [[Irritable bowel syndrome->Celiac disease - A]] [[Lactose intolerance->Celiac disease - D]] [[Tropical sprue->Celiac disease - C]]

<span class="ec-case-marker" hidden data-entry="Celiac disease. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Celiac disease.</div> Iron-deficiency anemia, chronic diarrhea, a positive tissue transglutaminase IgA, and dermatitis herpetiformis (grouped vesicles on extensor surfaces) are characteristic of celiac disease. Duodenal biopsy showing villous atrophy confirms the diagnosis. IBS does not cause weight loss or iron deficiency. Tropical sprue is geographically restricted. <div class="ec-src"><b>Source:</b> Rubio-Tapia A, et al. Am J Gastroenterol 2013;108(5):656-676.</div></div> [[Start another case->Hub]] [[Restart this case->Celiac disease - Dx]] [[Next case →->C difficile - Rx]]

<span class="ec-case-marker" hidden data-entry="Celiac disease. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is Celiac disease. Iron-deficiency anemia, chronic diarrhea, a positive tissue transglutaminase IgA, and dermatitis herpetiformis (grouped vesicles on extensor surfaces) are characteristic of celiac disease. Duodenal biopsy showing villous atrophy confirms the diagnosis. IBS does not cause weight loss or iron deficiency. Tropical sprue is geographically restricted. <div class="ec-src"><b>Source:</b> Rubio-Tapia A, et al. Am J Gastroenterol 2013;108(5):656-676.</div></div> [[Try this question again->Celiac disease - Dx]] [[Start another case->Hub]]

<div class="ec-scene">Movement disorders clinic · 13:15</div> A 70-year-old man with Parkinson disease has worsening bradykinesia and cogwheel rigidity despite carbidopa-levodopa therapy. His neurologist is considering adding a dopamine agonist. Loss of dopaminergic neurons in the substantia nigra pars compacta leads to excessive inhibitory output from the globus pallidus interna to the thalamus. <span class="ec-prompt">Which of the following clinical features is most directly explained by this increased thalamocortical inhibition?</span> [[Choreiform involuntary movements->Parkinson basal ganglia - D]] [[Difficulty initiating voluntary movements->Parkinson basal ganglia - Correct]] [[Intention tremor during finger-to-nose testing->Parkinson basal ganglia - C]] [[Resting tremor with pill-rolling character->Parkinson basal ganglia - A]] [[Sensory loss in a stocking-glove distribution->Parkinson basal ganglia - E]]

<span class="ec-case-marker" hidden data-entry="Parkinson basal ganglia. Mech"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Difficulty initiating voluntary movements.</div> Excessive GPi inhibition of the thalamus reduces thalamocortical excitation, directly producing akinesia/bradykinesia, difficulty initiating and executing voluntary movements. Resting tremor involves a different oscillatory circuit and is less directly linked to the GPi-thalamic pathway. Intention tremor localizes to the cerebellum, not basal ganglia. Chorea results from DECREASED GPi output (as in Huntington disease). Sensory loss is a peripheral nerve finding. <div class="ec-src"><b>Source:</b> DeLong MR, Wichmann T. JAMA Neurol 2015;72(11):1354-1360.</div></div> [[Start another case->Hub]] [[Restart this case->Parkinson basal ganglia - Mech]] [[Next case →->Delirium - Dx]]

<span class="ec-case-marker" hidden data-entry="Parkinson basal ganglia. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is Difficulty initiating voluntary movements. Excessive GPi inhibition of the thalamus reduces thalamocortical excitation, directly producing akinesia/bradykinesia, difficulty initiating and executing voluntary movements. Resting tremor involves a different oscillatory circuit and is less directly linked to the GPi-thalamic pathway. Intention tremor localizes to the cerebellum, not basal ganglia. Chorea results from DECREASED GPi output (as in Huntington disease). Sensory loss is a peripheral nerve finding. <div class="ec-src"><b>Source:</b> DeLong MR, Wichmann T. JAMA Neurol 2015;72(11):1354-1360.</div></div> [[Try this question again->Parkinson basal ganglia - Mech]] [[Start another case->Hub]]

<div class="ec-scene">Neurology clinic · 09:40</div> A 29-year-old woman presents with 4 weeks of episodic unilateral visual loss, followed 3 months later by numbness and tingling in her legs that ascended over several days. Neurologic examination shows a relative afferent pupillary defect in the right eye, hyperreflexia in the lower extremities, and a positive Babinski sign bilaterally. MRI of the brain and spinal cord is obtained. <span class="ec-prompt">Which of the following findings would most strongly support the suspected diagnosis?</span> [[Bilateral mesial temporal sclerosis->MS MRI findings - E]] [[Bilateral symmetric basal ganglia calcifications->MS MRI findings - B]] [[Diffuse cortical atrophy with widened sulci->MS MRI findings - C]] [[Periventricular and juxtacortical white matter lesions->MS MRI findings - Correct]] [[Single ring-enhancing lesion in the frontal lobe->MS MRI findings - D]]

<span class="ec-case-marker" hidden data-entry="MS MRI findings. Ix"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Periventricular and juxtacortical white matter lesions.</div> Relapsing neurologic deficits separated in time (optic neuritis → myelopathy) and space (optic nerve, spinal cord) with upper motor neuron signs strongly suggest multiple sclerosis. Periventricular and juxtacortical T2/FLAIR hyperintense lesions are characteristic MRI findings and part of the McDonald diagnostic criteria. Basal ganglia calcifications suggest Fahr disease. Diffuse atrophy suggests neurodegenerative disease. A single ring-enhancing lesion raises concern for abscess or tumor. Mesial temporal sclerosis is associated with temporal lobe epilepsy. <div class="ec-src"><b>Source:</b> Thompson AJ, et al. Lancet Neurol 2018;17(2):162-173.</div></div> [[Start another case->Hub]] [[Restart this case->MS MRI findings - Ix]] [[Next case →->Wernicke - Dx]]

<span class="ec-case-marker" hidden data-entry="MS MRI findings. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is Periventricular and juxtacortical white matter lesions. Relapsing neurologic deficits separated in time (optic neuritis → myelopathy) and space (optic nerve, spinal cord) with upper motor neuron signs strongly suggest multiple sclerosis. Periventricular and juxtacortical T2/FLAIR hyperintense lesions are characteristic MRI findings and part of the McDonald diagnostic criteria. Basal ganglia calcifications suggest Fahr disease. Diffuse atrophy suggests neurodegenerative disease. A single ring-enhancing lesion raises concern for abscess or tumor. Mesial temporal sclerosis is associated with temporal lobe epilepsy. <div class="ec-src"><b>Source:</b> Thompson AJ, et al. Lancet Neurol 2018;17(2):162-173.</div></div> [[Try this question again->MS MRI findings - Ix]] [[Start another case->Hub]]

<div class="ec-scene">Neurologic intensive care unit · 03:20</div> A 63-year-old man has a large left middle cerebral artery territory infarction involving most of the hemisphere. Temperature is 37.2°C (99.0°F), blood pressure is 168/94 mm Hg, and pulse is 82/min. 6 hours after onset, he becomes progressively more somnolent. <span class="ec-prompt">Which of the following complications is he at greatest risk of developing?</span> [[Cervical spinal cord infarction from hypoperfusion->Malignant MCA edema - E]] [[Delayed chronic subdural hematoma formation->Malignant MCA edema - C]] [[Malignant cerebral edema with transtentorial herniation->Malignant MCA edema - Correct]] [[Normal-pressure hydrocephalus with gait disturbance->Malignant MCA edema - D]] [[Obstructive hydrocephalus from aqueductal compression->Malignant MCA edema - A]]

<span class="ec-case-marker" hidden data-entry="Malignant MCA edema. Prog"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Malignant cerebral edema with transtentorial herniation.</div> Large MCA territory infarctions (malignant MCA syndrome) can produce massive cytotoxic edema peaking at 48–72 hours, causing midline shift, transtentorial herniation, and death in up to 80% of cases without intervention. The DECIMAL, DESTINY, and HAMLET trials demonstrated that decompressive craniectomy reduces mortality in selected patients. <div class="ec-src"><b>Source:</b> Vahedi K, et al. Lancet Neurol 2007;6(3):215-222.</div></div> [[Start another case->Hub]] [[Restart this case->Malignant MCA edema - Prog]] [[Next case →->Status epilepticus - Opening]]

<span class="ec-case-marker" hidden data-entry="Malignant MCA edema. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is Malignant cerebral edema with transtentorial herniation. Large MCA territory infarctions (malignant MCA syndrome) can produce massive cytotoxic edema peaking at 48–72 hours, causing midline shift, transtentorial herniation, and death in up to 80% of cases without intervention. The DECIMAL, DESTINY, and HAMLET trials demonstrated that decompressive craniectomy reduces mortality in selected patients. <div class="ec-src"><b>Source:</b> Vahedi K, et al. Lancet Neurol 2007;6(3):215-222.</div></div> [[Try this question again->Malignant MCA edema - Prog]] [[Start another case->Hub]]

<div class="ec-scene">Endocrinology clinic · 11:45</div> A 44-year-old woman has primary hyperparathyroidism with a serum calcium of 11.8 mg/dL and an elevated parathyroid hormone. <span class="ec-prompt">Which of the following renal effects does parathyroid hormone most directly produce, in addition to increasing distal tubular calcium reabsorption?</span> [[Decreased proximal tubular phosphate reabsorption->PTH phosphaturia - Correct]] [[Increased collecting-duct sodium reabsorption->PTH phosphaturia - D]] [[Increased proximal tubular phosphate reabsorption->PTH phosphaturia - A]] [[Inhibition of renal 1-alpha-hydroxylase activity->PTH phosphaturia - C]] [[Stimulation of renal erythropoietin production->PTH phosphaturia - E]]

<span class="ec-case-marker" hidden data-entry="PTH phosphaturia. Mech"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Decreased proximal tubular phosphate reabsorption.</div> PTH acts on the proximal tubule to downregulate the NaPi-IIa cotransporter, causing phosphaturia. PTH also stimulates 1-alpha-hydroxylase (not inhibits it), increasing active vitamin D production, and enhances distal tubular calcium reabsorption. The net result is hypercalcemia with hypophosphatemia, the classic biochemical signature of primary hyperparathyroidism. <div class="ec-src"><b>Source:</b> Juppner H, et al. The Parathyroids. 3rd ed. 2015.</div></div> [[Start another case->Hub]] [[Restart this case->PTH phosphaturia - Mech]] [[Next case →->Nephrolithiasis - Ix]]

<span class="ec-case-marker" hidden data-entry="PTH phosphaturia. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is Decreased proximal tubular phosphate reabsorption. PTH acts on the proximal tubule to downregulate the NaPi-IIa cotransporter, causing phosphaturia. PTH also stimulates 1-alpha-hydroxylase (not inhibits it), increasing active vitamin D production, and enhances distal tubular calcium reabsorption. The net result is hypercalcemia with hypophosphatemia, the classic biochemical signature of primary hyperparathyroidism. <div class="ec-src"><b>Source:</b> Juppner H, et al. The Parathyroids. 3rd ed. 2015.</div></div> [[Try this question again->PTH phosphaturia - Mech]] [[Start another case->Hub]]

<div class="ec-scene">Endocrinology clinic · 10:05</div> A 36-year-old woman has had weight loss, tremor, heat intolerance, and palpitations for 3 months. Pulse is 112/min and blood pressure is 148/72 mm Hg. TSH is undetectable and free T4 is elevated. Examination shows a diffuse nontender goiter and bilateral proptosis. <span class="ec-prompt">Which of the following tests would most specifically confirm the autoimmune etiology?</span> [[Elevated 24-hour urinary free cortisol->Graves TRAb - E]] [[Elevated serum calcitonin concentration->Graves TRAb - C]] [[Low radioactive iodine uptake on thyroid scan->Graves TRAb - A]] [[Positive anti-cyclic citrullinated peptide antibody->Graves TRAb - D]] [[Thyrotropin receptor antibody (TRAb) assay->Graves TRAb - Correct]]

<span class="ec-case-marker" hidden data-entry="Graves TRAb. Ix"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Thyrotropin receptor antibody (TRAb) assay.</div> TSH receptor (stimulating) antibodies are the most specific serologic test for Graves disease. While radioactive iodine uptake is diffusely increased (not decreased) in Graves, TRAb confirms the autoimmune etiology. Low uptake would suggest thyroiditis or exogenous thyroid hormone. Anti-CCP is specific for rheumatoid arthritis. <div class="ec-src"><b>Source:</b> Ross DS, et al. Thyroid 2016;26(10):1343-1421.</div></div> [[Start another case->Hub]] [[Restart this case->Graves TRAb - Ix]] [[Next case →->Papillary thyroid prognosis - Prog]]

<span class="ec-case-marker" hidden data-entry="Graves TRAb. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is Thyrotropin receptor antibody (TRAb) assay. TSH receptor (stimulating) antibodies are the most specific serologic test for Graves disease. While radioactive iodine uptake is diffusely increased (not decreased) in Graves, TRAb confirms the autoimmune etiology. Low uptake would suggest thyroiditis or exogenous thyroid hormone. Anti-CCP is specific for rheumatoid arthritis. <div class="ec-src"><b>Source:</b> Ross DS, et al. Thyroid 2016;26(10):1343-1421.</div></div> [[Try this question again->Graves TRAb - Ix]] [[Start another case->Hub]]

<div class="ec-scene">Endocrine surgery clinic · 15:30</div> A 52-year-old woman undergoes total thyroidectomy for a 1.5-cm papillary thyroid carcinoma confined to the thyroid gland with no lymph node involvement and no vascular invasion. Postoperative thyroglobulin is undetectable on levothyroxine suppression therapy. <span class="ec-prompt">Which of the following best describes her long-term prognosis?</span> [[Adjuvant external beam radiation is required to prevent recurrence->Papillary thyroid prognosis - D]] [[Distant metastases are expected within 2 years->Papillary thyroid prognosis - C]] [[The 10-year disease-specific survival exceeds 95%->Papillary thyroid prognosis - Correct]] [[The 5-year survival rate is approximately 40%->Papillary thyroid prognosis - B]] [[The tumor is likely to dedifferentiate into anaplastic carcinoma->Papillary thyroid prognosis - E]]

<span class="ec-case-marker" hidden data-entry="Papillary thyroid prognosis. Prog"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ The 10-year disease-specific survival exceeds 95%.</div> Low-risk papillary thyroid carcinoma (confined to the gland, <4 cm, no extrathyroidal extension, no vascular invasion, no nodal metastases) carries an excellent prognosis with 10-year disease-specific survival exceeding 95–98% (ATA 2015 guidelines). Undetectable postoperative thyroglobulin further supports a low-risk classification. Dedifferentiation to anaplastic carcinoma is rare. External beam radiation is not standard for low-risk disease. <div class="ec-src"><b>Source:</b> Haugen BR, et al. Thyroid 2016;26(1):1-133.</div></div> [[Start another case->Hub]] [[Restart this case->Papillary thyroid prognosis - Prog]] [[Next case →->Adrenal crisis - Dx]]

<span class="ec-case-marker" hidden data-entry="Papillary thyroid prognosis. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is The 10-year disease-specific survival exceeds 95%. Low-risk papillary thyroid carcinoma (confined to the gland, <4 cm, no extrathyroidal extension, no vascular invasion, no nodal metastases) carries an excellent prognosis with 10-year disease-specific survival exceeding 95–98% (ATA 2015 guidelines). Undetectable postoperative thyroglobulin further supports a low-risk classification. Dedifferentiation to anaplastic carcinoma is rare. External beam radiation is not standard for low-risk disease. <div class="ec-src"><b>Source:</b> Haugen BR, et al. Thyroid 2016;26(1):1-133.</div></div> [[Try this question again->Papillary thyroid prognosis - Prog]] [[Start another case->Hub]]

<div class="ec-scene">Hematology clinic · 09:15</div> A 19-year-old man with sickle cell disease presents with severe bilateral leg pain after becoming dehydrated during a track meet. Temperature is 37.8°C (100.0°F), blood pressure is 108/68 mm Hg, and pulse is 110/min. <span class="ec-prompt">Which of the following molecular event initiates the red-cell deformation responsible for vaso-occlusion?</span> [[Decreased renal erythropoietin production->HbS polymerization - D]] [[IgG-mediated complement fixation on red cells->HbS polymerization - C]] [[Oxidative denaturation of hemoglobin A->HbS polymerization - A]] [[Polymerization of deoxygenated hemoglobin S->HbS polymerization - Correct]] [[Proteolytic degradation of spectrin and ankyrin->HbS polymerization - E]]

<span class="ec-case-marker" hidden data-entry="HbS polymerization. Mech"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Polymerization of deoxygenated hemoglobin S.</div> HbS polymerizes upon deoxygenation, forming rigid fibers that distort the erythrocyte into a sickle shape. Dehydration increases intracellular HbS concentration, lowering the delay time to polymerization. This is not an immune-mediated hemolysis and is distinct from membrane protein defects like hereditary spherocytosis. <div class="ec-src"><b>Source:</b> Ware RE, et al. Lancet 2017;390(10091):311-323.</div></div> [[Start another case->Hub]] [[Restart this case->HbS polymerization - Mech]] [[Next case →->Acute chest syndrome - Dx]]

<span class="ec-case-marker" hidden data-entry="HbS polymerization. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is Polymerization of deoxygenated hemoglobin S. HbS polymerizes upon deoxygenation, forming rigid fibers that distort the erythrocyte into a sickle shape. Dehydration increases intracellular HbS concentration, lowering the delay time to polymerization. This is not an immune-mediated hemolysis and is distinct from membrane protein defects like hereditary spherocytosis. <div class="ec-src"><b>Source:</b> Ware RE, et al. Lancet 2017;390(10091):311-323.</div></div> [[Try this question again->HbS polymerization - Mech]] [[Start another case->Hub]]

<div class="ec-scene">Hematology-oncology clinic · 14:00</div> A 42-year-old woman with acute myeloid leukemia achieves morphologic complete remission after induction chemotherapy. Bone marrow biopsy shows <5% blasts. The medical team considers consolidation therapy options. <span class="ec-prompt">Which of the following post-remission findings most strongly predicts relapse?</span> [[Complex karyotype identified on pre-treatment bone marrow->AML MRD relapse - E]] [[Detectable measurable residual disease by flow cytometry->AML MRD relapse - Correct]] [[Elevated serum lactate dehydrogenase at remission assessment->AML MRD relapse - D]] [[FLT3-ITD mutation identified at initial diagnosis->AML MRD relapse - C]] [[Persistent t(8;21) translocation on cytogenetics->AML MRD relapse - A]]

<span class="ec-case-marker" hidden data-entry="AML MRD relapse. Prog"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Detectable measurable residual disease by flow cytometry.</div> Measurable residual disease (MRD) detected by multiparameter flow cytometry after achieving morphologic CR is the strongest independent predictor of relapse in AML. While FLT3-ITD and complex karyotype are adverse prognostic factors at diagnosis, they are pre-treatment risk stratifiers, not post-remission relapse predictors. t(8;21) is actually a favorable cytogenetic marker. Elevated LDH is nonspecific and less predictive than MRD assessment. <div class="ec-src"><b>Source:</b> Schuurhuis GJ, et al. Blood 2018;131(12):1275-1291.</div></div> [[Start another case->Hub]] [[Restart this case->AML MRD relapse - Prog]] [[Next case →->Hodgkin lymphoma - Dx]]

<span class="ec-case-marker" hidden data-entry="AML MRD relapse. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is Detectable measurable residual disease by flow cytometry. Measurable residual disease (MRD) detected by multiparameter flow cytometry after achieving morphologic CR is the strongest independent predictor of relapse in AML. While FLT3-ITD and complex karyotype are adverse prognostic factors at diagnosis, they are pre-treatment risk stratifiers, not post-remission relapse predictors. t(8;21) is actually a favorable cytogenetic marker. Elevated LDH is nonspecific and less predictive than MRD assessment. <div class="ec-src"><b>Source:</b> Schuurhuis GJ, et al. Blood 2018;131(12):1275-1291.</div></div> [[Try this question again->AML MRD relapse - Prog]] [[Start another case->Hub]]

<div class="ec-scene">Hematology clinic · 11:25</div> A 68-year-old man has had fatigue, recurrent bacterial infections, and worsening back pain for 4 months, with a normocytic anemia. Serum protein electrophoresis demonstrates a monoclonal spike in the gamma region. Serum creatinine is 2.1 mg/dL. <span class="ec-prompt">Which of the following tests is most appropriate to further characterize the suspected plasma-cell disorder?</span> [[Coagulation factor VIII activity level->Myeloma light chains - E]] [[Direct antiglobulin (Coombs) test->Myeloma light chains - D]] [[Glucose-6-phosphate dehydrogenase activity assay->Myeloma light chains - C]] [[Hemoglobin electrophoresis->Myeloma light chains - A]] [[Serum free light-chain assay with kappa/lambda ratio->Myeloma light chains - Correct]]

<span class="ec-case-marker" hidden data-entry="Myeloma light chains. Ix"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Serum free light-chain assay with kappa/lambda ratio.</div> Serum free light-chain assay with kappa/lambda ratio complements SPEP and immunofixation in the diagnostic workup of monoclonal gammopathies (IMWG guidelines). It is especially important for detecting light-chain-only myeloma. Hemoglobin electrophoresis evaluates hemoglobinopathies, not plasma-cell dyscrasias. <div class="ec-src"><b>Source:</b> Rajkumar SV, et al. Lancet Oncol 2014;15(12):e538-e548.</div></div> [[Start another case->Hub]] [[Restart this case->Myeloma light chains - Ix]] [[Next case →->ALL high risk - Dx]]

<span class="ec-case-marker" hidden data-entry="Myeloma light chains. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is Serum free light-chain assay with kappa/lambda ratio. Serum free light-chain assay with kappa/lambda ratio complements SPEP and immunofixation in the diagnostic workup of monoclonal gammopathies (IMWG guidelines). It is especially important for detecting light-chain-only myeloma. Hemoglobin electrophoresis evaluates hemoglobinopathies, not plasma-cell dyscrasias. <div class="ec-src"><b>Source:</b> Rajkumar SV, et al. Lancet Oncol 2014;15(12):e538-e548.</div></div> [[Try this question again->Myeloma light chains - Ix]] [[Start another case->Hub]]

<div class="ec-scene">Primary care clinic · 16:40</div> A 70-year-old man has had painless cervical and mediastinal lymphadenopathy for 6 weeks. He reports drenching night sweats and a 7-kg weight loss over 3 months. Lymph-node biopsy demonstrates scattered large binucleated cells with prominent eosinophilic nucleoli in a background of mixed inflammatory infiltrate. These cells express CD15 and CD30. <span class="ec-prompt">Which of the following is the most likely diagnosis?</span> [[Burkitt lymphoma->Hodgkin lymphoma - A]] [[Chronic lymphocytic leukemia->Hodgkin lymphoma - C]] [[Classical Hodgkin lymphoma->Hodgkin lymphoma - Correct]] [[Follicular lymphoma->Hodgkin lymphoma - E]] [[Mantle-cell lymphoma->Hodgkin lymphoma - D]]

<span class="ec-case-marker" hidden data-entry="Hodgkin lymphoma. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Classical Hodgkin lymphoma.</div> Reed-Sternberg cells, large binucleated cells with prominent nucleoli ("owl-eye" appearance) expressing CD15 and CD30 in a background of reactive inflammatory cells, are the hallmark of classical Hodgkin lymphoma. Burkitt lymphoma shows a "starry sky" pattern with MYC translocation. CLL shows small mature lymphocytes expressing CD5 and CD23. <div class="ec-src"><b>Source:</b> Swerdlow SH, et al. Blood 2016;127(20):2375-2390.</div></div> [[Start another case->Hub]] [[Restart this case->Hodgkin lymphoma - Dx]] [[Next case →->Tumor lysis - Ix]]

<span class="ec-case-marker" hidden data-entry="Hodgkin lymphoma. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is Classical Hodgkin lymphoma. Reed-Sternberg cells, large binucleated cells with prominent nucleoli ("owl-eye" appearance) expressing CD15 and CD30 in a background of reactive inflammatory cells, are the hallmark of classical Hodgkin lymphoma. Burkitt lymphoma shows a "starry sky" pattern with MYC translocation. CLL shows small mature lymphocytes expressing CD5 and CD23. <div class="ec-src"><b>Source:</b> Swerdlow SH, et al. Blood 2016;127(20):2375-2390.</div></div> [[Try this question again->Hodgkin lymphoma - Dx]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 20:22</div> A 23-year-old man develops fever, abdominal cramping, and bloody diarrhea 2 days after eating undercooked chicken at a barbecue. Temperature is 38.6°C (101.5°F), blood pressure is 118/72 mm Hg, and pulse is 96/min. Stool culture grows a curved, oxidase-positive, gram-negative rod at 42°C on selective media. <span class="ec-prompt">Which of the following is the most likely organism?</span> [[Campylobacter jejuni->Campylobacter - Correct]] [[Enterotoxigenic Escherichia coli->Campylobacter - E]] [[Shigella sonnei->Campylobacter - A]] [[Vibrio cholerae->Campylobacter - C]] [[Yersinia enterocolitica->Campylobacter - D]]

<span class="ec-case-marker" hidden data-entry="Campylobacter. Micro"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Campylobacter jejuni.</div> Campylobacter jejuni is a curved (or S-shaped) gram-negative rod that is oxidase-positive, microaerophilic, and grows optimally at 42°C. Poultry is the most common vehicle. Shigella is a straight rod that is oxidase-negative. Vibrio cholerae causes watery (not bloody) diarrhea. ETEC produces traveler's diarrhea, also typically watery. <div class="ec-src"><b>Source:</b> Kaakoush NO, et al. Clin Microbiol Rev 2015;28(3):687-720.</div></div> [[Start another case->Hub]] [[Restart this case->Campylobacter - Micro]] [[Next case →->Kawasaki treatment - Rx]]

<span class="ec-case-marker" hidden data-entry="Campylobacter. Micro"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is Campylobacter jejuni. Campylobacter jejuni is a curved (or S-shaped) gram-negative rod that is oxidase-positive, microaerophilic, and grows optimally at 42°C. Poultry is the most common vehicle. Shigella is a straight rod that is oxidase-negative. Vibrio cholerae causes watery (not bloody) diarrhea. ETEC produces traveler's diarrhea, also typically watery. <div class="ec-src"><b>Source:</b> Kaakoush NO, et al. Clin Microbiol Rev 2015;28(3):687-720.</div></div> [[Try this question again->Campylobacter - Micro]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 23:50</div> A 19-year-old college student has had fever, severe headache, and neck stiffness for 1 day. Temperature is 39.4°C (102.9°F), blood pressure is 96/62 mm Hg, and pulse is 118/min. A petechial rash is present on the trunk and extremities. CSF Gram stain demonstrates gram-negative diplococci within and around polymorphonuclear cells. <span class="ec-prompt">Which of the following is the most likely organism?</span> [[Group B Streptococcus (S. agalactiae)->N meningitidis - E]] [[Haemophilus influenzae type b->N meningitidis - C]] [[Listeria monocytogenes->N meningitidis - D]] [[Neisseria meningitidis->N meningitidis - Correct]] [[Streptococcus pneumoniae->N meningitidis - A]]

<span class="ec-case-marker" hidden data-entry="N meningitidis. Micro"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Neisseria meningitidis.</div> Gram-negative diplococci (kidney-bean-shaped pairs) in CSF in a young adult with meningitis and a petechial/purpuric rash is classic for Neisseria meningitidis. S. pneumoniae is gram-positive lancet-shaped diplococci. H. influenzae is a gram-negative coccobacillus. Listeria is a gram-positive rod. GBS causes neonatal meningitis. <div class="ec-src"><b>Source:</b> van de Beek D, et al. Nat Rev Dis Primers 2016;2:16074.</div></div> [[Start another case->Hub]] [[Restart this case->N meningitidis - Micro]] [[Next case →->Neonatal meningitis - Opening]]

<span class="ec-case-marker" hidden data-entry="N meningitidis. Micro"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is Neisseria meningitidis. Gram-negative diplococci (kidney-bean-shaped pairs) in CSF in a young adult with meningitis and a petechial/purpuric rash is classic for Neisseria meningitidis. S. pneumoniae is gram-positive lancet-shaped diplococci. H. influenzae is a gram-negative coccobacillus. Listeria is a gram-positive rod. GBS causes neonatal meningitis. <div class="ec-src"><b>Source:</b> van de Beek D, et al. Nat Rev Dis Primers 2016;2:16074.</div></div> [[Try this question again->N meningitidis - Micro]] [[Start another case->Hub]]

<div class="ec-scene">Medical ward · 07:25</div> A 72-year-old man with a prosthetic aortic valve develops fever, malaise, and a new regurgitant murmur 3 months after dental extraction. Blood cultures drawn from two separate sites grow gram-positive cocci in chains that are alpha-hemolytic, optochin-resistant, and bile esculin negative. <span class="ec-prompt">Which of the following is the most likely organism?</span> [[Coagulase-negative staphylococci->Viridans endocarditis - E]] [[Enterococcus faecalis->Viridans endocarditis - C]] [[Staphylococcus aureus->Viridans endocarditis - A]] [[Streptococcus pneumoniae->Viridans endocarditis - D]] [[Viridans group streptococci->Viridans endocarditis - Correct]]

<span class="ec-case-marker" hidden data-entry="Viridans endocarditis. Micro"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Viridans group streptococci.</div> Viridans group streptococci (e.g., S. mutans, S. sanguinis) are the most common cause of subacute infective endocarditis, particularly following dental procedures. They are alpha-hemolytic and optochin-resistant, distinguishing them from S. pneumoniae (alpha-hemolytic but optochin-sensitive). Bile esculin negativity excludes Enterococcus (bile esculin positive). S. aureus causes acute endocarditis with rapid valve destruction and appears as clusters, not chains. Coagulase-negative staphylococci also form clusters and typically cause early prosthetic valve endocarditis, most often within 60 days (and nearly always within the first year) after surgery, in contrast to late PVE (>1 year), which resembles native-valve endocarditis. <div class="ec-src"><b>Source:</b> Baddour LM, et al. Circulation 2015;132(15):1435-1486.</div></div> [[Start another case->Hub]] [[Restart this case->Viridans endocarditis - Micro]] [[Next case →->Acute rheumatic fever - Dx]]

<span class="ec-case-marker" hidden data-entry="Viridans endocarditis. Micro"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is Viridans group streptococci. Viridans group streptococci (e.g., S. mutans, S. sanguinis) are the most common cause of subacute infective endocarditis, particularly following dental procedures. They are alpha-hemolytic and optochin-resistant, distinguishing them from S. pneumoniae (alpha-hemolytic but optochin-sensitive). Bile esculin negativity excludes Enterococcus (bile esculin positive). S. aureus causes acute endocarditis with rapid valve destruction and appears as clusters, not chains. Coagulase-negative staphylococci also form clusters and typically cause early prosthetic valve endocarditis, most often within 60 days (and nearly always within the first year) after surgery, in contrast to late PVE (>1 year), which resembles native-valve endocarditis. <div class="ec-src"><b>Source:</b> Baddour LM, et al. Circulation 2015;132(15):1435-1486.</div></div> [[Try this question again->Viridans endocarditis - Micro]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 18:35</div> A 38-year-old man with advanced HIV infection (CD4 count 45 cells/mm3) presents with 2 weeks of headache, low-grade fever, and confusion. He is not taking prophylactic medications. MRI of the brain demonstrates multiple ring-enhancing lesions with surrounding edema, predominantly in the basal ganglia and corticomedullary junction. <span class="ec-prompt">Which of the following is the most likely diagnosis?</span> [[Cryptococcal meningoencephalitis->Toxoplasma AIDS - D]] [[Cytomegalovirus ventriculoencephalitis->Toxoplasma AIDS - E]] [[Primary CNS lymphoma->Toxoplasma AIDS - A]] [[Progressive multifocal leukoencephalopathy->Toxoplasma AIDS - C]] [[Toxoplasma gondii encephalitis->Toxoplasma AIDS - Correct]]

<span class="ec-case-marker" hidden data-entry="Toxoplasma AIDS. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Toxoplasma gondii encephalitis.</div> Multiple ring-enhancing lesions in an AIDS patient with CD4 <100 and no toxoplasma prophylaxis strongly suggests toxoplasma encephalitis. Primary CNS lymphoma typically presents as a single periventricular enhancing lesion. PML causes non-enhancing white matter lesions. Cryptococcus typically shows meningeal enhancement and rarely causes ring-enhancing parenchymal lesions. <div class="ec-src"><b>Source:</b> Panel on Opportunistic Infections in Adults and Adolescents with HIV. Guidelines for the Prevention and Treatment of Opportunistic Infections in Adults and Adolescents with HIV. Clinicalinfo.HIV.gov. 2024.</div></div> [[Start another case->Hub]] [[Restart this case->Toxoplasma AIDS - Dx]] [[Next case →->Gonorrhea treatment - Rx]]

<span class="ec-case-marker" hidden data-entry="Toxoplasma AIDS. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is Toxoplasma gondii encephalitis. Multiple ring-enhancing lesions in an AIDS patient with CD4 <100 and no toxoplasma prophylaxis strongly suggests toxoplasma encephalitis. Primary CNS lymphoma typically presents as a single periventricular enhancing lesion. PML causes non-enhancing white matter lesions. Cryptococcus typically shows meningeal enhancement and rarely causes ring-enhancing parenchymal lesions. <div class="ec-src"><b>Source:</b> Panel on Opportunistic Infections in Adults and Adolescents with HIV. Guidelines for the Prevention and Treatment of Opportunistic Infections in Adults and Adolescents with HIV. Clinicalinfo.HIV.gov. 2024.</div></div> [[Try this question again->Toxoplasma AIDS - Dx]] [[Start another case->Hub]]

<div class="ec-scene">Intensive care unit · 05:10</div> A 62-year-old man is hospitalized with community-acquired bacterial meningitis caused by Streptococcus pneumoniae. On admission, he has a Glasgow Coma Scale score of 9, requires intubation, and has seizure activity. Blood cultures are positive. Despite appropriate antibiotics and dexamethasone, he remains obtunded at 48 hours. <span class="ec-prompt">Which of the following admission features is most strongly associated with an unfavorable neurologic outcome?</span> [[Age over 60 years->Meningitis GCS prognosis - A]] [[Isolation of a gram-positive organism from cerebrospinal fluid->Meningitis GCS prognosis - D]] [[Low Glasgow Coma Scale score at presentation->Meningitis GCS prognosis - Correct]] [[Peripheral white blood cell count above 12,000/mm3->Meningitis GCS prognosis - E]] [[Presence of fever at the time of admission->Meningitis GCS prognosis - C]]

<span class="ec-case-marker" hidden data-entry="Meningitis GCS prognosis. Prog"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Low Glasgow Coma Scale score at presentation.</div> In bacterial meningitis, a low GCS at presentation is one of the strongest independent predictors of death and unfavorable neurologic outcome (van de Beek, N Engl J Med 2004; Bijlsma, Lancet Infect Dis 2016). Age is a risk factor but is weaker than depressed consciousness. Fever at admission is expected and does not independently predict poor outcome. Leukocytosis is a nonspecific marker of infection. <div class="ec-src"><b>Source:</b> van de Beek D, et al. N Engl J Med 2004;351(18):1849-1859.</div></div> [[Start another case->Hub]] [[Restart this case->Meningitis GCS prognosis - Prog]] [[Next case →->N meningitidis - Micro]]

<span class="ec-case-marker" hidden data-entry="Meningitis GCS prognosis. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is Low Glasgow Coma Scale score at presentation. In bacterial meningitis, a low GCS at presentation is one of the strongest independent predictors of death and unfavorable neurologic outcome (van de Beek, N Engl J Med 2004; Bijlsma, Lancet Infect Dis 2016). Age is a risk factor but is weaker than depressed consciousness. Fever at admission is expected and does not independently predict poor outcome. Leukocytosis is a nonspecific marker of infection. <div class="ec-src"><b>Source:</b> van de Beek D, et al. N Engl J Med 2004;351(18):1849-1859.</div></div> [[Try this question again->Meningitis GCS prognosis - Prog]] [[Start another case->Hub]]

<div class="ec-scene">Rheumatology clinic · 10:35</div> A 31-year-old woman with systemic lupus erythematosus has had proteinuria and hematuria for 6 weeks despite hydroxychloroquine therapy. Kidney biopsy shows granular immune-complex deposits along the glomerular basement membrane with complement activation on immunofluorescence. The nephrologist recommends mycophenolate mofetil. <span class="ec-prompt">Which of the following pathologic processes does this treatment primarily target?</span> [[Antibody-mediated receptor blockade on tubular epithelium->Lupus nephritis - E]] [[CD8+ T-cell-mediated direct cytotoxicity against podocytes->Lupus nephritis - D]] [[Cytotoxic antibody binding to basement membrane antigens->Lupus nephritis - B]] [[IgE-mediated mast-cell degranulation causing vascular leak->Lupus nephritis - A]] [[Immune-complex deposition with complement-mediated inflammation->Lupus nephritis - Correct]]

<span class="ec-case-marker" hidden data-entry="Lupus nephritis. Mech"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Immune-complex deposition with complement-mediated inflammation.</div> Lupus nephritis is driven by type III hypersensitivity: circulating immune complexes (anti-dsDNA/DNA) deposit in the glomerular basement membrane and activate complement, producing inflammation. Mycophenolate suppresses the immune response generating these complexes. The granular ("lumpy-bumpy") immunofluorescence pattern distinguishes immune-complex disease from the linear pattern of anti-GBM disease (type II). IgE-mediated (type I) and direct T-cell (type IV) mechanisms are not the primary drivers of lupus nephritis. <div class="ec-src"><b>Source:</b> Hahn BH, et al. Arthritis Care Res 2012;64(6):797-808.</div></div> [[Start another case->Hub]] [[Restart this case->Lupus nephritis - Mech]] [[Next case →->Albuminuria progression - Prog]]

<span class="ec-case-marker" hidden data-entry="Lupus nephritis. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is Immune-complex deposition with complement-mediated inflammation. Lupus nephritis is driven by type III hypersensitivity: circulating immune complexes (anti-dsDNA/DNA) deposit in the glomerular basement membrane and activate complement, producing inflammation. Mycophenolate suppresses the immune response generating these complexes. The granular ("lumpy-bumpy") immunofluorescence pattern distinguishes immune-complex disease from the linear pattern of anti-GBM disease (type II). IgE-mediated (type I) and direct T-cell (type IV) mechanisms are not the primary drivers of lupus nephritis. <div class="ec-src"><b>Source:</b> Hahn BH, et al. Arthritis Care Res 2012;64(6):797-808.</div></div> [[Try this question again->Lupus nephritis - Mech]] [[Start another case->Hub]]

<div class="ec-scene">Rheumatology clinic · 13:50</div> A 49-year-old woman has symmetric pain and swelling of the metacarpophalangeal and proximal interphalangeal joints with morning stiffness lasting more than 90 minutes daily for 3 months. Rheumatoid factor is positive. <span class="ec-prompt">Which of the following antibody tests is most specific for rheumatoid arthritis?</span> [[Anti-centromere antibody->Anti-CCP RA - D]] [[Anti-cyclic citrullinated peptide (anti-CCP)->Anti-CCP RA - Correct]] [[Anti-double-stranded DNA (anti-dsDNA)->Anti-CCP RA - B]] [[Anti-topoisomerase I (anti-Scl-70)->Anti-CCP RA - E]] [[Antinuclear antibody (ANA)->Anti-CCP RA - A]]

<span class="ec-case-marker" hidden data-entry="Anti-CCP RA. Ix"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Anti-cyclic citrullinated peptide (anti-CCP).</div> Anti-CCP has a specificity of approximately 95% for RA, significantly higher than rheumatoid factor (~85%). ANA is sensitive but nonspecific. Anti-dsDNA is specific for SLE. Anti-centromere is associated with limited cutaneous systemic sclerosis. Anti-Scl-70 is associated with diffuse cutaneous systemic sclerosis. <div class="ec-src"><b>Source:</b> Aletaha D, et al. Arthritis Rheum 2010;62(9):2569-2581.</div></div> [[Start another case->Hub]] [[Restart this case->Anti-CCP RA - Ix]] [[Next case →->Giant cell arteritis - Rx]]

<span class="ec-case-marker" hidden data-entry="Anti-CCP RA. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is Anti-cyclic citrullinated peptide (anti-CCP). Anti-CCP has a specificity of approximately 95% for RA, significantly higher than rheumatoid factor (~85%). ANA is sensitive but nonspecific. Anti-dsDNA is specific for SLE. Anti-centromere is associated with limited cutaneous systemic sclerosis. Anti-Scl-70 is associated with diffuse cutaneous systemic sclerosis. <div class="ec-src"><b>Source:</b> Aletaha D, et al. Arthritis Rheum 2010;62(9):2569-2581.</div></div> [[Try this question again->Anti-CCP RA - Ix]] [[Start another case->Hub]]

<div class="ec-scene">Rheumatology clinic · 09:55</div> A 52-year-old woman with systemic sclerosis (diffuse cutaneous type) develops progressive exertional dyspnea over 6 months. Pulmonary function testing shows a restrictive pattern with forced vital capacity 62% of predicted and diffusing capacity 44% of predicted. CT of the chest demonstrates bilateral ground-glass opacities and early honeycombing at the bases. <span class="ec-prompt">Which of the following pulmonary complications is the leading cause of disease-related death in systemic sclerosis?</span> [[Bronchiolitis obliterans organizing pneumonia->SSc-ILD mortality - E]] [[Interstitial lung disease->SSc-ILD mortality - Correct]] [[Pulmonary arterial hypertension->SSc-ILD mortality - B]] [[Recurrent aspiration pneumonia from esophageal dysmotility->SSc-ILD mortality - C]] [[Scleroderma renal crisis with secondary pulmonary edema->SSc-ILD mortality - D]]

<span class="ec-case-marker" hidden data-entry="SSc-ILD mortality. Prog"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Interstitial lung disease.</div> Interstitial lung disease (most commonly NSIP pattern) is the leading cause of disease-related death in systemic sclerosis. Pulmonary arterial hypertension is the second leading cause, distinguishing between the two requires clinical reasoning because management differs (immunosuppression for ILD vs pulmonary vasodilators for PAH). The SENSCIS trial demonstrated that nintedanib slows FVC decline in SSc-ILD. Scleroderma renal crisis has become less lethal since ACE inhibitors became available. BOOP is an uncommon association with SSc. <div class="ec-src"><b>Source:</b> Elhai M, et al. Trends in mortality in patients with systemic sclerosis over 40 years: a systematic literature review and EUSTAR database analysis. Ann Rheum Dis 2017;76(11):1897-1905 (mortality data). Distler O, et al. N Engl J Med 2019;380(26):2518-2528 (SENSCIS trial, nintedanib for SSc-ILD).</div></div> [[Start another case->Hub]] [[Restart this case->SSc-ILD mortality - Prog]] [[Next case →->Bronchiolitis - Dx]]

<span class="ec-case-marker" hidden data-entry="SSc-ILD mortality. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is Interstitial lung disease. Interstitial lung disease (most commonly NSIP pattern) is the leading cause of disease-related death in systemic sclerosis. Pulmonary arterial hypertension is the second leading cause, distinguishing between the two requires clinical reasoning because management differs (immunosuppression for ILD vs pulmonary vasodilators for PAH). The SENSCIS trial demonstrated that nintedanib slows FVC decline in SSc-ILD. Scleroderma renal crisis has become less lethal since ACE inhibitors became available. BOOP is an uncommon association with SSc. <div class="ec-src"><b>Source:</b> Elhai M, et al. Trends in mortality in patients with systemic sclerosis over 40 years: a systematic literature review and EUSTAR database analysis. Ann Rheum Dis 2017;76(11):1897-1905 (mortality data). Distler O, et al. N Engl J Med 2019;380(26):2518-2528 (SENSCIS trial, nintedanib for SSc-ILD).</div></div> [[Try this question again->SSc-ILD mortality - Prog]] [[Start another case->Hub]]

<div class="ec-scene">Pediatric immunology clinic · 11:05</div> A 7-month-old boy has recurrent sinopulmonary bacterial infections and chronic diarrhea since age 5 months. Maternal history is unremarkable. Serum IgG, IgA, and IgM are profoundly decreased. Flow cytometry shows an absence of mature CD19+ B cells with normal T-cell numbers. <span class="ec-prompt">Which of the following defects best explains his immunodeficiency?</span> [[22q11.2 microdeletion with thymic aplasia->XLA BTK - E]] [[Bruton tyrosine kinase (BTK) deficiency->XLA BTK - Correct]] [[Failure of T-cell receptor gene rearrangement->XLA BTK - A]] [[NADPH oxidase complex deficiency->XLA BTK - C]] [[Terminal complement component (C5–C9) deficiency->XLA BTK - D]]

<span class="ec-case-marker" hidden data-entry="XLA BTK. Mech"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Bruton tyrosine kinase (BTK) deficiency.</div> BTK deficiency causes X-linked agammaglobulinemia: a block in pre-B to immature B-cell transition produces absent mature B cells and profoundly low immunoglobulins. Infections begin after maternal IgG wanes at ~6 months. NADPH oxidase deficiency (chronic granulomatous disease) causes defective intracellular killing with normal immunoglobulins. 22q11.2 deletion (DiGeorge) causes T-cell, not B-cell, deficiency. <div class="ec-src"><b>Source:</b> Conley ME, et al. Stiehm's Immune Deficiencies. 2nd ed. 2020.</div></div> [[Start another case->Hub]] [[Restart this case->XLA BTK - Mech]] [[Next case →->Wound healing phases - Mech]]

<span class="ec-case-marker" hidden data-entry="XLA BTK. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is Bruton tyrosine kinase (BTK) deficiency. BTK deficiency causes X-linked agammaglobulinemia: a block in pre-B to immature B-cell transition produces absent mature B cells and profoundly low immunoglobulins. Infections begin after maternal IgG wanes at ~6 months. NADPH oxidase deficiency (chronic granulomatous disease) causes defective intracellular killing with normal immunoglobulins. 22q11.2 deletion (DiGeorge) causes T-cell, not B-cell, deficiency. <div class="ec-src"><b>Source:</b> Conley ME, et al. Stiehm's Immune Deficiencies. 2nd ed. 2020.</div></div> [[Try this question again->XLA BTK - Mech]] [[Start another case->Hub]]

<div class="ec-scene">Pediatric clinic · 15:45</div> A 9-year-old boy develops migratory pain and swelling of several large joints 3 weeks after an episode of pharyngitis treated with ibuprofen alone. He now has a low-grade fever and a new holosystolic murmur best heard at the apex with radiation to the axilla. ASO titer is elevated. <span class="ec-prompt">Which of the following is the most likely diagnosis?</span> [[Acute rheumatic fever->Acute rheumatic fever - Correct]] [[IgA vasculitis (Henoch-Schönlein purpura)->Acute rheumatic fever - E]] [[Infective endocarditis->Acute rheumatic fever - D]] [[Juvenile idiopathic arthritis->Acute rheumatic fever - C]] [[Kawasaki disease->Acute rheumatic fever - A]]

<span class="ec-case-marker" hidden data-entry="Acute rheumatic fever. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Acute rheumatic fever.</div> Migratory large-joint polyarthritis and new-onset mitral regurgitation (pancarditis) following group A streptococcal pharyngitis with an elevated ASO titer satisfy the revised Jones criteria for acute rheumatic fever. Kawasaki disease occurs in younger children (<5 years) with different mucocutaneous findings. JIA is a diagnosis of exclusion requiring ≥6 weeks of symptoms. <div class="ec-src"><b>Source:</b> Gewitz MH, et al. Circulation 2015;131(20):1806-1818.</div></div> [[Start another case->Hub]] [[Restart this case->Acute rheumatic fever - Dx]] [[Next case →->HFrEF pillars - Rx]]

<span class="ec-case-marker" hidden data-entry="Acute rheumatic fever. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is Acute rheumatic fever. Migratory large-joint polyarthritis and new-onset mitral regurgitation (pancarditis) following group A streptococcal pharyngitis with an elevated ASO titer satisfy the revised Jones criteria for acute rheumatic fever. Kawasaki disease occurs in younger children (<5 years) with different mucocutaneous findings. JIA is a diagnosis of exclusion requiring ≥6 weeks of symptoms. <div class="ec-src"><b>Source:</b> Gewitz MH, et al. Circulation 2015;131(20):1806-1818.</div></div> [[Try this question again->Acute rheumatic fever - Dx]] [[Start another case->Hub]]

<div class="ec-scene">Gynecology clinic · 10:40</div> A 29-year-old woman presents with secondary amenorrhea of 6 months' duration. Pregnancy test is negative. TSH and prolactin are normal. After a progestin challenge test, she has no withdrawal bleeding. <span class="ec-prompt">Which of the following tests is most appropriate next to distinguish between inadequate estrogen production and an outflow-tract abnormality?</span> [[Combined estrogen-progestin challenge->Amenorrhea workup - Correct]] [[High-sensitivity C-reactive protein->Amenorrhea workup - E]] [[Morning serum cortisol level->Amenorrhea workup - C]] [[Pelvic CT with intravenous contrast->Amenorrhea workup - D]] [[Repeat serum β-hCG in 48 hours->Amenorrhea workup - A]]

<span class="ec-case-marker" hidden data-entry="Amenorrhea workup. Ix"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Combined estrogen-progestin challenge.</div> If a progestin challenge produces no withdrawal bleeding, the next step is to add exogenous estrogen followed by progestin. If bleeding occurs, the endometrium is responsive and the problem is hypoestrogenism (hypothalamic, pituitary, or ovarian). If no bleeding occurs despite adequate estrogen and progestin, an outflow-tract obstruction (e.g., Asherman syndrome) is likely. <div class="ec-src"><b>Source:</b> Klein DA, Poth MA. Am Fam Physician 2013;87(11):781-788.</div></div> [[Start another case->Hub]] [[Restart this case->Amenorrhea workup - Ix]] [[Next case →->Ovarian torsion - Opening]]

<span class="ec-case-marker" hidden data-entry="Amenorrhea workup. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is Combined estrogen-progestin challenge. If a progestin challenge produces no withdrawal bleeding, the next step is to add exogenous estrogen followed by progestin. If bleeding occurs, the endometrium is responsive and the problem is hypoestrogenism (hypothalamic, pituitary, or ovarian). If no bleeding occurs despite adequate estrogen and progestin, an outflow-tract obstruction (e.g., Asherman syndrome) is likely. <div class="ec-src"><b>Source:</b> Klein DA, Poth MA. Am Fam Physician 2013;87(11):781-788.</div></div> [[Try this question again->Amenorrhea workup - Ix]] [[Start another case->Hub]]

<div class="ec-scene">Labor and delivery unit · 22:10</div> A 28-year-old woman at 24 weeks' gestation develops severe preeclampsia with blood pressure 168/110 mm Hg, proteinuria, and headache. She is started on magnesium sulfate and antihypertensive therapy. Fetal heart tracing is reassuring and estimated fetal weight is appropriate for gestational age. The medical team considers expectant management to prolong gestation. <span class="ec-prompt">Which of the following maternal complication represents the greatest risk of expectant management at this gestational age?</span> [[Acute kidney injury from renal cortical necrosis->Preeclampsia expectant - C]] [[Placental abruption with hemorrhage->Preeclampsia expectant - B]] [[Posterior reversible encephalopathy syndrome->Preeclampsia expectant - D]] [[Progression to eclamptic seizures or HELLP syndrome->Preeclampsia expectant - Correct]] [[Pulmonary edema from capillary leak->Preeclampsia expectant - E]]

<span class="ec-case-marker" hidden data-entry="Preeclampsia expectant. Prog"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Progression to eclamptic seizures or HELLP syndrome.</div> Expectant management of early severe preeclampsia carries risk of progression to eclampsia, HELLP syndrome, placental abruption, and end-organ damage. While abruption, AKI, PRES, and pulmonary edema are all real complications of severe preeclampsia, progression to eclampsia/HELLP is the most frequent and most dangerous maternal risk driving the decision to deliver. In late preterm hypertensive disease, from 34 to 37 weeks, the HYPITAT-II trial found that expectant management reduced neonatal respiratory distress but increased adverse maternal outcomes, which is why delivery is favored once severe features are present. <div class="ec-src"><b>Source:</b> ACOG Practice Bulletin 222. Obstet Gynecol 2020;135(6):e237-e260.</div></div> [[Start another case->Hub]] [[Restart this case->Preeclampsia expectant - Prog]] [[Next case →->Placenta previa - Ix]]

<span class="ec-case-marker" hidden data-entry="Preeclampsia expectant. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is Progression to eclamptic seizures or HELLP syndrome. Expectant management of early severe preeclampsia carries risk of progression to eclampsia, HELLP syndrome, placental abruption, and end-organ damage. While abruption, AKI, PRES, and pulmonary edema are all real complications of severe preeclampsia, progression to eclampsia/HELLP is the most frequent and most dangerous maternal risk driving the decision to deliver. In late preterm hypertensive disease, from 34 to 37 weeks, the HYPITAT-II trial found that expectant management reduced neonatal respiratory distress but increased adverse maternal outcomes, which is why delivery is favored once severe features are present. <div class="ec-src"><b>Source:</b> ACOG Practice Bulletin 222. Obstet Gynecol 2020;135(6):e237-e260.</div></div> [[Try this question again->Preeclampsia expectant - Prog]] [[Start another case->Hub]]

<div class="ec-scene">Psychiatry clinic · 14:25</div> A 24-year-old man has had auditory hallucinations, paranoid delusions, and disorganized speech for 8 months. He has no history of substance use. His symptoms are most improved by a medication that blocks D2 receptors. <span class="ec-prompt">Which of the following neurotransmitter pathway alterations is most strongly associated with his positive symptoms?</span> [[Decreased cholinergic activity in the hippocampus->Schizophrenia dopamine - D]] [[Decreased dopaminergic activity in the mesocortical pathway->Schizophrenia dopamine - A]] [[Increased dopaminergic activity in the mesolimbic pathway->Schizophrenia dopamine - Correct]] [[Increased GABAergic activity in the nigrostriatal pathway->Schizophrenia dopamine - C]] [[Increased serotonergic activity in the raphe nuclei->Schizophrenia dopamine - E]]

<span class="ec-case-marker" hidden data-entry="Schizophrenia dopamine. Mech"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Increased dopaminergic activity in the mesolimbic pathway.</div> The dopamine hypothesis of schizophrenia attributes positive symptoms (hallucinations, delusions, disorganized thinking) to excessive dopaminergic transmission in the mesolimbic pathway. Antipsychotics that block D2 receptors in this pathway reduce positive symptoms. Negative symptoms and cognitive deficits are associated with decreased dopamine in the mesocortical pathway, this distinction is high-yield. <div class="ec-src"><b>Source:</b> Howes OD, Kapur S. Schizophr Bull 2009;35(3):549-562.</div></div> [[Start another case->Hub]] [[Restart this case->Schizophrenia dopamine - Mech]] [[Next case →->Serotonin syndrome - Dx]]

<span class="ec-case-marker" hidden data-entry="Schizophrenia dopamine. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is Increased dopaminergic activity in the mesolimbic pathway. The dopamine hypothesis of schizophrenia attributes positive symptoms (hallucinations, delusions, disorganized thinking) to excessive dopaminergic transmission in the mesolimbic pathway. Antipsychotics that block D2 receptors in this pathway reduce positive symptoms. Negative symptoms and cognitive deficits are associated with decreased dopamine in the mesocortical pathway, this distinction is high-yield. <div class="ec-src"><b>Source:</b> Howes OD, Kapur S. Schizophr Bull 2009;35(3):549-562.</div></div> [[Try this question again->Schizophrenia dopamine - Mech]] [[Start another case->Hub]]

<div class="ec-scene">Surgical clinic · 08:30</div> A 45-year-old man undergoes a clean surgical incision that is closed primarily. On postoperative day 5, the wound edges are well approximated and healing without complication. <span class="ec-prompt">Which of the following processes is primarily responsible for the wound's tensile strength at this stage?</span> [[Angiogenesis restoring the original capillary network->Wound healing phases - E]] [[Fibrin clot contraction and platelet aggregation->Wound healing phases - A]] [[Fibroblast proliferation and type III collagen deposition->Wound healing phases - Correct]] [[Re-epithelialization of the epidermal surface->Wound healing phases - D]] [[Type I collagen cross-linking and scar maturation->Wound healing phases - C]]

<span class="ec-case-marker" hidden data-entry="Wound healing phases. Mech"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Fibroblast proliferation and type III collagen deposition.</div> At postoperative day 5, the wound is in the proliferative phase: fibroblasts migrate into the wound bed and synthesize type III collagen, forming granulation tissue that provides early tensile strength. The remodeling phase (type III → type I collagen replacement with cross-linking) begins around week 3 and continues for months. The initial inflammatory/hemostatic phase (fibrin, platelets) occurs in the first 48–72 hours. <div class="ec-src"><b>Source:</b> Gurtner GC, et al. Nature 2008;453(7193):314-321.</div></div> [[Start another case->Hub]] [[Restart this case->Wound healing phases - Mech]] [[Next case →->Goals of care - Opening]]

<span class="ec-case-marker" hidden data-entry="Wound healing phases. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is Fibroblast proliferation and type III collagen deposition. At postoperative day 5, the wound is in the proliferative phase: fibroblasts migrate into the wound bed and synthesize type III collagen, forming granulation tissue that provides early tensile strength. The remodeling phase (type III → type I collagen replacement with cross-linking) begins around week 3 and continues for months. The initial inflammatory/hemostatic phase (fibrin, platelets) occurs in the first 48–72 hours. <div class="ec-src"><b>Source:</b> Gurtner GC, et al. Nature 2008;453(7193):314-321.</div></div> [[Try this question again->Wound healing phases - Mech]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 03:15</div> <div class="ec-seq-badge">Sequential Case. Question 1 of 3</div> A 62-year-old man with a history of cirrhosis presents with large-volume hematemesis. He is pale, diaphoretic, and confused. Temperature is 36.4°C (97.5°F), blood pressure is 78/52 mm Hg, pulse is 124/min, and respirations are 22/min. Hemoglobin is 6.8 g/dL. <span class="ec-prompt">Which of the following is the most appropriate initial step?</span> [[CT angiography of the abdomen to localize the bleeding source->Acute GI bleed - Q1 E]] [[Emergent upper endoscopy before any resuscitation->Acute GI bleed - Q1 A]] [[Immediate surgical consultation for exploratory laparotomy->Acute GI bleed - Q1 D]] [[Oral proton pump inhibitor and observation->Acute GI bleed - Q1 C]] [[Volume resuscitation with crystalloid and packed RBC transfusion->Acute GI bleed - Q1 Correct]]

<span class="ec-case-marker" hidden data-entry="Acute GI bleed (Sequential, 3 Questions). Ix"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Volume resuscitation with crystalloid and packed RBC transfusion.</div> In acute upper GI hemorrhage with hemodynamic instability (tachycardia, hypotension, altered mental status) and severe anemia (Hgb 6.8), the immediate priority is hemodynamic resuscitation. IV crystalloid and packed RBC transfusion to restore circulating volume and oxygen-carrying capacity. Endoscopy is essential but should follow initial stabilization. Oral PPI is insufficient for active hemorrhage. Surgery is premature before endoscopic assessment. CT angiography delays resuscitation without changing the immediate management. <div class="ec-src"><b>Source:</b> Laine L, et al. ACG Clinical Guideline: upper gastrointestinal and ulcer bleeding. Am J Gastroenterol 2021;116(5):899-917. Villanueva C, et al. Transfusion strategies for acute upper gastrointestinal bleeding. N Engl J Med 2013;368(1):11-21.</div></div> [[Next question →->Acute GI bleed - Q2]] [[Start another case->Hub]] [[Restart this case->Acute GI bleed - Q2]]

<span class="ec-case-marker" hidden data-entry="Acute GI bleed (Sequential, 3 Questions). Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is Volume resuscitation with crystalloid and packed RBC transfusion. In acute upper GI hemorrhage with hemodynamic instability (tachycardia, hypotension, altered mental status) and severe anemia (Hgb 6.8), the immediate priority is hemodynamic resuscitation. IV crystalloid and packed RBC transfusion to restore circulating volume and oxygen-carrying capacity. Endoscopy is essential but should follow initial stabilization. Oral PPI is insufficient for active hemorrhage. Surgery is premature before endoscopic assessment. CT angiography delays resuscitation without changing the immediate management. <div class="ec-src"><b>Source:</b> Laine L, et al. ACG Clinical Guideline: upper gastrointestinal and ulcer bleeding. Am J Gastroenterol 2021;116(5):899-917. Villanueva C, et al. Transfusion strategies for acute upper gastrointestinal bleeding. N Engl J Med 2013;368(1):11-21.</div></div> [[Try this question again->Acute GI bleed (Sequential - 3 Questions) - Ix]] [[Next question →->Acute GI bleed - Q2]] [[Start another case->Hub]]

<div class="ec-scene">Endoscopy suite · 02:20</div> <div class="ec-seq-badge">Sequential Case. Question 2 of 3</div> After resuscitation, blood pressure improves to 102/64 mm Hg and heart rate decreases to 98/min. Octreotide infusion is started. Upper endoscopy is performed and reveals three columns of large esophageal varices with active spurting from one varix. <span class="ec-prompt">Which of the following endoscopic interventions is most appropriate?</span> [[Application of hemostatic clips to the varix->Acute GI bleed - Q2 C]] [[Argon plasma coagulation of all three columns->Acute GI bleed - Q2 D]] [[Endoscopic sclerotherapy with ethanolamine oleate as first-line->Acute GI bleed - Q2 E]] [[Endoscopic variceal band ligation->Acute GI bleed - Q2 Correct]] [[Epinephrine injection into the varix->Acute GI bleed - Q2 B]]

<span class="ec-case-marker" hidden data-entry="Acute GI bleed (Sequential, 3 Questions). Ix"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Endoscopic variceal band ligation.</div> Endoscopic variceal band ligation (EVL) is the recommended first-line endoscopic treatment for acute esophageal variceal hemorrhage (Baveno VII consensus, AASLD guidelines). It has superior efficacy and fewer complications compared to endoscopic sclerotherapy. Epinephrine injection and hemostatic clips are used for non-variceal bleeding (peptic ulcers). Argon plasma coagulation is used for vascular ectasias and is not appropriate for variceal bleeding. <div class="ec-src"><b>Source:</b> de Franchis R, et al. Baveno VII. Renewing consensus in portal hypertension. J Hepatol 2022;76(4):959-974. Garcia-Tsao G, et al. Portal hypertensive bleeding in cirrhosis: risk stratification, diagnosis, and management (AASLD). Hepatology 2017;65(1):310-335.</div></div> [[Next question →->Acute GI bleed - Q3]] [[Start another case->Hub]] [[Restart this case->Acute GI bleed - Q2]]

<span class="ec-case-marker" hidden data-entry="Acute GI bleed (Sequential, 3 Questions). Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is Endoscopic variceal band ligation. Endoscopic variceal band ligation (EVL) is the recommended first-line endoscopic treatment for acute esophageal variceal hemorrhage (Baveno VII consensus, AASLD guidelines). It has superior efficacy and fewer complications compared to endoscopic sclerotherapy. Epinephrine injection and hemostatic clips are used for non-variceal bleeding (peptic ulcers). Argon plasma coagulation is used for vascular ectasias and is not appropriate for variceal bleeding. <div class="ec-src"><b>Source:</b> de Franchis R, et al. Baveno VII. Renewing consensus in portal hypertension. J Hepatol 2022;76(4):959-974. Garcia-Tsao G, et al. Portal hypertensive bleeding in cirrhosis: risk stratification, diagnosis, and management (AASLD). Hepatology 2017;65(1):310-335.</div></div> [[Try this question again->Acute GI bleed - Q2]] [[Next question →->Acute GI bleed - Q3]] [[Start another case->Hub]]

<div class="ec-scene">Intensive care unit · 06:45</div> <div class="ec-seq-badge">Sequential Case. Question 3 of 3</div> Band ligation is successfully performed. Forty-8 hours later, the patient has another episode of large-volume hematemesis with recurrent hemodynamic instability. Repeat endoscopy shows rebleeding from the variceal site despite banding. <span class="ec-prompt">Which of the following is the most appropriate next step?</span> [[Balloon tamponade as definitive long-term therapy->Acute GI bleed - Q3 D]] [[Initiation of oral propranolol for portal pressure reduction->Acute GI bleed - Q3 C]] [[Placement of a transjugular intrahepatic portosystemic shunt (TIPS)->Acute GI bleed - Q3 Correct]] [[Repeat band ligation a third time->Acute GI bleed - Q3 A]] [[Watchful waiting with continued octreotide alone->Acute GI bleed - Q3 E]]

<span class="ec-case-marker" hidden data-entry="Acute GI bleed (Sequential, 3 Questions). Ix"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Placement of a transjugular intrahepatic portosystemic shunt (TIPS).</div> When variceal bleeding is refractory to endoscopic therapy (defined as failure to control bleeding or early rebleeding despite two endoscopic attempts), salvage TIPS is indicated (Baveno VII). Balloon tamponade (Sengstaken-Blakemore or Minnesota tube) is a temporizing bridge to TIPS, not definitive therapy. Propranolol is for secondary prophylaxis, not acute rebleeding. Watchful waiting with octreotide alone is inadequate for refractory hemorrhage. <div class="ec-src"><b>Source:</b> de Franchis R, et al. Baveno VII. Renewing consensus in portal hypertension. J Hepatol 2022;76(4):959-974. Garcia-Pagán JC, et al. Early use of TIPS in patients with cirrhosis and variceal bleeding. N Engl J Med 2010;362(25):2370-2379.</div></div> [[Start another case->Hub]] [[Restart this case->Acute GI bleed - Q2]] [[Next case →->Upper GI bleed - Rx]]

<span class="ec-case-marker" hidden data-entry="Acute GI bleed (Sequential, 3 Questions). Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is Placement of a transjugular intrahepatic portosystemic shunt (TIPS). When variceal bleeding is refractory to endoscopic therapy (defined as failure to control bleeding or early rebleeding despite two endoscopic attempts), salvage TIPS is indicated (Baveno VII). Balloon tamponade (Sengstaken-Blakemore or Minnesota tube) is a temporizing bridge to TIPS, not definitive therapy. Propranolol is for secondary prophylaxis, not acute rebleeding. Watchful waiting with octreotide alone is inadequate for refractory hemorrhage. <div class="ec-src"><b>Source:</b> de Franchis R, et al. Baveno VII. Renewing consensus in portal hypertension. J Hepatol 2022;76(4):959-974. Garcia-Pagán JC, et al. Early use of TIPS in patients with cirrhosis and variceal bleeding. N Engl J Med 2010;362(25):2370-2379.</div></div> [[Try this question again->Acute GI bleed - Q3]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 14:37</div> <div class="ec-seq-badge">Sequential Case. Question 1 of 2</div> A 28-year-old woman with type 1 diabetes presents with nausea, vomiting, and abdominal pain for 2 days. She ran out of insulin 3 days ago. Temperature is 37.2°C (99.0°F), blood pressure is 96/62 mm Hg, pulse is 118/min, and respirations are 28/min with Kussmaul pattern. Glucose is 520 mg/dL, arterial pH is 7.08, serum bicarbonate is 6 mEq/L, anion gap is 28, and serum potassium is 5.6 mEq/L. Serum osmolality is 305 mOsm/kg. <span class="ec-prompt">Which of the following diagnoses best explains these findings?</span> [[Alcoholic ketoacidosis->Diabetic emergency - Q1 D]] [[Diabetic ketoacidosis->Diabetic emergency - Q1 Correct]] [[Hyperosmolar hyperglycemic state->Diabetic emergency - Q1 A]] [[Lactic acidosis from sepsis->Diabetic emergency - Q1 C]] [[Salicylate toxicity->Diabetic emergency - Q1 E]]

<span class="ec-case-marker" hidden data-entry="Diabetic emergency (Sequential, 2 Questions). Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Diabetic ketoacidosis.</div> Severe anion-gap metabolic acidosis (pH 7.08, bicarbonate 6, anion gap 28) with hyperglycemia (520 mg/dL) in a type 1 diabetic who stopped insulin is classic DKA. HHS typically presents with glucose >600 mg/dL, serum osmolality >320 mOsm/kg, and minimal acidosis. The osmolality of 305 is not in the HHS range. Alcoholic ketoacidosis occurs in malnourished chronic alcohol users, usually with low or normal glucose. Kussmaul respirations reflect respiratory compensation for metabolic acidosis. <div class="ec-src"><b>Source:</b> Kitabchi AE, et al. Hyperglycemic crises in adult patients with diabetes. Diabetes Care 2009;32(7):1335-1343.</div></div> [[Next question →->Diabetic emergency - Q2]] [[Start another case->Hub]] [[Restart this case->Diabetic emergency - Q2]]

<span class="ec-case-marker" hidden data-entry="Diabetic emergency (Sequential, 2 Questions). Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is Diabetic ketoacidosis. Severe anion-gap metabolic acidosis (pH 7.08, bicarbonate 6, anion gap 28) with hyperglycemia (520 mg/dL) in a type 1 diabetic who stopped insulin is classic DKA. HHS typically presents with glucose >600 mg/dL, serum osmolality >320 mOsm/kg, and minimal acidosis. The osmolality of 305 is not in the HHS range. Alcoholic ketoacidosis occurs in malnourished chronic alcohol users, usually with low or normal glucose. Kussmaul respirations reflect respiratory compensation for metabolic acidosis. <div class="ec-src"><b>Source:</b> Kitabchi AE, et al. Hyperglycemic crises in adult patients with diabetes. Diabetes Care 2009;32(7):1335-1343.</div></div> [[Try this question again->Diabetic emergency (Sequential - 2 Questions) - Dx]] [[Next question →->Diabetic emergency - Q2]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 04:17</div> <div class="ec-seq-badge">Sequential Case. Question 2 of 2</div> Intravenous insulin infusion and aggressive fluid resuscitation are initiated. 3 hours later, glucose has decreased to 280 mg/dL and pH has improved to 7.22. However, repeat serum potassium is now 3.1 mEq/L. The patient develops new U waves on telemetry. <span class="ec-prompt">Which of the following is the most appropriate next step?</span> [[Administer intravenous sodium bicarbonate to correct the remaining acidosis->Diabetic emergency - Q2 D]] [[Aggressive intravenous potassium replacement before continuing insulin->Diabetic emergency - Q2 Correct]] [[Continue the current insulin infusion rate without changes->Diabetic emergency - Q2 A]] [[Discontinue insulin and switch to subcutaneous long-acting insulin->Diabetic emergency - Q2 E]] [[Increase the insulin infusion rate to accelerate glucose correction->Diabetic emergency - Q2 B]]

<span class="ec-case-marker" hidden data-entry="Diabetic emergency (Sequential, 2 Questions). Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Aggressive intravenous potassium replacement before continuing insulin.</div> Hypokalemia during DKA treatment is a critical and potentially fatal complication. Insulin drives potassium intracellularly, and fluid resuscitation dilutes serum potassium and increases renal potassium excretion. When potassium falls below 3.5 mEq/L, insulin should be held until potassium is repleted to avoid life-threatening cardiac arrhythmias (U waves are an early ECG sign of hypokalemia). ADA guidelines specify that potassium must be ≥3.5 mEq/L before insulin infusion continues. Sodium bicarbonate is not routinely recommended in DKA unless pH <7.0. <div class="ec-src"><b>Source:</b> Umpierrez GE, et al. Hyperglycemic Crises in Adults With Diabetes. Diabetes Care 2024;47(8):1257-1275.</div></div> [[Start another case->Hub]] [[Restart this case->Diabetic emergency - Q2]] [[Next case →->Diabetic foot - Rx]]

<span class="ec-case-marker" hidden data-entry="Diabetic emergency (Sequential, 2 Questions). Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The correct answer is Aggressive intravenous potassium replacement before continuing insulin. Hypokalemia during DKA treatment is a critical and potentially fatal complication. Insulin drives potassium intracellularly, and fluid resuscitation dilutes serum potassium and increases renal potassium excretion. When potassium falls below 3.5 mEq/L, insulin should be held until potassium is repleted to avoid life-threatening cardiac arrhythmias (U waves are an early ECG sign of hypokalemia). ADA guidelines specify that potassium must be ≥3.5 mEq/L before insulin infusion continues. Sodium bicarbonate is not routinely recommended in DKA unless pH <7.0. <div class="ec-src"><b>Source:</b> Umpierrez GE, et al. Hyperglycemic Crises in Adults With Diabetes. Diabetes Care 2024;47(8):1257-1275.</div></div> [[Try this question again->Diabetic emergency - Q2]] [[Start another case->Hub]]

<div class="ec-scene">Journal club · 07:40</div> A randomized trial of a new lipid-lowering agent enrolls 8,000 adults with established coronary disease and follows them for 4 years. Recurrent myocardial infarction occurs in 240 of 4,000 patients in the treatment arm and in 360 of 4,000 patients in the placebo arm. The difference is statistically significant. A resident asks how many patients would need to be treated for 4 years to prevent one recurrent infarction. <span class="ec-prompt">Which of the following is the number needed to treat?</span> [[120->NNT interpretation - Biostat D4]] [[17->NNT interpretation - Biostat D2]] [[3->NNT interpretation - Biostat D1]] [[33->NNT interpretation - Biostat correct]] [[333->NNT interpretation - Biostat D5]] [[60->NNT interpretation - Biostat D3]]

<span class="ec-case-marker" hidden data-entry="NNT interpretation. Biostat"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ 33</div> Event rates are 240/4,000 = 6.0% with treatment and 360/4,000 = 9.0% with placebo. The absolute risk reduction is 9.0% minus 6.0%, or 3.0%. The number needed to treat is the reciprocal of the absolute risk reduction: 1 divided by 0.03 is 33.3, which rounds to an NNT of approximately 33 patients. Note that the relative risk reduction here is 33%, a much more impressive-sounding number derived from the same data, which is why absolute measures are preferred for judging clinical impact. <div class="ec-src"><b>Source:</b> Laupacis A, Sackett DL, Roberts RS. An assessment of clinically useful measures of the consequences of treatment. N Engl J Med 1988;319(26):1728-1733.</div></div> [[Start another case->Hub]] [[Restart this case->NNT interpretation - Biostat]] [[Next case →->Predictive value and prevalence - Biostat]]

<span class="ec-case-marker" hidden data-entry="NNT interpretation. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This is the absolute risk reduction expressed as a percentage, not its reciprocal. The number needed to treat inverts the absolute risk reduction, so a 3% difference corresponds to roughly 33 patients treated, not 3. <div class="ec-teach"><div class="th">What the findings point to</div> Event rates are 240/4,000 = 6.0% with treatment and 360/4,000 = 9.0% with placebo. The absolute risk reduction is 9.0% minus 6.0%, or 3.0%. The number needed to treat is the reciprocal of the absolute risk reduction: 1 divided by 0.03 is 33.3, which rounds to an NNT of approximately 33 patients. Note that the relative risk reduction here is 33%, a much more impressive-sounding number derived from the same data, which is why absolute measures are preferred for judging clinical impact. <div class="ec-src"><b>Source:</b> Laupacis A, Sackett DL, Roberts RS. An assessment of clinically useful measures of the consequences of treatment. N Engl J Med 1988;319(26):1728-1733.</div></div></div> [[Try this question again->NNT interpretation - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="NNT interpretation. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This would be the number needed to treat if the absolute risk reduction were about 6%, which is the event rate in the treatment arm rather than the difference between arms. Using a single arm's event rate instead of the between-arm difference is the most common error in this calculation. <div class="ec-teach"><div class="th">What the findings point to</div> Event rates are 240/4,000 = 6.0% with treatment and 360/4,000 = 9.0% with placebo. The absolute risk reduction is 9.0% minus 6.0%, or 3.0%. The number needed to treat is the reciprocal of the absolute risk reduction: 1 divided by 0.03 is 33.3, which rounds to an NNT of approximately 33 patients. Note that the relative risk reduction here is 33%, a much more impressive-sounding number derived from the same data, which is why absolute measures are preferred for judging clinical impact. <div class="ec-src"><b>Source:</b> Laupacis A, Sackett DL, Roberts RS. An assessment of clinically useful measures of the consequences of treatment. N Engl J Med 1988;319(26):1728-1733.</div></div></div> [[Try this question again->NNT interpretation - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="NNT interpretation. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This value does not follow from either the absolute or the relative difference in this trial. It would correspond to an absolute risk reduction near 1.7%, roughly half the observed difference. <div class="ec-teach"><div class="th">What the findings point to</div> Event rates are 240/4,000 = 6.0% with treatment and 360/4,000 = 9.0% with placebo. The absolute risk reduction is 9.0% minus 6.0%, or 3.0%. The number needed to treat is the reciprocal of the absolute risk reduction: 1 divided by 0.03 is 33.3, which rounds to an NNT of approximately 33 patients. Note that the relative risk reduction here is 33%, a much more impressive-sounding number derived from the same data, which is why absolute measures are preferred for judging clinical impact. <div class="ec-src"><b>Source:</b> Laupacis A, Sackett DL, Roberts RS. An assessment of clinically useful measures of the consequences of treatment. N Engl J Med 1988;319(26):1728-1733.</div></div></div> [[Try this question again->NNT interpretation - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="NNT interpretation. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This is the raw difference in the number of events between arms, 360 minus 240. The count of events prevented in the whole trial is not the number needed to treat, which is expressed per patient treated. <div class="ec-teach"><div class="th">What the findings point to</div> Event rates are 240/4,000 = 6.0% with treatment and 360/4,000 = 9.0% with placebo. The absolute risk reduction is 9.0% minus 6.0%, or 3.0%. The number needed to treat is the reciprocal of the absolute risk reduction: 1 divided by 0.03 is 33.3, which rounds to an NNT of approximately 33 patients. Note that the relative risk reduction here is 33%, a much more impressive-sounding number derived from the same data, which is why absolute measures are preferred for judging clinical impact. <div class="ec-src"><b>Source:</b> Laupacis A, Sackett DL, Roberts RS. An assessment of clinically useful measures of the consequences of treatment. N Engl J Med 1988;319(26):1728-1733.</div></div></div> [[Try this question again->NNT interpretation - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="NNT interpretation. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This is the reciprocal of 0.3% rather than 3%, an order-of-magnitude slip. Converting the percentage to a decimal before inverting avoids it. <div class="ec-teach"><div class="th">What the findings point to</div> Event rates are 240/4,000 = 6.0% with treatment and 360/4,000 = 9.0% with placebo. The absolute risk reduction is 9.0% minus 6.0%, or 3.0%. The number needed to treat is the reciprocal of the absolute risk reduction: 1 divided by 0.03 is 33.3, which rounds to an NNT of approximately 33 patients. Note that the relative risk reduction here is 33%, a much more impressive-sounding number derived from the same data, which is why absolute measures are preferred for judging clinical impact. <div class="ec-src"><b>Source:</b> Laupacis A, Sackett DL, Roberts RS. An assessment of clinically useful measures of the consequences of treatment. N Engl J Med 1988;319(26):1728-1733.</div></div></div> [[Try this question again->NNT interpretation - Biostat]] [[Start another case->Hub]]

<div class="ec-scene">Ambulatory clinic · 11:15</div> A screening assay for a chronic infection has a sensitivity of 99% and a specificity of 98%. It performed well in a high-risk urban cohort in which the prevalence of infection was 10%. A public health agency now proposes deploying the identical assay, unchanged, in a rural population in which the prevalence is 0.1%. The laboratory director is asked what will happen to test performance. <span class="ec-prompt">Which of the following parameters will change most as a result of this deployment?</span> [[Likelihood ratio of a negative result->Predictive value and prevalence - Biostat D1]] [[Likelihood ratio of a positive result->Predictive value and prevalence - Biostat D2]] [[Positive predictive value->Predictive value and prevalence - Biostat correct]] [[Sensitivity->Predictive value and prevalence - Biostat D3]] [[Specificity->Predictive value and prevalence - Biostat D4]] [[Test-retest reliability->Predictive value and prevalence - Biostat D5]]

<span class="ec-case-marker" hidden data-entry="Predictive value and prevalence. Biostat"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Positive predictive value</div> Sensitivity and specificity are properties of the test itself and are essentially independent of prevalence. Predictive values are not. At 10% prevalence this assay yields a positive predictive value near 85%. At 0.1% prevalence, most positives are drawn from the far larger uninfected pool, and the positive predictive value collapses to roughly 5%, meaning about nineteen of every twenty positive results are false. This is the central argument against applying a good test to a low-prevalence population without a confirmatory strategy. <div class="ec-src"><b>Source:</b> Sackett DL, Haynes RB. The architecture of diagnostic research. BMJ 2002;324(7336):539-541.</div></div> [[Start another case->Hub]] [[Restart this case->Predictive value and prevalence - Biostat]] [[Next case →->Lung cancer screening eligibility - Prevention]]

<span class="ec-case-marker" hidden data-entry="Predictive value and prevalence. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Likelihood ratios are calculated from sensitivity and specificity alone and therefore do not vary with prevalence. Their stability is precisely why they are useful for moving between populations. <div class="ec-teach"><div class="th">What the findings point to</div> Sensitivity and specificity are properties of the test itself and are essentially independent of prevalence. Predictive values are not. At 10% prevalence this assay yields a positive predictive value near 85%. At 0.1% prevalence, most positives are drawn from the far larger uninfected pool, and the positive predictive value collapses to roughly 5%, meaning about nineteen of every twenty positive results are false. This is the central argument against applying a good test to a low-prevalence population without a confirmatory strategy. <div class="ec-src"><b>Source:</b> Sackett DL, Haynes RB. The architecture of diagnostic research. BMJ 2002;324(7336):539-541.</div></div></div> [[Try this question again->Predictive value and prevalence - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Predictive value and prevalence. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This equals sensitivity divided by one minus specificity, both intrinsic test properties, and is unchanged by the prevalence of disease in the population tested. <div class="ec-teach"><div class="th">What the findings point to</div> Sensitivity and specificity are properties of the test itself and are essentially independent of prevalence. Predictive values are not. At 10% prevalence this assay yields a positive predictive value near 85%. At 0.1% prevalence, most positives are drawn from the far larger uninfected pool, and the positive predictive value collapses to roughly 5%, meaning about nineteen of every twenty positive results are false. This is the central argument against applying a good test to a low-prevalence population without a confirmatory strategy. <div class="ec-src"><b>Source:</b> Sackett DL, Haynes RB. The architecture of diagnostic research. BMJ 2002;324(7336):539-541.</div></div></div> [[Try this question again->Predictive value and prevalence - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Predictive value and prevalence. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Sensitivity is the proportion of truly infected people the test identifies. It is a property of the assay measured among diseased patients and does not shift because fewer diseased patients are present, although spectrum effects can alter it when the severity distribution changes. <div class="ec-teach"><div class="th">What the findings point to</div> Sensitivity and specificity are properties of the test itself and are essentially independent of prevalence. Predictive values are not. At 10% prevalence this assay yields a positive predictive value near 85%. At 0.1% prevalence, most positives are drawn from the far larger uninfected pool, and the positive predictive value collapses to roughly 5%, meaning about nineteen of every twenty positive results are false. This is the central argument against applying a good test to a low-prevalence population without a confirmatory strategy. <div class="ec-src"><b>Source:</b> Sackett DL, Haynes RB. The architecture of diagnostic research. BMJ 2002;324(7336):539-541.</div></div></div> [[Try this question again->Predictive value and prevalence - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Predictive value and prevalence. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Specificity is measured among uninfected people and remains approximately 98% regardless of how many uninfected people are tested. What changes is the absolute number of false positives generated. <div class="ec-teach"><div class="th">What the findings point to</div> Sensitivity and specificity are properties of the test itself and are essentially independent of prevalence. Predictive values are not. At 10% prevalence this assay yields a positive predictive value near 85%. At 0.1% prevalence, most positives are drawn from the far larger uninfected pool, and the positive predictive value collapses to roughly 5%, meaning about nineteen of every twenty positive results are false. This is the central argument against applying a good test to a low-prevalence population without a confirmatory strategy. <div class="ec-src"><b>Source:</b> Sackett DL, Haynes RB. The architecture of diagnostic research. BMJ 2002;324(7336):539-541.</div></div></div> [[Try this question again->Predictive value and prevalence - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Predictive value and prevalence. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Reliability describes reproducibility of the assay on repeated measurement and is a laboratory characteristic unaffected by the prevalence of disease in the sampled population. <div class="ec-teach"><div class="th">What the findings point to</div> Sensitivity and specificity are properties of the test itself and are essentially independent of prevalence. Predictive values are not. At 10% prevalence this assay yields a positive predictive value near 85%. At 0.1% prevalence, most positives are drawn from the far larger uninfected pool, and the positive predictive value collapses to roughly 5%, meaning about nineteen of every twenty positive results are false. This is the central argument against applying a good test to a low-prevalence population without a confirmatory strategy. <div class="ec-src"><b>Source:</b> Sackett DL, Haynes RB. The architecture of diagnostic research. BMJ 2002;324(7336):539-541.</div></div></div> [[Try this question again->Predictive value and prevalence - Biostat]] [[Start another case->Hub]]

<div class="ec-scene">Adolescent medicine clinic · 15:20</div> A 16-year-old girl is seen for a sports physical. Her mother steps out at the request and the patient then discloses that she is sexually active with one partner, uses condoms inconsistently, and would like testing for sexually transmitted infections and a prescription for contraception. She is doing well in school, denies coercion, denies substance use, and denies any thoughts of self-harm. She asks that her mother not be told. In this state, minors may consent to their own testing and treatment for sexually transmitted infections and to contraceptive services. <span class="ec-prompt">Which of the following is the most appropriate next step?</span> [[Defer testing until she agrees to inform her mother->Adolescent confidentiality - Ethics D1]] [[Inform her mother because the patient is a minor->Adolescent confidentiality - Ethics D2]] [[Obtain written parental consent before prescribing contraception->Adolescent confidentiality - Ethics D3]] [[Provide the requested testing and contraception without disclosing to her mother->Adolescent confidentiality - Ethics correct]] [[Refer her to a confidential public health clinic instead of treating her->Adolescent confidentiality - Ethics D5]] [[Report the sexual activity to child protective services->Adolescent confidentiality - Ethics D4]]

<span class="ec-case-marker" hidden data-entry="Adolescent confidentiality. Ethics"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Provide the requested testing and contraception without disclosing to her mother</div> The patient falls squarely within a category of care that minors may consent to independently, she has no features suggesting abuse, coercion, or danger to herself, and confidentiality is the condition on which adolescents seek this care at all. Providing services directly is both legally permitted and clinically correct. It is good practice to encourage her to involve a parent, and to warn her in advance that an explanation of benefits mailed to the policyholder may inadvertently disclose the visit, but neither converts into a requirement to inform. <div class="ec-src"><b>Source:</b> English A, Ford CA. The HIPAA privacy rule and adolescents: legal questions and clinical challenges. Perspect Sex Reprod Health 2004;36(2):80-86.</div></div> [[Start another case->Hub]] [[Restart this case->Adolescent confidentiality - Ethics]] [[Next case →->Decision-making capacity - Ethics]]

<span class="ec-case-marker" hidden data-entry="Adolescent confidentiality. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Conditioning care on parental disclosure is the intervention most reliably shown to make adolescents forgo care entirely. She has independent authority to consent here, so withholding testing has no legal basis and predictable clinical harm. <div class="ec-teach"><div class="th">What the findings point to</div> The patient falls squarely within a category of care that minors may consent to independently, she has no features suggesting abuse, coercion, or danger to herself, and confidentiality is the condition on which adolescents seek this care at all. Providing services directly is both legally permitted and clinically correct. It is good practice to encourage her to involve a parent, and to warn her in advance that an explanation of benefits mailed to the policyholder may inadvertently disclose the visit, but neither converts into a requirement to inform. <div class="ec-src"><b>Source:</b> English A, Ford CA. The HIPAA privacy rule and adolescents: legal questions and clinical challenges. Perspect Sex Reprod Health 2004;36(2):80-86.</div></div></div> [[Try this question again->Adolescent confidentiality - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Adolescent confidentiality. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Minor status does not override the specific statutory carve-outs for sexually transmitted infection and contraceptive services, which exist in every state in some form. Disclosing against her wishes here breaches confidentiality without justification. <div class="ec-teach"><div class="th">What the findings point to</div> The patient falls squarely within a category of care that minors may consent to independently, she has no features suggesting abuse, coercion, or danger to herself, and confidentiality is the condition on which adolescents seek this care at all. Providing services directly is both legally permitted and clinically correct. It is good practice to encourage her to involve a parent, and to warn her in advance that an explanation of benefits mailed to the policyholder may inadvertently disclose the visit, but neither converts into a requirement to inform. <div class="ec-src"><b>Source:</b> English A, Ford CA. The HIPAA privacy rule and adolescents: legal questions and clinical challenges. Perspect Sex Reprod Health 2004;36(2):80-86.</div></div></div> [[Try this question again->Adolescent confidentiality - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Adolescent confidentiality. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> No parental consent is required for a service the minor may consent to herself. Requiring it functions as a refusal. <div class="ec-teach"><div class="th">What the findings point to</div> The patient falls squarely within a category of care that minors may consent to independently, she has no features suggesting abuse, coercion, or danger to herself, and confidentiality is the condition on which adolescents seek this care at all. Providing services directly is both legally permitted and clinically correct. It is good practice to encourage her to involve a parent, and to warn her in advance that an explanation of benefits mailed to the policyholder may inadvertently disclose the visit, but neither converts into a requirement to inform. <div class="ec-src"><b>Source:</b> English A, Ford CA. The HIPAA privacy rule and adolescents: legal questions and clinical challenges. Perspect Sex Reprod Health 2004;36(2):80-86.</div></div></div> [[Try this question again->Adolescent confidentiality - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Adolescent confidentiality. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Consensual activity between similarly aged adolescents, absent coercion or a reporting threshold under state law, is not a reportable finding. Reflexive reporting of ordinary adolescent sexual activity misuses the child protection system. <div class="ec-teach"><div class="th">What the findings point to</div> The patient falls squarely within a category of care that minors may consent to independently, she has no features suggesting abuse, coercion, or danger to herself, and confidentiality is the condition on which adolescents seek this care at all. Providing services directly is both legally permitted and clinically correct. It is good practice to encourage her to involve a parent, and to warn her in advance that an explanation of benefits mailed to the policyholder may inadvertently disclose the visit, but neither converts into a requirement to inform. <div class="ec-src"><b>Source:</b> English A, Ford CA. The HIPAA privacy rule and adolescents: legal questions and clinical challenges. Perspect Sex Reprod Health 2004;36(2):80-86.</div></div></div> [[Try this question again->Adolescent confidentiality - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Adolescent confidentiality. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Referral elsewhere is reasonable only if one cannot provide the service. Deflecting a patient who is already present introduces delay and signals that the request was unwelcome. <div class="ec-teach"><div class="th">What the findings point to</div> The patient falls squarely within a category of care that minors may consent to independently, she has no features suggesting abuse, coercion, or danger to herself, and confidentiality is the condition on which adolescents seek this care at all. Providing services directly is both legally permitted and clinically correct. It is good practice to encourage her to involve a parent, and to warn her in advance that an explanation of benefits mailed to the policyholder may inadvertently disclose the visit, but neither converts into a requirement to inform. <div class="ec-src"><b>Source:</b> English A, Ford CA. The HIPAA privacy rule and adolescents: legal questions and clinical challenges. Perspect Sex Reprod Health 2004;36(2):80-86.</div></div></div> [[Try this question again->Adolescent confidentiality - Ethics]] [[Start another case->Hub]]

<div class="ec-scene">Hospital ward · 09:05</div> A nurse administers 10 times the intended dose of intravenous morphine to a postoperative patient. The patient becomes apneic, is given naloxone, and recovers fully. Review shows that the pharmacy stocks morphine in two concentrations in identically sized vials with nearly identical labels, that the automated dispensing cabinet did not prompt a concentration check, and that the nurse was covering an unusually high patient load on the night shift. The nurse has no prior safety events and reported the error herself within minutes. <span class="ec-prompt">Which of the following is the most appropriate initial institutional response?</span> [[Add a mandatory second-nurse verification for all opioid doses->Just culture after error - QI D1]] [[Convene a root cause analysis of the medication system->Just culture after error - QI correct]] [[Issue a written warning to the nurse and require remedial training->Just culture after error - QI D2]] [[Report the nurse to the state board of nursing->Just culture after error - QI D3]] [[Survey staff about their perceptions of the event->Just culture after error - QI D5]] [[Suspend the nurse pending investigation->Just culture after error - QI D4]]

<span class="ec-case-marker" hidden data-entry="Just culture after error. QI"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Convene a root cause analysis of the medication system</div> The event has multiple latent system defects: look-alike vials at differing concentrations, absent forcing functions in the dispensing cabinet, and unsafe staffing. A root cause analysis is designed to surface exactly these and generate durable fixes such as removing the concentrated vial from floor stock and adding a hard stop at dispensing. Punishing an individual who self-reported an error produced by a hazardous system fixes nothing and suppresses the reporting that safety work depends on. <div class="ec-src"><b>Source:</b> Institute of Medicine, Committee on Quality of Health Care in America. To Err Is Human: Building a Safer Health System. Washington, DC: National Academies Press, 2000.</div></div> [[Start another case->Hub]] [[Restart this case->Just culture after error - QI]] [[Next case →->Catheter infection bundle - QI]]

<span class="ec-case-marker" hidden data-entry="Just culture after error. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Layering a human double-check onto a hazardous supply is a weak intervention that degrades with workload and habituation. Removing the look-alike vial is a stronger fix, and adding checks before analysis skips the step that identifies which fix matters. <div class="ec-teach"><div class="th">What the findings point to</div> The event has multiple latent system defects: look-alike vials at differing concentrations, absent forcing functions in the dispensing cabinet, and unsafe staffing. A root cause analysis is designed to surface exactly these and generate durable fixes such as removing the concentrated vial from floor stock and adding a hard stop at dispensing. Punishing an individual who self-reported an error produced by a hazardous system fixes nothing and suppresses the reporting that safety work depends on. <div class="ec-src"><b>Source:</b> Institute of Medicine, Committee on Quality of Health Care in America. To Err Is Human: Building a Safer Health System. Washington, DC: National Academies Press, 2000.</div></div></div> [[Try this question again->Just culture after error - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Just culture after error. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Blame directed at a self-reporting clinician in a system stacked with hazards drives future errors underground and leaves every latent defect in place for the next nurse. <div class="ec-teach"><div class="th">What the findings point to</div> The event has multiple latent system defects: look-alike vials at differing concentrations, absent forcing functions in the dispensing cabinet, and unsafe staffing. A root cause analysis is designed to surface exactly these and generate durable fixes such as removing the concentrated vial from floor stock and adding a hard stop at dispensing. Punishing an individual who self-reported an error produced by a hazardous system fixes nothing and suppresses the reporting that safety work depends on. <div class="ec-src"><b>Source:</b> Institute of Medicine, Committee on Quality of Health Care in America. To Err Is Human: Building a Safer Health System. Washington, DC: National Academies Press, 2000.</div></div></div> [[Try this question again->Just culture after error - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Just culture after error. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Board referral is reserved for reckless conduct, impairment, or willful violation. This was a systems-driven error, promptly disclosed, in a clinician with no prior events. <div class="ec-teach"><div class="th">What the findings point to</div> The event has multiple latent system defects: look-alike vials at differing concentrations, absent forcing functions in the dispensing cabinet, and unsafe staffing. A root cause analysis is designed to surface exactly these and generate durable fixes such as removing the concentrated vial from floor stock and adding a hard stop at dispensing. Punishing an individual who self-reported an error produced by a hazardous system fixes nothing and suppresses the reporting that safety work depends on. <div class="ec-src"><b>Source:</b> Institute of Medicine, Committee on Quality of Health Care in America. To Err Is Human: Building a Safer Health System. Washington, DC: National Academies Press, 2000.</div></div></div> [[Try this question again->Just culture after error - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Just culture after error. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Suspension is a punitive measure disproportionate to a self-reported systems error and communicates to the entire unit that reporting carries personal risk. <div class="ec-teach"><div class="th">What the findings point to</div> The event has multiple latent system defects: look-alike vials at differing concentrations, absent forcing functions in the dispensing cabinet, and unsafe staffing. A root cause analysis is designed to surface exactly these and generate durable fixes such as removing the concentrated vial from floor stock and adding a hard stop at dispensing. Punishing an individual who self-reported an error produced by a hazardous system fixes nothing and suppresses the reporting that safety work depends on. <div class="ec-src"><b>Source:</b> Institute of Medicine, Committee on Quality of Health Care in America. To Err Is Human: Building a Safer Health System. Washington, DC: National Academies Press, 2000.</div></div></div> [[Try this question again->Just culture after error - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Just culture after error. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Perception data has a role in safety culture measurement but does not identify the mechanical failure points that caused this specific event. <div class="ec-teach"><div class="th">What the findings point to</div> The event has multiple latent system defects: look-alike vials at differing concentrations, absent forcing functions in the dispensing cabinet, and unsafe staffing. A root cause analysis is designed to surface exactly these and generate durable fixes such as removing the concentrated vial from floor stock and adding a hard stop at dispensing. Punishing an individual who self-reported an error produced by a hazardous system fixes nothing and suppresses the reporting that safety work depends on. <div class="ec-src"><b>Source:</b> Institute of Medicine, Committee on Quality of Health Care in America. To Err Is Human: Building a Safer Health System. Washington, DC: National Academies Press, 2000.</div></div></div> [[Try this question again->Just culture after error - QI]] [[Start another case->Hub]]

<div class="ec-scene">Primary care clinic · 08:50</div> A 55-year-old man presents to establish care. He smoked one pack of cigarettes daily for 22 years and quit 9 years ago. He is asymptomatic, walks two miles daily, and has no chronic illness. His father died of lung cancer at 70. He asks whether he should be screened for lung cancer. Vital signs and physical examination are normal. <span class="ec-prompt">Which of the following is the most appropriate recommendation?</span> [[Annual chest radiography->Lung cancer screening eligibility - Prevention D1]] [[Annual low-dose CT of the chest->Lung cancer screening eligibility - Prevention correct]] [[No screening because he quit more than 5 years ago->Lung cancer screening eligibility - Prevention D2]] [[No screening because his pack-year history is below the threshold->Lung cancer screening eligibility - Prevention D3]] [[Screening sputum cytology every 3 years->Lung cancer screening eligibility - Prevention D4]] [[Serum tumor marker panel every 12 months->Lung cancer screening eligibility - Prevention D5]]

<span class="ec-case-marker" hidden data-entry="Lung cancer screening eligibility. Prevention"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Annual low-dose CT of the chest</div> Current US Preventive Services Task Force criteria are age 50 to 80 years, at least a 20 pack-year history, and current smoking or cessation within the past 15 years. He is 55, has 22 pack-years, and quit 9 years ago, so he meets all three. Screening is annual low-dose CT and continues through age 80, accumulates 15 years of abstinence, or develops a condition that would preclude curative treatment. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Screening for Lung Cancer: US Preventive Services Task Force Recommendation Statement. JAMA 2021;325(10):962-970.</div></div> [[Start another case->Hub]] [[Restart this case->Lung cancer screening eligibility - Prevention]] [[Next case →->Osteoporosis screening - Prevention]]

<span class="ec-case-marker" hidden data-entry="Lung cancer screening eligibility. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Chest radiography was tested directly against usual care in the PLCO trial and did not reduce lung cancer mortality. Only low-dose CT has shown a mortality benefit. <div class="ec-teach"><div class="th">What the findings point to</div> Current US Preventive Services Task Force criteria are age 50 to 80 years, at least a 20 pack-year history, and current smoking or cessation within the past 15 years. He is 55, has 22 pack-years, and quit 9 years ago, so he meets all three. Screening is annual low-dose CT and continues through age 80, accumulates 15 years of abstinence, or develops a condition that would preclude curative treatment. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Screening for Lung Cancer: US Preventive Services Task Force Recommendation Statement. JAMA 2021;325(10):962-970.</div></div></div> [[Try this question again->Lung cancer screening eligibility - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Lung cancer screening eligibility. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The cessation cutoff is 15 years, not 5. At 9 years out he remains within the eligible window. <div class="ec-teach"><div class="th">What the findings point to</div> Current US Preventive Services Task Force criteria are age 50 to 80 years, at least a 20 pack-year history, and current smoking or cessation within the past 15 years. He is 55, has 22 pack-years, and quit 9 years ago, so he meets all three. Screening is annual low-dose CT and continues through age 80, accumulates 15 years of abstinence, or develops a condition that would preclude curative treatment. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Screening for Lung Cancer: US Preventive Services Task Force Recommendation Statement. JAMA 2021;325(10):962-970.</div></div></div> [[Try this question again->Lung cancer screening eligibility - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Lung cancer screening eligibility. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> One pack daily for 22 years is 22 pack-years, above the 20 pack-year threshold set in the 2021 update, which lowered the previous 30 pack-year requirement. <div class="ec-teach"><div class="th">What the findings point to</div> Current US Preventive Services Task Force criteria are age 50 to 80 years, at least a 20 pack-year history, and current smoking or cessation within the past 15 years. He is 55, has 22 pack-years, and quit 9 years ago, so he meets all three. Screening is annual low-dose CT and continues through age 80, accumulates 15 years of abstinence, or develops a condition that would preclude curative treatment. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Screening for Lung Cancer: US Preventive Services Task Force Recommendation Statement. JAMA 2021;325(10):962-970.</div></div></div> [[Try this question again->Lung cancer screening eligibility - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Lung cancer screening eligibility. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Sputum cytology has been studied as a screening modality and does not reduce lung cancer mortality. It has no role in asymptomatic screening. <div class="ec-teach"><div class="th">What the findings point to</div> Current US Preventive Services Task Force criteria are age 50 to 80 years, at least a 20 pack-year history, and current smoking or cessation within the past 15 years. He is 55, has 22 pack-years, and quit 9 years ago, so he meets all three. Screening is annual low-dose CT and continues through age 80, accumulates 15 years of abstinence, or develops a condition that would preclude curative treatment. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Screening for Lung Cancer: US Preventive Services Task Force Recommendation Statement. JAMA 2021;325(10):962-970.</div></div></div> [[Try this question again->Lung cancer screening eligibility - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Lung cancer screening eligibility. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> No serum marker has demonstrated adequate performance for lung cancer screening in asymptomatic adults, and marker panels generate false positives that lead to unnecessary imaging. <div class="ec-teach"><div class="th">What the findings point to</div> Current US Preventive Services Task Force criteria are age 50 to 80 years, at least a 20 pack-year history, and current smoking or cessation within the past 15 years. He is 55, has 22 pack-years, and quit 9 years ago, so he meets all three. Screening is annual low-dose CT and continues through age 80, accumulates 15 years of abstinence, or develops a condition that would preclude curative treatment. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Screening for Lung Cancer: US Preventive Services Task Force Recommendation Statement. JAMA 2021;325(10):962-970.</div></div></div> [[Try this question again->Lung cancer screening eligibility - Prevention]] [[Start another case->Hub]]

<div class="ec-scene">Allergy clinic · 13:30</div> A 38-year-old woman has a 6-year history of asthma requiring daily inhaled corticosteroid, chronic nasal congestion with anosmia, and two prior endoscopic resections of nasal polyps. Ninety minutes after taking ibuprofen for a headache she developed profuse rhinorrhea, facial flushing, and wheezing requiring nebulized albuterol. She tolerates acetaminophen in standard doses. Skin testing to ibuprofen is negative and serum specific IgE is undetectable. <span class="ec-prompt">Which of the following best explains this patient's reaction?</span> [[Complement activation with anaphylatoxin release->Aspirin-exacerbated respiratory disease - Mech D1]] [[Cross-linking of drug-specific IgE on mast cells->Aspirin-exacerbated respiratory disease - Mech D2]] [[Cyclooxygenase-1 inhibition shunting toward leukotrienes->Aspirin-exacerbated respiratory disease - Mech correct]] [[Direct mast cell degranulation through MRGPRX2->Aspirin-exacerbated respiratory disease - Mech D3]] [[Selective cyclooxygenase-2 inhibition reducing prostacyclin->Aspirin-exacerbated respiratory disease - Mech D4]] [[T cell-mediated delayed hypersensitivity to the drug->Aspirin-exacerbated respiratory disease - Mech D5]]

<span class="ec-case-marker" hidden data-entry="Aspirin-exacerbated respiratory disease. Mech"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Cyclooxygenase-1 inhibition shunting toward leukotrienes</div> This is aspirin-exacerbated respiratory disease, the triad of asthma, nasal polyposis, and reactions to cyclooxygenase-1 inhibitors. The mechanism is pharmacologic, not allergic. Blocking cyclooxygenase-1 removes prostaglandin E2's normal brake on mast cells, which shifts arachidonic acid down the 5-lipoxygenase pathway and floods an already overactive receptor population with cysteinyl leukotrienes. That explains three things: skin testing and specific IgE are negative because no antibody is involved; any drug that blocks cyclooxygenase-1 sets it off, even ones structurally unrelated to aspirin; and acetaminophen, a weak cyclooxygenase-1 inhibitor at normal doses, is usually tolerated. <div class="ec-src"><b>Source:</b> Laidlaw TM, Boyce JA. Aspirin-Exacerbated Respiratory Disease. New Prime Suspects. N Engl J Med 2016;374(5):484-488.</div></div> [[Start another case->Hub]] [[Restart this case->Aspirin-exacerbated respiratory disease - Mech]] [[Next case →->Incidental pulmonary nodule - Ix]]

<span class="ec-case-marker" hidden data-entry="Aspirin-exacerbated respiratory disease. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Complement-mediated pseudoallergy occurs with some infused agents and solubilizing excipients but does not explain a reproducible reaction to every cyclooxygenase-1 inhibitor while a structurally similar non-inhibitor is tolerated. <div class="ec-teach"><div class="th">What the findings point to</div> This is aspirin-exacerbated respiratory disease, the triad of asthma, nasal polyposis, and reactions to cyclooxygenase-1 inhibitors. The mechanism is pharmacologic, not allergic. Blocking cyclooxygenase-1 removes prostaglandin E2's normal brake on mast cells, which shifts arachidonic acid down the 5-lipoxygenase pathway and floods an already overactive receptor population with cysteinyl leukotrienes. That explains three things: skin testing and specific IgE are negative because no antibody is involved; any drug that blocks cyclooxygenase-1 sets it off, even ones structurally unrelated to aspirin; and acetaminophen, a weak cyclooxygenase-1 inhibitor at normal doses, is usually tolerated. <div class="ec-src"><b>Source:</b> Laidlaw TM, Boyce JA. Aspirin-Exacerbated Respiratory Disease. New Prime Suspects. N Engl J Med 2016;374(5):484-488.</div></div></div> [[Try this question again->Aspirin-exacerbated respiratory disease - Mech]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Aspirin-exacerbated respiratory disease. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> An IgE-mediated reaction would be drug-specific rather than shared across chemically unrelated inhibitors, and it would be expected to yield positive skin testing or detectable specific IgE, neither of which is present. <div class="ec-teach"><div class="th">What the findings point to</div> This is aspirin-exacerbated respiratory disease, the triad of asthma, nasal polyposis, and reactions to cyclooxygenase-1 inhibitors. The mechanism is pharmacologic, not allergic. Blocking cyclooxygenase-1 removes prostaglandin E2's normal brake on mast cells, which shifts arachidonic acid down the 5-lipoxygenase pathway and floods an already overactive receptor population with cysteinyl leukotrienes. That explains three things: skin testing and specific IgE are negative because no antibody is involved; any drug that blocks cyclooxygenase-1 sets it off, even ones structurally unrelated to aspirin; and acetaminophen, a weak cyclooxygenase-1 inhibitor at normal doses, is usually tolerated. <div class="ec-src"><b>Source:</b> Laidlaw TM, Boyce JA. Aspirin-Exacerbated Respiratory Disease. New Prime Suspects. N Engl J Med 2016;374(5):484-488.</div></div></div> [[Try this question again->Aspirin-exacerbated respiratory disease - Mech]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Aspirin-exacerbated respiratory disease. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> MRGPRX2 activation underlies pseudoallergic reactions to agents such as vancomycin and certain neuromuscular blockers. It does not account for a class effect defined by enzyme inhibition or for the coexisting polyposis. <div class="ec-teach"><div class="th">What the findings point to</div> This is aspirin-exacerbated respiratory disease, the triad of asthma, nasal polyposis, and reactions to cyclooxygenase-1 inhibitors. The mechanism is pharmacologic, not allergic. Blocking cyclooxygenase-1 removes prostaglandin E2's normal brake on mast cells, which shifts arachidonic acid down the 5-lipoxygenase pathway and floods an already overactive receptor population with cysteinyl leukotrienes. That explains three things: skin testing and specific IgE are negative because no antibody is involved; any drug that blocks cyclooxygenase-1 sets it off, even ones structurally unrelated to aspirin; and acetaminophen, a weak cyclooxygenase-1 inhibitor at normal doses, is usually tolerated. <div class="ec-src"><b>Source:</b> Laidlaw TM, Boyce JA. Aspirin-Exacerbated Respiratory Disease. New Prime Suspects. N Engl J Med 2016;374(5):484-488.</div></div></div> [[Try this question again->Aspirin-exacerbated respiratory disease - Mech]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Aspirin-exacerbated respiratory disease. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Selective cyclooxygenase-2 inhibitors are generally tolerated in this disease precisely because they spare cyclooxygenase-1, which is the enzyme whose inhibition triggers the reaction. <div class="ec-teach"><div class="th">What the findings point to</div> This is aspirin-exacerbated respiratory disease, the triad of asthma, nasal polyposis, and reactions to cyclooxygenase-1 inhibitors. The mechanism is pharmacologic, not allergic. Blocking cyclooxygenase-1 removes prostaglandin E2's normal brake on mast cells, which shifts arachidonic acid down the 5-lipoxygenase pathway and floods an already overactive receptor population with cysteinyl leukotrienes. That explains three things: skin testing and specific IgE are negative because no antibody is involved; any drug that blocks cyclooxygenase-1 sets it off, even ones structurally unrelated to aspirin; and acetaminophen, a weak cyclooxygenase-1 inhibitor at normal doses, is usually tolerated. <div class="ec-src"><b>Source:</b> Laidlaw TM, Boyce JA. Aspirin-Exacerbated Respiratory Disease. New Prime Suspects. N Engl J Med 2016;374(5):484-488.</div></div></div> [[Try this question again->Aspirin-exacerbated respiratory disease - Mech]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Aspirin-exacerbated respiratory disease. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Delayed hypersensitivity develops over days and manifests as cutaneous or organ-specific inflammation, not as rhinorrhea and bronchospasm within 90 minutes. <div class="ec-teach"><div class="th">What the findings point to</div> This is aspirin-exacerbated respiratory disease, the triad of asthma, nasal polyposis, and reactions to cyclooxygenase-1 inhibitors. The mechanism is pharmacologic, not allergic. Blocking cyclooxygenase-1 removes prostaglandin E2's normal brake on mast cells, which shifts arachidonic acid down the 5-lipoxygenase pathway and floods an already overactive receptor population with cysteinyl leukotrienes. That explains three things: skin testing and specific IgE are negative because no antibody is involved; any drug that blocks cyclooxygenase-1 sets it off, even ones structurally unrelated to aspirin; and acetaminophen, a weak cyclooxygenase-1 inhibitor at normal doses, is usually tolerated. <div class="ec-src"><b>Source:</b> Laidlaw TM, Boyce JA. Aspirin-Exacerbated Respiratory Disease. New Prime Suspects. N Engl J Med 2016;374(5):484-488.</div></div></div> [[Try this question again->Aspirin-exacerbated respiratory disease - Mech]] [[Start another case->Hub]]

<div class="ec-scene">Surgical ward · 06:40</div> A 64-year-old man is on day 6 after elective hip arthroplasty and has received subcutaneous unfractionated heparin since surgery. His platelet count has fallen from 262,000/mm3 on admission to 88,000/mm3. He is afebrile. The right calf is swollen and tender, and ultrasonography confirms an occlusive popliteal vein thrombosis. There is no bleeding. Fibrinogen is 380 mg/dL, prothrombin time is 13 seconds, and the peripheral smear shows no schistocytes. <span class="ec-prompt">Which of the following best explains the thrombosis in this patient?</span> [[ADAMTS13 deficiency with ultra-large von Willebrand factor multimers->Heparin-induced thrombocytopenia mechanism - Mech D1]] [[Antiphospholipid antibodies prolonging phospholipid-dependent clotting assays->Heparin-induced thrombocytopenia mechanism - Mech D2]] [[Consumptive coagulopathy from systemic tissue factor release->Heparin-induced thrombocytopenia mechanism - Mech D3]] [[Direct heparin binding to platelets causing non-immune aggregation->Heparin-induced thrombocytopenia mechanism - Mech D4]] [[IgG against platelet factor 4-heparin complexes->Heparin-induced thrombocytopenia mechanism - Mech correct]] [[Splenic sequestration of platelets from postoperative inflammation->Heparin-induced thrombocytopenia mechanism - Mech D5]]

<span class="ec-case-marker" hidden data-entry="Heparin-induced thrombocytopenia mechanism. Mech"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ IgG against platelet factor 4-heparin complexes</div> Heparin-induced thrombocytopenia is caused by IgG directed at neoepitopes on platelet factor 4 bound to heparin. These immune complexes bind platelet FcgammaRIIa receptors, activating the platelets and triggering release of procoagulant microparticles. At the same time, monocytes and endothelium are activated and generate tissue factor. The result is a paradoxical prothrombotic state despite a falling platelet count, typically appearing 5 to 10 days after exposure with a drop of more than 50% from baseline. Normal fibrinogen, normal prothrombin time, and absent schistocytes separate it from disseminated intravascular coagulation and the thrombotic microangiopathies. <div class="ec-src"><b>Source:</b> Arepally GM. Heparin-induced thrombocytopenia. Blood 2017;129(21):2864-2872.</div></div> [[Start another case->Hub]] [[Restart this case->Heparin-induced thrombocytopenia mechanism - Mech]] [[Next case →->Warfarin skin necrosis - Mech]]

<span class="ec-case-marker" hidden data-entry="Heparin-induced thrombocytopenia mechanism. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This is the mechanism of thrombotic thrombocytopenic purpura, which produces microangiopathic hemolysis with schistocytes on smear and typically neurologic or renal involvement rather than a single large-vein thrombosis. <div class="ec-teach"><div class="th">What the findings point to</div> Heparin-induced thrombocytopenia is caused by IgG directed at neoepitopes on platelet factor 4 bound to heparin. These immune complexes bind platelet FcgammaRIIa receptors, activating the platelets and triggering release of procoagulant microparticles. At the same time, monocytes and endothelium are activated and generate tissue factor. The result is a paradoxical prothrombotic state despite a falling platelet count, typically appearing 5 to 10 days after exposure with a drop of more than 50% from baseline. Normal fibrinogen, normal prothrombin time, and absent schistocytes separate it from disseminated intravascular coagulation and the thrombotic microangiopathies. <div class="ec-src"><b>Source:</b> Arepally GM. Heparin-induced thrombocytopenia. Blood 2017;129(21):2864-2872.</div></div></div> [[Try this question again->Heparin-induced thrombocytopenia mechanism - Mech]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Heparin-induced thrombocytopenia mechanism. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Antiphospholipid syndrome causes thrombosis and can lower platelets, but it does not have a 5 to 10 day temporal relationship to a first heparin exposure and does not resolve with heparin withdrawal. <div class="ec-teach"><div class="th">What the findings point to</div> Heparin-induced thrombocytopenia is caused by IgG directed at neoepitopes on platelet factor 4 bound to heparin. These immune complexes bind platelet FcgammaRIIa receptors, activating the platelets and triggering release of procoagulant microparticles. At the same time, monocytes and endothelium are activated and generate tissue factor. The result is a paradoxical prothrombotic state despite a falling platelet count, typically appearing 5 to 10 days after exposure with a drop of more than 50% from baseline. Normal fibrinogen, normal prothrombin time, and absent schistocytes separate it from disseminated intravascular coagulation and the thrombotic microangiopathies. <div class="ec-src"><b>Source:</b> Arepally GM. Heparin-induced thrombocytopenia. Blood 2017;129(21):2864-2872.</div></div></div> [[Try this question again->Heparin-induced thrombocytopenia mechanism - Mech]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Heparin-induced thrombocytopenia mechanism. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Disseminated intravascular coagulation consumes fibrinogen and prolongs the prothrombin time. Both are normal here, which argues directly against it. <div class="ec-teach"><div class="th">What the findings point to</div> Heparin-induced thrombocytopenia is caused by IgG directed at neoepitopes on platelet factor 4 bound to heparin. These immune complexes bind platelet FcgammaRIIa receptors, activating the platelets and triggering release of procoagulant microparticles. At the same time, monocytes and endothelium are activated and generate tissue factor. The result is a paradoxical prothrombotic state despite a falling platelet count, typically appearing 5 to 10 days after exposure with a drop of more than 50% from baseline. Normal fibrinogen, normal prothrombin time, and absent schistocytes separate it from disseminated intravascular coagulation and the thrombotic microangiopathies. <div class="ec-src"><b>Source:</b> Arepally GM. Heparin-induced thrombocytopenia. Blood 2017;129(21):2864-2872.</div></div></div> [[Try this question again->Heparin-induced thrombocytopenia mechanism - Mech]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Heparin-induced thrombocytopenia mechanism. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Non-immune heparin-associated thrombocytopenia occurs early, is mild, and is not associated with thrombosis. It does not produce a 66% fall in platelet count with an occlusive clot. <div class="ec-teach"><div class="th">What the findings point to</div> Heparin-induced thrombocytopenia is caused by IgG directed at neoepitopes on platelet factor 4 bound to heparin. These immune complexes bind platelet FcgammaRIIa receptors, activating the platelets and triggering release of procoagulant microparticles. At the same time, monocytes and endothelium are activated and generate tissue factor. The result is a paradoxical prothrombotic state despite a falling platelet count, typically appearing 5 to 10 days after exposure with a drop of more than 50% from baseline. Normal fibrinogen, normal prothrombin time, and absent schistocytes separate it from disseminated intravascular coagulation and the thrombotic microangiopathies. <div class="ec-src"><b>Source:</b> Arepally GM. Heparin-induced thrombocytopenia. Blood 2017;129(21):2864-2872.</div></div></div> [[Try this question again->Heparin-induced thrombocytopenia mechanism - Mech]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Heparin-induced thrombocytopenia mechanism. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Sequestration lowers the circulating count without conferring a prothrombotic state and would not explain a new occlusive venous thrombosis in a patient receiving prophylaxis. <div class="ec-teach"><div class="th">What the findings point to</div> Heparin-induced thrombocytopenia is caused by IgG directed at neoepitopes on platelet factor 4 bound to heparin. These immune complexes bind platelet FcgammaRIIa receptors, activating the platelets and triggering release of procoagulant microparticles. At the same time, monocytes and endothelium are activated and generate tissue factor. The result is a paradoxical prothrombotic state despite a falling platelet count, typically appearing 5 to 10 days after exposure with a drop of more than 50% from baseline. Normal fibrinogen, normal prothrombin time, and absent schistocytes separate it from disseminated intravascular coagulation and the thrombotic microangiopathies. <div class="ec-src"><b>Source:</b> Arepally GM. Heparin-induced thrombocytopenia. Blood 2017;129(21):2864-2872.</div></div></div> [[Try this question again->Heparin-induced thrombocytopenia mechanism - Mech]] [[Start another case->Hub]]

<div class="ec-scene">Heart failure clinic · 10:25</div> A 62-year-old man had an anterior myocardial infarction 5 months ago treated with primary percutaneous coronary intervention. He is adherent to a beta blocker, an angiotensin receptor-neprilysin inhibitor, a mineralocorticoid receptor antagonist, an SGLT2 inhibitor, and a statin. He walks on level ground without dyspnea but is short of breath climbing a flight of stairs. Blood pressure is 118/72 mm Hg and pulse is 62/min. Repeat echocardiography today shows a left ventricular ejection fraction of 28%. Electrocardiography shows sinus rhythm with a QRS duration of 96 milliseconds. <span class="ec-prompt">Which of the following interventions will most reduce this patient's risk of death?</span> [[Amiodarone therapy for suppression of ventricular ectopy->Post-MI sudden death risk - Prog D1]] [[Cardiac resynchronization therapy->Post-MI sudden death risk - Prog D2]] [[Digoxin therapy->Post-MI sudden death risk - Prog D3]] [[Implantable cardioverter-defibrillator placement->Post-MI sudden death risk - Prog correct]] [[Referral for cardiac transplantation->Post-MI sudden death risk - Prog D4]] [[Supervised aerobic exercise training->Post-MI sudden death risk - Prog D5]]

<span class="ec-case-marker" hidden data-entry="Post-MI sudden death risk. Prog"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Implantable cardioverter-defibrillator placement</div> He has ischemic cardiomyopathy with an ejection fraction of 28% persisting beyond 40 days after infarction, New York Heart Association class II symptoms, and optimal medical therapy. This is the population in which prophylactic defibrillator implantation reduced all-cause mortality, driven by prevention of sudden arrhythmic death. The 40-day interval matters: implantation immediately after infarction has not shown benefit, because early mortality is dominated by non-arrhythmic mechanisms, which is why reassessment of ejection fraction after a period of guideline-directed therapy is the required step before implantation. <div class="ec-src"><b>Source:</b> Moss AJ, Zareba W, Hall WJ, et al. Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction. N Engl J Med 2002;346(12):877-883.</div></div> [[Start another case->Hub]] [[Restart this case->Post-MI sudden death risk - Prog]] [[Next case →->ACE inhibitor angioedema - Mech]]

<span class="ec-case-marker" hidden data-entry="Post-MI sudden death risk. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Antiarrhythmic drug therapy has not reduced mortality in this setting and carries substantial thyroid, pulmonary, and hepatic toxicity with long-term use. <div class="ec-teach"><div class="th">What the findings point to</div> He has ischemic cardiomyopathy with an ejection fraction of 28% persisting beyond 40 days after infarction, New York Heart Association class II symptoms, and optimal medical therapy. This is the population in which prophylactic defibrillator implantation reduced all-cause mortality, driven by prevention of sudden arrhythmic death. The 40-day interval matters: implantation immediately after infarction has not shown benefit, because early mortality is dominated by non-arrhythmic mechanisms, which is why reassessment of ejection fraction after a period of guideline-directed therapy is the required step before implantation. <div class="ec-src"><b>Source:</b> Moss AJ, Zareba W, Hall WJ, et al. Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction. N Engl J Med 2002;346(12):877-883.</div></div></div> [[Try this question again->Post-MI sudden death risk - Prog]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Post-MI sudden death risk. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Resynchronization benefits patients with a wide QRS, generally 150 milliseconds or greater with left bundle branch block. At 96 milliseconds there is no dyssynchrony to correct. <div class="ec-teach"><div class="th">What the findings point to</div> He has ischemic cardiomyopathy with an ejection fraction of 28% persisting beyond 40 days after infarction, New York Heart Association class II symptoms, and optimal medical therapy. This is the population in which prophylactic defibrillator implantation reduced all-cause mortality, driven by prevention of sudden arrhythmic death. The 40-day interval matters: implantation immediately after infarction has not shown benefit, because early mortality is dominated by non-arrhythmic mechanisms, which is why reassessment of ejection fraction after a period of guideline-directed therapy is the required step before implantation. <div class="ec-src"><b>Source:</b> Moss AJ, Zareba W, Hall WJ, et al. Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction. N Engl J Med 2002;346(12):877-883.</div></div></div> [[Try this question again->Post-MI sudden death risk - Prog]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Post-MI sudden death risk. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Digoxin reduces heart failure hospitalizations but has a neutral effect on mortality and does not address sudden arrhythmic death. <div class="ec-teach"><div class="th">What the findings point to</div> He has ischemic cardiomyopathy with an ejection fraction of 28% persisting beyond 40 days after infarction, New York Heart Association class II symptoms, and optimal medical therapy. This is the population in which prophylactic defibrillator implantation reduced all-cause mortality, driven by prevention of sudden arrhythmic death. The 40-day interval matters: implantation immediately after infarction has not shown benefit, because early mortality is dominated by non-arrhythmic mechanisms, which is why reassessment of ejection fraction after a period of guideline-directed therapy is the required step before implantation. <div class="ec-src"><b>Source:</b> Moss AJ, Zareba W, Hall WJ, et al. Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction. N Engl J Med 2002;346(12):877-883.</div></div></div> [[Try this question again->Post-MI sudden death risk - Prog]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Post-MI sudden death risk. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> He is ambulatory with class II symptoms on full therapy. Transplantation is considered for advanced, refractory disease, which he does not have. <div class="ec-teach"><div class="th">What the findings point to</div> He has ischemic cardiomyopathy with an ejection fraction of 28% persisting beyond 40 days after infarction, New York Heart Association class II symptoms, and optimal medical therapy. This is the population in which prophylactic defibrillator implantation reduced all-cause mortality, driven by prevention of sudden arrhythmic death. The 40-day interval matters: implantation immediately after infarction has not shown benefit, because early mortality is dominated by non-arrhythmic mechanisms, which is why reassessment of ejection fraction after a period of guideline-directed therapy is the required step before implantation. <div class="ec-src"><b>Source:</b> Moss AJ, Zareba W, Hall WJ, et al. Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction. N Engl J Med 2002;346(12):877-883.</div></div></div> [[Try this question again->Post-MI sudden death risk - Prog]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Post-MI sudden death risk. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Exercise training improves functional capacity and quality of life and is appropriate for him, but it has not demonstrated a significant reduction in mortality. <div class="ec-teach"><div class="th">What the findings point to</div> He has ischemic cardiomyopathy with an ejection fraction of 28% persisting beyond 40 days after infarction, New York Heart Association class II symptoms, and optimal medical therapy. This is the population in which prophylactic defibrillator implantation reduced all-cause mortality, driven by prevention of sudden arrhythmic death. The 40-day interval matters: implantation immediately after infarction has not shown benefit, because early mortality is dominated by non-arrhythmic mechanisms, which is why reassessment of ejection fraction after a period of guideline-directed therapy is the required step before implantation. <div class="ec-src"><b>Source:</b> Moss AJ, Zareba W, Hall WJ, et al. Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction. N Engl J Med 2002;346(12):877-883.</div></div></div> [[Try this question again->Post-MI sudden death risk - Prog]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 19:10</div> A 54-year-old man with a 20-year history of heavy alcohol use presents with 3 weeks of abdominal distention and ankle swelling. Temperature is 37.1°C, blood pressure 104/62 mm Hg, pulse 96/min, and respirations 18/min. He has spider angiomata, a shifting dullness, and 2+ pitting edema. Serum albumin is 2.4 g/dL, total bilirubin 2.8 mg/dL, and platelet count 82,000/mm3. Diagnostic paracentesis yields clear yellow fluid with 180 leukocytes/mm3 (12% neutrophils) and an ascitic albumin of 0.9 g/dL. <span class="ec-prompt">Which of the following best characterizes the cause of this patient's ascites?</span> [[Malignant peritoneal seeding->Ascites SAAG - Ix D1]] [[Nephrotic syndrome->Ascites SAAG - Ix D2]] [[Pancreatic duct disruption->Ascites SAAG - Ix D3]] [[Portal hypertension->Ascites SAAG - Ix correct]] [[Spontaneous bacterial peritonitis->Ascites SAAG - Ix D4]] [[Tuberculous peritonitis->Ascites SAAG - Ix D5]]

<span class="ec-case-marker" hidden data-entry="Ascites SAAG. Ix"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Portal hypertension</div> The serum-ascites albumin gradient is serum albumin minus ascitic albumin, here 2.4 minus 0.9, or 1.5 g/dL. A gradient of 1.1 g/dL or greater indicates portal hypertension with approximately 97% accuracy and is the single most useful ascitic fluid calculation. Total ascitic protein then separates cardiac ascites, which is high gradient and protein-rich at 2.5 g/dL or more, from cirrhotic ascites, which is high gradient and protein-poor. The neutrophil count of 22/mm3 is far below the 250/mm3 threshold, so spontaneous bacterial peritonitis is excluded. <div class="ec-src"><b>Source:</b> Runyon BA; AASLD. Introduction to the revised AASLD Practice Guideline management of adult patients with ascites due to cirrhosis 2012. Hepatology 2013;57(4):1651-1653.</div></div> [[Start another case->Hub]] [[Restart this case->Ascites SAAG - Ix]] [[Next case →->Pancreatitis severity - Prog]]

<span class="ec-case-marker" hidden data-entry="Ascites SAAG. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Peritoneal carcinomatosis produces a low gradient, below 1.1 g/dL, because the ascites forms from tumor-studded peritoneal surfaces rather than sinusoidal hypertension. The calculated gradient of 1.5 g/dL argues against it. <div class="ec-teach"><div class="th">What the findings point to</div> The serum-ascites albumin gradient is serum albumin minus ascitic albumin, here 2.4 minus 0.9, or 1.5 g/dL. A gradient of 1.1 g/dL or greater indicates portal hypertension with approximately 97% accuracy and is the single most useful ascitic fluid calculation. Total ascitic protein then separates cardiac ascites, which is high gradient and protein-rich at 2.5 g/dL or more, from cirrhotic ascites, which is high gradient and protein-poor. The neutrophil count of 22/mm3 is far below the 250/mm3 threshold, so spontaneous bacterial peritonitis is excluded. <div class="ec-src"><b>Source:</b> Runyon BA; AASLD. Introduction to the revised AASLD Practice Guideline management of adult patients with ascites due to cirrhosis 2012. Hepatology 2013;57(4):1651-1653.</div></div></div> [[Try this question again->Ascites SAAG - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Ascites SAAG. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Nephrotic ascites is low gradient and would be accompanied by heavy proteinuria and hyperlipidemia. Hypoalbuminemia alone does not produce a high gradient. <div class="ec-teach"><div class="th">What the findings point to</div> The serum-ascites albumin gradient is serum albumin minus ascitic albumin, here 2.4 minus 0.9, or 1.5 g/dL. A gradient of 1.1 g/dL or greater indicates portal hypertension with approximately 97% accuracy and is the single most useful ascitic fluid calculation. Total ascitic protein then separates cardiac ascites, which is high gradient and protein-rich at 2.5 g/dL or more, from cirrhotic ascites, which is high gradient and protein-poor. The neutrophil count of 22/mm3 is far below the 250/mm3 threshold, so spontaneous bacterial peritonitis is excluded. <div class="ec-src"><b>Source:</b> Runyon BA; AASLD. Introduction to the revised AASLD Practice Guideline management of adult patients with ascites due to cirrhosis 2012. Hepatology 2013;57(4):1651-1653.</div></div></div> [[Try this question again->Ascites SAAG - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Ascites SAAG. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Pancreatic ascites is low gradient with a markedly elevated ascitic amylase, typically over 1,000 U/L, and usually follows a documented episode of pancreatitis or ductal injury. <div class="ec-teach"><div class="th">What the findings point to</div> The serum-ascites albumin gradient is serum albumin minus ascitic albumin, here 2.4 minus 0.9, or 1.5 g/dL. A gradient of 1.1 g/dL or greater indicates portal hypertension with approximately 97% accuracy and is the single most useful ascitic fluid calculation. Total ascitic protein then separates cardiac ascites, which is high gradient and protein-rich at 2.5 g/dL or more, from cirrhotic ascites, which is high gradient and protein-poor. The neutrophil count of 22/mm3 is far below the 250/mm3 threshold, so spontaneous bacterial peritonitis is excluded. <div class="ec-src"><b>Source:</b> Runyon BA; AASLD. Introduction to the revised AASLD Practice Guideline management of adult patients with ascites due to cirrhosis 2012. Hepatology 2013;57(4):1651-1653.</div></div></div> [[Try this question again->Ascites SAAG - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Ascites SAAG. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Diagnosis requires an ascitic neutrophil count of 250/mm3 or greater. This fluid contains 22 neutrophils/mm3. <div class="ec-teach"><div class="th">What the findings point to</div> The serum-ascites albumin gradient is serum albumin minus ascitic albumin, here 2.4 minus 0.9, or 1.5 g/dL. A gradient of 1.1 g/dL or greater indicates portal hypertension with approximately 97% accuracy and is the single most useful ascitic fluid calculation. Total ascitic protein then separates cardiac ascites, which is high gradient and protein-rich at 2.5 g/dL or more, from cirrhotic ascites, which is high gradient and protein-poor. The neutrophil count of 22/mm3 is far below the 250/mm3 threshold, so spontaneous bacterial peritonitis is excluded. <div class="ec-src"><b>Source:</b> Runyon BA; AASLD. Introduction to the revised AASLD Practice Guideline management of adult patients with ascites due to cirrhosis 2012. Hepatology 2013;57(4):1651-1653.</div></div></div> [[Try this question again->Ascites SAAG - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Ascites SAAG. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Tuberculous ascites is low gradient with lymphocytic predominance and an elevated adenosine deaminase. The gradient here excludes a peritoneal process as the primary driver. <div class="ec-teach"><div class="th">What the findings point to</div> The serum-ascites albumin gradient is serum albumin minus ascitic albumin, here 2.4 minus 0.9, or 1.5 g/dL. A gradient of 1.1 g/dL or greater indicates portal hypertension with approximately 97% accuracy and is the single most useful ascitic fluid calculation. Total ascitic protein then separates cardiac ascites, which is high gradient and protein-rich at 2.5 g/dL or more, from cirrhotic ascites, which is high gradient and protein-poor. The neutrophil count of 22/mm3 is far below the 250/mm3 threshold, so spontaneous bacterial peritonitis is excluded. <div class="ec-src"><b>Source:</b> Runyon BA; AASLD. Introduction to the revised AASLD Practice Guideline management of adult patients with ascites due to cirrhosis 2012. Hepatology 2013;57(4):1651-1653.</div></div></div> [[Try this question again->Ascites SAAG - Ix]] [[Start another case->Hub]]

<div class="ec-scene">Primary care clinic · 14:05</div> A 58-year-old woman undergoes CT of the abdomen for right upper quadrant pain, and the lung bases show an incidental solid nodule in the right lower lobe measuring 5 mm. She has never smoked, has no occupational exposures, no family history of malignancy, and no prior chest imaging. She is asymptomatic. Dedicated CT of the chest confirms a single solid 5-mm nodule with smooth margins and no other abnormality. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[CT-guided percutaneous biopsy->Incidental pulmonary nodule - Ix D1]] [[No routine follow-up imaging->Incidental pulmonary nodule - Ix correct]] [[Positron emission tomography->Incidental pulmonary nodule - Ix D2]] [[Repeat CT of the chest in 3 months->Incidental pulmonary nodule - Ix D3]] [[Serum carcinoembryonic antigen measurement->Incidental pulmonary nodule - Ix D4]] [[Video-assisted thoracoscopic wedge resection->Incidental pulmonary nodule - Ix D5]]

<span class="ec-case-marker" hidden data-entry="Incidental pulmonary nodule. Ix"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ No routine follow-up imaging</div> For a single solid nodule smaller than 6 mm in a low-risk patient, Fleischner Society criteria call for no routine follow-up, because the estimated risk of malignancy is under 1% and serial imaging delivers radiation and downstream procedures without benefit. Optional CT at 12 months is offered only for nodules with suspicious morphology or in patients at higher risk. Her never-smoker status, smooth margins, and absent family history place her firmly in the low-risk group. <div class="ec-src"><b>Source:</b> MacMahon H, Naidich DP, Goo JM, et al. Guidelines for Management of Incidental Pulmonary Nodules Detected on CT Images: From the Fleischner Society 2017. Radiology 2017;284(1):228-243.</div></div> [[Start another case->Hub]] [[Restart this case->Incidental pulmonary nodule - Ix]] [[Next case →->Pulmonary embolism risk stratification - Prog]]

<span class="ec-case-marker" hidden data-entry="Incidental pulmonary nodule. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A 5-mm nodule is at the lower limit of what can be reliably targeted, and biopsy carries a pneumothorax rate of roughly 15% to 25%. Subjecting a sub-1% pretest probability lesion to biopsy inverts the risk-benefit balance. <div class="ec-teach"><div class="th">What the findings point to</div> For a single solid nodule smaller than 6 mm in a low-risk patient, Fleischner Society criteria call for no routine follow-up, because the estimated risk of malignancy is under 1% and serial imaging delivers radiation and downstream procedures without benefit. Optional CT at 12 months is offered only for nodules with suspicious morphology or in patients at higher risk. Her never-smoker status, smooth margins, and absent family history place her firmly in the low-risk group. <div class="ec-src"><b>Source:</b> MacMahon H, Naidich DP, Goo JM, et al. Guidelines for Management of Incidental Pulmonary Nodules Detected on CT Images: From the Fleischner Society 2017. Radiology 2017;284(1):228-243.</div></div></div> [[Try this question again->Incidental pulmonary nodule - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Incidental pulmonary nodule. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Metabolic imaging has poor sensitivity below 8 mm because of partial volume effects, and a negative study in a nodule this size does not meaningfully change management. <div class="ec-teach"><div class="th">What the findings point to</div> For a single solid nodule smaller than 6 mm in a low-risk patient, Fleischner Society criteria call for no routine follow-up, because the estimated risk of malignancy is under 1% and serial imaging delivers radiation and downstream procedures without benefit. Optional CT at 12 months is offered only for nodules with suspicious morphology or in patients at higher risk. Her never-smoker status, smooth margins, and absent family history place her firmly in the low-risk group. <div class="ec-src"><b>Source:</b> MacMahon H, Naidich DP, Goo JM, et al. Guidelines for Management of Incidental Pulmonary Nodules Detected on CT Images: From the Fleischner Society 2017. Radiology 2017;284(1):228-243.</div></div></div> [[Try this question again->Incidental pulmonary nodule - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Incidental pulmonary nodule. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> 3-month interval imaging is reserved for nodules with intermediate suspicion or for subsolid lesions requiring persistence assessment, not for a smooth solid nodule under 6 mm in a low-risk patient. <div class="ec-teach"><div class="th">What the findings point to</div> For a single solid nodule smaller than 6 mm in a low-risk patient, Fleischner Society criteria call for no routine follow-up, because the estimated risk of malignancy is under 1% and serial imaging delivers radiation and downstream procedures without benefit. Optional CT at 12 months is offered only for nodules with suspicious morphology or in patients at higher risk. Her never-smoker status, smooth margins, and absent family history place her firmly in the low-risk group. <div class="ec-src"><b>Source:</b> MacMahon H, Naidich DP, Goo JM, et al. Guidelines for Management of Incidental Pulmonary Nodules Detected on CT Images: From the Fleischner Society 2017. Radiology 2017;284(1):228-243.</div></div></div> [[Try this question again->Incidental pulmonary nodule - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Incidental pulmonary nodule. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> No serum tumor marker has adequate sensitivity or specificity to characterize a small pulmonary nodule, and an abnormal result would prompt investigation unrelated to the nodule. <div class="ec-teach"><div class="th">What the findings point to</div> For a single solid nodule smaller than 6 mm in a low-risk patient, Fleischner Society criteria call for no routine follow-up, because the estimated risk of malignancy is under 1% and serial imaging delivers radiation and downstream procedures without benefit. Optional CT at 12 months is offered only for nodules with suspicious morphology or in patients at higher risk. Her never-smoker status, smooth margins, and absent family history place her firmly in the low-risk group. <div class="ec-src"><b>Source:</b> MacMahon H, Naidich DP, Goo JM, et al. Guidelines for Management of Incidental Pulmonary Nodules Detected on CT Images: From the Fleischner Society 2017. Radiology 2017;284(1):228-243.</div></div></div> [[Try this question again->Incidental pulmonary nodule - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Incidental pulmonary nodule. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Surgical resection of a sub-6-mm nodule in a never-smoker commits a patient with a very low probability of malignancy to general anesthesia and lung resection. <div class="ec-teach"><div class="th">What the findings point to</div> For a single solid nodule smaller than 6 mm in a low-risk patient, Fleischner Society criteria call for no routine follow-up, because the estimated risk of malignancy is under 1% and serial imaging delivers radiation and downstream procedures without benefit. Optional CT at 12 months is offered only for nodules with suspicious morphology or in patients at higher risk. Her never-smoker status, smooth margins, and absent family history place her firmly in the low-risk group. <div class="ec-src"><b>Source:</b> MacMahon H, Naidich DP, Goo JM, et al. Guidelines for Management of Incidental Pulmonary Nodules Detected on CT Images: From the Fleischner Society 2017. Radiology 2017;284(1):228-243.</div></div></div> [[Try this question again->Incidental pulmonary nodule - Ix]] [[Start another case->Hub]]

<div class="ec-scene">Primary care clinic · 10:40</div> A 63-year-old man is found to have 8 red blood cells per high-power field on microscopy of a urine specimen obtained during a preoperative evaluation. He is asymptomatic. He smoked one pack daily for 30 years and quit last year. He takes no anticoagulants and has no history of stones, trauma, catheterization, or recent vigorous exercise. Blood pressure is 128/78 mm Hg. Serum creatinine is 0.9 mg/dL. Urinalysis shows no proteinuria, no dysmorphic erythrocytes, and no casts. Repeat microscopy 2 weeks later confirms 7 red blood cells per high-power field, and urine culture is negative. <span class="ec-prompt">Which of the following is the most appropriate next step in evaluation?</span> [[Cystoscopy and CT urography->Microscopic hematuria - Ix correct]] [[Empiric antibiotic therapy for presumed urinary tract infection->Microscopic hematuria - Ix D1]] [[Reassurance and repeat urinalysis in 12 months->Microscopic hematuria - Ix D2]] [[Referral for renal biopsy->Microscopic hematuria - Ix D3]] [[Renal ultrasonography alone->Microscopic hematuria - Ix D4]] [[Urine cytology->Microscopic hematuria - Ix D5]]

<span class="ec-case-marker" hidden data-entry="Microscopic hematuria. Ix"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Cystoscopy and CT urography</div> Confirmed microhematuria without an identified benign cause, in a 63-year-old man with a 30 pack-year history, places him in the high-risk category. High-risk patients undergo cystoscopy together with upper tract imaging by CT urography. The absence of proteinuria, dysmorphic erythrocytes, and casts argues against a glomerular source and directs the workup toward the urothelium, where his smoking history is the dominant risk factor for bladder cancer. <div class="ec-src"><b>Source:</b> Barocas DA, Boorjian SA, Alvarez RD, et al. Microhematuria: AUA/SUFU Guideline. J Urol 2020;204(4):778-786.</div></div> [[Start another case->Hub]] [[Restart this case->Microscopic hematuria - Ix]] [[Next case →->DKA - Ix]]

<span class="ec-case-marker" hidden data-entry="Microscopic hematuria. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> He is asymptomatic and the urine culture is negative. Treating a negative culture delays the evaluation and exposes him to antibiotics without indication. <div class="ec-teach"><div class="th">What the findings point to</div> Confirmed microhematuria without an identified benign cause, in a 63-year-old man with a 30 pack-year history, places him in the high-risk category. High-risk patients undergo cystoscopy together with upper tract imaging by CT urography. The absence of proteinuria, dysmorphic erythrocytes, and casts argues against a glomerular source and directs the workup toward the urothelium, where his smoking history is the dominant risk factor for bladder cancer. <div class="ec-src"><b>Source:</b> Barocas DA, Boorjian SA, Alvarez RD, et al. Microhematuria: AUA/SUFU Guideline. J Urol 2020;204(4):778-786.</div></div></div> [[Try this question again->Microscopic hematuria - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Microscopic hematuria. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Deferred surveillance is appropriate only for low-risk patients, defined by younger age and minimal smoking exposure. A 63-year-old former smoker with 30 pack-years does not qualify. <div class="ec-teach"><div class="th">What the findings point to</div> Confirmed microhematuria without an identified benign cause, in a 63-year-old man with a 30 pack-year history, places him in the high-risk category. High-risk patients undergo cystoscopy together with upper tract imaging by CT urography. The absence of proteinuria, dysmorphic erythrocytes, and casts argues against a glomerular source and directs the workup toward the urothelium, where his smoking history is the dominant risk factor for bladder cancer. <div class="ec-src"><b>Source:</b> Barocas DA, Boorjian SA, Alvarez RD, et al. Microhematuria: AUA/SUFU Guideline. J Urol 2020;204(4):778-786.</div></div></div> [[Try this question again->Microscopic hematuria - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Microscopic hematuria. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Biopsy is indicated when findings suggest glomerular disease: proteinuria, dysmorphic erythrocytes, red cell casts, or a rising creatinine. None is present. <div class="ec-teach"><div class="th">What the findings point to</div> Confirmed microhematuria without an identified benign cause, in a 63-year-old man with a 30 pack-year history, places him in the high-risk category. High-risk patients undergo cystoscopy together with upper tract imaging by CT urography. The absence of proteinuria, dysmorphic erythrocytes, and casts argues against a glomerular source and directs the workup toward the urothelium, where his smoking history is the dominant risk factor for bladder cancer. <div class="ec-src"><b>Source:</b> Barocas DA, Boorjian SA, Alvarez RD, et al. Microhematuria: AUA/SUFU Guideline. J Urol 2020;204(4):778-786.</div></div></div> [[Try this question again->Microscopic hematuria - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Microscopic hematuria. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Ultrasonography is the imaging option for intermediate-risk patients and misses small upper tract urothelial lesions. It also does not evaluate the bladder mucosa, which cystoscopy is required for. <div class="ec-teach"><div class="th">What the findings point to</div> Confirmed microhematuria without an identified benign cause, in a 63-year-old man with a 30 pack-year history, places him in the high-risk category. High-risk patients undergo cystoscopy together with upper tract imaging by CT urography. The absence of proteinuria, dysmorphic erythrocytes, and casts argues against a glomerular source and directs the workup toward the urothelium, where his smoking history is the dominant risk factor for bladder cancer. <div class="ec-src"><b>Source:</b> Barocas DA, Boorjian SA, Alvarez RD, et al. Microhematuria: AUA/SUFU Guideline. J Urol 2020;204(4):778-786.</div></div></div> [[Try this question again->Microscopic hematuria - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Microscopic hematuria. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Cytology is not recommended as part of the initial evaluation of microhematuria because its sensitivity for low-grade disease is poor. It is reserved for persistent hematuria after a negative workup or for irritative symptoms. <div class="ec-teach"><div class="th">What the findings point to</div> Confirmed microhematuria without an identified benign cause, in a 63-year-old man with a 30 pack-year history, places him in the high-risk category. High-risk patients undergo cystoscopy together with upper tract imaging by CT urography. The absence of proteinuria, dysmorphic erythrocytes, and casts argues against a glomerular source and directs the workup toward the urothelium, where his smoking history is the dominant risk factor for bladder cancer. <div class="ec-src"><b>Source:</b> Barocas DA, Boorjian SA, Alvarez RD, et al. Microhematuria: AUA/SUFU Guideline. J Urol 2020;204(4):778-786.</div></div></div> [[Try this question again->Microscopic hematuria - Ix]] [[Start another case->Hub]]

<div class="ec-scene">Endocrinology clinic · 09:30</div> A 44-year-old woman noticed a lump in her neck 3 weeks ago. She has no dysphagia, hoarseness, or neck irradiation, and no family history of thyroid cancer. Examination shows a firm, mobile 2.5-cm nodule in the right thyroid lobe and no palpable cervical lymphadenopathy. Ultrasonography shows a solid hypoechoic nodule measuring 2.4 cm with smooth margins and no microcalcifications. Serum thyroid-stimulating hormone concentration has not yet been obtained. <span class="ec-prompt">Which of the following is the most appropriate next step in evaluation?</span> [[Fine-needle aspiration biopsy of the nodule->Thyroid nodule workup - Ix D1]] [[Measurement of serum calcitonin->Thyroid nodule workup - Ix D2]] [[Measurement of serum thyroglobulin->Thyroid nodule workup - Ix D3]] [[Measurement of serum thyroid-stimulating hormone->Thyroid nodule workup - Ix correct]] [[Radionuclide thyroid scintigraphy->Thyroid nodule workup - Ix D4]] [[Surgical excision of the right thyroid lobe->Thyroid nodule workup - Ix D5]]

<span class="ec-case-marker" hidden data-entry="Thyroid nodule workup. Ix"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Measurement of serum thyroid-stimulating hormone</div> Thyroid-stimulating hormone is the required first test for any thyroid nodule, because the result determines the entire subsequent pathway. If it is suppressed, a radionuclide scan is performed and an autonomously functioning nodule requires no cytology, since hyperfunctioning nodules are almost never malignant. If it is normal or elevated, ultrasound risk stratification proceeds and fine-needle aspiration is decided by sonographic pattern and size. Ordering aspiration before the thyroid-stimulating hormone risks biopsying a nodule that never needed it. <div class="ec-src"><b>Source:</b> Haugen BR, Alexander EK, Bible KC, et al. 2015 American Thyroid Association Management Guidelines for Adult Patients with Thyroid Nodules and Differentiated Thyroid Cancer. Thyroid 2016;26(1):1-133.</div></div> [[Start another case->Hub]] [[Restart this case->Thyroid nodule workup - Ix]] [[Next case →->Diabetes screening - Prevention]]

<span class="ec-case-marker" hidden data-entry="Thyroid nodule workup. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Aspiration is very likely to be needed, but only after the thyroid-stimulating hormone is known. A suppressed value redirects to scintigraphy and can spare the patient a biopsy altogether. <div class="ec-teach"><div class="th">What the findings point to</div> Thyroid-stimulating hormone is the required first test for any thyroid nodule, because the result determines the entire subsequent pathway. If it is suppressed, a radionuclide scan is performed and an autonomously functioning nodule requires no cytology, since hyperfunctioning nodules are almost never malignant. If it is normal or elevated, ultrasound risk stratification proceeds and fine-needle aspiration is decided by sonographic pattern and size. Ordering aspiration before the thyroid-stimulating hormone risks biopsying a nodule that never needed it. <div class="ec-src"><b>Source:</b> Haugen BR, Alexander EK, Bible KC, et al. 2015 American Thyroid Association Management Guidelines for Adult Patients with Thyroid Nodules and Differentiated Thyroid Cancer. Thyroid 2016;26(1):1-133.</div></div></div> [[Try this question again->Thyroid nodule workup - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Thyroid nodule workup. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Routine calcitonin screening is not recommended in the United States. It is reserved for suspected medullary carcinoma or multiple endocrine neoplasia syndromes. <div class="ec-teach"><div class="th">What the findings point to</div> Thyroid-stimulating hormone is the required first test for any thyroid nodule, because the result determines the entire subsequent pathway. If it is suppressed, a radionuclide scan is performed and an autonomously functioning nodule requires no cytology, since hyperfunctioning nodules are almost never malignant. If it is normal or elevated, ultrasound risk stratification proceeds and fine-needle aspiration is decided by sonographic pattern and size. Ordering aspiration before the thyroid-stimulating hormone risks biopsying a nodule that never needed it. <div class="ec-src"><b>Source:</b> Haugen BR, Alexander EK, Bible KC, et al. 2015 American Thyroid Association Management Guidelines for Adult Patients with Thyroid Nodules and Differentiated Thyroid Cancer. Thyroid 2016;26(1):1-133.</div></div></div> [[Try this question again->Thyroid nodule workup - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Thyroid nodule workup. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Thyroglobulin is a postoperative surveillance marker for differentiated thyroid cancer. It has no role in the initial evaluation of a nodule because it is elevated in many benign conditions. <div class="ec-teach"><div class="th">What the findings point to</div> Thyroid-stimulating hormone is the required first test for any thyroid nodule, because the result determines the entire subsequent pathway. If it is suppressed, a radionuclide scan is performed and an autonomously functioning nodule requires no cytology, since hyperfunctioning nodules are almost never malignant. If it is normal or elevated, ultrasound risk stratification proceeds and fine-needle aspiration is decided by sonographic pattern and size. Ordering aspiration before the thyroid-stimulating hormone risks biopsying a nodule that never needed it. <div class="ec-src"><b>Source:</b> Haugen BR, Alexander EK, Bible KC, et al. 2015 American Thyroid Association Management Guidelines for Adult Patients with Thyroid Nodules and Differentiated Thyroid Cancer. Thyroid 2016;26(1):1-133.</div></div></div> [[Try this question again->Thyroid nodule workup - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Thyroid nodule workup. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Scintigraphy is performed only when the thyroid-stimulating hormone is below the reference range. Obtaining it first exposes the patient to radioisotope for a question that a serum test answers. <div class="ec-teach"><div class="th">What the findings point to</div> Thyroid-stimulating hormone is the required first test for any thyroid nodule, because the result determines the entire subsequent pathway. If it is suppressed, a radionuclide scan is performed and an autonomously functioning nodule requires no cytology, since hyperfunctioning nodules are almost never malignant. If it is normal or elevated, ultrasound risk stratification proceeds and fine-needle aspiration is decided by sonographic pattern and size. Ordering aspiration before the thyroid-stimulating hormone risks biopsying a nodule that never needed it. <div class="ec-src"><b>Source:</b> Haugen BR, Alexander EK, Bible KC, et al. 2015 American Thyroid Association Management Guidelines for Adult Patients with Thyroid Nodules and Differentiated Thyroid Cancer. Thyroid 2016;26(1):1-133.</div></div></div> [[Try this question again->Thyroid nodule workup - Ix]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Thyroid nodule workup. Ix"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Lobectomy before any biochemical or cytologic assessment commits a patient with a probably benign nodule to operative risk and possible lifelong hormone replacement. <div class="ec-teach"><div class="th">What the findings point to</div> Thyroid-stimulating hormone is the required first test for any thyroid nodule, because the result determines the entire subsequent pathway. If it is suppressed, a radionuclide scan is performed and an autonomously functioning nodule requires no cytology, since hyperfunctioning nodules are almost never malignant. If it is normal or elevated, ultrasound risk stratification proceeds and fine-needle aspiration is decided by sonographic pattern and size. Ordering aspiration before the thyroid-stimulating hormone risks biopsying a nodule that never needed it. <div class="ec-src"><b>Source:</b> Haugen BR, Alexander EK, Bible KC, et al. 2015 American Thyroid Association Management Guidelines for Adult Patients with Thyroid Nodules and Differentiated Thyroid Cancer. Thyroid 2016;26(1):1-133.</div></div></div> [[Try this question again->Thyroid nodule workup - Ix]] [[Start another case->Hub]]

<div class="ec-scene">Intensive care unit · 04:15</div> A 47-year-old man was admitted 3 days ago with gallstone pancreatitis. He initially required 4 L of intravenous fluid. On hospital day 3 he is on 60% oxygen by face mask with a PaO2 of 62 mm Hg, blood pressure of 88/50 mm Hg despite fluid resuscitation, and a serum creatinine that has risen from 0.9 to 2.6 mg/dL. These abnormalities have persisted for 52 hours. CT of the abdomen shows peripancreatic fluid without necrosis. Serum lipase is 240 U/L, down from a peak of 3,100 U/L. <span class="ec-prompt">Which of the following findings best predicts this patient's mortality risk?</span> [[Duration of multiorgan failure->Pancreatitis severity - Prog correct]] [[Extent of peripancreatic fluid on CT->Pancreatitis severity - Prog D1]] [[Gallstone rather than alcoholic etiology->Pancreatitis severity - Prog D2]] [[Peak serum lipase concentration->Pancreatitis severity - Prog D3]] [[Serum creatinine value on admission->Pancreatitis severity - Prog D4]] [[Volume of fluid administered in the first 24 hours->Pancreatitis severity - Prog D5]]

<span class="ec-case-marker" hidden data-entry="Pancreatitis severity. Prog"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Duration of multiorgan failure</div> Under the revised Atlanta classification, severity is defined by organ failure and its duration, not by imaging or enzyme levels. Organ failure lasting more than 48 hours defines severe acute pancreatitis and carries mortality in the range of 30% or higher, whereas transient failure resolving within 48 hours defines moderately severe disease with a far better outlook. He has respiratory, cardiovascular, and renal failure persisting past 48 hours, which is the finding that drives his prognosis. <div class="ec-src"><b>Source:</b> Banks PA, Bollen TL, Dervenis C, et al. Classification of acute pancreatitis 2012: revision of the Atlanta classification and definitions by international consensus. Gut 2013;62(1):102-111.</div></div> [[Start another case->Hub]] [[Restart this case->Pancreatitis severity - Prog]] [[Next case →->Cirrhosis surgical risk - Prog]]

<span class="ec-case-marker" hidden data-entry="Pancreatitis severity. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Morphologic findings define local complications and guide drainage decisions but correlate poorly with death. CT severity indices add little to organ failure assessment in the first week. <div class="ec-teach"><div class="th">What the findings point to</div> Under the revised Atlanta classification, severity is defined by organ failure and its duration, not by imaging or enzyme levels. Organ failure lasting more than 48 hours defines severe acute pancreatitis and carries mortality in the range of 30% or higher, whereas transient failure resolving within 48 hours defines moderately severe disease with a far better outlook. He has respiratory, cardiovascular, and renal failure persisting past 48 hours, which is the finding that drives his prognosis. <div class="ec-src"><b>Source:</b> Banks PA, Bollen TL, Dervenis C, et al. Classification of acute pancreatitis 2012: revision of the Atlanta classification and definitions by international consensus. Gut 2013;62(1):102-111.</div></div></div> [[Try this question again->Pancreatitis severity - Prog]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Pancreatitis severity. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Etiology determines definitive management, including cholecystectomy before discharge, but it is not an independent predictor of mortality once organ failure is established. <div class="ec-teach"><div class="th">What the findings point to</div> Under the revised Atlanta classification, severity is defined by organ failure and its duration, not by imaging or enzyme levels. Organ failure lasting more than 48 hours defines severe acute pancreatitis and carries mortality in the range of 30% or higher, whereas transient failure resolving within 48 hours defines moderately severe disease with a far better outlook. He has respiratory, cardiovascular, and renal failure persisting past 48 hours, which is the finding that drives his prognosis. <div class="ec-src"><b>Source:</b> Banks PA, Bollen TL, Dervenis C, et al. Classification of acute pancreatitis 2012: revision of the Atlanta classification and definitions by international consensus. Gut 2013;62(1):102-111.</div></div></div> [[Try this question again->Pancreatitis severity - Prog]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Pancreatitis severity. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Enzyme levels establish the diagnosis and bear no relationship to severity or outcome. His lipase is falling while he deteriorates, which illustrates the point. <div class="ec-teach"><div class="th">What the findings point to</div> Under the revised Atlanta classification, severity is defined by organ failure and its duration, not by imaging or enzyme levels. Organ failure lasting more than 48 hours defines severe acute pancreatitis and carries mortality in the range of 30% or higher, whereas transient failure resolving within 48 hours defines moderately severe disease with a far better outlook. He has respiratory, cardiovascular, and renal failure persisting past 48 hours, which is the finding that drives his prognosis. <div class="ec-src"><b>Source:</b> Banks PA, Bollen TL, Dervenis C, et al. Classification of acute pancreatitis 2012: revision of the Atlanta classification and definitions by international consensus. Gut 2013;62(1):102-111.</div></div></div> [[Try this question again->Pancreatitis severity - Prog]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Pancreatitis severity. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A single early creatinine reflects volume status more than intrinsic injury. It is the persistence of renal failure through 48 hours of resuscitation that carries prognostic weight. <div class="ec-teach"><div class="th">What the findings point to</div> Under the revised Atlanta classification, severity is defined by organ failure and its duration, not by imaging or enzyme levels. Organ failure lasting more than 48 hours defines severe acute pancreatitis and carries mortality in the range of 30% or higher, whereas transient failure resolving within 48 hours defines moderately severe disease with a far better outlook. He has respiratory, cardiovascular, and renal failure persisting past 48 hours, which is the finding that drives his prognosis. <div class="ec-src"><b>Source:</b> Banks PA, Bollen TL, Dervenis C, et al. Classification of acute pancreatitis 2012: revision of the Atlanta classification and definitions by international consensus. Gut 2013;62(1):102-111.</div></div></div> [[Try this question again->Pancreatitis severity - Prog]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Pancreatitis severity. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Resuscitation volume is a treatment variable, and both under-resuscitation and aggressive overfilling cause harm. It is not a validated prognostic marker. <div class="ec-teach"><div class="th">What the findings point to</div> Under the revised Atlanta classification, severity is defined by organ failure and its duration, not by imaging or enzyme levels. Organ failure lasting more than 48 hours defines severe acute pancreatitis and carries mortality in the range of 30% or higher, whereas transient failure resolving within 48 hours defines moderately severe disease with a far better outlook. He has respiratory, cardiovascular, and renal failure persisting past 48 hours, which is the finding that drives his prognosis. <div class="ec-src"><b>Source:</b> Banks PA, Bollen TL, Dervenis C, et al. Classification of acute pancreatitis 2012: revision of the Atlanta classification and definitions by international consensus. Gut 2013;62(1):102-111.</div></div></div> [[Try this question again->Pancreatitis severity - Prog]] [[Start another case->Hub]]

<div class="ec-scene">Preoperative clinic · 11:50</div> A 61-year-old woman with cirrhosis from chronic hepatitis C is referred before elective open cholecystectomy for recurrent biliary colic. She has no ascites, no encephalopathy, and no variceal bleeding. Total bilirubin is 2.9 mg/dL, serum creatinine 1.6 mg/dL, international normalized ratio 1.9, serum sodium 133 mEq/L, and serum albumin 3.1 g/dL. Esophagogastroduodenoscopy 6 months ago showed small varices. She walks a mile daily without limitation. <span class="ec-prompt">Which of the following best estimates this patient's perioperative mortality risk?</span> [[Duke Activity Status Index->Cirrhosis surgical risk - Prog D1]] [[Model for End-Stage Liver Disease score->Cirrhosis surgical risk - Prog correct]] [[Presence of esophageal varices on endoscopy->Cirrhosis surgical risk - Prog D2]] [[Revised Cardiac Risk Index->Cirrhosis surgical risk - Prog D3]] [[Serum albumin concentration->Cirrhosis surgical risk - Prog D4]] [[Serum sodium concentration->Cirrhosis surgical risk - Prog D5]]

<span class="ec-case-marker" hidden data-entry="Cirrhosis surgical risk. Prog"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Model for End-Stage Liver Disease score</div> The Model for End-Stage Liver Disease score, calculated from bilirubin, creatinine, and international normalized ratio, is the best-validated predictor of mortality after surgery in cirrhosis and outperforms subjective staging. In the Mayo model, each 1-point rise in MELD is associated with roughly a 14% relative increase in postoperative mortality, so risk climbs steeply rather than by a flat 1% per point: 30-day mortality is about 5.5% below a MELD of 8, climbs into the 25-45% range through the high teens, and approaches 90% once the score exceeds 25. Because it uses only objective laboratory values, it avoids the interobserver variability introduced by grading ascites and encephalopathy. <div class="ec-src"><b>Source:</b> Teh SH, Nagorney DM, Stevens SR, et al. Risk factors for mortality after surgery in patients with cirrhosis. Gastroenterology 2007;132(4):1261-1269.</div></div> [[Start another case->Hub]] [[Restart this case->Cirrhosis surgical risk - Prog]] [[Next case →->Acute kidney injury - Ix]]

<span class="ec-case-marker" hidden data-entry="Cirrhosis surgical risk. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Functional capacity indices predict cardiac events in noncardiac surgery. They do not capture hepatic synthetic failure, which is the dominant risk in cirrhosis. <div class="ec-teach"><div class="th">What the findings point to</div> The Model for End-Stage Liver Disease score, calculated from bilirubin, creatinine, and international normalized ratio, is the best-validated predictor of mortality after surgery in cirrhosis and outperforms subjective staging. In the Mayo model, each 1-point rise in MELD is associated with roughly a 14% relative increase in postoperative mortality, so risk climbs steeply rather than by a flat 1% per point: 30-day mortality is about 5.5% below a MELD of 8, climbs into the 25-45% range through the high teens, and approaches 90% once the score exceeds 25. Because it uses only objective laboratory values, it avoids the interobserver variability introduced by grading ascites and encephalopathy. <div class="ec-src"><b>Source:</b> Teh SH, Nagorney DM, Stevens SR, et al. Risk factors for mortality after surgery in patients with cirrhosis. Gastroenterology 2007;132(4):1261-1269.</div></div></div> [[Try this question again->Cirrhosis surgical risk - Prog]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Cirrhosis surgical risk. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Varices indicate portal hypertension and guide bleeding prophylaxis, but their presence alone is not a graded predictor of perioperative death. <div class="ec-teach"><div class="th">What the findings point to</div> The Model for End-Stage Liver Disease score, calculated from bilirubin, creatinine, and international normalized ratio, is the best-validated predictor of mortality after surgery in cirrhosis and outperforms subjective staging. In the Mayo model, each 1-point rise in MELD is associated with roughly a 14% relative increase in postoperative mortality, so risk climbs steeply rather than by a flat 1% per point: 30-day mortality is about 5.5% below a MELD of 8, climbs into the 25-45% range through the high teens, and approaches 90% once the score exceeds 25. Because it uses only objective laboratory values, it avoids the interobserver variability introduced by grading ascites and encephalopathy. <div class="ec-src"><b>Source:</b> Teh SH, Nagorney DM, Stevens SR, et al. Risk factors for mortality after surgery in patients with cirrhosis. Gastroenterology 2007;132(4):1261-1269.</div></div></div> [[Try this question again->Cirrhosis surgical risk - Prog]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Cirrhosis surgical risk. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This index estimates perioperative cardiac complications and does not account for coagulopathy, hyperbilirubinemia, or renal dysfunction from liver disease. <div class="ec-teach"><div class="th">What the findings point to</div> The Model for End-Stage Liver Disease score, calculated from bilirubin, creatinine, and international normalized ratio, is the best-validated predictor of mortality after surgery in cirrhosis and outperforms subjective staging. In the Mayo model, each 1-point rise in MELD is associated with roughly a 14% relative increase in postoperative mortality, so risk climbs steeply rather than by a flat 1% per point: 30-day mortality is about 5.5% below a MELD of 8, climbs into the 25-45% range through the high teens, and approaches 90% once the score exceeds 25. Because it uses only objective laboratory values, it avoids the interobserver variability introduced by grading ascites and encephalopathy. <div class="ec-src"><b>Source:</b> Teh SH, Nagorney DM, Stevens SR, et al. Risk factors for mortality after surgery in patients with cirrhosis. Gastroenterology 2007;132(4):1261-1269.</div></div></div> [[Try this question again->Cirrhosis surgical risk - Prog]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Cirrhosis surgical risk. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Albumin contributes to older staging systems and is a general marker of nutrition and inflammation, but as a single value it discriminates poorly compared with a composite score. <div class="ec-teach"><div class="th">What the findings point to</div> The Model for End-Stage Liver Disease score, calculated from bilirubin, creatinine, and international normalized ratio, is the best-validated predictor of mortality after surgery in cirrhosis and outperforms subjective staging. In the Mayo model, each 1-point rise in MELD is associated with roughly a 14% relative increase in postoperative mortality, so risk climbs steeply rather than by a flat 1% per point: 30-day mortality is about 5.5% below a MELD of 8, climbs into the 25-45% range through the high teens, and approaches 90% once the score exceeds 25. Because it uses only objective laboratory values, it avoids the interobserver variability introduced by grading ascites and encephalopathy. <div class="ec-src"><b>Source:</b> Teh SH, Nagorney DM, Stevens SR, et al. Risk factors for mortality after surgery in patients with cirrhosis. Gastroenterology 2007;132(4):1261-1269.</div></div></div> [[Try this question again->Cirrhosis surgical risk - Prog]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Cirrhosis surgical risk. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Hyponatremia reflects severity of portal hypertension and refines transplant listing, but by itself it is a weak predictor of surgical mortality. <div class="ec-teach"><div class="th">What the findings point to</div> The Model for End-Stage Liver Disease score, calculated from bilirubin, creatinine, and international normalized ratio, is the best-validated predictor of mortality after surgery in cirrhosis and outperforms subjective staging. In the Mayo model, each 1-point rise in MELD is associated with roughly a 14% relative increase in postoperative mortality, so risk climbs steeply rather than by a flat 1% per point: 30-day mortality is about 5.5% below a MELD of 8, climbs into the 25-45% range through the high teens, and approaches 90% once the score exceeds 25. Because it uses only objective laboratory values, it avoids the interobserver variability introduced by grading ascites and encephalopathy. <div class="ec-src"><b>Source:</b> Teh SH, Nagorney DM, Stevens SR, et al. Risk factors for mortality after surgery in patients with cirrhosis. Gastroenterology 2007;132(4):1261-1269.</div></div></div> [[Try this question again->Cirrhosis surgical risk - Prog]] [[Start another case->Hub]]

<div class="ec-scene">Intensive care unit · 23:40</div> A 58-year-old man had an out-of-hospital cardiac arrest with 18 minutes of downtime before return of spontaneous circulation. He was cooled to a target temperature of 34°C and rewarmed 24 hours ago. He received propofol and fentanyl during cooling, both discontinued 12 hours ago, and a single dose of rocuronium 20 hours ago. Now, 60 hours after return of circulation, he does not open his eyes, has absent corneal reflexes, and shows extensor posturing to noxious stimulation. Temperature is 36.8°C, blood pressure 118/70 mm Hg. His family asks whether he will recover. <span class="ec-prompt">Which of the following is the most appropriate response regarding prognosis?</span> [[A brain death evaluation should be performed now->Post-arrest neuroprognostication - Prog D5]] [[Absent corneal reflexes at this time indicate irreversible injury->Post-arrest neuroprognostication - Prog D1]] [[Defer prognostication for at least 72 hours->Post-arrest neuroprognostication - Prog correct]] [[Extensor posturing establishes a poor neurologic outcome->Post-arrest neuroprognostication - Prog D2]] [[Prolonged downtime before return of circulation predicts nonrecovery->Post-arrest neuroprognostication - Prog D3]] [[Withdrawal of life-sustaining therapy should be discussed today->Post-arrest neuroprognostication - Prog D4]]

<span class="ec-case-marker" hidden data-entry="Post-arrest neuroprognostication. Prog"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Defer prognostication for at least 72 hours</div> Neurologic examination performed too early is unreliable, because sedatives, analgesics, and neuromuscular blockade have prolonged clearance after hypothermia and can mimic devastating injury. Guidelines call for multimodal assessment no sooner than 72 hours after return to normothermia, in a patient free of confounders, combining examination with somatosensory evoked potentials, electroencephalography, neuron-specific enolase, and imaging. He is 60 hours out with recently discontinued sedation and a paralytic within the past 24 hours, so no reliable statement can be made now. <div class="ec-src"><b>Source:</b> Nolan JP, Sandroni C, Böttiger BW, et al. European Resuscitation Council and European Society of Intensive Care Medicine Guidelines 2021: Post-resuscitation Care. Resuscitation 2021;161:220-269.</div></div> [[Start another case->Hub]] [[Restart this case->Post-arrest neuroprognostication - Prog]] [[Next case →->Suicide risk - Opening]]

<span class="ec-case-marker" hidden data-entry="Post-arrest neuroprognostication. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Corneal reflexes are among the findings most easily suppressed by residual sedation and by hypothermia itself. Their absence at 36 hours has an unacceptably high false-positive rate for poor outcome. <div class="ec-teach"><div class="th">What the findings point to</div> Neurologic examination performed too early is unreliable, because sedatives, analgesics, and neuromuscular blockade have prolonged clearance after hypothermia and can mimic devastating injury. Guidelines call for multimodal assessment no sooner than 72 hours after return to normothermia, in a patient free of confounders, combining examination with somatosensory evoked potentials, electroencephalography, neuron-specific enolase, and imaging. He is 60 hours out with recently discontinued sedation and a paralytic within the past 24 hours, so no reliable statement can be made now. <div class="ec-src"><b>Source:</b> Nolan JP, Sandroni C, Böttiger BW, et al. European Resuscitation Council and European Society of Intensive Care Medicine Guidelines 2021: Post-resuscitation Care. Resuscitation 2021;161:220-269.</div></div></div> [[Try this question again->Post-arrest neuroprognostication - Prog]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Post-arrest neuroprognostication. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Motor response is the least reliable component of the post-arrest examination and is explicitly not recommended as a standalone predictor at any time point. <div class="ec-teach"><div class="th">What the findings point to</div> Neurologic examination performed too early is unreliable, because sedatives, analgesics, and neuromuscular blockade have prolonged clearance after hypothermia and can mimic devastating injury. Guidelines call for multimodal assessment no sooner than 72 hours after return to normothermia, in a patient free of confounders, combining examination with somatosensory evoked potentials, electroencephalography, neuron-specific enolase, and imaging. He is 60 hours out with recently discontinued sedation and a paralytic within the past 24 hours, so no reliable statement can be made now. <div class="ec-src"><b>Source:</b> Nolan JP, Sandroni C, Böttiger BW, et al. European Resuscitation Council and European Society of Intensive Care Medicine Guidelines 2021: Post-resuscitation Care. Resuscitation 2021;161:220-269.</div></div></div> [[Try this question again->Post-arrest neuroprognostication - Prog]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Post-arrest neuroprognostication. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Downtime correlates with outcome across populations but has poor discrimination for the individual patient, and good recoveries occur after prolonged arrest. <div class="ec-teach"><div class="th">What the findings point to</div> Neurologic examination performed too early is unreliable, because sedatives, analgesics, and neuromuscular blockade have prolonged clearance after hypothermia and can mimic devastating injury. Guidelines call for multimodal assessment no sooner than 72 hours after return to normothermia, in a patient free of confounders, combining examination with somatosensory evoked potentials, electroencephalography, neuron-specific enolase, and imaging. He is 60 hours out with recently discontinued sedation and a paralytic within the past 24 hours, so no reliable statement can be made now. <div class="ec-src"><b>Source:</b> Nolan JP, Sandroni C, Böttiger BW, et al. European Resuscitation Council and European Society of Intensive Care Medicine Guidelines 2021: Post-resuscitation Care. Resuscitation 2021;161:220-269.</div></div></div> [[Try this question again->Post-arrest neuroprognostication - Prog]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Post-arrest neuroprognostication. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Raising withdrawal while the examination is confounded risks a self-fulfilling prophecy, the principal bias affecting outcome studies in this population. <div class="ec-teach"><div class="th">What the findings point to</div> Neurologic examination performed too early is unreliable, because sedatives, analgesics, and neuromuscular blockade have prolonged clearance after hypothermia and can mimic devastating injury. Guidelines call for multimodal assessment no sooner than 72 hours after return to normothermia, in a patient free of confounders, combining examination with somatosensory evoked potentials, electroencephalography, neuron-specific enolase, and imaging. He is 60 hours out with recently discontinued sedation and a paralytic within the past 24 hours, so no reliable statement can be made now. <div class="ec-src"><b>Source:</b> Nolan JP, Sandroni C, Böttiger BW, et al. European Resuscitation Council and European Society of Intensive Care Medicine Guidelines 2021: Post-resuscitation Care. Resuscitation 2021;161:220-269.</div></div></div> [[Try this question again->Post-arrest neuroprognostication - Prog]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Post-arrest neuroprognostication. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Brain death determination requires the absence of confounders including sedatives and neuromuscular blockade, and he received both within the last 24 hours. <div class="ec-teach"><div class="th">What the findings point to</div> Neurologic examination performed too early is unreliable, because sedatives, analgesics, and neuromuscular blockade have prolonged clearance after hypothermia and can mimic devastating injury. Guidelines call for multimodal assessment no sooner than 72 hours after return to normothermia, in a patient free of confounders, combining examination with somatosensory evoked potentials, electroencephalography, neuron-specific enolase, and imaging. He is 60 hours out with recently discontinued sedation and a paralytic within the past 24 hours, so no reliable statement can be made now. <div class="ec-src"><b>Source:</b> Nolan JP, Sandroni C, Böttiger BW, et al. European Resuscitation Council and European Society of Intensive Care Medicine Guidelines 2021: Post-resuscitation Care. Resuscitation 2021;161:220-269.</div></div></div> [[Try this question again->Post-arrest neuroprognostication - Prog]] [[Start another case->Hub]]

<div class="ec-scene">Surgical ward · 16:20</div> A 72-year-old man with type 2 diabetes mellitus has a necrotic forefoot ulcer with osteomyelitis. Vascular surgery recommends transmetatarsal amputation. He declines. He states that he understands the infection is in the bone, that refusing surgery is likely to lead to spreading infection and possibly death, and that antibiotics alone may not clear it. He says he has watched two relatives decline after amputation and would rather accept a shorter life with an intact foot. He is alert, oriented, and consistent in this position across three conversations. His daughter demands that surgery proceed. <span class="ec-prompt">Which of the following is the most appropriate next step?</span> [[Honor the refusal and offer intravenous antibiotics->Decision-making capacity - Ethics correct]] [[Obtain a court order to authorize the amputation->Decision-making capacity - Ethics D1]] [[Obtain consent from his daughter as surrogate->Decision-making capacity - Ethics D2]] [[Perform a Mini-Mental State Examination to determine capacity->Decision-making capacity - Ethics D3]] [[Proceed to surgery under the emergency exception->Decision-making capacity - Ethics D4]] [[Request psychiatric evaluation for competence->Decision-making capacity - Ethics D5]]

<span class="ec-case-marker" hidden data-entry="Decision-making capacity. Ethics"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Honor the refusal and offer intravenous antibiotics</div> Capacity requires that a patient communicate a choice, understand the relevant information, appreciate how it applies to his own situation, and reason among options. He satisfies all four, and the fact that his choice carries a high risk of death does not negate capacity. A capacitated refusal binds regardless of family objection, so the correct step is to accept it and offer the best available alternative, keeping the door open to reconsider. <div class="ec-src"><b>Source:</b> Appelbaum PS. Assessment of patients' competence to consent to treatment. N Engl J Med 2007;357(18):1834-1840.</div></div> [[Start another case->Hub]] [[Restart this case->Decision-making capacity - Ethics]] [[Next case →->Disclosure of medical error - Ethics]]

<span class="ec-case-marker" hidden data-entry="Decision-making capacity. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Judicial intervention is reserved for patients who lack capacity and have no surrogate, or for disputes among surrogates. Overriding a capacitated adult's refusal has no legal footing. <div class="ec-teach"><div class="th">What the findings point to</div> Capacity requires that a patient communicate a choice, understand the relevant information, appreciate how it applies to his own situation, and reason among options. He satisfies all four, and the fact that his choice carries a high risk of death does not negate capacity. A capacitated refusal binds regardless of family objection, so the correct step is to accept it and offer the best available alternative, keeping the door open to reconsider. <div class="ec-src"><b>Source:</b> Appelbaum PS. Assessment of patients' competence to consent to treatment. N Engl J Med 2007;357(18):1834-1840.</div></div></div> [[Try this question again->Decision-making capacity - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Decision-making capacity. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Surrogate decision-making is activated only when a patient lacks capacity. A daughter's wishes do not supersede those of a capacitated parent. <div class="ec-teach"><div class="th">What the findings point to</div> Capacity requires that a patient communicate a choice, understand the relevant information, appreciate how it applies to his own situation, and reason among options. He satisfies all four, and the fact that his choice carries a high risk of death does not negate capacity. A capacitated refusal binds regardless of family objection, so the correct step is to accept it and offer the best available alternative, keeping the door open to reconsider. <div class="ec-src"><b>Source:</b> Appelbaum PS. Assessment of patients' competence to consent to treatment. N Engl J Med 2007;357(18):1834-1840.</div></div></div> [[Try this question again->Decision-making capacity - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Decision-making capacity. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Cognitive screening instruments measure global cognition, not the four decision-specific abilities. A normal or abnormal score does not establish or refute capacity for a particular decision. <div class="ec-teach"><div class="th">What the findings point to</div> Capacity requires that a patient communicate a choice, understand the relevant information, appreciate how it applies to his own situation, and reason among options. He satisfies all four, and the fact that his choice carries a high risk of death does not negate capacity. A capacitated refusal binds regardless of family objection, so the correct step is to accept it and offer the best available alternative, keeping the door open to reconsider. <div class="ec-src"><b>Source:</b> Appelbaum PS. Assessment of patients' competence to consent to treatment. N Engl J Med 2007;357(18):1834-1840.</div></div></div> [[Try this question again->Decision-making capacity - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Decision-making capacity. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The emergency exception applies when a patient cannot consent and delay threatens life or limb. It does not apply to an alert patient who has explicitly refused. <div class="ec-teach"><div class="th">What the findings point to</div> Capacity requires that a patient communicate a choice, understand the relevant information, appreciate how it applies to his own situation, and reason among options. He satisfies all four, and the fact that his choice carries a high risk of death does not negate capacity. A capacitated refusal binds regardless of family objection, so the correct step is to accept it and offer the best available alternative, keeping the door open to reconsider. <div class="ec-src"><b>Source:</b> Appelbaum PS. Assessment of patients' competence to consent to treatment. N Engl J Med 2007;357(18):1834-1840.</div></div></div> [[Try this question again->Decision-making capacity - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Decision-making capacity. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Competence is a legal determination made by a court. Psychiatric consultation is useful when capacity is genuinely in doubt, but it should not be deployed simply because a clinician disagrees with a clear and reasoned choice. <div class="ec-teach"><div class="th">What the findings point to</div> Capacity requires that a patient communicate a choice, understand the relevant information, appreciate how it applies to his own situation, and reason among options. He satisfies all four, and the fact that his choice carries a high risk of death does not negate capacity. A capacitated refusal binds regardless of family objection, so the correct step is to accept it and offer the best available alternative, keeping the door open to reconsider. <div class="ec-src"><b>Source:</b> Appelbaum PS. Assessment of patients' competence to consent to treatment. N Engl J Med 2007;357(18):1834-1840.</div></div></div> [[Try this question again->Decision-making capacity - Ethics]] [[Start another case->Hub]]

<div class="ec-scene">Medical ward · 08:15</div> A hospitalized 68-year-old woman receives a dose of penicillin despite a documented history of anaphylaxis to it. She develops urticaria and mild wheezing, is treated with intramuscular epinephrine and an antihistamine, and recovers fully within an hour. Review shows the allergy was recorded in the chart but was not carried into the electronic order set. The attending physician who wrote the order asks whether the patient needs to be told, noting that she is now well and that raising it may frighten her and invite litigation. <span class="ec-prompt">Which of the following is the most appropriate course of action?</span> [[Consult the hospital attorney before deciding whether to inform her->Disclosure of medical error - Ethics D1]] [[Disclose the error promptly, explain what happened, and apologize->Disclosure of medical error - Ethics correct]] [[Disclose the event only if the patient asks about the rash->Disclosure of medical error - Ethics D2]] [[Document the reaction in the chart without informing the patient->Disclosure of medical error - Ethics D3]] [[Inform the patient's family and let them decide whether to tell her->Disclosure of medical error - Ethics D4]] [[Report the event to the safety committee and defer disclosure until the review concludes->Disclosure of medical error - Ethics D5]]

<span class="ec-case-marker" hidden data-entry="Disclosure of medical error. Ethics"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Disclose the error promptly, explain what happened, and apologize</div> Patients are entitled to know about errors that reach them, including those causing transient harm. Disclosure should be timely, should state the facts and the consequence, should include an explicit apology, and should describe what will be done to prevent recurrence. Withholding this information is a breach of the therapeutic relationship, and evidence indicates that open disclosure does not increase, and may reduce, the likelihood of litigation. <div class="ec-src"><b>Source:</b> Gallagher TH, Studdert D, Levinson W. Disclosing harmful medical errors to patients. N Engl J Med 2007;356(26):2713-2719.</div></div> [[Start another case->Hub]] [[Restart this case->Disclosure of medical error - Ethics]] [[Next case →->Transfusion refusal - Ethics]]

<span class="ec-case-marker" hidden data-entry="Disclosure of medical error. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Risk management input can help with wording, but making disclosure conditional on legal clearance inverts the duty. The obligation to inform arises from the patient relationship, not from liability exposure. <div class="ec-teach"><div class="th">What the findings point to</div> Patients are entitled to know about errors that reach them, including those causing transient harm. Disclosure should be timely, should state the facts and the consequence, should include an explicit apology, and should describe what will be done to prevent recurrence. Withholding this information is a breach of the therapeutic relationship, and evidence indicates that open disclosure does not increase, and may reduce, the likelihood of litigation. <div class="ec-src"><b>Source:</b> Gallagher TH, Studdert D, Levinson W. Disclosing harmful medical errors to patients. N Engl J Med 2007;356(26):2713-2719.</div></div></div> [[Try this question again->Disclosure of medical error - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Disclosure of medical error. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Conditioning honesty on a patient's ability to detect the error is not disclosure. She has no way to know that an allergy documented in her chart was overridden. <div class="ec-teach"><div class="th">What the findings point to</div> Patients are entitled to know about errors that reach them, including those causing transient harm. Disclosure should be timely, should state the facts and the consequence, should include an explicit apology, and should describe what will be done to prevent recurrence. Withholding this information is a breach of the therapeutic relationship, and evidence indicates that open disclosure does not increase, and may reduce, the likelihood of litigation. <div class="ec-src"><b>Source:</b> Gallagher TH, Studdert D, Levinson W. Disclosing harmful medical errors to patients. N Engl J Med 2007;356(26):2713-2719.</div></div></div> [[Try this question again->Disclosure of medical error - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Disclosure of medical error. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Documentation serves the record. It does not discharge the obligation owed directly to the person who was harmed. <div class="ec-teach"><div class="th">What the findings point to</div> Patients are entitled to know about errors that reach them, including those causing transient harm. Disclosure should be timely, should state the facts and the consequence, should include an explicit apology, and should describe what will be done to prevent recurrence. Withholding this information is a breach of the therapeutic relationship, and evidence indicates that open disclosure does not increase, and may reduce, the likelihood of litigation. <div class="ec-src"><b>Source:</b> Gallagher TH, Studdert D, Levinson W. Disclosing harmful medical errors to patients. N Engl J Med 2007;356(26):2713-2719.</div></div></div> [[Try this question again->Disclosure of medical error - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Disclosure of medical error. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Redirecting disclosure through relatives bypasses a capacitated adult and compounds the original breach of trust. <div class="ec-teach"><div class="th">What the findings point to</div> Patients are entitled to know about errors that reach them, including those causing transient harm. Disclosure should be timely, should state the facts and the consequence, should include an explicit apology, and should describe what will be done to prevent recurrence. Withholding this information is a breach of the therapeutic relationship, and evidence indicates that open disclosure does not increase, and may reduce, the likelihood of litigation. <div class="ec-src"><b>Source:</b> Gallagher TH, Studdert D, Levinson W. Disclosing harmful medical errors to patients. N Engl J Med 2007;356(26):2713-2719.</div></div></div> [[Try this question again->Disclosure of medical error - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Disclosure of medical error. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Incident reporting and disclosure are parallel duties, not sequential ones. Waiting weeks for a review to close leaves the patient uninformed about something that already happened to her. <div class="ec-teach"><div class="th">What the findings point to</div> Patients are entitled to know about errors that reach them, including those causing transient harm. Disclosure should be timely, should state the facts and the consequence, should include an explicit apology, and should describe what will be done to prevent recurrence. Withholding this information is a breach of the therapeutic relationship, and evidence indicates that open disclosure does not increase, and may reduce, the likelihood of litigation. <div class="ec-src"><b>Source:</b> Gallagher TH, Studdert D, Levinson W. Disclosing harmful medical errors to patients. N Engl J Med 2007;356(26):2713-2719.</div></div></div> [[Try this question again->Disclosure of medical error - Ethics]] [[Start another case->Hub]]

<div class="ec-scene">Quality committee · 12:07</div> An intensive care unit reports a central line-associated bloodstream infection rate of 7.1 per 1,000 catheter-days, well above the national benchmark. Audit shows that operators vary in skin antisepsis agent, that full-barrier drapes are stocked in a supply room two corridors away, that femoral sites are chosen for convenience during night shifts, and that no one reviews daily whether existing catheters are still needed. Nursing staff report reluctance to interrupt physicians during insertion. <span class="ec-prompt">Which of the following interventions is most likely to reduce the infection rate?</span> [[Distribute monthly infection rate reports to each physician->Catheter infection bundle - QI D1]] [[Insertion checklist with bedside supplies and stop authority->Catheter infection bundle - QI correct]] [[Post signage on hand hygiene at every unit entrance->Catheter infection bundle - QI D2]] [[Require an attending physician to perform all central line insertions->Catheter infection bundle - QI D3]] [[Routinely exchange central catheters over a guidewire every 7 days->Catheter infection bundle - QI D4]] [[Use antibiotic-impregnated catheters for all insertions->Catheter infection bundle - QI D5]]

<span class="ec-case-marker" hidden data-entry="Catheter infection bundle. QI"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Insertion checklist with bedside supplies and stop authority</div> The intervention with demonstrated large and sustained reductions combines specific practices with the system changes that make them happen: hand hygiene, chlorhexidine antisepsis, full-barrier precautions, avoiding the femoral site, and daily review for catheter removal, delivered through a cart that places every item at the bedside and an explicit mandate empowering nurses to stop a violation. Each element addresses one of the observed defects. <div class="ec-src"><b>Source:</b> Pronovost P, Needham D, Berenholtz S, et al. An intervention to decrease catheter-related bloodstream infections in the ICU. N Engl J Med 2006;355(26):2725-2732.</div></div> [[Start another case->Hub]] [[Restart this case->Catheter infection bundle - QI]] [[Next case →->Latent system failure - QI]]

<span class="ec-case-marker" hidden data-entry="Catheter infection bundle. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Feedback alone changes behavior weakly and does nothing about drapes stored two corridors away or the reluctance to speak up during a procedure. <div class="ec-teach"><div class="th">What the findings point to</div> The intervention with demonstrated large and sustained reductions combines specific practices with the system changes that make them happen: hand hygiene, chlorhexidine antisepsis, full-barrier precautions, avoiding the femoral site, and daily review for catheter removal, delivered through a cart that places every item at the bedside and an explicit mandate empowering nurses to stop a violation. Each element addresses one of the observed defects. <div class="ec-src"><b>Source:</b> Pronovost P, Needham D, Berenholtz S, et al. An intervention to decrease catheter-related bloodstream infections in the ICU. N Engl J Med 2006;355(26):2725-2732.</div></div></div> [[Try this question again->Catheter infection bundle - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Catheter infection bundle. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Reminders are among the weakest interventions in the hierarchy of controls and are quickly filtered out by staff working under time pressure. <div class="ec-teach"><div class="th">What the findings point to</div> The intervention with demonstrated large and sustained reductions combines specific practices with the system changes that make them happen: hand hygiene, chlorhexidine antisepsis, full-barrier precautions, avoiding the femoral site, and daily review for catheter removal, delivered through a cart that places every item at the bedside and an explicit mandate empowering nurses to stop a violation. Each element addresses one of the observed defects. <div class="ec-src"><b>Source:</b> Pronovost P, Needham D, Berenholtz S, et al. An intervention to decrease catheter-related bloodstream infections in the ICU. N Engl J Med 2006;355(26):2725-2732.</div></div></div> [[Try this question again->Catheter infection bundle - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Catheter infection bundle. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Restricting the operator pool delays access, does not address technique variation or supply availability, and is unsustainable in a unit placing lines around the clock. <div class="ec-teach"><div class="th">What the findings point to</div> The intervention with demonstrated large and sustained reductions combines specific practices with the system changes that make them happen: hand hygiene, chlorhexidine antisepsis, full-barrier precautions, avoiding the femoral site, and daily review for catheter removal, delivered through a cart that places every item at the bedside and an explicit mandate empowering nurses to stop a violation. Each element addresses one of the observed defects. <div class="ec-src"><b>Source:</b> Pronovost P, Needham D, Berenholtz S, et al. An intervention to decrease catheter-related bloodstream infections in the ICU. N Engl J Med 2006;355(26):2725-2732.</div></div></div> [[Try this question again->Catheter infection bundle - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Catheter infection bundle. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Scheduled catheter exchange does not reduce infection and introduces mechanical complications. Guidewire exchange through an infected site propagates the infection. <div class="ec-teach"><div class="th">What the findings point to</div> The intervention with demonstrated large and sustained reductions combines specific practices with the system changes that make them happen: hand hygiene, chlorhexidine antisepsis, full-barrier precautions, avoiding the femoral site, and daily review for catheter removal, delivered through a cart that places every item at the bedside and an explicit mandate empowering nurses to stop a violation. Each element addresses one of the observed defects. <div class="ec-src"><b>Source:</b> Pronovost P, Needham D, Berenholtz S, et al. An intervention to decrease catheter-related bloodstream infections in the ICU. N Engl J Med 2006;355(26):2725-2732.</div></div></div> [[Try this question again->Catheter infection bundle - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Catheter infection bundle. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Impregnated catheters have a role when rates remain high after a full bundle is implemented. Deploying them first substitutes a costly device for the process fixes that produce most of the benefit. <div class="ec-teach"><div class="th">What the findings point to</div> The intervention with demonstrated large and sustained reductions combines specific practices with the system changes that make them happen: hand hygiene, chlorhexidine antisepsis, full-barrier precautions, avoiding the femoral site, and daily review for catheter removal, delivered through a cart that places every item at the bedside and an explicit mandate empowering nurses to stop a violation. Each element addresses one of the observed defects. <div class="ec-src"><b>Source:</b> Pronovost P, Needham D, Berenholtz S, et al. An intervention to decrease catheter-related bloodstream infections in the ICU. N Engl J Med 2006;355(26):2725-2732.</div></div></div> [[Try this question again->Catheter infection bundle - QI]] [[Start another case->Hub]]

<div class="ec-scene">Primary care clinic · 15:40</div> A 67-year-old woman presents for routine care. She is postmenopausal since age 51, has never taken hormone therapy or glucocorticoids, has no fractures, does not smoke, and drinks alcohol rarely. Her mother sustained a hip fracture at age 80. She walks daily. Body mass index is 24 kg/m2. She has never had bone densitometry. Physical examination is normal. <span class="ec-prompt">Which of the following is the most appropriate screening recommendation?</span> [[Calcaneal quantitative ultrasonography->Osteoporosis screening - Prevention D1]] [[Dual-energy x-ray absorptiometry of the hip and lumbar spine->Osteoporosis screening - Prevention correct]] [[Fracture risk assessment alone without imaging->Osteoporosis screening - Prevention D2]] [[No screening in the absence of a personal fracture history->Osteoporosis screening - Prevention D3]] [[Serum bone turnover marker panel->Osteoporosis screening - Prevention D4]] [[Vertebral radiography of the thoracic and lumbar spine->Osteoporosis screening - Prevention D5]]

<span class="ec-case-marker" hidden data-entry="Osteoporosis screening. Prevention"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Dual-energy x-ray absorptiometry of the hip and lumbar spine</div> The US Preventive Services Task Force recommends screening for osteoporosis with bone measurement testing in all women 65 years and older. She is 67 and has never been tested, so densitometry is indicated on age alone, independent of her additional risk factors. Central densitometry of the hip and spine is the reference standard because those are the sites at which fracture risk is best predicted and treatment thresholds are defined. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Screening for Osteoporosis to Prevent Fractures: US Preventive Services Task Force Recommendation Statement. JAMA 2018;319(24):2521-2531.</div></div> [[Start another case->Hub]] [[Restart this case->Osteoporosis screening - Prevention]] [[Next case →->Lead-time bias - Biostat]]

<span class="ec-case-marker" hidden data-entry="Osteoporosis screening. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Peripheral measurement can identify people at risk but cannot be used to diagnose osteoporosis or to define treatment thresholds, which are anchored to central densitometry. <div class="ec-teach"><div class="th">What the findings point to</div> The US Preventive Services Task Force recommends screening for osteoporosis with bone measurement testing in all women 65 years and older. She is 67 and has never been tested, so densitometry is indicated on age alone, independent of her additional risk factors. Central densitometry of the hip and spine is the reference standard because those are the sites at which fracture risk is best predicted and treatment thresholds are defined. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Screening for Osteoporosis to Prevent Fractures: US Preventive Services Task Force Recommendation Statement. JAMA 2018;319(24):2521-2531.</div></div></div> [[Try this question again->Osteoporosis screening - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Osteoporosis screening. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The fracture risk tool is used to decide whether to screen women younger than 65. Once a woman reaches 65, screening is recommended directly and the tool does not substitute for measurement. <div class="ec-teach"><div class="th">What the findings point to</div> The US Preventive Services Task Force recommends screening for osteoporosis with bone measurement testing in all women 65 years and older. She is 67 and has never been tested, so densitometry is indicated on age alone, independent of her additional risk factors. Central densitometry of the hip and spine is the reference standard because those are the sites at which fracture risk is best predicted and treatment thresholds are defined. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Screening for Osteoporosis to Prevent Fractures: US Preventive Services Task Force Recommendation Statement. JAMA 2018;319(24):2521-2531.</div></div></div> [[Try this question again->Osteoporosis screening - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Osteoporosis screening. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Screening exists precisely to identify women before a first fracture. Waiting for a fracture defeats the purpose of the recommendation. <div class="ec-teach"><div class="th">What the findings point to</div> The US Preventive Services Task Force recommends screening for osteoporosis with bone measurement testing in all women 65 years and older. She is 67 and has never been tested, so densitometry is indicated on age alone, independent of her additional risk factors. Central densitometry of the hip and spine is the reference standard because those are the sites at which fracture risk is best predicted and treatment thresholds are defined. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Screening for Osteoporosis to Prevent Fractures: US Preventive Services Task Force Recommendation Statement. JAMA 2018;319(24):2521-2531.</div></div></div> [[Try this question again->Osteoporosis screening - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Osteoporosis screening. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Turnover markers can monitor response to therapy in selected patients. They are not accurate enough to screen for or diagnose osteoporosis. <div class="ec-teach"><div class="th">What the findings point to</div> The US Preventive Services Task Force recommends screening for osteoporosis with bone measurement testing in all women 65 years and older. She is 67 and has never been tested, so densitometry is indicated on age alone, independent of her additional risk factors. Central densitometry of the hip and spine is the reference standard because those are the sites at which fracture risk is best predicted and treatment thresholds are defined. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Screening for Osteoporosis to Prevent Fractures: US Preventive Services Task Force Recommendation Statement. JAMA 2018;319(24):2521-2531.</div></div></div> [[Try this question again->Osteoporosis screening - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Osteoporosis screening. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Plain films detect deformity only after substantial bone loss and cannot quantify density. They are used to identify occult vertebral fractures, not for screening. <div class="ec-teach"><div class="th">What the findings point to</div> The US Preventive Services Task Force recommends screening for osteoporosis with bone measurement testing in all women 65 years and older. She is 67 and has never been tested, so densitometry is indicated on age alone, independent of her additional risk factors. Central densitometry of the hip and spine is the reference standard because those are the sites at which fracture risk is best predicted and treatment thresholds are defined. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Screening for Osteoporosis to Prevent Fractures: US Preventive Services Task Force Recommendation Statement. JAMA 2018;319(24):2521-2531.</div></div></div> [[Try this question again->Osteoporosis screening - Prevention]] [[Start another case->Hub]]

<div class="ec-scene">Journal club · 07:30</div> An observational study compares two hospital systems. In the system that introduced a new imaging-based screening program for a slow-growing cancer, median survival after diagnosis is 6.2 years. In the system without the program, median survival after diagnosis is 3.4 years. The number of cancer deaths per 100,000 population per year is 24 in both systems and has not changed in either over the 15-year study period. The authors conclude that screening improves survival. <span class="ec-prompt">Which of the following best explains the observed difference in survival?</span> [[Confounding by differences in baseline health between the populations->Lead-time bias - Biostat D1]] [[Detection of slowly progressive tumors that would never have caused symptoms->Lead-time bias - Biostat D2]] [[Differential loss to follow-up between the two systems->Lead-time bias - Biostat D3]] [[Earlier detection lengthens survival without postponing death->Lead-time bias - Biostat correct]] [[Improved treatment introduced alongside the screening program->Lead-time bias - Biostat D4]] [[Random variation in a study of insufficient size->Lead-time bias - Biostat D5]]

<span class="ec-case-marker" hidden data-entry="Lead-time bias. Biostat"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Earlier detection lengthens survival without postponing death</div> This is lead-time bias. Screening advances the moment of diagnosis, so survival measured from that moment lengthens automatically even when the date of death is unchanged. The decisive clue is that mortality per 100,000 population is identical in both systems and stable over 15 years. Mortality rate in the source population, not survival from diagnosis, is the outcome that can distinguish genuine benefit from an artifact of measurement. <div class="ec-src"><b>Source:</b> Welch HG, Black WC. Overdiagnosis in cancer. J Natl Cancer Inst 2010;102(9):605-613.</div></div> [[Start another case->Hub]] [[Restart this case->Lead-time bias - Biostat]] [[Next case →->Ruling out with a sensitive test - Biostat]]

<span class="ec-case-marker" hidden data-entry="Lead-time bias. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Confounding is plausible in any observational comparison, but it would not produce identical mortality rates in the two systems alongside a large survival difference. <div class="ec-teach"><div class="th">What the findings point to</div> This is lead-time bias. Screening advances the moment of diagnosis, so survival measured from that moment lengthens automatically even when the date of death is unchanged. The decisive clue is that mortality per 100,000 population is identical in both systems and stable over 15 years. Mortality rate in the source population, not survival from diagnosis, is the outcome that can distinguish genuine benefit from an artifact of measurement. <div class="ec-src"><b>Source:</b> Welch HG, Black WC. Overdiagnosis in cancer. J Natl Cancer Inst 2010;102(9):605-613.</div></div></div> [[Try this question again->Lead-time bias - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Lead-time bias. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This describes length-time bias and overdiagnosis, which also inflate apparent survival. It is a real contributor, but the stem specifies a difference in survival from diagnosis with unchanged mortality, which defines lead time as the primary explanation. <div class="ec-teach"><div class="th">What the findings point to</div> This is lead-time bias. Screening advances the moment of diagnosis, so survival measured from that moment lengthens automatically even when the date of death is unchanged. The decisive clue is that mortality per 100,000 population is identical in both systems and stable over 15 years. Mortality rate in the source population, not survival from diagnosis, is the outcome that can distinguish genuine benefit from an artifact of measurement. <div class="ec-src"><b>Source:</b> Welch HG, Black WC. Overdiagnosis in cancer. J Natl Cancer Inst 2010;102(9):605-613.</div></div></div> [[Try this question again->Lead-time bias - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Lead-time bias. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Attrition bias would distort survival estimates, but the stem gives no indication that follow-up differed, and it would not explain stable population mortality. <div class="ec-teach"><div class="th">What the findings point to</div> This is lead-time bias. Screening advances the moment of diagnosis, so survival measured from that moment lengthens automatically even when the date of death is unchanged. The decisive clue is that mortality per 100,000 population is identical in both systems and stable over 15 years. Mortality rate in the source population, not survival from diagnosis, is the outcome that can distinguish genuine benefit from an artifact of measurement. <div class="ec-src"><b>Source:</b> Welch HG, Black WC. Overdiagnosis in cancer. J Natl Cancer Inst 2010;102(9):605-613.</div></div></div> [[Try this question again->Lead-time bias - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Lead-time bias. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A genuine treatment effect would reduce cancer deaths per 100,000 population. That figure is unchanged. <div class="ec-teach"><div class="th">What the findings point to</div> This is lead-time bias. Screening advances the moment of diagnosis, so survival measured from that moment lengthens automatically even when the date of death is unchanged. The decisive clue is that mortality per 100,000 population is identical in both systems and stable over 15 years. Mortality rate in the source population, not survival from diagnosis, is the outcome that can distinguish genuine benefit from an artifact of measurement. <div class="ec-src"><b>Source:</b> Welch HG, Black WC. Overdiagnosis in cancer. J Natl Cancer Inst 2010;102(9):605-613.</div></div></div> [[Try this question again->Lead-time bias - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Lead-time bias. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A survival difference of nearly 3 years sustained across 15 years and two health systems is not attributable to chance. <div class="ec-teach"><div class="th">What the findings point to</div> This is lead-time bias. Screening advances the moment of diagnosis, so survival measured from that moment lengthens automatically even when the date of death is unchanged. The decisive clue is that mortality per 100,000 population is identical in both systems and stable over 15 years. Mortality rate in the source population, not survival from diagnosis, is the outcome that can distinguish genuine benefit from an artifact of measurement. <div class="ec-src"><b>Source:</b> Welch HG, Black WC. Overdiagnosis in cancer. J Natl Cancer Inst 2010;102(9):605-613.</div></div></div> [[Try this question again->Lead-time bias - Biostat]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 02:42</div> A 56-year-old man awakens with swelling of the lips and tongue. He has taken lisinopril for hypertension for 14 months without difficulty. There is no urticaria, no pruritus, and no wheezing. Temperature is 36.9°C, blood pressure 152/88 mm Hg, pulse 92/min, and oxygen saturation 97% on room air. The tongue is markedly swollen and his voice is muffled. Serum tryptase measured on arrival is within the reference range. C4 concentration is normal. <span class="ec-prompt">Which of the following best explains this patient's presentation?</span> [[Accumulation of bradykinin from inhibited degradation->ACE inhibitor angioedema - Mech correct]] [[Consumption of C1 inhibitor by an underlying lymphoproliferative disorder->ACE inhibitor angioedema - Mech D1]] [[Drug-specific IgE cross-linking on mast cells->ACE inhibitor angioedema - Mech D2]] [[Hereditary deficiency of C1 inhibitor->ACE inhibitor angioedema - Mech D3]] [[Immune complex deposition in dermal vessels->ACE inhibitor angioedema - Mech D4]] [[Mast cell activation through MRGPRX2->ACE inhibitor angioedema - Mech D5]]

<span class="ec-case-marker" hidden data-entry="ACE inhibitor angioedema. Mech"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Accumulation of bradykinin from inhibited degradation</div> Angiotensin-converting enzyme, also called kininase II, degrades bradykinin. Inhibiting it allows bradykinin to accumulate and act on B2 receptors, producing vascular permeability and localized edema. The reaction is not immunologic, which is why it can appear months to years after starting the drug, why urticaria and pruritus are absent, and why tryptase is normal. Normal C4 separates it from hereditary and acquired C1 inhibitor deficiency. Management is airway assessment and permanent discontinuation of the entire drug class. <div class="ec-src"><b>Source:</b> Bas M, Greve J, Stelter K, et al. A randomized trial of icatibant in ACE-inhibitor-induced angioedema. N Engl J Med 2015;372(5):418-425.</div></div> [[Start another case->Hub]] [[Restart this case->ACE inhibitor angioedema - Mech]] [[Next case →->Stroke risk in atrial fibrillation - Prog]]

<span class="ec-case-marker" hidden data-entry="ACE inhibitor angioedema. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Acquired C1 inhibitor deficiency lowers C4, which is normal here, and typically presents with recurrent episodes rather than a single event tied to an ongoing drug exposure. <div class="ec-teach"><div class="th">What the findings point to</div> Angiotensin-converting enzyme, also called kininase II, degrades bradykinin. Inhibiting it allows bradykinin to accumulate and act on B2 receptors, producing vascular permeability and localized edema. The reaction is not immunologic, which is why it can appear months to years after starting the drug, why urticaria and pruritus are absent, and why tryptase is normal. Normal C4 separates it from hereditary and acquired C1 inhibitor deficiency. Management is airway assessment and permanent discontinuation of the entire drug class. <div class="ec-src"><b>Source:</b> Bas M, Greve J, Stelter K, et al. A randomized trial of icatibant in ACE-inhibitor-induced angioedema. N Engl J Med 2015;372(5):418-425.</div></div></div> [[Try this question again->ACE inhibitor angioedema - Mech]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="ACE inhibitor angioedema. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> An IgE-mediated reaction would be expected to produce urticaria, pruritus, and an elevated tryptase, and it would not first appear after 14 months of uneventful daily use. <div class="ec-teach"><div class="th">What the findings point to</div> Angiotensin-converting enzyme, also called kininase II, degrades bradykinin. Inhibiting it allows bradykinin to accumulate and act on B2 receptors, producing vascular permeability and localized edema. The reaction is not immunologic, which is why it can appear months to years after starting the drug, why urticaria and pruritus are absent, and why tryptase is normal. Normal C4 separates it from hereditary and acquired C1 inhibitor deficiency. Management is airway assessment and permanent discontinuation of the entire drug class. <div class="ec-src"><b>Source:</b> Bas M, Greve J, Stelter K, et al. A randomized trial of icatibant in ACE-inhibitor-induced angioedema. N Engl J Med 2015;372(5):418-425.</div></div></div> [[Try this question again->ACE inhibitor angioedema - Mech]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="ACE inhibitor angioedema. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Hereditary angioedema also acts through bradykinin but presents in childhood or adolescence with recurrent attacks and a low C4 between episodes. <div class="ec-teach"><div class="th">What the findings point to</div> Angiotensin-converting enzyme, also called kininase II, degrades bradykinin. Inhibiting it allows bradykinin to accumulate and act on B2 receptors, producing vascular permeability and localized edema. The reaction is not immunologic, which is why it can appear months to years after starting the drug, why urticaria and pruritus are absent, and why tryptase is normal. Normal C4 separates it from hereditary and acquired C1 inhibitor deficiency. Management is airway assessment and permanent discontinuation of the entire drug class. <div class="ec-src"><b>Source:</b> Bas M, Greve J, Stelter K, et al. A randomized trial of icatibant in ACE-inhibitor-induced angioedema. N Engl J Med 2015;372(5):418-425.</div></div></div> [[Try this question again->ACE inhibitor angioedema - Mech]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="ACE inhibitor angioedema. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A type III reaction produces palpable purpura, arthralgia, and fever over days, not isolated mucosal swelling within hours. <div class="ec-teach"><div class="th">What the findings point to</div> Angiotensin-converting enzyme, also called kininase II, degrades bradykinin. Inhibiting it allows bradykinin to accumulate and act on B2 receptors, producing vascular permeability and localized edema. The reaction is not immunologic, which is why it can appear months to years after starting the drug, why urticaria and pruritus are absent, and why tryptase is normal. Normal C4 separates it from hereditary and acquired C1 inhibitor deficiency. Management is airway assessment and permanent discontinuation of the entire drug class. <div class="ec-src"><b>Source:</b> Bas M, Greve J, Stelter K, et al. A randomized trial of icatibant in ACE-inhibitor-induced angioedema. N Engl J Med 2015;372(5):418-425.</div></div></div> [[Try this question again->ACE inhibitor angioedema - Mech]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="ACE inhibitor angioedema. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This receptor mediates pseudoallergic degranulation to agents such as vancomycin and produces flushing and urticaria with elevated tryptase, none of which is present. <div class="ec-teach"><div class="th">What the findings point to</div> Angiotensin-converting enzyme, also called kininase II, degrades bradykinin. Inhibiting it allows bradykinin to accumulate and act on B2 receptors, producing vascular permeability and localized edema. The reaction is not immunologic, which is why it can appear months to years after starting the drug, why urticaria and pruritus are absent, and why tryptase is normal. Normal C4 separates it from hereditary and acquired C1 inhibitor deficiency. Management is airway assessment and permanent discontinuation of the entire drug class. <div class="ec-src"><b>Source:</b> Bas M, Greve J, Stelter K, et al. A randomized trial of icatibant in ACE-inhibitor-induced angioedema. N Engl J Med 2015;372(5):418-425.</div></div></div> [[Try this question again->ACE inhibitor angioedema - Mech]] [[Start another case->Hub]]

<div class="ec-scene">Trauma bay · 22:40</div> A 34-year-old man is brought in 30 minutes after a motorcycle collision. He is alert, oriented, and in pain. Blood pressure is 96/58 mm Hg, pulse 118/min, and hemoglobin is 7.2 g/dL with ongoing intraabdominal bleeding on ultrasonography. He carries a signed card identifying him as a Jehovah's Witness and states clearly that he refuses all blood products, including in a life-threatening situation. He consents to surgery and to all other treatments. His wife, present at the bedside, begs the team to transfuse him. <span class="ec-prompt">Which of the following is the most appropriate next step?</span> [[Consult the hospital ethics committee before operating->Transfusion refusal - Ethics D1]] [[Obtain an emergency court order authorizing transfusion->Transfusion refusal - Ethics D2]] [[Proceed to surgery without transfusion->Transfusion refusal - Ethics correct]] [[Seek consent to transfuse from his wife->Transfusion refusal - Ethics D3]] [[Transfuse once he is anesthetized and cannot object->Transfusion refusal - Ethics D4]] [[Transfuse under the emergency exception to consent->Transfusion refusal - Ethics D5]]

<span class="ec-case-marker" hidden data-entry="Transfusion refusal. Ethics"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Proceed to surgery without transfusion</div> A capacitated adult may refuse any specific treatment, including one that is life-sustaining, and the refusal remains binding when he becomes unable to speak for himself during the operation. He is alert, has stated the refusal directly, and has consented to everything else. The obligation is to proceed with the surgery he has accepted while using every bloodless alternative available: cell salvage, tranexamic acid, meticulous hemostasis, and tolerance of a lower hemoglobin threshold. <div class="ec-src"><b>Source:</b> American Medical Association. Code of Medical Ethics Opinion 2.1.1: Informed Consent.</div></div> [[Start another case->Hub]] [[Restart this case->Transfusion refusal - Ethics]] [[Next case →->Substituted judgment - Ethics]]

<span class="ec-case-marker" hidden data-entry="Transfusion refusal. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Ethics consultation is valuable when the right course is genuinely unclear. Here the refusal is contemporaneous, informed, and unambiguous, and delaying a bleeding trauma patient to convene a committee causes harm without resolving anything. <div class="ec-teach"><div class="th">What the findings point to</div> A capacitated adult may refuse any specific treatment, including one that is life-sustaining, and the refusal remains binding when he becomes unable to speak for himself during the operation. He is alert, has stated the refusal directly, and has consented to everything else. The obligation is to proceed with the surgery he has accepted while using every bloodless alternative available: cell salvage, tranexamic acid, meticulous hemostasis, and tolerance of a lower hemoglobin threshold. <div class="ec-src"><b>Source:</b> American Medical Association. Code of Medical Ethics Opinion 2.1.1: Informed Consent.</div></div></div> [[Try this question again->Transfusion refusal - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Transfusion refusal. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Courts have consistently upheld the refusal of blood by capacitated adult Jehovah's Witnesses. Judicial override applies to minors, not to competent adults. <div class="ec-teach"><div class="th">What the findings point to</div> A capacitated adult may refuse any specific treatment, including one that is life-sustaining, and the refusal remains binding when he becomes unable to speak for himself during the operation. He is alert, has stated the refusal directly, and has consented to everything else. The obligation is to proceed with the surgery he has accepted while using every bloodless alternative available: cell salvage, tranexamic acid, meticulous hemostasis, and tolerance of a lower hemoglobin threshold. <div class="ec-src"><b>Source:</b> American Medical Association. Code of Medical Ethics Opinion 2.1.1: Informed Consent.</div></div></div> [[Try this question again->Transfusion refusal - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Transfusion refusal. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Spousal authority arises only when a patient cannot decide for himself. It does not permit reversal of a decision the patient has already made while capacitated. <div class="ec-teach"><div class="th">What the findings point to</div> A capacitated adult may refuse any specific treatment, including one that is life-sustaining, and the refusal remains binding when he becomes unable to speak for himself during the operation. He is alert, has stated the refusal directly, and has consented to everything else. The obligation is to proceed with the surgery he has accepted while using every bloodless alternative available: cell salvage, tranexamic acid, meticulous hemostasis, and tolerance of a lower hemoglobin threshold. <div class="ec-src"><b>Source:</b> American Medical Association. Code of Medical Ethics Opinion 2.1.1: Informed Consent.</div></div></div> [[Try this question again->Transfusion refusal - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Transfusion refusal. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Acting against a known refusal while the patient is unconscious is battery. Loss of consciousness does not revoke a prior competent decision. <div class="ec-teach"><div class="th">What the findings point to</div> A capacitated adult may refuse any specific treatment, including one that is life-sustaining, and the refusal remains binding when he becomes unable to speak for himself during the operation. He is alert, has stated the refusal directly, and has consented to everything else. The obligation is to proceed with the surgery he has accepted while using every bloodless alternative available: cell salvage, tranexamic acid, meticulous hemostasis, and tolerance of a lower hemoglobin threshold. <div class="ec-src"><b>Source:</b> American Medical Association. Code of Medical Ethics Opinion 2.1.1: Informed Consent.</div></div></div> [[Try this question again->Transfusion refusal - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Transfusion refusal. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> That exception presumes consent when a patient's wishes are unknown. His wishes are known and explicitly to the contrary. <div class="ec-teach"><div class="th">What the findings point to</div> A capacitated adult may refuse any specific treatment, including one that is life-sustaining, and the refusal remains binding when he becomes unable to speak for himself during the operation. He is alert, has stated the refusal directly, and has consented to everything else. The obligation is to proceed with the surgery he has accepted while using every bloodless alternative available: cell salvage, tranexamic acid, meticulous hemostasis, and tolerance of a lower hemoglobin threshold. <div class="ec-src"><b>Source:</b> American Medical Association. Code of Medical Ethics Opinion 2.1.1: Informed Consent.</div></div></div> [[Try this question again->Transfusion refusal - Ethics]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 03:05</div> A 9-year-old boy is brought in by a neighbor 40 minutes after falling from a second-story window. He is somnolent with a Glasgow Coma Scale score of 10. Blood pressure is 88/50 mm Hg and pulse is 142/min. CT of the head shows an expanding epidural hematoma, and neurosurgery recommends immediate craniotomy. His parents are traveling internationally and cannot be reached by phone. The neighbor has no legal authority to consent. <span class="ec-prompt">Which of the following is the most appropriate next step?</span> [[Ask the neighbor to sign the consent form->Emergency care of a minor - Ethics D1]] [[Contact child protective services for consent->Emergency care of a minor - Ethics D2]] [[Delay surgery until a parent can be reached->Emergency care of a minor - Ethics D3]] [[Obtain a court order appointing a temporary guardian->Emergency care of a minor - Ethics D4]] [[Proceed with surgery immediately->Emergency care of a minor - Ethics correct]] [[Treat medically with mannitol and defer the operation->Emergency care of a minor - Ethics D5]]

<span class="ec-case-marker" hidden data-entry="Emergency care of a minor. Ethics"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Proceed with surgery immediately</div> Emergency treatment necessary to prevent death or serious harm to a minor may proceed without parental consent when a parent is unavailable. Consent is presumed on the reasoning that a parent would authorize life-saving care. Continued attempts to reach the parents should occur in parallel, but they do not gate the operation. An expanding epidural hematoma is the paradigm of a lesion in which delay converts a survivable injury into death or severe disability. <div class="ec-src"><b>Source:</b> Committee on Pediatric Emergency Medicine, American Academy of Pediatrics. Consent for emergency medical services for children and adolescents. Pediatrics 2011;128(2):427-433.</div></div> [[Start another case->Hub]] [[Restart this case->Emergency care of a minor - Ethics]] [[Next case →->Major burn - Opening]]

<span class="ec-case-marker" hidden data-entry="Emergency care of a minor. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A neighbor has no legal standing to authorize surgery. Obtaining a meaningless signature adds a false record without providing valid consent. <div class="ec-teach"><div class="th">What the findings point to</div> Emergency treatment necessary to prevent death or serious harm to a minor may proceed without parental consent when a parent is unavailable. Consent is presumed on the reasoning that a parent would authorize life-saving care. Continued attempts to reach the parents should occur in parallel, but they do not gate the operation. An expanding epidural hematoma is the paradigm of a lesion in which delay converts a survivable injury into death or severe disability. <div class="ec-src"><b>Source:</b> Committee on Pediatric Emergency Medicine, American Academy of Pediatrics. Consent for emergency medical services for children and adolescents. Pediatrics 2011;128(2):427-433.</div></div></div> [[Try this question again->Emergency care of a minor - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Emergency care of a minor. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Protective services can assume custody in cases of neglect or abuse, but that pathway takes hours and does not apply to parents who are simply unreachable while traveling. <div class="ec-teach"><div class="th">What the findings point to</div> Emergency treatment necessary to prevent death or serious harm to a minor may proceed without parental consent when a parent is unavailable. Consent is presumed on the reasoning that a parent would authorize life-saving care. Continued attempts to reach the parents should occur in parallel, but they do not gate the operation. An expanding epidural hematoma is the paradigm of a lesion in which delay converts a survivable injury into death or severe disability. <div class="ec-src"><b>Source:</b> Committee on Pediatric Emergency Medicine, American Academy of Pediatrics. Consent for emergency medical services for children and adolescents. Pediatrics 2011;128(2):427-433.</div></div></div> [[Try this question again->Emergency care of a minor - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Emergency care of a minor. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> An expanding epidural hematoma produces herniation within hours. Waiting for a phone call is the decision most likely to kill him. <div class="ec-teach"><div class="th">What the findings point to</div> Emergency treatment necessary to prevent death or serious harm to a minor may proceed without parental consent when a parent is unavailable. Consent is presumed on the reasoning that a parent would authorize life-saving care. Continued attempts to reach the parents should occur in parallel, but they do not gate the operation. An expanding epidural hematoma is the paradigm of a lesion in which delay converts a survivable injury into death or severe disability. <div class="ec-src"><b>Source:</b> Committee on Pediatric Emergency Medicine, American Academy of Pediatrics. Consent for emergency medical services for children and adolescents. Pediatrics 2011;128(2):427-433.</div></div></div> [[Try this question again->Emergency care of a minor - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Emergency care of a minor. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Judicial appointment is appropriate for elective or contested decisions. It cannot be completed inside the window this injury allows. <div class="ec-teach"><div class="th">What the findings point to</div> Emergency treatment necessary to prevent death or serious harm to a minor may proceed without parental consent when a parent is unavailable. Consent is presumed on the reasoning that a parent would authorize life-saving care. Continued attempts to reach the parents should occur in parallel, but they do not gate the operation. An expanding epidural hematoma is the paradigm of a lesion in which delay converts a survivable injury into death or severe disability. <div class="ec-src"><b>Source:</b> Committee on Pediatric Emergency Medicine, American Academy of Pediatrics. Consent for emergency medical services for children and adolescents. Pediatrics 2011;128(2):427-433.</div></div></div> [[Try this question again->Emergency care of a minor - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Emergency care of a minor. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Osmotic therapy is a temporizing measure while the patient goes to the operating room. It is not an alternative to evacuating the clot. <div class="ec-teach"><div class="th">What the findings point to</div> Emergency treatment necessary to prevent death or serious harm to a minor may proceed without parental consent when a parent is unavailable. Consent is presumed on the reasoning that a parent would authorize life-saving care. Continued attempts to reach the parents should occur in parallel, but they do not gate the operation. An expanding epidural hematoma is the paradigm of a lesion in which delay converts a survivable injury into death or severe disability. <div class="ec-src"><b>Source:</b> Committee on Pediatric Emergency Medicine, American Academy of Pediatrics. Consent for emergency medical services for children and adolescents. Pediatrics 2011;128(2):427-433.</div></div></div> [[Try this question again->Emergency care of a minor - Ethics]] [[Start another case->Hub]]

<div class="ec-scene">Intensive care unit · 17:30</div> An 81-year-old woman with advanced dementia is admitted with aspiration pneumonia and respiratory failure requiring mechanical ventilation. She has no written advance directive. Her son, the designated health care proxy, recalls that she said repeatedly over many years that she never wanted to be kept alive on machines and that she had watched her own sister die that way. Her daughter, who lives out of state, insists that everything be done because she believes her mother would want to fight. <span class="ec-prompt">Which of the following standards should guide the decision?</span> [[Best interests as assessed by the treating team->Substituted judgment - Ethics D1]] [[Consensus of all immediate family members->Substituted judgment - Ethics D2]] [[Preservation of life as the default in the absence of a written directive->Substituted judgment - Ethics D3]] [[Substituted judgment based on her previously expressed wishes->Substituted judgment - Ethics correct]] [[The physician's clinical judgment about likely benefit->Substituted judgment - Ethics D4]] [[The proxy's own assessment of what he would want->Substituted judgment - Ethics D5]]

<span class="ec-case-marker" hidden data-entry="Substituted judgment. Ethics"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Substituted judgment based on her previously expressed wishes</div> When a patient lacks capacity, the decision is made as she would have made it, using her own previously expressed values and statements. Her repeated and specific statements about not wanting mechanical support are the controlling evidence. The best interests standard applies only when the patient's wishes cannot be reconstructed. The daughter's belief about how her mother would feel is not evidence of what the patient actually said, and the proxy, not the family at large, holds decisional authority. <div class="ec-src"><b>Source:</b> Torke AM, Alexander GC, Lantos J. Substituted judgment: the limitations of autonomy in surrogate decision making. J Gen Intern Med 2008;23(9):1514-1517.</div></div> [[Start another case->Hub]] [[Restart this case->Substituted judgment - Ethics]] [[Next case →->Potentially inappropriate treatment - Ethics]]

<span class="ec-case-marker" hidden data-entry="Substituted judgment. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This standard governs only when a patient's preferences are unknown, such as in a never-competent adult. Here her preferences were stated clearly and repeatedly. <div class="ec-teach"><div class="th">What the findings point to</div> When a patient lacks capacity, the decision is made as she would have made it, using her own previously expressed values and statements. Her repeated and specific statements about not wanting mechanical support are the controlling evidence. The best interests standard applies only when the patient's wishes cannot be reconstructed. The daughter's belief about how her mother would feel is not evidence of what the patient actually said, and the proxy, not the family at large, holds decisional authority. <div class="ec-src"><b>Source:</b> Torke AM, Alexander GC, Lantos J. Substituted judgment: the limitations of autonomy in surrogate decision making. J Gen Intern Med 2008;23(9):1514-1517.</div></div></div> [[Try this question again->Substituted judgment - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Substituted judgment. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Requiring unanimity gives an absent relative veto power over a designated proxy and over the patient's own recorded values. <div class="ec-teach"><div class="th">What the findings point to</div> When a patient lacks capacity, the decision is made as she would have made it, using her own previously expressed values and statements. Her repeated and specific statements about not wanting mechanical support are the controlling evidence. The best interests standard applies only when the patient's wishes cannot be reconstructed. The daughter's belief about how her mother would feel is not evidence of what the patient actually said, and the proxy, not the family at large, holds decisional authority. <div class="ec-src"><b>Source:</b> Torke AM, Alexander GC, Lantos J. Substituted judgment: the limitations of autonomy in surrogate decision making. J Gen Intern Med 2008;23(9):1514-1517.</div></div></div> [[Try this question again->Substituted judgment - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Substituted judgment. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> No jurisdiction requires a written document before honoring known wishes. Oral statements to a proxy are valid evidence of preference. <div class="ec-teach"><div class="th">What the findings point to</div> When a patient lacks capacity, the decision is made as she would have made it, using her own previously expressed values and statements. Her repeated and specific statements about not wanting mechanical support are the controlling evidence. The best interests standard applies only when the patient's wishes cannot be reconstructed. The daughter's belief about how her mother would feel is not evidence of what the patient actually said, and the proxy, not the family at large, holds decisional authority. <div class="ec-src"><b>Source:</b> Torke AM, Alexander GC, Lantos J. Substituted judgment: the limitations of autonomy in surrogate decision making. J Gen Intern Med 2008;23(9):1514-1517.</div></div></div> [[Try this question again->Substituted judgment - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Substituted judgment. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Prognostic input informs the discussion and is owed to the family, but the choice among medically reasonable options belongs to the patient through her surrogate. <div class="ec-teach"><div class="th">What the findings point to</div> When a patient lacks capacity, the decision is made as she would have made it, using her own previously expressed values and statements. Her repeated and specific statements about not wanting mechanical support are the controlling evidence. The best interests standard applies only when the patient's wishes cannot be reconstructed. The daughter's belief about how her mother would feel is not evidence of what the patient actually said, and the proxy, not the family at large, holds decisional authority. <div class="ec-src"><b>Source:</b> Torke AM, Alexander GC, Lantos J. Substituted judgment: the limitations of autonomy in surrogate decision making. J Gen Intern Med 2008;23(9):1514-1517.</div></div></div> [[Try this question again->Substituted judgment - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Substituted judgment. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A proxy is required to reason from the patient's values, not to substitute his own preferences for hers. <div class="ec-teach"><div class="th">What the findings point to</div> When a patient lacks capacity, the decision is made as she would have made it, using her own previously expressed values and statements. Her repeated and specific statements about not wanting mechanical support are the controlling evidence. The best interests standard applies only when the patient's wishes cannot be reconstructed. The daughter's belief about how her mother would feel is not evidence of what the patient actually said, and the proxy, not the family at large, holds decisional authority. <div class="ec-src"><b>Source:</b> Torke AM, Alexander GC, Lantos J. Substituted judgment: the limitations of autonomy in surrogate decision making. J Gen Intern Med 2008;23(9):1514-1517.</div></div></div> [[Try this question again->Substituted judgment - Ethics]] [[Start another case->Hub]]

<div class="ec-scene">Intensive care unit · 13:15</div> A 76-year-old man with metastatic pancreatic cancer, refractory septic shock on three vasopressors, and progressive multiorgan failure has had no response to 9 days of maximal support. The oncology team states there is no remaining disease-directed therapy. His wife, his legal surrogate, insists that cardiopulmonary resuscitation be performed if his heart stops and refuses to discuss any limitation. The intensivist believes resuscitation cannot achieve any of the patient's stated goals. <span class="ec-prompt">Which of the following is the most appropriate next step?</span> [[Ask the wife to sign a form acknowledging that resuscitation is futile->Potentially inappropriate treatment - Ethics D1]] [[Comply fully with the request without further discussion->Potentially inappropriate treatment - Ethics D2]] [[Continue current support and start a formal conflict resolution process->Potentially inappropriate treatment - Ethics correct]] [[Transfer decision-making authority to the patient's adult children->Potentially inappropriate treatment - Ethics D3]] [[Withdraw vasopressors and transition to comfort care today->Potentially inappropriate treatment - Ethics D5]] [[Write a do-not-resuscitate order over the surrogate's objection->Potentially inappropriate treatment - Ethics D4]]

<span class="ec-case-marker" hidden data-entry="Potentially inappropriate treatment. Ethics"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Continue current support and start a formal conflict resolution process</div> When a surrogate requests treatment clinicians judge inappropriate, the recommended pathway is procedural rather than unilateral: continue support while enlisting expert consultation, obtaining a second medical opinion, involving the ethics committee, offering transfer to a willing institution, and informing the surrogate of the process and her right to appeal. Unilateral refusal short-circuits safeguards that exist precisely because clinician prognostic judgment is fallible. <div class="ec-src"><b>Source:</b> Bosslet GT, Pope TM, Rubenfeld GD, et al. An Official ATS/AACN/ACCP/ESICM/SCCM Policy Statement: Responding to Requests for Potentially Inappropriate Treatments in Intensive Care Units. Am J Respir Crit Care Med 2015;191(11):1318-1330.</div></div> [[Start another case->Hub]] [[Restart this case->Potentially inappropriate treatment - Ethics]] [[Next case →->Industry gifts - Ethics]]

<span class="ec-case-marker" hidden data-entry="Potentially inappropriate treatment. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Documentation of disagreement is not a resolution process and does nothing to address the underlying conflict or to protect the patient. <div class="ec-teach"><div class="th">What the findings point to</div> When a surrogate requests treatment clinicians judge inappropriate, the recommended pathway is procedural rather than unilateral: continue support while enlisting expert consultation, obtaining a second medical opinion, involving the ethics committee, offering transfer to a willing institution, and informing the surrogate of the process and her right to appeal. Unilateral refusal short-circuits safeguards that exist precisely because clinician prognostic judgment is fallible. <div class="ec-src"><b>Source:</b> Bosslet GT, Pope TM, Rubenfeld GD, et al. An Official ATS/AACN/ACCP/ESICM/SCCM Policy Statement: Responding to Requests for Potentially Inappropriate Treatments in Intensive Care Units. Am J Respir Crit Care Med 2015;191(11):1318-1330.</div></div></div> [[Try this question again->Potentially inappropriate treatment - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Potentially inappropriate treatment. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Acquiescence without engagement abandons both the clinician's professional judgment and the family's need for honest prognostic information. <div class="ec-teach"><div class="th">What the findings point to</div> When a surrogate requests treatment clinicians judge inappropriate, the recommended pathway is procedural rather than unilateral: continue support while enlisting expert consultation, obtaining a second medical opinion, involving the ethics committee, offering transfer to a willing institution, and informing the surrogate of the process and her right to appeal. Unilateral refusal short-circuits safeguards that exist precisely because clinician prognostic judgment is fallible. <div class="ec-src"><b>Source:</b> Bosslet GT, Pope TM, Rubenfeld GD, et al. An Official ATS/AACN/ACCP/ESICM/SCCM Policy Statement: Responding to Requests for Potentially Inappropriate Treatments in Intensive Care Units. Am J Respir Crit Care Med 2015;191(11):1318-1330.</div></div></div> [[Try this question again->Potentially inappropriate treatment - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Potentially inappropriate treatment. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Surrogate authority follows a defined hierarchy. Bypassing a spouse because clinicians dislike her decision is not permissible. <div class="ec-teach"><div class="th">What the findings point to</div> When a surrogate requests treatment clinicians judge inappropriate, the recommended pathway is procedural rather than unilateral: continue support while enlisting expert consultation, obtaining a second medical opinion, involving the ethics committee, offering transfer to a willing institution, and informing the surrogate of the process and her right to appeal. Unilateral refusal short-circuits safeguards that exist precisely because clinician prognostic judgment is fallible. <div class="ec-src"><b>Source:</b> Bosslet GT, Pope TM, Rubenfeld GD, et al. An Official ATS/AACN/ACCP/ESICM/SCCM Policy Statement: Responding to Requests for Potentially Inappropriate Treatments in Intensive Care Units. Am J Respir Crit Care Med 2015;191(11):1318-1330.</div></div></div> [[Try this question again->Potentially inappropriate treatment - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Potentially inappropriate treatment. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Unilateral orders against an explicit surrogate refusal, without exhausting the procedural pathway, are indefensible except where a professional standard clearly and narrowly applies. <div class="ec-teach"><div class="th">What the findings point to</div> When a surrogate requests treatment clinicians judge inappropriate, the recommended pathway is procedural rather than unilateral: continue support while enlisting expert consultation, obtaining a second medical opinion, involving the ethics committee, offering transfer to a willing institution, and informing the surrogate of the process and her right to appeal. Unilateral refusal short-circuits safeguards that exist precisely because clinician prognostic judgment is fallible. <div class="ec-src"><b>Source:</b> Bosslet GT, Pope TM, Rubenfeld GD, et al. An Official ATS/AACN/ACCP/ESICM/SCCM Policy Statement: Responding to Requests for Potentially Inappropriate Treatments in Intensive Care Units. Am J Respir Crit Care Med 2015;191(11):1318-1330.</div></div></div> [[Try this question again->Potentially inappropriate treatment - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Potentially inappropriate treatment. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Withdrawing support the surrogate has not agreed to is a more drastic unilateral action than the one already at issue. <div class="ec-teach"><div class="th">What the findings point to</div> When a surrogate requests treatment clinicians judge inappropriate, the recommended pathway is procedural rather than unilateral: continue support while enlisting expert consultation, obtaining a second medical opinion, involving the ethics committee, offering transfer to a willing institution, and informing the surrogate of the process and her right to appeal. Unilateral refusal short-circuits safeguards that exist precisely because clinician prognostic judgment is fallible. <div class="ec-src"><b>Source:</b> Bosslet GT, Pope TM, Rubenfeld GD, et al. An Official ATS/AACN/ACCP/ESICM/SCCM Policy Statement: Responding to Requests for Potentially Inappropriate Treatments in Intensive Care Units. Am J Respir Crit Care Med 2015;191(11):1318-1330.</div></div></div> [[Try this question again->Potentially inappropriate treatment - Ethics]] [[Start another case->Hub]]

<div class="ec-scene">Clinic office · 12:20</div> A pharmaceutical representative offers to sponsor a weekly catered lunch for the practice, provide branded stationery and pens, and fund the registration and travel to an international conference at which the company's new anticoagulant will be discussed. She notes that no obligation is attached and that many practices in the area accept the same arrangement. The practice currently prescribes a competing anticoagulant as first line. <span class="ec-prompt">Which of the following is the most appropriate response?</span> [[Accept everything but disclose it to patients->Industry gifts - Ethics D1]] [[Accept only the branded pens and stationery->Industry gifts - Ethics D2]] [[Accept only the catered lunches for the staff->Industry gifts - Ethics D3]] [[Accept the conference travel because it is educational->Industry gifts - Ethics D4]] [[Ask the representative to donate an equivalent sum to the clinic->Industry gifts - Ethics D5]] [[Decline all of the offers->Industry gifts - Ethics correct]]

<span class="ec-case-marker" hidden data-entry="Industry gifts. Ethics"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Decline all of the offers</div> Gifts from industry, including modest ones, generate reciprocity that measurably shifts prescribing even when physicians believe themselves unaffected. Meals, branded items, and subsidized travel all carry this effect, and the fact that other practices accept them does not change the analysis. Continuing education should be funded through channels that do not tie support to a specific product, and any industry relationship that remains must be disclosed. <div class="ec-src"><b>Source:</b> American Medical Association. Code of Medical Ethics Opinion 9.6.2: Gifts to Physicians from Industry.</div></div> [[Start another case->Hub]] [[Restart this case->Industry gifts - Ethics]] [[Next case →->Medical interpretation - Ethics]]

<span class="ec-case-marker" hidden data-entry="Industry gifts. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Disclosure does not neutralize the influence of a gift and can paradoxically license the recipient to feel absolved while still being affected. <div class="ec-teach"><div class="th">What the findings point to</div> Gifts from industry, including modest ones, generate reciprocity that measurably shifts prescribing even when physicians believe themselves unaffected. Meals, branded items, and subsidized travel all carry this effect, and the fact that other practices accept them does not change the analysis. Continuing education should be funded through channels that do not tie support to a specific product, and any industry relationship that remains must be disclosed. <div class="ec-src"><b>Source:</b> American Medical Association. Code of Medical Ethics Opinion 9.6.2: Gifts to Physicians from Industry.</div></div></div> [[Try this question again->Industry gifts - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Industry gifts. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Small branded items are among the best-documented drivers of prescribing change precisely because they are dismissed as trivial. <div class="ec-teach"><div class="th">What the findings point to</div> Gifts from industry, including modest ones, generate reciprocity that measurably shifts prescribing even when physicians believe themselves unaffected. Meals, branded items, and subsidized travel all carry this effect, and the fact that other practices accept them does not change the analysis. Continuing education should be funded through channels that do not tie support to a specific product, and any industry relationship that remains must be disclosed. <div class="ec-src"><b>Source:</b> American Medical Association. Code of Medical Ethics Opinion 9.6.2: Gifts to Physicians from Industry.</div></div></div> [[Try this question again->Industry gifts - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Industry gifts. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Sponsored meals are associated with increased prescribing of the sponsor's drug in a dose-dependent fashion. <div class="ec-teach"><div class="th">What the findings point to</div> Gifts from industry, including modest ones, generate reciprocity that measurably shifts prescribing even when physicians believe themselves unaffected. Meals, branded items, and subsidized travel all carry this effect, and the fact that other practices accept them does not change the analysis. Continuing education should be funded through channels that do not tie support to a specific product, and any industry relationship that remains must be disclosed. <div class="ec-src"><b>Source:</b> American Medical Association. Code of Medical Ethics Opinion 9.6.2: Gifts to Physicians from Industry.</div></div></div> [[Try this question again->Industry gifts - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Industry gifts. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Product-linked travel funding is the most valuable form of the offer and creates the strongest obligation. <div class="ec-teach"><div class="th">What the findings point to</div> Gifts from industry, including modest ones, generate reciprocity that measurably shifts prescribing even when physicians believe themselves unaffected. Meals, branded items, and subsidized travel all carry this effect, and the fact that other practices accept them does not change the analysis. Continuing education should be funded through channels that do not tie support to a specific product, and any industry relationship that remains must be disclosed. <div class="ec-src"><b>Source:</b> American Medical Association. Code of Medical Ethics Opinion 9.6.2: Gifts to Physicians from Industry.</div></div></div> [[Try this question again->Industry gifts - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Industry gifts. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Redirecting the money preserves the reciprocal relationship with the manufacturer while adding an appearance of impropriety. <div class="ec-teach"><div class="th">What the findings point to</div> Gifts from industry, including modest ones, generate reciprocity that measurably shifts prescribing even when physicians believe themselves unaffected. Meals, branded items, and subsidized travel all carry this effect, and the fact that other practices accept them does not change the analysis. Continuing education should be funded through channels that do not tie support to a specific product, and any industry relationship that remains must be disclosed. <div class="ec-src"><b>Source:</b> American Medical Association. Code of Medical Ethics Opinion 9.6.2: Gifts to Physicians from Industry.</div></div></div> [[Try this question again->Industry gifts - Ethics]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 20:17</div> A 58-year-old woman who speaks only Mandarin presents with 3 months of rectal bleeding and weight loss. Her 15-year-old grandson, who is bilingual, offers to translate. A certified telephone interpreter service is available and reaches a Mandarin interpreter in under 3 minutes. The physician needs to take a history, discuss the possibility of colorectal cancer, and obtain consent for colonoscopy. <span class="ec-prompt">Which of the following is the most appropriate next step?</span> [[Ask a bilingual member of the housekeeping staff to help->Medical interpretation - Ethics D3]] [[Proceed in English with written materials in Mandarin->Medical interpretation - Ethics D4]] [[Use a machine translation application on a mobile device->Medical interpretation - Ethics D5]] [[Use the certified interpreter service->Medical interpretation - Ethics correct]] [[Use the grandson because he knows her medical history->Medical interpretation - Ethics D1]] [[Use the grandson for the history and an interpreter for consent->Medical interpretation - Ethics D2]]

<span class="ec-case-marker" hidden data-entry="Medical interpretation. Ethics"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Use the certified interpreter service</div> Professional interpretation reduces communication errors with clinical consequences, improves comprehension and adherence, and is required for meaningful access under federal civil rights law. Using a 15-year-old family member introduces omission and substitution errors at a far higher rate, places a child in the position of relaying a cancer discussion about his grandmother, and predictably causes the patient to withhold sensitive information. A 3-minute wait is not a justification. <div class="ec-src"><b>Source:</b> Flores G. The impact of medical interpreter services on the quality of health care: a systematic review. Med Care Res Rev 2005;62(3):255-299.</div></div> [[Start another case->Hub]] [[Restart this case->Medical interpretation - Ethics]] [[Next case →->Advance directive conflict - Ethics]]

<span class="ec-case-marker" hidden data-entry="Medical interpretation. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Familiarity does not confer interpreting competence, and personal involvement is the source of the filtering that makes family interpretation unreliable. <div class="ec-teach"><div class="th">What the findings point to</div> Professional interpretation reduces communication errors with clinical consequences, improves comprehension and adherence, and is required for meaningful access under federal civil rights law. Using a 15-year-old family member introduces omission and substitution errors at a far higher rate, places a child in the position of relaying a cancer discussion about his grandmother, and predictably causes the patient to withhold sensitive information. A 3-minute wait is not a justification. <div class="ec-src"><b>Source:</b> Flores G. The impact of medical interpreter services on the quality of health care: a systematic review. Med Care Res Rev 2005;62(3):255-299.</div></div></div> [[Try this question again->Medical interpretation - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Medical interpretation. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Splitting the encounter still routes the diagnostic discussion through a child and produces an incomplete and possibly inaccurate history. <div class="ec-teach"><div class="th">What the findings point to</div> Professional interpretation reduces communication errors with clinical consequences, improves comprehension and adherence, and is required for meaningful access under federal civil rights law. Using a 15-year-old family member introduces omission and substitution errors at a far higher rate, places a child in the position of relaying a cancer discussion about his grandmother, and predictably causes the patient to withhold sensitive information. A 3-minute wait is not a justification. <div class="ec-src"><b>Source:</b> Flores G. The impact of medical interpreter services on the quality of health care: a systematic review. Med Care Res Rev 2005;62(3):255-299.</div></div></div> [[Try this question again->Medical interpretation - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Medical interpretation. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Untrained bilingual staff produce error rates comparable to family members and are not authorized to interpret clinical information. <div class="ec-teach"><div class="th">What the findings point to</div> Professional interpretation reduces communication errors with clinical consequences, improves comprehension and adherence, and is required for meaningful access under federal civil rights law. Using a 15-year-old family member introduces omission and substitution errors at a far higher rate, places a child in the position of relaying a cancer discussion about his grandmother, and predictably causes the patient to withhold sensitive information. A 3-minute wait is not a justification. <div class="ec-src"><b>Source:</b> Flores G. The impact of medical interpreter services on the quality of health care: a systematic review. Med Care Res Rev 2005;62(3):255-299.</div></div></div> [[Try this question again->Medical interpretation - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Medical interpretation. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Written translation does not permit dialogue, and literacy in the written language cannot be assumed. <div class="ec-teach"><div class="th">What the findings point to</div> Professional interpretation reduces communication errors with clinical consequences, improves comprehension and adherence, and is required for meaningful access under federal civil rights law. Using a 15-year-old family member introduces omission and substitution errors at a far higher rate, places a child in the position of relaying a cancer discussion about his grandmother, and predictably causes the patient to withhold sensitive information. A 3-minute wait is not a justification. <div class="ec-src"><b>Source:</b> Flores G. The impact of medical interpreter services on the quality of health care: a systematic review. Med Care Res Rev 2005;62(3):255-299.</div></div></div> [[Try this question again->Medical interpretation - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Medical interpretation. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Machine translation is not validated for clinical consent discussions and fails on the idiomatic and emotionally weighted content this conversation requires. <div class="ec-teach"><div class="th">What the findings point to</div> Professional interpretation reduces communication errors with clinical consequences, improves comprehension and adherence, and is required for meaningful access under federal civil rights law. Using a 15-year-old family member introduces omission and substitution errors at a far higher rate, places a child in the position of relaying a cancer discussion about his grandmother, and predictably causes the patient to withhold sensitive information. A 3-minute wait is not a justification. <div class="ec-src"><b>Source:</b> Flores G. The impact of medical interpreter services on the quality of health care: a systematic review. Med Care Res Rev 2005;62(3):255-299.</div></div></div> [[Try this question again->Medical interpretation - Ethics]] [[Start another case->Hub]]

<div class="ec-scene">Outpatient psychiatry · 16:45</div> A 29-year-old man in weekly psychotherapy describes escalating rage toward a named former coworker. He states that he has purchased a weapon, has driven past the coworker's home twice this week, and intends to confront and kill him within days. He is fully oriented, is not psychotic, and asks the physician to keep this confidential because it was said in therapy. He has no prior violent convictions. <span class="ec-prompt">Which of the following is the most appropriate next step?</span> [[Increase the frequency of therapy sessions and reassess in 1 week->Duty to warn - Ethics D1]] [[Maintain confidentiality because the disclosure occurred in therapy->Duty to warn - Ethics D2]] [[Notify only the patient's family so they can intervene->Duty to warn - Ethics D3]] [[Notify the identified person and law enforcement->Duty to warn - Ethics correct]] [[Obtain a signed no-harm contract from the patient->Duty to warn - Ethics D4]] [[Report the threat to the state licensing board->Duty to warn - Ethics D5]]

<span class="ec-case-marker" hidden data-entry="Duty to warn. Ethics"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Notify the identified person and law enforcement</div> When a patient makes a credible threat of serious violence against an identifiable victim, the therapeutic obligation to protect overrides confidentiality. The specificity here is what makes the threat actionable: a named target, a stated intent, a means already acquired, and reconnaissance already performed. The required action is to take reasonable steps to protect, which includes warning the intended victim and notifying police, and to consider whether the patient meets criteria for involuntary hold. <div class="ec-src"><b>Source:</b> Tarasoff v. Regents of the University of California, 17 Cal.3d 425 (1976).</div></div> [[Start another case->Hub]] [[Restart this case->Duty to warn - Ethics]] [[Next case →->Tobacco cessation pharmacotherapy - Prevention]]

<span class="ec-case-marker" hidden data-entry="Duty to warn. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Intensifying treatment does not protect a named third party during the interval in which the patient has stated he intends to act. <div class="ec-teach"><div class="th">What the findings point to</div> When a patient makes a credible threat of serious violence against an identifiable victim, the therapeutic obligation to protect overrides confidentiality. The specificity here is what makes the threat actionable: a named target, a stated intent, a means already acquired, and reconnaissance already performed. The required action is to take reasonable steps to protect, which includes warning the intended victim and notifying police, and to consider whether the patient meets criteria for involuntary hold. <div class="ec-src"><b>Source:</b> Tarasoff v. Regents of the University of California, 17 Cal.3d 425 (1976).</div></div></div> [[Try this question again->Duty to warn - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Duty to warn. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Privilege is not absolute. It yields when a specific person faces a serious risk of harm that disclosure could prevent. <div class="ec-teach"><div class="th">What the findings point to</div> When a patient makes a credible threat of serious violence against an identifiable victim, the therapeutic obligation to protect overrides confidentiality. The specificity here is what makes the threat actionable: a named target, a stated intent, a means already acquired, and reconnaissance already performed. The required action is to take reasonable steps to protect, which includes warning the intended victim and notifying police, and to consider whether the patient meets criteria for involuntary hold. <div class="ec-src"><b>Source:</b> Tarasoff v. Regents of the University of California, 17 Cal.3d 425 (1976).</div></div></div> [[Try this question again->Duty to warn - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Duty to warn. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Relatives have no capacity to protect the target and no authority to act, and this discloses confidential material without accomplishing the protective purpose. <div class="ec-teach"><div class="th">What the findings point to</div> When a patient makes a credible threat of serious violence against an identifiable victim, the therapeutic obligation to protect overrides confidentiality. The specificity here is what makes the threat actionable: a named target, a stated intent, a means already acquired, and reconnaissance already performed. The required action is to take reasonable steps to protect, which includes warning the intended victim and notifying police, and to consider whether the patient meets criteria for involuntary hold. <div class="ec-src"><b>Source:</b> Tarasoff v. Regents of the University of California, 17 Cal.3d 425 (1976).</div></div></div> [[Try this question again->Duty to warn - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Duty to warn. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Written agreements of this kind have no demonstrated protective effect and provide false reassurance. <div class="ec-teach"><div class="th">What the findings point to</div> When a patient makes a credible threat of serious violence against an identifiable victim, the therapeutic obligation to protect overrides confidentiality. The specificity here is what makes the threat actionable: a named target, a stated intent, a means already acquired, and reconnaissance already performed. The required action is to take reasonable steps to protect, which includes warning the intended victim and notifying police, and to consider whether the patient meets criteria for involuntary hold. <div class="ec-src"><b>Source:</b> Tarasoff v. Regents of the University of California, 17 Cal.3d 425 (1976).</div></div></div> [[Try this question again->Duty to warn - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Duty to warn. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Licensing boards regulate clinicians. They have no role in protecting a threatened member of the public. <div class="ec-teach"><div class="th">What the findings point to</div> When a patient makes a credible threat of serious violence against an identifiable victim, the therapeutic obligation to protect overrides confidentiality. The specificity here is what makes the threat actionable: a named target, a stated intent, a means already acquired, and reconnaissance already performed. The required action is to take reasonable steps to protect, which includes warning the intended victim and notifying police, and to consider whether the patient meets criteria for involuntary hold. <div class="ec-src"><b>Source:</b> Tarasoff v. Regents of the University of California, 17 Cal.3d 425 (1976).</div></div></div> [[Try this question again->Duty to warn - Ethics]] [[Start another case->Hub]]

<div class="ec-scene">Infectious disease clinic · 14:00</div> A 31-year-old man is newly diagnosed with HIV infection. His CD4 count is 410/mm3 and viral load is 62,000 copies/mL. He has one regular female partner of 2 years and reports condomless intercourse. He starts antiretroviral therapy. He refuses to tell his partner, saying he fears she will leave him, and asks that she not be contacted. He has no history of violence toward her. <span class="ec-prompt">Which of the following is the most appropriate next step?</span> [[Accept his refusal and continue counseling him at each visit->Partner notification - Ethics D1]] [[Contact the partner directly and disclose his diagnosis->Partner notification - Ethics D2]] [[Defer notification until his viral load becomes undetectable->Partner notification - Ethics D3]] [[Discharge him from the practice for refusing to disclose->Partner notification - Ethics D4]] [[Involve the health department partner services program->Partner notification - Ethics correct]] [[Prescribe preexposure prophylaxis for the partner without telling her why->Partner notification - Ethics D5]]

<span class="ec-case-marker" hidden data-entry="Partner notification. Ethics"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Involve the health department partner services program</div> Partner notification is a public health function. The correct route is to report the case as required and engage partner services, which contacts exposed partners confidentially and without naming the index patient. This protects a person at ongoing risk of a serious transmissible infection while preserving as much of the patient's confidentiality as possible. Counseling him to disclose himself should continue in parallel, but his refusal does not end the obligation to the partner. <div class="ec-src"><b>Source:</b> Centers for Disease Control and Prevention. Recommendations for partner services programs for HIV infection, syphilis, gonorrhea, and chlamydial infection. MMWR Recomm Rep 2008;57(RR-9):1-83.</div></div> [[Start another case->Hub]] [[Restart this case->Partner notification - Ethics]] [[Next case →->Hepatitis C screening - Prevention]]

<span class="ec-case-marker" hidden data-entry="Partner notification. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Repeated counseling without any notification pathway leaves an identifiable person exposed indefinitely to a preventable infection. <div class="ec-teach"><div class="th">What the findings point to</div> Partner notification is a public health function. The correct route is to report the case as required and engage partner services, which contacts exposed partners confidentially and without naming the index patient. This protects a person at ongoing risk of a serious transmissible infection while preserving as much of the patient's confidentiality as possible. Counseling him to disclose himself should continue in parallel, but his refusal does not end the obligation to the partner. <div class="ec-src"><b>Source:</b> Centers for Disease Control and Prevention. Recommendations for partner services programs for HIV infection, syphilis, gonorrhea, and chlamydial infection. MMWR Recomm Rep 2008;57(RR-9):1-83.</div></div></div> [[Try this question again->Partner notification - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Partner notification. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Direct disclosure by the treating physician names the index patient unnecessarily when a confidential public health mechanism exists for exactly this purpose. <div class="ec-teach"><div class="th">What the findings point to</div> Partner notification is a public health function. The correct route is to report the case as required and engage partner services, which contacts exposed partners confidentially and without naming the index patient. This protects a person at ongoing risk of a serious transmissible infection while preserving as much of the patient's confidentiality as possible. Counseling him to disclose himself should continue in parallel, but his refusal does not end the obligation to the partner. <div class="ec-src"><b>Source:</b> Centers for Disease Control and Prevention. Recommendations for partner services programs for HIV infection, syphilis, gonorrhea, and chlamydial infection. MMWR Recomm Rep 2008;57(RR-9):1-83.</div></div></div> [[Try this question again->Partner notification - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Partner notification. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Suppression takes months and is not guaranteed. The partner's exposure is occurring now. <div class="ec-teach"><div class="th">What the findings point to</div> Partner notification is a public health function. The correct route is to report the case as required and engage partner services, which contacts exposed partners confidentially and without naming the index patient. This protects a person at ongoing risk of a serious transmissible infection while preserving as much of the patient's confidentiality as possible. Counseling him to disclose himself should continue in parallel, but his refusal does not end the obligation to the partner. <div class="ec-src"><b>Source:</b> Centers for Disease Control and Prevention. Recommendations for partner services programs for HIV infection, syphilis, gonorrhea, and chlamydial infection. MMWR Recomm Rep 2008;57(RR-9):1-83.</div></div></div> [[Try this question again->Partner notification - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Partner notification. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Terminating care removes the one person able to counsel him and to keep him virally suppressed, increasing risk to his partner. <div class="ec-teach"><div class="th">What the findings point to</div> Partner notification is a public health function. The correct route is to report the case as required and engage partner services, which contacts exposed partners confidentially and without naming the index patient. This protects a person at ongoing risk of a serious transmissible infection while preserving as much of the patient's confidentiality as possible. Counseling him to disclose himself should continue in parallel, but his refusal does not end the obligation to the partner. <div class="ec-src"><b>Source:</b> Centers for Disease Control and Prevention. Recommendations for partner services programs for HIV infection, syphilis, gonorrhea, and chlamydial infection. MMWR Recomm Rep 2008;57(RR-9):1-83.</div></div></div> [[Try this question again->Partner notification - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Partner notification. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Prescribing to a person who has not been evaluated, tested, or informed is not possible and would itself be a serious breach. <div class="ec-teach"><div class="th">What the findings point to</div> Partner notification is a public health function. The correct route is to report the case as required and engage partner services, which contacts exposed partners confidentially and without naming the index patient. This protects a person at ongoing risk of a serious transmissible infection while preserving as much of the patient's confidentiality as possible. Counseling him to disclose himself should continue in parallel, but his refusal does not end the obligation to the partner. <div class="ec-src"><b>Source:</b> Centers for Disease Control and Prevention. Recommendations for partner services programs for HIV infection, syphilis, gonorrhea, and chlamydial infection. MMWR Recomm Rep 2008;57(RR-9):1-83.</div></div></div> [[Try this question again->Partner notification - Ethics]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 01:20</div> A 79-year-old woman with end-stage chronic obstructive pulmonary disease arrives in severe respiratory distress. She is obtunded with a respirations are 8/min and a PaCO2 of 88 mm Hg. Her chart contains a valid state advance directive, signed 2 years ago and witnessed, declining intubation and mechanical ventilation under any circumstance. Her son arrives and demands that she be intubated, saying she was confused when she signed it, although she was documented as fully capacitated at the time. <span class="ec-prompt">Which of the following is the most appropriate next step?</span> [[Ask the hospital attorney whether the directive is enforceable->Advance directive conflict - Ethics D3]] [[Consider the directive void because it is 2 years old->Advance directive conflict - Ethics D4]] [[Honor the directive and provide noninvasive support and comfort measures->Advance directive conflict - Ethics correct]] [[Intubate because the son is the next of kin->Advance directive conflict - Ethics D2]] [[Intubate now and address the directive after stabilization->Advance directive conflict - Ethics D1]] [[Perform a trial of intubation with planned extubation in 48 hours->Advance directive conflict - Ethics D5]]

<span class="ec-case-marker" hidden data-entry="Advance directive conflict. Ethics"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Honor the directive and provide noninvasive support and comfort measures</div> A valid advance directive executed while the patient had capacity governs when she can no longer speak. The son may not override it, and his belief about her state of mind at signing is contradicted by the contemporaneous documentation. The correct course is to follow the document while treating aggressively within its limits, which for hypercapnic respiratory failure means noninvasive ventilation if she has not declined it, bronchodilators, steroids, and symptom control. <div class="ec-src"><b>Source:</b> American Medical Association. Code of Medical Ethics Opinion 5.2: Advance Directives.</div></div> [[Start another case->Hub]] [[Restart this case->Advance directive conflict - Ethics]] [[Next case →->Family request for nondisclosure - Ethics]]

<span class="ec-case-marker" hidden data-entry="Advance directive conflict. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Intubating against a valid refusal is the specific act she prohibited, and reversing it later does not undo the violation. <div class="ec-teach"><div class="th">What the findings point to</div> A valid advance directive executed while the patient had capacity governs when she can no longer speak. The son may not override it, and his belief about her state of mind at signing is contradicted by the contemporaneous documentation. The correct course is to follow the document while treating aggressively within its limits, which for hypercapnic respiratory failure means noninvasive ventilation if she has not declined it, bronchodilators, steroids, and symptom control. <div class="ec-src"><b>Source:</b> American Medical Association. Code of Medical Ethics Opinion 5.2: Advance Directives.</div></div></div> [[Try this question again->Advance directive conflict - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Advance directive conflict. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Next-of-kin authority applies when a patient's wishes are unknown. A valid directive displaces surrogate discretion on the question it addresses. <div class="ec-teach"><div class="th">What the findings point to</div> A valid advance directive executed while the patient had capacity governs when she can no longer speak. The son may not override it, and his belief about her state of mind at signing is contradicted by the contemporaneous documentation. The correct course is to follow the document while treating aggressively within its limits, which for hypercapnic respiratory failure means noninvasive ventilation if she has not declined it, bronchodilators, steroids, and symptom control. <div class="ec-src"><b>Source:</b> American Medical Association. Code of Medical Ethics Opinion 5.2: Advance Directives.</div></div></div> [[Try this question again->Advance directive conflict - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Advance directive conflict. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A directive that is signed, witnessed, and valid under state law does not require legal review at the bedside during respiratory failure. <div class="ec-teach"><div class="th">What the findings point to</div> A valid advance directive executed while the patient had capacity governs when she can no longer speak. The son may not override it, and his belief about her state of mind at signing is contradicted by the contemporaneous documentation. The correct course is to follow the document while treating aggressively within its limits, which for hypercapnic respiratory failure means noninvasive ventilation if she has not declined it, bronchodilators, steroids, and symptom control. <div class="ec-src"><b>Source:</b> American Medical Association. Code of Medical Ethics Opinion 5.2: Advance Directives.</div></div></div> [[Try this question again->Advance directive conflict - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Advance directive conflict. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Advance directives do not expire with time. They remain effective until revoked by the patient. <div class="ec-teach"><div class="th">What the findings point to</div> A valid advance directive executed while the patient had capacity governs when she can no longer speak. The son may not override it, and his belief about her state of mind at signing is contradicted by the contemporaneous documentation. The correct course is to follow the document while treating aggressively within its limits, which for hypercapnic respiratory failure means noninvasive ventilation if she has not declined it, bronchodilators, steroids, and symptom control. <div class="ec-src"><b>Source:</b> American Medical Association. Code of Medical Ethics Opinion 5.2: Advance Directives.</div></div></div> [[Try this question again->Advance directive conflict - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Advance directive conflict. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A time-limited trial is a reasonable tool when goals are uncertain. Here the patient has already answered the question. <div class="ec-teach"><div class="th">What the findings point to</div> A valid advance directive executed while the patient had capacity governs when she can no longer speak. The son may not override it, and his belief about her state of mind at signing is contradicted by the contemporaneous documentation. The correct course is to follow the document while treating aggressively within its limits, which for hypercapnic respiratory failure means noninvasive ventilation if she has not declined it, bronchodilators, steroids, and symptom control. <div class="ec-src"><b>Source:</b> American Medical Association. Code of Medical Ethics Opinion 5.2: Advance Directives.</div></div></div> [[Try this question again->Advance directive conflict - Ethics]] [[Start another case->Hub]]

<div class="ec-scene">Oncology clinic · 10:05</div> Biopsy confirms metastatic gastric adenocarcinoma in a 68-year-old woman. Before the physician enter the room, her two adult children intercept the physician and ask that she not be told the diagnosis, explaining that in their family bad news is shared with relatives and that hearing it will destroy her will to live. The patient is alert, fully oriented, and has previously asked the physician directly to tell her everything the tests show. <span class="ec-prompt">Which of the following is the most appropriate next step?</span> [[Agree to withhold the diagnosis at the family's request->Family request for nondisclosure - Ethics D1]] [[Ask her children to deliver the diagnosis themselves->Family request for nondisclosure - Ethics D5]] [[Ask the patient how much she wishes to know->Family request for nondisclosure - Ethics correct]] [[Disclose the diagnosis immediately without further preparation->Family request for nondisclosure - Ethics D2]] [[Refer the family to the ethics committee before speaking with her->Family request for nondisclosure - Ethics D3]] [[Tell her only that the results were abnormal and require treatment->Family request for nondisclosure - Ethics D4]]

<span class="ec-case-marker" hidden data-entry="Family request for nondisclosure. Ethics"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Ask the patient how much she wishes to know</div> Information belongs to the patient, and only she can waive her right to it. The correct step is to ask her directly how much she wants to know and whom she wants involved, which respects both her autonomy and the family's cultural framing without presuming either answer. If she asks not to be told and to have her children decide, that is a valid waiver. Her prior statement that she wants everything disclosed makes concealment indefensible. <div class="ec-src"><b>Source:</b> American Medical Association. Code of Medical Ethics Opinion 2.1.3: Withholding Information from Patients.</div></div> [[Start another case->Hub]] [[Restart this case->Family request for nondisclosure - Ethics]] [[Next case →->Inappropriate antibiotic request - Ethics]]

<span class="ec-case-marker" hidden data-entry="Family request for nondisclosure. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Relatives cannot waive a capacitated patient's right to her own medical information, and she has already asked to be told. <div class="ec-teach"><div class="th">What the findings point to</div> Information belongs to the patient, and only she can waive her right to it. The correct step is to ask her directly how much she wants to know and whom she wants involved, which respects both her autonomy and the family's cultural framing without presuming either answer. If she asks not to be told and to have her children decide, that is a valid waiver. Her prior statement that she wants everything disclosed makes concealment indefensible. <div class="ec-src"><b>Source:</b> American Medical Association. Code of Medical Ethics Opinion 2.1.3: Withholding Information from Patients.</div></div></div> [[Try this question again->Family request for nondisclosure - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Family request for nondisclosure. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Blunt disclosure without first establishing what she wants to know and preparing her ignores the sequencing that makes bad news survivable to hear. <div class="ec-teach"><div class="th">What the findings point to</div> Information belongs to the patient, and only she can waive her right to it. The correct step is to ask her directly how much she wants to know and whom she wants involved, which respects both her autonomy and the family's cultural framing without presuming either answer. If she asks not to be told and to have her children decide, that is a valid waiver. Her prior statement that she wants everything disclosed makes concealment indefensible. <div class="ec-src"><b>Source:</b> American Medical Association. Code of Medical Ethics Opinion 2.1.3: Withholding Information from Patients.</div></div></div> [[Try this question again->Family request for nondisclosure - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Family request for nondisclosure. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Consultation is unnecessary for a question the patient herself can answer in the next few minutes. <div class="ec-teach"><div class="th">What the findings point to</div> Information belongs to the patient, and only she can waive her right to it. The correct step is to ask her directly how much she wants to know and whom she wants involved, which respects both her autonomy and the family's cultural framing without presuming either answer. If she asks not to be told and to have her children decide, that is a valid waiver. Her prior statement that she wants everything disclosed makes concealment indefensible. <div class="ec-src"><b>Source:</b> American Medical Association. Code of Medical Ethics Opinion 2.1.3: Withholding Information from Patients.</div></div></div> [[Try this question again->Family request for nondisclosure - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Family request for nondisclosure. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Vague euphemism leaves her unable to make decisions about therapy she may or may not want and is a form of deception. <div class="ec-teach"><div class="th">What the findings point to</div> Information belongs to the patient, and only she can waive her right to it. The correct step is to ask her directly how much she wants to know and whom she wants involved, which respects both her autonomy and the family's cultural framing without presuming either answer. If she asks not to be told and to have her children decide, that is a valid waiver. Her prior statement that she wants everything disclosed makes concealment indefensible. <div class="ec-src"><b>Source:</b> American Medical Association. Code of Medical Ethics Opinion 2.1.3: Withholding Information from Patients.</div></div></div> [[Try this question again->Family request for nondisclosure - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Family request for nondisclosure. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Delegating disclosure to family who have stated they intend to conceal it guarantees she is not informed. <div class="ec-teach"><div class="th">What the findings point to</div> Information belongs to the patient, and only she can waive her right to it. The correct step is to ask her directly how much she wants to know and whom she wants involved, which respects both her autonomy and the family's cultural framing without presuming either answer. If she asks not to be told and to have her children decide, that is a valid waiver. Her prior statement that she wants everything disclosed makes concealment indefensible. <div class="ec-src"><b>Source:</b> American Medical Association. Code of Medical Ethics Opinion 2.1.3: Withholding Information from Patients.</div></div></div> [[Try this question again->Family request for nondisclosure - Ethics]] [[Start another case->Hub]]

<div class="ec-scene">Urgent care · 18:30</div> A 41-year-old woman requests antibiotics for 3 days of nasal congestion, sore throat, and a nonproductive cough. Temperature is 37.2°C. Examination shows clear nasal discharge, a mildly erythematous pharynx without exudate, and clear lungs. She has no comorbidities. She states that antibiotics always cure this for her, that she has an important presentation on Monday, and that she will simply go elsewhere if the physician refuse. Rapid streptococcal antigen testing is negative. <span class="ec-prompt">Which of the following is the most appropriate response?</span> [[Explain why antibiotics are not indicated and offer symptomatic treatment->Inappropriate antibiotic request - Ethics correct]] [[Order sinus radiography to justify the decision->Inappropriate antibiotic request - Ethics D4]] [[Prescribe a nasal antibiotic preparation as a compromise->Inappropriate antibiotic request - Ethics D5]] [[Prescribe amoxicillin because she will otherwise obtain it elsewhere->Inappropriate antibiotic request - Ethics D1]] [[Prescribe azithromycin as a lower-risk compromise->Inappropriate antibiotic request - Ethics D2]] [[Provide a delayed prescription to fill if she is not better in 3 days->Inappropriate antibiotic request - Ethics D3]]

<span class="ec-case-marker" hidden data-entry="Inappropriate antibiotic request. Ethics"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Explain why antibiotics are not indicated and offer symptomatic treatment</div> Prescribing an antibiotic for a viral upper respiratory infection provides no benefit, exposes her to adverse effects and Clostridioides difficile risk, and contributes to resistance that harms other patients. Patient satisfaction is not an indication. The effective response pairs a clear explanation with a positive treatment plan and specific return precautions, which achieves satisfaction comparable to prescribing while avoiding the harm. <div class="ec-src"><b>Source:</b> Fleming-Dutra KE, Hersh AL, Shapiro DJ, et al. Prevalence of inappropriate antibiotic prescriptions among US ambulatory care visits, 2010-2011. JAMA 2016;315(17):1864-1873.</div></div> [[Start another case->Hub]] [[Restart this case->Inappropriate antibiotic request - Ethics]] [[Next case →->Diagnostic error - Opening]]

<span class="ec-case-marker" hidden data-entry="Inappropriate antibiotic request. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The possibility that another clinician will prescribe inappropriately does not create a justification to do so yourself. <div class="ec-teach"><div class="th">What the findings point to</div> Prescribing an antibiotic for a viral upper respiratory infection provides no benefit, exposes her to adverse effects and Clostridioides difficile risk, and contributes to resistance that harms other patients. Patient satisfaction is not an indication. The effective response pairs a clear explanation with a positive treatment plan and specific return precautions, which achieves satisfaction comparable to prescribing while avoiding the harm. <div class="ec-src"><b>Source:</b> Fleming-Dutra KE, Hersh AL, Shapiro DJ, et al. Prevalence of inappropriate antibiotic prescriptions among US ambulatory care visits, 2010-2011. JAMA 2016;315(17):1864-1873.</div></div></div> [[Try this question again->Inappropriate antibiotic request - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Inappropriate antibiotic request. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Macrolides carry QT prolongation and resistance concerns and are no more indicated than any other antibiotic for a viral illness. <div class="ec-teach"><div class="th">What the findings point to</div> Prescribing an antibiotic for a viral upper respiratory infection provides no benefit, exposes her to adverse effects and Clostridioides difficile risk, and contributes to resistance that harms other patients. Patient satisfaction is not an indication. The effective response pairs a clear explanation with a positive treatment plan and specific return precautions, which achieves satisfaction comparable to prescribing while avoiding the harm. <div class="ec-src"><b>Source:</b> Fleming-Dutra KE, Hersh AL, Shapiro DJ, et al. Prevalence of inappropriate antibiotic prescriptions among US ambulatory care visits, 2010-2011. JAMA 2016;315(17):1864-1873.</div></div></div> [[Try this question again->Inappropriate antibiotic request - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Inappropriate antibiotic request. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Delayed prescribing has a role in selected cases such as acute otitis media, but here the illness is clearly viral and most such prescriptions are filled. <div class="ec-teach"><div class="th">What the findings point to</div> Prescribing an antibiotic for a viral upper respiratory infection provides no benefit, exposes her to adverse effects and Clostridioides difficile risk, and contributes to resistance that harms other patients. Patient satisfaction is not an indication. The effective response pairs a clear explanation with a positive treatment plan and specific return precautions, which achieves satisfaction comparable to prescribing while avoiding the harm. <div class="ec-src"><b>Source:</b> Fleming-Dutra KE, Hersh AL, Shapiro DJ, et al. Prevalence of inappropriate antibiotic prescriptions among US ambulatory care visits, 2010-2011. JAMA 2016;315(17):1864-1873.</div></div></div> [[Try this question again->Inappropriate antibiotic request - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Inappropriate antibiotic request. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Imaging cannot distinguish viral from bacterial sinusitis at 3 days and adds cost and radiation to support a decision already clear on history. <div class="ec-teach"><div class="th">What the findings point to</div> Prescribing an antibiotic for a viral upper respiratory infection provides no benefit, exposes her to adverse effects and Clostridioides difficile risk, and contributes to resistance that harms other patients. Patient satisfaction is not an indication. The effective response pairs a clear explanation with a positive treatment plan and specific return precautions, which achieves satisfaction comparable to prescribing while avoiding the harm. <div class="ec-src"><b>Source:</b> Fleming-Dutra KE, Hersh AL, Shapiro DJ, et al. Prevalence of inappropriate antibiotic prescriptions among US ambulatory care visits, 2010-2011. JAMA 2016;315(17):1864-1873.</div></div></div> [[Try this question again->Inappropriate antibiotic request - Ethics]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Inappropriate antibiotic request. Ethics"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Topical antibiotics have no role in viral upper respiratory infection and normalize the expectation that an antibiotic is owed. <div class="ec-teach"><div class="th">What the findings point to</div> Prescribing an antibiotic for a viral upper respiratory infection provides no benefit, exposes her to adverse effects and Clostridioides difficile risk, and contributes to resistance that harms other patients. Patient satisfaction is not an indication. The effective response pairs a clear explanation with a positive treatment plan and specific return precautions, which achieves satisfaction comparable to prescribing while avoiding the harm. <div class="ec-src"><b>Source:</b> Fleming-Dutra KE, Hersh AL, Shapiro DJ, et al. Prevalence of inappropriate antibiotic prescriptions among US ambulatory care visits, 2010-2011. JAMA 2016;315(17):1864-1873.</div></div></div> [[Try this question again->Inappropriate antibiotic request - Ethics]] [[Start another case->Hub]]

<div class="ec-scene">Morbidity and mortality conference · 07:00</div> A patient received a 10-fold overdose of insulin. Review shows the order was written as "10U" and read as 100 units, that the ordering system permitted free-text insulin orders, that the unit had no independent double-check policy for high-alert medications, and that the nurse who administered the dose had been redeployed from another floor without orientation. The nurse and the prescriber were both experienced and had no prior events. <span class="ec-prompt">Which of the following best describes the primary contributor to this event?</span> [[A knowledge deficit in the administering nurse->Latent system failure - QI D1]] [[A lapse in attention by the prescribing physician->Latent system failure - QI D2]] [[Inadequate staffing on the receiving unit->Latent system failure - QI D3]] [[Insufficient pharmacist review of the order->Latent system failure - QI D4]] [[Latent conditions built into the system->Latent system failure - QI correct]] [[Violation of established medication policy->Latent system failure - QI D5]]

<span class="ec-case-marker" hidden data-entry="Latent system failure. QI"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Latent conditions built into the system</div> Active failures are the unsafe acts at the sharp end. Latent conditions are the decisions embedded in the system long before, which lie dormant until they combine with an active failure to produce harm. Here the free-text order field, the abbreviation permitted in the order set, the absence of a double-check policy, and the unoriented float nurse were all present before anyone touched the patient. Defenses fail when holes in successive layers align, and correcting only the sharp-end act leaves every hole open. <div class="ec-src"><b>Source:</b> Reason J. Human error: models and management. BMJ 2000;320(7237):768-770.</div></div> [[Start another case->Hub]] [[Restart this case->Latent system failure - QI]] [[Next case →->Proactive risk analysis - QI]]

<span class="ec-case-marker" hidden data-entry="Latent system failure. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> She was experienced and the misreading arose from an ambiguous abbreviation the system permitted, not from a gap in her knowledge of insulin. <div class="ec-teach"><div class="th">What the findings point to</div> Active failures are the unsafe acts at the sharp end. Latent conditions are the decisions embedded in the system long before, which lie dormant until they combine with an active failure to produce harm. Here the free-text order field, the abbreviation permitted in the order set, the absence of a double-check policy, and the unoriented float nurse were all present before anyone touched the patient. Defenses fail when holes in successive layers align, and correcting only the sharp-end act leaves every hole open. <div class="ec-src"><b>Source:</b> Reason J. Human error: models and management. BMJ 2000;320(7237):768-770.</div></div></div> [[Try this question again->Latent system failure - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Latent system failure. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The abbreviation is a recognized hazard specifically because attentive practitioners misread it. Attributing the event to inattention stops the analysis where it should begin. <div class="ec-teach"><div class="th">What the findings point to</div> Active failures are the unsafe acts at the sharp end. Latent conditions are the decisions embedded in the system long before, which lie dormant until they combine with an active failure to produce harm. Here the free-text order field, the abbreviation permitted in the order set, the absence of a double-check policy, and the unoriented float nurse were all present before anyone touched the patient. Defenses fail when holes in successive layers align, and correcting only the sharp-end act leaves every hole open. <div class="ec-src"><b>Source:</b> Reason J. Human error: models and management. BMJ 2000;320(7237):768-770.</div></div></div> [[Try this question again->Latent system failure - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Latent system failure. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Staffing contributed, but it is one of several latent conditions rather than the framework explaining how they combined. <div class="ec-teach"><div class="th">What the findings point to</div> Active failures are the unsafe acts at the sharp end. Latent conditions are the decisions embedded in the system long before, which lie dormant until they combine with an active failure to produce harm. Here the free-text order field, the abbreviation permitted in the order set, the absence of a double-check policy, and the unoriented float nurse were all present before anyone touched the patient. Defenses fail when holes in successive layers align, and correcting only the sharp-end act leaves every hole open. <div class="ec-src"><b>Source:</b> Reason J. Human error: models and management. BMJ 2000;320(7237):768-770.</div></div></div> [[Try this question again->Latent system failure - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Latent system failure. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Missing verification is another absent defense, again one hole among several rather than the primary explanatory factor. <div class="ec-teach"><div class="th">What the findings point to</div> Active failures are the unsafe acts at the sharp end. Latent conditions are the decisions embedded in the system long before, which lie dormant until they combine with an active failure to produce harm. Here the free-text order field, the abbreviation permitted in the order set, the absence of a double-check policy, and the unoriented float nurse were all present before anyone touched the patient. Defenses fail when holes in successive layers align, and correcting only the sharp-end act leaves every hole open. <div class="ec-src"><b>Source:</b> Reason J. Human error: models and management. BMJ 2000;320(7237):768-770.</div></div></div> [[Try this question again->Latent system failure - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Latent system failure. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> No policy requiring an independent double-check existed to violate, which is itself part of the problem. <div class="ec-teach"><div class="th">What the findings point to</div> Active failures are the unsafe acts at the sharp end. Latent conditions are the decisions embedded in the system long before, which lie dormant until they combine with an active failure to produce harm. Here the free-text order field, the abbreviation permitted in the order set, the absence of a double-check policy, and the unoriented float nurse were all present before anyone touched the patient. Defenses fail when holes in successive layers align, and correcting only the sharp-end act leaves every hole open. <div class="ec-src"><b>Source:</b> Reason J. Human error: models and management. BMJ 2000;320(7237):768-770.</div></div></div> [[Try this question again->Latent system failure - QI]] [[Start another case->Hub]]

<div class="ec-scene">Quality office · 09:45</div> A hospital is preparing to launch a new outpatient chemotherapy infusion unit. No patient has yet been treated there. Leadership wants to identify, before the first patient arrives, where the ordering, verification, compounding, and administration process is most likely to fail, and to rank potential failures so that resources are directed at those with the greatest combination of likelihood and severity. <span class="ec-prompt">Which of the following methods is most appropriate for this purpose?</span> [[Failure mode and effects analysis->Proactive risk analysis - QI correct]] [[Incident report trend analysis->Proactive risk analysis - QI D3]] [[Morbidity and mortality conference review->Proactive risk analysis - QI D4]] [[Patient satisfaction survey of the existing infusion service->Proactive risk analysis - QI D5]] [[Root cause analysis->Proactive risk analysis - QI D1]] [[Statistical process control charting->Proactive risk analysis - QI D2]]

<span class="ec-case-marker" hidden data-entry="Proactive risk analysis. QI"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Failure mode and effects analysis</div> This method is prospective. A multidisciplinary team maps each step of a planned process, enumerates the ways each step could fail, scores each failure mode for frequency, severity, and detectability, and directs redesign at the highest-scoring modes before any patient is exposed. It is the standard tool when the question is what could go wrong rather than what did go wrong. <div class="ec-src"><b>Source:</b> DeRosier J, Stalhandske E, Bagian JP, Nudell T. Using health care failure mode and effect analysis. Jt Comm J Qual Improv 2002;28(5):248-267.</div></div> [[Start another case->Hub]] [[Restart this case->Proactive risk analysis - QI]] [[Next case →->Improvement cycle - QI]]

<span class="ec-case-marker" hidden data-entry="Proactive risk analysis. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Root cause analysis is retrospective and is triggered by an event that has already occurred. There has been no event here to analyze. <div class="ec-teach"><div class="th">What the findings point to</div> This method is prospective. A multidisciplinary team maps each step of a planned process, enumerates the ways each step could fail, scores each failure mode for frequency, severity, and detectability, and directs redesign at the highest-scoring modes before any patient is exposed. It is the standard tool when the question is what could go wrong rather than what did go wrong. <div class="ec-src"><b>Source:</b> DeRosier J, Stalhandske E, Bagian JP, Nudell T. Using health care failure mode and effect analysis. Jt Comm J Qual Improv 2002;28(5):248-267.</div></div></div> [[Try this question again->Proactive risk analysis - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Proactive risk analysis. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Control charts detect whether a process is stable over time and require accumulated data from a running process, which does not yet exist. <div class="ec-teach"><div class="th">What the findings point to</div> This method is prospective. A multidisciplinary team maps each step of a planned process, enumerates the ways each step could fail, scores each failure mode for frequency, severity, and detectability, and directs redesign at the highest-scoring modes before any patient is exposed. It is the standard tool when the question is what could go wrong rather than what did go wrong. <div class="ec-src"><b>Source:</b> DeRosier J, Stalhandske E, Bagian JP, Nudell T. Using health care failure mode and effect analysis. Jt Comm J Qual Improv 2002;28(5):248-267.</div></div></div> [[Try this question again->Proactive risk analysis - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Proactive risk analysis. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Trend analysis depends on reports generated by care already delivered and cannot anticipate hazards in a process not yet started. <div class="ec-teach"><div class="th">What the findings point to</div> This method is prospective. A multidisciplinary team maps each step of a planned process, enumerates the ways each step could fail, scores each failure mode for frequency, severity, and detectability, and directs redesign at the highest-scoring modes before any patient is exposed. It is the standard tool when the question is what could go wrong rather than what did go wrong. <div class="ec-src"><b>Source:</b> DeRosier J, Stalhandske E, Bagian JP, Nudell T. Using health care failure mode and effect analysis. Jt Comm J Qual Improv 2002;28(5):248-267.</div></div></div> [[Try this question again->Proactive risk analysis - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Proactive risk analysis. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This forum examines individual adverse outcomes after the fact and does not systematically enumerate potential failure modes. <div class="ec-teach"><div class="th">What the findings point to</div> This method is prospective. A multidisciplinary team maps each step of a planned process, enumerates the ways each step could fail, scores each failure mode for frequency, severity, and detectability, and directs redesign at the highest-scoring modes before any patient is exposed. It is the standard tool when the question is what could go wrong rather than what did go wrong. <div class="ec-src"><b>Source:</b> DeRosier J, Stalhandske E, Bagian JP, Nudell T. Using health care failure mode and effect analysis. Jt Comm J Qual Improv 2002;28(5):248-267.</div></div></div> [[Try this question again->Proactive risk analysis - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Proactive risk analysis. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Satisfaction data captures experience in a different unit and does not identify latent hazards in a newly designed process. <div class="ec-teach"><div class="th">What the findings point to</div> This method is prospective. A multidisciplinary team maps each step of a planned process, enumerates the ways each step could fail, scores each failure mode for frequency, severity, and detectability, and directs redesign at the highest-scoring modes before any patient is exposed. It is the standard tool when the question is what could go wrong rather than what did go wrong. <div class="ec-src"><b>Source:</b> DeRosier J, Stalhandske E, Bagian JP, Nudell T. Using health care failure mode and effect analysis. Jt Comm J Qual Improv 2002;28(5):248-267.</div></div></div> [[Try this question again->Proactive risk analysis - QI]] [[Start another case->Hub]]

<div class="ec-scene">Clinic quality meeting · 08:20</div> A primary care clinic with 14 physicians has a hemoglobin A1c testing rate of 54% among patients with diabetes mellitus. The team hypothesizes that a nurse-driven standing order for testing at check-in will raise the rate. They want to learn quickly whether the idea works and what problems it creates before committing the whole clinic. <span class="ec-prompt">Which of the following is the most appropriate next step?</span> [[Add a reminder to the electronic record and monitor for 12 months->Improvement cycle - QI D5]] [[Benchmark the clinic against regional testing rates->Improvement cycle - QI D4]] [[Conduct a randomized trial across the 14 physicians->Improvement cycle - QI D2]] [[Implement the standing order clinic-wide immediately->Improvement cycle - QI D1]] [[Survey the physicians about barriers before making any change->Improvement cycle - QI D3]] [[Test the standing order with one nurse for 1 week->Improvement cycle - QI correct]]

<span class="ec-case-marker" hidden data-entry="Improvement cycle. QI"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Test the standing order with one nurse for 1 week</div> Improvement proceeds through small, rapid cycles: plan a change, run it on a deliberately small scale, study what the data and the participants show, then act by adopting, adapting, or abandoning it. Testing with one nurse for one week surfaces the practical failures, such as which patients get missed at check-in and how the result is routed, at negligible cost and with the ability to revise before wider spread. <div class="ec-src"><b>Source:</b> Langley GJ, Moen RD, Nolan KM, et al. The Improvement Guide: A Practical Approach to Enhancing Organizational Performance. 2nd ed. San Francisco: Jossey-Bass, 2009.</div></div> [[Start another case->Hub]] [[Restart this case->Improvement cycle - QI]] [[Next case →->Hierarchy of controls - QI]]

<span class="ec-case-marker" hidden data-entry="Improvement cycle. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Full-scale implementation of an untested change spreads its defects to every patient and makes it politically difficult to withdraw. <div class="ec-teach"><div class="th">What the findings point to</div> Improvement proceeds through small, rapid cycles: plan a change, run it on a deliberately small scale, study what the data and the participants show, then act by adopting, adapting, or abandoning it. Testing with one nurse for one week surfaces the practical failures, such as which patients get missed at check-in and how the result is routed, at negligible cost and with the ability to revise before wider spread. <div class="ec-src"><b>Source:</b> Langley GJ, Moen RD, Nolan KM, et al. The Improvement Guide: A Practical Approach to Enhancing Organizational Performance. 2nd ed. San Francisco: Jossey-Bass, 2009.</div></div></div> [[Try this question again->Improvement cycle - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Improvement cycle. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A formal trial answers a research question at high cost and over months. Improvement work needs a usable answer this week. <div class="ec-teach"><div class="th">What the findings point to</div> Improvement proceeds through small, rapid cycles: plan a change, run it on a deliberately small scale, study what the data and the participants show, then act by adopting, adapting, or abandoning it. Testing with one nurse for one week surfaces the practical failures, such as which patients get missed at check-in and how the result is routed, at negligible cost and with the ability to revise before wider spread. <div class="ec-src"><b>Source:</b> Langley GJ, Moen RD, Nolan KM, et al. The Improvement Guide: A Practical Approach to Enhancing Organizational Performance. 2nd ed. San Francisco: Jossey-Bass, 2009.</div></div></div> [[Try this question again->Improvement cycle - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Improvement cycle. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Opinion gathering can inform design but generates no data on whether the change actually moves the measure. <div class="ec-teach"><div class="th">What the findings point to</div> Improvement proceeds through small, rapid cycles: plan a change, run it on a deliberately small scale, study what the data and the participants show, then act by adopting, adapting, or abandoning it. Testing with one nurse for one week surfaces the practical failures, such as which patients get missed at check-in and how the result is routed, at negligible cost and with the ability to revise before wider spread. <div class="ec-src"><b>Source:</b> Langley GJ, Moen RD, Nolan KM, et al. The Improvement Guide: A Practical Approach to Enhancing Organizational Performance. 2nd ed. San Francisco: Jossey-Bass, 2009.</div></div></div> [[Try this question again->Improvement cycle - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Improvement cycle. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Comparison establishes that a gap exists, which the team already knows, and does nothing to test the proposed remedy. <div class="ec-teach"><div class="th">What the findings point to</div> Improvement proceeds through small, rapid cycles: plan a change, run it on a deliberately small scale, study what the data and the participants show, then act by adopting, adapting, or abandoning it. Testing with one nurse for one week surfaces the practical failures, such as which patients get missed at check-in and how the result is routed, at negligible cost and with the ability to revise before wider spread. <div class="ec-src"><b>Source:</b> Langley GJ, Moen RD, Nolan KM, et al. The Improvement Guide: A Practical Approach to Enhancing Organizational Performance. 2nd ed. San Francisco: Jossey-Bass, 2009.</div></div></div> [[Try this question again->Improvement cycle - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Improvement cycle. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A year-long observation period without staged testing forfeits the chance to correct the intervention early. <div class="ec-teach"><div class="th">What the findings point to</div> Improvement proceeds through small, rapid cycles: plan a change, run it on a deliberately small scale, study what the data and the participants show, then act by adopting, adapting, or abandoning it. Testing with one nurse for one week surfaces the practical failures, such as which patients get missed at check-in and how the result is routed, at negligible cost and with the ability to revise before wider spread. <div class="ec-src"><b>Source:</b> Langley GJ, Moen RD, Nolan KM, et al. The Improvement Guide: A Practical Approach to Enhancing Organizational Performance. 2nd ed. San Francisco: Jossey-Bass, 2009.</div></div></div> [[Try this question again->Improvement cycle - QI]] [[Start another case->Hub]]

<div class="ec-scene">Pharmacy and therapeutics committee · 15:10</div> Over 18 months a hospital has recorded three events in which concentrated potassium chloride was infused undiluted, one of them fatal. In each case a nurse withdrew the vial from ward floor stock intending to dilute it. Staff have already received two rounds of mandatory education and warning stickers have been applied to the vials. <span class="ec-prompt">Which of the following interventions is most likely to prevent recurrence?</span> [[Add a third mandatory education module for nursing staff->Hierarchy of controls - QI D1]] [[Apply larger and more prominent warning labels to the vials->Hierarchy of controls - QI D2]] [[Institute disciplinary action for nurses involved in future events->Hierarchy of controls - QI D5]] [[Remove concentrated potassium chloride from floor stock->Hierarchy of controls - QI correct]] [[Require a second nurse to verify every potassium infusion->Hierarchy of controls - QI D3]] [[Require pharmacist approval before each dose is dispensed->Hierarchy of controls - QI D4]]

<span class="ec-case-marker" hidden data-entry="Hierarchy of controls. QI"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Remove concentrated potassium chloride from floor stock</div> Interventions differ enormously in durability. Education, reminders, and warning labels depend on human vigilance and decay quickly, which is why two rounds of training and stickers have already failed. Removing the hazardous concentrate from the units and supplying only premixed dilute solutions is a forcing function: it makes the error physically impossible rather than merely discouraged. This is the highest-reliability class of intervention available. <div class="ec-src"><b>Source:</b> The Joint Commission. Sentinel Event Alert, Issue 1: Medication error prevention, potassium chloride. February 27, 1998.</div></div> [[Start another case->Hub]] [[Restart this case->Hierarchy of controls - QI]] [[Next case →->Care transitions - QI]]

<span class="ec-case-marker" hidden data-entry="Hierarchy of controls. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Two prior rounds have not worked. Repeating the weakest intervention class predicts a fourth event rather than preventing one. <div class="ec-teach"><div class="th">What the findings point to</div> Interventions differ enormously in durability. Education, reminders, and warning labels depend on human vigilance and decay quickly, which is why two rounds of training and stickers have already failed. Removing the hazardous concentrate from the units and supplying only premixed dilute solutions is a forcing function: it makes the error physically impossible rather than merely discouraged. This is the highest-reliability class of intervention available. <div class="ec-src"><b>Source:</b> The Joint Commission. Sentinel Event Alert, Issue 1: Medication error prevention, potassium chloride. February 27, 1998.</div></div></div> [[Try this question again->Hierarchy of controls - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Hierarchy of controls. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Labeling has already been tried, and warnings are filtered out with repeated exposure under time pressure. <div class="ec-teach"><div class="th">What the findings point to</div> Interventions differ enormously in durability. Education, reminders, and warning labels depend on human vigilance and decay quickly, which is why two rounds of training and stickers have already failed. Removing the hazardous concentrate from the units and supplying only premixed dilute solutions is a forcing function: it makes the error physically impossible rather than merely discouraged. This is the highest-reliability class of intervention available. <div class="ec-src"><b>Source:</b> The Joint Commission. Sentinel Event Alert, Issue 1: Medication error prevention, potassium chloride. February 27, 1998.</div></div></div> [[Try this question again->Hierarchy of controls - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Hierarchy of controls. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Independent double-checks are moderately effective but degrade with workload and do not remove the hazard from the environment. <div class="ec-teach"><div class="th">What the findings point to</div> Interventions differ enormously in durability. Education, reminders, and warning labels depend on human vigilance and decay quickly, which is why two rounds of training and stickers have already failed. Removing the hazardous concentrate from the units and supplying only premixed dilute solutions is a forcing function: it makes the error physically impossible rather than merely discouraged. This is the highest-reliability class of intervention available. <div class="ec-src"><b>Source:</b> The Joint Commission. Sentinel Event Alert, Issue 1: Medication error prevention, potassium chloride. February 27, 1998.</div></div></div> [[Try this question again->Hierarchy of controls - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Hierarchy of controls. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Approval steps add delay and can be bypassed in urgent situations, leaving the concentrate available on the unit. <div class="ec-teach"><div class="th">What the findings point to</div> Interventions differ enormously in durability. Education, reminders, and warning labels depend on human vigilance and decay quickly, which is why two rounds of training and stickers have already failed. Removing the hazardous concentrate from the units and supplying only premixed dilute solutions is a forcing function: it makes the error physically impossible rather than merely discouraged. This is the highest-reliability class of intervention available. <div class="ec-src"><b>Source:</b> The Joint Commission. Sentinel Event Alert, Issue 1: Medication error prevention, potassium chloride. February 27, 1998.</div></div></div> [[Try this question again->Hierarchy of controls - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Hierarchy of controls. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Punishment suppresses reporting, does not alter the physical hazard, and has no demonstrated effect on error rates. <div class="ec-teach"><div class="th">What the findings point to</div> Interventions differ enormously in durability. Education, reminders, and warning labels depend on human vigilance and decay quickly, which is why two rounds of training and stickers have already failed. Removing the hazardous concentrate from the units and supplying only premixed dilute solutions is a forcing function: it makes the error physically impossible rather than merely discouraged. This is the highest-reliability class of intervention available. <div class="ec-src"><b>Source:</b> The Joint Commission. Sentinel Event Alert, Issue 1: Medication error prevention, potassium chloride. February 27, 1998.</div></div></div> [[Try this question again->Hierarchy of controls - QI]] [[Start another case->Hub]]

<div class="ec-scene">Hospital leadership meeting · 11:30</div> A hospital has a 30-day readmission rate of 24% among patients discharged with heart failure. Chart review shows that discharge summaries reach primary care physicians a median of 11 days after discharge, that 40% of patients have at least one medication discrepancy between the discharge list and what they are taking at home, and that only a third have an outpatient appointment scheduled at the time of discharge. <span class="ec-prompt">Which of the following interventions is most likely to reduce readmissions?</span> [[Extend the average length of stay by 1 day->Care transitions - QI D1]] [[Institute a telephone survey of patient satisfaction after discharge->Care transitions - QI D4]] [[Mail the discharge summary to patients as well as physicians->Care transitions - QI D2]] [[Provide written heart failure education pamphlets at discharge->Care transitions - QI D3]] [[Restrict discharges to weekdays when more staff are available->Care transitions - QI D5]] [[Transitional care with reconciliation and early follow-up->Care transitions - QI correct]]

<span class="ec-case-marker" hidden data-entry="Care transitions. QI"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Transitional care with reconciliation and early follow-up</div> The defects identified are all in the transition itself, and the intervention with the best evidence targets exactly that interval: reconciling medications at discharge, giving the patient a personal health record and a self-management plan, arranging follow-up before discharge, and providing a transition coach who contacts the patient in the first days at home. Programs built on these elements have produced significant reductions in readmission. <div class="ec-src"><b>Source:</b> Coleman EA, Parry C, Chalmers S, Min SJ. The care transitions intervention: results of a randomized controlled trial. Arch Intern Med 2006;166(17):1822-1828.</div></div> [[Start another case->Hub]] [[Restart this case->Care transitions - QI]] [[Next case →->Failure to rescue - QI]]

<span class="ec-case-marker" hidden data-entry="Care transitions. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Longer stays increase exposure to hospital-acquired complications and do not fix an information handoff that fails after the patient leaves. <div class="ec-teach"><div class="th">What the findings point to</div> The defects identified are all in the transition itself, and the intervention with the best evidence targets exactly that interval: reconciling medications at discharge, giving the patient a personal health record and a self-management plan, arranging follow-up before discharge, and providing a transition coach who contacts the patient in the first days at home. Programs built on these elements have produced significant reductions in readmission. <div class="ec-src"><b>Source:</b> Coleman EA, Parry C, Chalmers S, Min SJ. The care transitions intervention: results of a randomized controlled trial. Arch Intern Med 2006;166(17):1822-1828.</div></div></div> [[Try this question again->Care transitions - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Care transitions. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Adding a recipient to a document that arrives 11 days late does not close the gap in the first week, which is when most readmissions begin. <div class="ec-teach"><div class="th">What the findings point to</div> The defects identified are all in the transition itself, and the intervention with the best evidence targets exactly that interval: reconciling medications at discharge, giving the patient a personal health record and a self-management plan, arranging follow-up before discharge, and providing a transition coach who contacts the patient in the first days at home. Programs built on these elements have produced significant reductions in readmission. <div class="ec-src"><b>Source:</b> Coleman EA, Parry C, Chalmers S, Min SJ. The care transitions intervention: results of a randomized controlled trial. Arch Intern Med 2006;166(17):1822-1828.</div></div></div> [[Try this question again->Care transitions - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Care transitions. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Print education alone has little effect on readmission and does not address medication discrepancies or missing appointments. <div class="ec-teach"><div class="th">What the findings point to</div> The defects identified are all in the transition itself, and the intervention with the best evidence targets exactly that interval: reconciling medications at discharge, giving the patient a personal health record and a self-management plan, arranging follow-up before discharge, and providing a transition coach who contacts the patient in the first days at home. Programs built on these elements have produced significant reductions in readmission. <div class="ec-src"><b>Source:</b> Coleman EA, Parry C, Chalmers S, Min SJ. The care transitions intervention: results of a randomized controlled trial. Arch Intern Med 2006;166(17):1822-1828.</div></div></div> [[Try this question again->Care transitions - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Care transitions. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Satisfaction measurement produces data but delivers no clinical intervention during the vulnerable period. <div class="ec-teach"><div class="th">What the findings point to</div> The defects identified are all in the transition itself, and the intervention with the best evidence targets exactly that interval: reconciling medications at discharge, giving the patient a personal health record and a self-management plan, arranging follow-up before discharge, and providing a transition coach who contacts the patient in the first days at home. Programs built on these elements have produced significant reductions in readmission. <div class="ec-src"><b>Source:</b> Coleman EA, Parry C, Chalmers S, Min SJ. The care transitions intervention: results of a randomized controlled trial. Arch Intern Med 2006;166(17):1822-1828.</div></div></div> [[Try this question again->Care transitions - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Care transitions. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Limiting discharge days lengthens stays and creates capacity problems without correcting the underlying process failures. <div class="ec-teach"><div class="th">What the findings point to</div> The defects identified are all in the transition itself, and the intervention with the best evidence targets exactly that interval: reconciling medications at discharge, giving the patient a personal health record and a self-management plan, arranging follow-up before discharge, and providing a transition coach who contacts the patient in the first days at home. Programs built on these elements have produced significant reductions in readmission. <div class="ec-src"><b>Source:</b> Coleman EA, Parry C, Chalmers S, Min SJ. The care transitions intervention: results of a randomized controlled trial. Arch Intern Med 2006;166(17):1822-1828.</div></div></div> [[Try this question again->Care transitions - QI]] [[Start another case->Hub]]

<div class="ec-scene">Patient safety committee · 13:40</div> Review of eight in-hospital cardiac arrests on general wards shows that in seven, documented vital sign abnormalities were present for 6 to 12 hours before the arrest: rising respiratory rate, falling blood pressure, or new confusion. Nurses recorded the abnormalities. In five cases the covering intern was paged but did not attend for more than an hour, and in three the nurse reported feeling unable to escalate above the intern. <span class="ec-prompt">Which of the following interventions most directly addresses this pattern?</span> [[Add an automated alert to the electronic record for abnormal vital signs->Failure to rescue - QI D5]] [[Implement a rapid response team activated by defined criteria->Failure to rescue - QI correct]] [[Increase the frequency of routine vital sign measurement->Failure to rescue - QI D1]] [[Provide additional advanced life support training for ward nurses->Failure to rescue - QI D2]] [[Require attending physicians to round twice daily on all patients->Failure to rescue - QI D3]] [[Transfer all patients with any abnormal vital sign to the intensive care unit->Failure to rescue - QI D4]]

<span class="ec-case-marker" hidden data-entry="Failure to rescue. QI"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Implement a rapid response team activated by defined criteria</div> The pattern is failure to rescue: deterioration was detectable and documented, but the response system did not bring skilled help to the bedside in time. A rapid response team with explicit physiologic activation criteria, callable by any staff member without going through the ward hierarchy, targets both defects at once. It converts a recognized abnormality into an immediate bedside evaluation and removes the requirement to persuade a junior physician first. <div class="ec-src"><b>Source:</b> Berwick DM, Calkins DR, McCannon CJ, Hackbarth AD. The 100,000 Lives Campaign: setting a goal and a deadline for improving health care quality. JAMA 2006;295(3):324-327.</div></div> [[Start another case->Hub]] [[Restart this case->Failure to rescue - QI]] [[Next case →->Handoff standardization - QI]]

<span class="ec-case-marker" hidden data-entry="Failure to rescue. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The abnormalities were already measured and charted. Measuring more often without changing the response adds data to a system that failed to act on it. <div class="ec-teach"><div class="th">What the findings point to</div> The pattern is failure to rescue: deterioration was detectable and documented, but the response system did not bring skilled help to the bedside in time. A rapid response team with explicit physiologic activation criteria, callable by any staff member without going through the ward hierarchy, targets both defects at once. It converts a recognized abnormality into an immediate bedside evaluation and removes the requirement to persuade a junior physician first. <div class="ec-src"><b>Source:</b> Berwick DM, Calkins DR, McCannon CJ, Hackbarth AD. The 100,000 Lives Campaign: setting a goal and a deadline for improving health care quality. JAMA 2006;295(3):324-327.</div></div></div> [[Try this question again->Failure to rescue - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Failure to rescue. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Resuscitation training improves care after the arrest. The opportunity here lies in the hours before it. <div class="ec-teach"><div class="th">What the findings point to</div> The pattern is failure to rescue: deterioration was detectable and documented, but the response system did not bring skilled help to the bedside in time. A rapid response team with explicit physiologic activation criteria, callable by any staff member without going through the ward hierarchy, targets both defects at once. It converts a recognized abnormality into an immediate bedside evaluation and removes the requirement to persuade a junior physician first. <div class="ec-src"><b>Source:</b> Berwick DM, Calkins DR, McCannon CJ, Hackbarth AD. The 100,000 Lives Campaign: setting a goal and a deadline for improving health care quality. JAMA 2006;295(3):324-327.</div></div></div> [[Try this question again->Failure to rescue - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Failure to rescue. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Scheduled rounds do not coincide with unscheduled deterioration and consume large amounts of physician time inefficiently. <div class="ec-teach"><div class="th">What the findings point to</div> The pattern is failure to rescue: deterioration was detectable and documented, but the response system did not bring skilled help to the bedside in time. A rapid response team with explicit physiologic activation criteria, callable by any staff member without going through the ward hierarchy, targets both defects at once. It converts a recognized abnormality into an immediate bedside evaluation and removes the requirement to persuade a junior physician first. <div class="ec-src"><b>Source:</b> Berwick DM, Calkins DR, McCannon CJ, Hackbarth AD. The 100,000 Lives Campaign: setting a goal and a deadline for improving health care quality. JAMA 2006;295(3):324-327.</div></div></div> [[Try this question again->Failure to rescue - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Failure to rescue. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Blanket transfer is not feasible on capacity grounds and would overwhelm critical care without triaging who actually needs it. <div class="ec-teach"><div class="th">What the findings point to</div> The pattern is failure to rescue: deterioration was detectable and documented, but the response system did not bring skilled help to the bedside in time. A rapid response team with explicit physiologic activation criteria, callable by any staff member without going through the ward hierarchy, targets both defects at once. It converts a recognized abnormality into an immediate bedside evaluation and removes the requirement to persuade a junior physician first. <div class="ec-src"><b>Source:</b> Berwick DM, Calkins DR, McCannon CJ, Hackbarth AD. The 100,000 Lives Campaign: setting a goal and a deadline for improving health care quality. JAMA 2006;295(3):324-327.</div></div></div> [[Try this question again->Failure to rescue - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Failure to rescue. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Alerts without a defined responder and an obligation to attend generate fatigue and reproduce the same failure to respond. <div class="ec-teach"><div class="th">What the findings point to</div> The pattern is failure to rescue: deterioration was detectable and documented, but the response system did not bring skilled help to the bedside in time. A rapid response team with explicit physiologic activation criteria, callable by any staff member without going through the ward hierarchy, targets both defects at once. It converts a recognized abnormality into an immediate bedside evaluation and removes the requirement to persuade a junior physician first. <div class="ec-src"><b>Source:</b> Berwick DM, Calkins DR, McCannon CJ, Hackbarth AD. The 100,000 Lives Campaign: setting a goal and a deadline for improving health care quality. JAMA 2006;295(3):324-327.</div></div></div> [[Try this question again->Failure to rescue - QI]] [[Start another case->Hub]]

<div class="ec-scene">Residency program office · 16:00</div> An internal medicine program finds that preventable adverse events cluster after shift change. Audit of 40 handoffs shows that illness severity is stated in 30%, that a contingency plan for anticipated problems is given in 25%, that the receiving resident summarizes back what was heard in 5%, and that handoffs occur in a corridor with frequent interruptions. <span class="ec-prompt">Which of the following interventions is most likely to reduce these events?</span> [[Adopt a structured handoff bundle with mandatory read-back->Handoff standardization - QI correct]] [[Have attending physicians conduct all handoffs personally->Handoff standardization - QI D4]] [[Lengthen the time allotted for handoff by 15 minutes->Handoff standardization - QI D1]] [[Reduce the number of patients each resident covers overnight->Handoff standardization - QI D3]] [[Require the outgoing resident to write a detailed note->Handoff standardization - QI D2]] [[Send an automated patient list from the electronic record at each shift change->Handoff standardization - QI D5]]

<span class="ec-case-marker" hidden data-entry="Handoff standardization. QI"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Adopt a structured handoff bundle with mandatory read-back</div> The measured defects map onto the components of a validated handoff structure: an explicit illness severity statement, a patient summary, an action list, situation awareness with contingency planning, and synthesis by the receiver in the form of a read-back. Implementing this bundle with training, a printed structure, and a protected location has been associated with a substantial reduction in medical errors and preventable adverse events without lengthening handoffs. <div class="ec-src"><b>Source:</b> Starmer AJ, Spector ND, Srivastava R, et al. Changes in medical errors after implementation of a handoff program. N Engl J Med 2014;371(19):1803-1812.</div></div> [[Start another case->Hub]] [[Restart this case->Handoff standardization - QI]] [[Next case →->Alarm fatigue - QI]]

<span class="ec-case-marker" hidden data-entry="Handoff standardization. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> More time spent on an unstructured process does not reliably add the missing elements and increases duty hour pressure. <div class="ec-teach"><div class="th">What the findings point to</div> The measured defects map onto the components of a validated handoff structure: an explicit illness severity statement, a patient summary, an action list, situation awareness with contingency planning, and synthesis by the receiver in the form of a read-back. Implementing this bundle with training, a printed structure, and a protected location has been associated with a substantial reduction in medical errors and preventable adverse events without lengthening handoffs. <div class="ec-src"><b>Source:</b> Starmer AJ, Spector ND, Srivastava R, et al. Changes in medical errors after implementation of a handoff program. N Engl J Med 2014;371(19):1803-1812.</div></div></div> [[Try this question again->Handoff standardization - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Handoff standardization. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Written documentation supplements but does not replace verbal transfer, and it provides no opportunity for the receiver to confirm understanding. <div class="ec-teach"><div class="th">What the findings point to</div> The measured defects map onto the components of a validated handoff structure: an explicit illness severity statement, a patient summary, an action list, situation awareness with contingency planning, and synthesis by the receiver in the form of a read-back. Implementing this bundle with training, a printed structure, and a protected location has been associated with a substantial reduction in medical errors and preventable adverse events without lengthening handoffs. <div class="ec-src"><b>Source:</b> Starmer AJ, Spector ND, Srivastava R, et al. Changes in medical errors after implementation of a handoff program. N Engl J Med 2014;371(19):1803-1812.</div></div></div> [[Try this question again->Handoff standardization - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Handoff standardization. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Lower census may help but is constrained by staffing and does not fix the content or setting of the transfer. <div class="ec-teach"><div class="th">What the findings point to</div> The measured defects map onto the components of a validated handoff structure: an explicit illness severity statement, a patient summary, an action list, situation awareness with contingency planning, and synthesis by the receiver in the form of a read-back. Implementing this bundle with training, a printed structure, and a protected location has been associated with a substantial reduction in medical errors and preventable adverse events without lengthening handoffs. <div class="ec-src"><b>Source:</b> Starmer AJ, Spector ND, Srivastava R, et al. Changes in medical errors after implementation of a handoff program. N Engl J Med 2014;371(19):1803-1812.</div></div></div> [[Try this question again->Handoff standardization - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Handoff standardization. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Substituting a more senior speaker does not supply structure, and it removes a core educational activity from training. <div class="ec-teach"><div class="th">What the findings point to</div> The measured defects map onto the components of a validated handoff structure: an explicit illness severity statement, a patient summary, an action list, situation awareness with contingency planning, and synthesis by the receiver in the form of a read-back. Implementing this bundle with training, a printed structure, and a protected location has been associated with a substantial reduction in medical errors and preventable adverse events without lengthening handoffs. <div class="ec-src"><b>Source:</b> Starmer AJ, Spector ND, Srivastava R, et al. Changes in medical errors after implementation of a handoff program. N Engl J Med 2014;371(19):1803-1812.</div></div></div> [[Try this question again->Handoff standardization - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Handoff standardization. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> An automated list carries data but omits illness severity judgment and contingency planning, which are the elements most often missing. <div class="ec-teach"><div class="th">What the findings point to</div> The measured defects map onto the components of a validated handoff structure: an explicit illness severity statement, a patient summary, an action list, situation awareness with contingency planning, and synthesis by the receiver in the form of a read-back. Implementing this bundle with training, a printed structure, and a protected location has been associated with a substantial reduction in medical errors and preventable adverse events without lengthening handoffs. <div class="ec-src"><b>Source:</b> Starmer AJ, Spector ND, Srivastava R, et al. Changes in medical errors after implementation of a handoff program. N Engl J Med 2014;371(19):1803-1812.</div></div></div> [[Try this question again->Handoff standardization - QI]] [[Start another case->Hub]]

<div class="ec-scene">Telemetry unit · 02:50</div> A patient on continuous cardiac monitoring died after ventricular fibrillation went unrecognized for 19 minutes. Audit of the unit shows an average of 942 audible alarms per patient per day, that 88% are technical or nonactionable, that default alarm limits are used for every patient regardless of baseline, and that staff routinely lower alarm volume at night. Two nurses reported that they no longer distinguish among alarm tones. <span class="ec-prompt">Which of the following interventions is most likely to prevent recurrence?</span> [[Add a secondary alarm notification to staff mobile phones->Alarm fatigue - QI D5]] [[Assign a dedicated technician to watch the central monitor->Alarm fatigue - QI D2]] [[Customize alarm limits and remove nonactionable alarms->Alarm fatigue - QI correct]] [[Discipline staff who reduce alarm volume->Alarm fatigue - QI D3]] [[Extend continuous monitoring to all patients on the unit->Alarm fatigue - QI D4]] [[Increase the minimum audible volume of all alarms->Alarm fatigue - QI D1]]

<span class="ec-case-marker" hidden data-entry="Alarm fatigue. QI"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Customize alarm limits and remove nonactionable alarms</div> The failure is desensitization produced by alarm burden. Reducing the number of alarms is what restores the signal: setting limits appropriate to the individual patient rather than device defaults, disabling nonactionable alarm categories, changing electrodes daily to reduce artifact, and reviewing which patients still require monitoring. Interventions that add alarms or add staff to respond to them leave the underlying burden intact. <div class="ec-src"><b>Source:</b> The Joint Commission. Sentinel Event Alert, Issue 50: Medical device alarm safety in hospitals. April 8, 2013.</div></div> [[Start another case->Hub]] [[Restart this case->Alarm fatigue - QI]] [[Next case →->Catheter-associated infection - QI]]

<span class="ec-case-marker" hidden data-entry="Alarm fatigue. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Louder alarms in a unit already generating 942 per patient per day accelerate desensitization rather than reversing it. <div class="ec-teach"><div class="th">What the findings point to</div> The failure is desensitization produced by alarm burden. Reducing the number of alarms is what restores the signal: setting limits appropriate to the individual patient rather than device defaults, disabling nonactionable alarm categories, changing electrodes daily to reduce artifact, and reviewing which patients still require monitoring. Interventions that add alarms or add staff to respond to them leave the underlying burden intact. <div class="ec-src"><b>Source:</b> The Joint Commission. Sentinel Event Alert, Issue 50: Medical device alarm safety in hospitals. April 8, 2013.</div></div></div> [[Try this question again->Alarm fatigue - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Alarm fatigue. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A monitor watcher may help, but with 88% nonactionable alarms the watcher becomes desensitized in the same way the nurses did. <div class="ec-teach"><div class="th">What the findings point to</div> The failure is desensitization produced by alarm burden. Reducing the number of alarms is what restores the signal: setting limits appropriate to the individual patient rather than device defaults, disabling nonactionable alarm categories, changing electrodes daily to reduce artifact, and reviewing which patients still require monitoring. Interventions that add alarms or add staff to respond to them leave the underlying burden intact. <div class="ec-src"><b>Source:</b> The Joint Commission. Sentinel Event Alert, Issue 50: Medical device alarm safety in hospitals. April 8, 2013.</div></div></div> [[Try this question again->Alarm fatigue - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Alarm fatigue. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Volume reduction is a predictable adaptation to an unmanageable alarm load. Punishing the symptom leaves the cause untouched. <div class="ec-teach"><div class="th">What the findings point to</div> The failure is desensitization produced by alarm burden. Reducing the number of alarms is what restores the signal: setting limits appropriate to the individual patient rather than device defaults, disabling nonactionable alarm categories, changing electrodes daily to reduce artifact, and reviewing which patients still require monitoring. Interventions that add alarms or add staff to respond to them leave the underlying burden intact. <div class="ec-src"><b>Source:</b> The Joint Commission. Sentinel Event Alert, Issue 50: Medical device alarm safety in hospitals. April 8, 2013.</div></div></div> [[Try this question again->Alarm fatigue - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Alarm fatigue. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Monitoring patients who do not need it adds alarms and worsens the exact problem identified. <div class="ec-teach"><div class="th">What the findings point to</div> The failure is desensitization produced by alarm burden. Reducing the number of alarms is what restores the signal: setting limits appropriate to the individual patient rather than device defaults, disabling nonactionable alarm categories, changing electrodes daily to reduce artifact, and reviewing which patients still require monitoring. Interventions that add alarms or add staff to respond to them leave the underlying burden intact. <div class="ec-src"><b>Source:</b> The Joint Commission. Sentinel Event Alert, Issue 50: Medical device alarm safety in hospitals. April 8, 2013.</div></div></div> [[Try this question again->Alarm fatigue - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Alarm fatigue. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Secondary notification without first reducing nonactionable alarms transmits the noise to a second device. <div class="ec-teach"><div class="th">What the findings point to</div> The failure is desensitization produced by alarm burden. Reducing the number of alarms is what restores the signal: setting limits appropriate to the individual patient rather than device defaults, disabling nonactionable alarm categories, changing electrodes daily to reduce artifact, and reviewing which patients still require monitoring. Interventions that add alarms or add staff to respond to them leave the underlying burden intact. <div class="ec-src"><b>Source:</b> The Joint Commission. Sentinel Event Alert, Issue 50: Medical device alarm safety in hospitals. April 8, 2013.</div></div></div> [[Try this question again->Alarm fatigue - QI]] [[Start another case->Hub]]

<div class="ec-scene">Infection prevention rounds · 10:15</div> A medical ward reports a catheter-associated urinary tract infection rate above the national benchmark. Point prevalence audit finds that 38% of inpatients have an indwelling urinary catheter, that the documented indication is absent or inappropriate in more than half, that the most common recorded reason is nursing convenience for incontinence, and that median catheter duration is 6 days. <span class="ec-prompt">Which of the following interventions is most likely to reduce the infection rate?</span> [[Administer prophylactic antibiotics for the duration of catheterization->Catheter-associated infection - QI D4]] [[Daily review with nurse-driven catheter removal->Catheter-associated infection - QI correct]] [[Irrigate catheters daily with antiseptic solution->Catheter-associated infection - QI D2]] [[Obtain routine surveillance urine cultures twice weekly->Catheter-associated infection - QI D3]] [[Replace every indwelling catheter every 72 hours->Catheter-associated infection - QI D5]] [[Use antimicrobial-impregnated urinary catheters for all patients->Catheter-associated infection - QI D1]]

<span class="ec-case-marker" hidden data-entry="Catheter-associated infection. QI"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Daily review with nurse-driven catheter removal</div> Risk of infection rises with each catheter day, so the dominant lever is device days rather than catheter care technique. Restricting insertion to appropriate indications and empowering nurses to remove catheters that no longer meet criteria, without waiting for a physician order, reduces both prevalence and duration. Incontinence alone is not an indication, and external collection devices serve that purpose without entering the bladder. <div class="ec-src"><b>Source:</b> Meddings J, Rogers MA, Krein SL, et al. Reducing unnecessary urinary catheter use and other strategies to prevent catheter-associated urinary tract infection. BMJ Qual Saf 2014;23(4):277-289.</div></div> [[Start another case->Hub]] [[Restart this case->Catheter-associated infection - QI]] [[Next case →->Second victim - QI]]

<span class="ec-case-marker" hidden data-entry="Catheter-associated infection. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Coated catheters have not shown a consistent reduction in symptomatic infection and do nothing about the large share of catheters that should not be present at all. <div class="ec-teach"><div class="th">What the findings point to</div> Risk of infection rises with each catheter day, so the dominant lever is device days rather than catheter care technique. Restricting insertion to appropriate indications and empowering nurses to remove catheters that no longer meet criteria, without waiting for a physician order, reduces both prevalence and duration. Incontinence alone is not an indication, and external collection devices serve that purpose without entering the bladder. <div class="ec-src"><b>Source:</b> Meddings J, Rogers MA, Krein SL, et al. Reducing unnecessary urinary catheter use and other strategies to prevent catheter-associated urinary tract infection. BMJ Qual Saf 2014;23(4):277-289.</div></div></div> [[Try this question again->Catheter-associated infection - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Catheter-associated infection. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Bladder irrigation does not prevent infection, breaks the closed drainage system, and is explicitly discouraged. <div class="ec-teach"><div class="th">What the findings point to</div> Risk of infection rises with each catheter day, so the dominant lever is device days rather than catheter care technique. Restricting insertion to appropriate indications and empowering nurses to remove catheters that no longer meet criteria, without waiting for a physician order, reduces both prevalence and duration. Incontinence alone is not an indication, and external collection devices serve that purpose without entering the bladder. <div class="ec-src"><b>Source:</b> Meddings J, Rogers MA, Krein SL, et al. Reducing unnecessary urinary catheter use and other strategies to prevent catheter-associated urinary tract infection. BMJ Qual Saf 2014;23(4):277-289.</div></div></div> [[Try this question again->Catheter-associated infection - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Catheter-associated infection. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Culturing asymptomatic patients detects bacteriuria that should not be treated and drives unnecessary antibiotic use. <div class="ec-teach"><div class="th">What the findings point to</div> Risk of infection rises with each catheter day, so the dominant lever is device days rather than catheter care technique. Restricting insertion to appropriate indications and empowering nurses to remove catheters that no longer meet criteria, without waiting for a physician order, reduces both prevalence and duration. Incontinence alone is not an indication, and external collection devices serve that purpose without entering the bladder. <div class="ec-src"><b>Source:</b> Meddings J, Rogers MA, Krein SL, et al. Reducing unnecessary urinary catheter use and other strategies to prevent catheter-associated urinary tract infection. BMJ Qual Saf 2014;23(4):277-289.</div></div></div> [[Try this question again->Catheter-associated infection - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Catheter-associated infection. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Prophylaxis selects resistant organisms and does not prevent catheter-associated infection. <div class="ec-teach"><div class="th">What the findings point to</div> Risk of infection rises with each catheter day, so the dominant lever is device days rather than catheter care technique. Restricting insertion to appropriate indications and empowering nurses to remove catheters that no longer meet criteria, without waiting for a physician order, reduces both prevalence and duration. Incontinence alone is not an indication, and external collection devices serve that purpose without entering the bladder. <div class="ec-src"><b>Source:</b> Meddings J, Rogers MA, Krein SL, et al. Reducing unnecessary urinary catheter use and other strategies to prevent catheter-associated urinary tract infection. BMJ Qual Saf 2014;23(4):277-289.</div></div></div> [[Try this question again->Catheter-associated infection - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Catheter-associated infection. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Scheduled replacement introduces repeated instrumentation without reducing infection and increases trauma. <div class="ec-teach"><div class="th">What the findings point to</div> Risk of infection rises with each catheter day, so the dominant lever is device days rather than catheter care technique. Restricting insertion to appropriate indications and empowering nurses to remove catheters that no longer meet criteria, without waiting for a physician order, reduces both prevalence and duration. Incontinence alone is not an indication, and external collection devices serve that purpose without entering the bladder. <div class="ec-src"><b>Source:</b> Meddings J, Rogers MA, Krein SL, et al. Reducing unnecessary urinary catheter use and other strategies to prevent catheter-associated urinary tract infection. BMJ Qual Saf 2014;23(4):277-289.</div></div></div> [[Try this question again->Catheter-associated infection - QI]] [[Start another case->Hub]]

<div class="ec-scene">Department office · 17:20</div> A second-year resident miscalculated a heparin infusion rate, contributing to a fatal intracranial hemorrhage. She disclosed the error immediately, participated in the disclosure conversation with the family, and has since been tearful, sleeping poorly, avoiding the intensive care unit, and asking to be removed from clinical duties. A root cause analysis is underway and has identified a nonstandard concentration and an absent dosing calculator. <span class="ec-prompt">Which of the following is the most appropriate institutional response toward the resident?</span> [[Advise her to avoid discussing the event with colleagues->Second victim - QI D4]] [[Assign her to nonclinical duties for the remainder of the year->Second victim - QI D3]] [[Place her on administrative leave pending the analysis->Second victim - QI D1]] [[Provide structured peer support and confidential counseling->Second victim - QI correct]] [[Require her to complete a remedial pharmacology course->Second victim - QI D2]] [[Take no specific action because the analysis found system causes->Second victim - QI D5]]

<span class="ec-case-marker" hidden data-entry="Second victim. QI"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Provide structured peer support and confidential counseling</div> Clinicians involved in harmful errors experience predictable and severe distress, with risks including depression, burnout, attrition, and subsequent errors driven by impairment. Institutions that pair systems analysis with structured peer support and confidential counseling retain clinicians and sustain reporting. Support is not in tension with accountability here: the analysis has already identified system defects, and she disclosed the error herself. <div class="ec-src"><b>Source:</b> Wu AW. Medical error: the second victim. BMJ 2000;320(7237):726-727.</div></div> [[Start another case->Hub]] [[Restart this case->Second victim - QI]] [[Next case →->Risk reduction measures - Opening]]

<span class="ec-case-marker" hidden data-entry="Second victim. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Removal framed as suspension is experienced as punishment and reinforces the message that reporting an error ends a career. <div class="ec-teach"><div class="th">What the findings point to</div> Clinicians involved in harmful errors experience predictable and severe distress, with risks including depression, burnout, attrition, and subsequent errors driven by impairment. Institutions that pair systems analysis with structured peer support and confidential counseling retain clinicians and sustain reporting. Support is not in tension with accountability here: the analysis has already identified system defects, and she disclosed the error herself. <div class="ec-src"><b>Source:</b> Wu AW. Medical error: the second victim. BMJ 2000;320(7237):726-727.</div></div></div> [[Try this question again->Second victim - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Second victim. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Remediation targeted at an individual implies a knowledge deficit that the analysis has not identified and that the nonstandard concentration argues against. <div class="ec-teach"><div class="th">What the findings point to</div> Clinicians involved in harmful errors experience predictable and severe distress, with risks including depression, burnout, attrition, and subsequent errors driven by impairment. Institutions that pair systems analysis with structured peer support and confidential counseling retain clinicians and sustain reporting. Support is not in tension with accountability here: the analysis has already identified system defects, and she disclosed the error herself. <div class="ec-src"><b>Source:</b> Wu AW. Medical error: the second victim. BMJ 2000;320(7237):726-727.</div></div></div> [[Try this question again->Second victim - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Second victim. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Prolonged removal from patient care compounds isolation and shame without addressing the distress or the system defect. <div class="ec-teach"><div class="th">What the findings point to</div> Clinicians involved in harmful errors experience predictable and severe distress, with risks including depression, burnout, attrition, and subsequent errors driven by impairment. Institutions that pair systems analysis with structured peer support and confidential counseling retain clinicians and sustain reporting. Support is not in tension with accountability here: the analysis has already identified system defects, and she disclosed the error herself. <div class="ec-src"><b>Source:</b> Wu AW. Medical error: the second victim. BMJ 2000;320(7237):726-727.</div></div></div> [[Try this question again->Second victim - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Second victim. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Enforced silence is the condition under which second victim distress becomes most severe and most persistent. <div class="ec-teach"><div class="th">What the findings point to</div> Clinicians involved in harmful errors experience predictable and severe distress, with risks including depression, burnout, attrition, and subsequent errors driven by impairment. Institutions that pair systems analysis with structured peer support and confidential counseling retain clinicians and sustain reporting. Support is not in tension with accountability here: the analysis has already identified system defects, and she disclosed the error herself. <div class="ec-src"><b>Source:</b> Wu AW. Medical error: the second victim. BMJ 2000;320(7237):726-727.</div></div></div> [[Try this question again->Second victim - QI]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Second victim. QI"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Identifying system causes addresses the next patient. It does not address the clinician who is currently symptomatic and asking for help. <div class="ec-teach"><div class="th">What the findings point to</div> Clinicians involved in harmful errors experience predictable and severe distress, with risks including depression, burnout, attrition, and subsequent errors driven by impairment. Institutions that pair systems analysis with structured peer support and confidential counseling retain clinicians and sustain reporting. Support is not in tension with accountability here: the analysis has already identified system defects, and she disclosed the error herself. <div class="ec-src"><b>Source:</b> Wu AW. Medical error: the second victim. BMJ 2000;320(7237):726-727.</div></div></div> [[Try this question again->Second victim - QI]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 23:22</div> A 28-year-old woman has had pleuritic chest pain for 4 hours. She has no risk factors for venous thromboembolism, a pulse is 78/min, an oxygen saturation of 99% on room air, and no leg swelling. Her clinical probability of pulmonary embolism is low. A high-sensitivity D-dimer assay with a sensitivity of 98% and a specificity of 42% returns a negative result. <span class="ec-prompt">Which of the following best justifies withholding further imaging?</span> [[A likelihood ratio near 1 indicates the test is uninformative->Ruling out with a sensitive test - Biostat D3]] [[High sensitivity makes a negative result effective for exclusion->Ruling out with a sensitive test - Biostat correct]] [[High specificity makes a negative result effective for exclusion->Ruling out with a sensitive test - Biostat D1]] [[Specificity rises as prevalence falls in the tested population->Ruling out with a sensitive test - Biostat D5]] [[The assay has a low false-positive rate->Ruling out with a sensitive test - Biostat D4]] [[The negative predictive value is independent of pretest probability->Ruling out with a sensitive test - Biostat D2]]

<span class="ec-case-marker" hidden data-entry="Ruling out with a sensitive test. Biostat"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ High sensitivity makes a negative result effective for exclusion</div> A test with very high sensitivity produces few false negatives, so a negative result in a patient with low pretest probability drives the posttest probability of disease below the threshold at which further testing does more harm than good. The low specificity is irrelevant to this use, because a negative result is what is being interpreted. The same assay would be a poor choice for confirming disease, which is why it is deployed only after clinical probability has been assessed as low. <div class="ec-src"><b>Source:</b> Jaeschke R, Guyatt GH, Sackett DL. Users' guides to the medical literature. III. How to use an article about a diagnostic test. JAMA 1994;271(9):703-707.</div></div> [[Start another case->Hub]] [[Restart this case->Ruling out with a sensitive test - Biostat]] [[Next case →->Type II error - Biostat]]

<span class="ec-case-marker" hidden data-entry="Ruling out with a sensitive test. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Specificity governs the interpretation of positive results. It is 42% here, which is why a positive D-dimer in this patient would mean very little. <div class="ec-teach"><div class="th">What the findings point to</div> A test with very high sensitivity produces few false negatives, so a negative result in a patient with low pretest probability drives the posttest probability of disease below the threshold at which further testing does more harm than good. The low specificity is irrelevant to this use, because a negative result is what is being interpreted. The same assay would be a poor choice for confirming disease, which is why it is deployed only after clinical probability has been assessed as low. <div class="ec-src"><b>Source:</b> Jaeschke R, Guyatt GH, Sackett DL. Users' guides to the medical literature. III. How to use an article about a diagnostic test. JAMA 1994;271(9):703-707.</div></div></div> [[Try this question again->Ruling out with a sensitive test - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Ruling out with a sensitive test. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Predictive values depend heavily on prevalence. It is precisely because her pretest probability is low that the negative result is decisive. <div class="ec-teach"><div class="th">What the findings point to</div> A test with very high sensitivity produces few false negatives, so a negative result in a patient with low pretest probability drives the posttest probability of disease below the threshold at which further testing does more harm than good. The low specificity is irrelevant to this use, because a negative result is what is being interpreted. The same assay would be a poor choice for confirming disease, which is why it is deployed only after clinical probability has been assessed as low. <div class="ec-src"><b>Source:</b> Jaeschke R, Guyatt GH, Sackett DL. Users' guides to the medical literature. III. How to use an article about a diagnostic test. JAMA 1994;271(9):703-707.</div></div></div> [[Try this question again->Ruling out with a sensitive test - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Ruling out with a sensitive test. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The negative likelihood ratio here is approximately 0.05, which is strongly informative. A value near 1 would indicate the opposite. <div class="ec-teach"><div class="th">What the findings point to</div> A test with very high sensitivity produces few false negatives, so a negative result in a patient with low pretest probability drives the posttest probability of disease below the threshold at which further testing does more harm than good. The low specificity is irrelevant to this use, because a negative result is what is being interpreted. The same assay would be a poor choice for confirming disease, which is why it is deployed only after clinical probability has been assessed as low. <div class="ec-src"><b>Source:</b> Jaeschke R, Guyatt GH, Sackett DL. Users' guides to the medical literature. III. How to use an article about a diagnostic test. JAMA 1994;271(9):703-707.</div></div></div> [[Try this question again->Ruling out with a sensitive test - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Ruling out with a sensitive test. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The false-positive rate is 58%, which is high. False positives are the reason this test is not used in patients with high pretest probability. <div class="ec-teach"><div class="th">What the findings point to</div> A test with very high sensitivity produces few false negatives, so a negative result in a patient with low pretest probability drives the posttest probability of disease below the threshold at which further testing does more harm than good. The low specificity is irrelevant to this use, because a negative result is what is being interpreted. The same assay would be a poor choice for confirming disease, which is why it is deployed only after clinical probability has been assessed as low. <div class="ec-src"><b>Source:</b> Jaeschke R, Guyatt GH, Sackett DL. Users' guides to the medical literature. III. How to use an article about a diagnostic test. JAMA 1994;271(9):703-707.</div></div></div> [[Try this question again->Ruling out with a sensitive test - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Ruling out with a sensitive test. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Specificity is an intrinsic property of the test and does not vary systematically with prevalence. <div class="ec-teach"><div class="th">What the findings point to</div> A test with very high sensitivity produces few false negatives, so a negative result in a patient with low pretest probability drives the posttest probability of disease below the threshold at which further testing does more harm than good. The low specificity is irrelevant to this use, because a negative result is what is being interpreted. The same assay would be a poor choice for confirming disease, which is why it is deployed only after clinical probability has been assessed as low. <div class="ec-src"><b>Source:</b> Jaeschke R, Guyatt GH, Sackett DL. Users' guides to the medical literature. III. How to use an article about a diagnostic test. JAMA 1994;271(9):703-707.</div></div></div> [[Try this question again->Ruling out with a sensitive test - Biostat]] [[Start another case->Hub]]

<div class="ec-scene">Journal club · 07:42</div> A randomized trial compares a new antiemetic with placebo in 60 patients undergoing chemotherapy. Complete response occurs in 62% of the treatment group and 41% of the placebo group. The reported P value is 0.11 and the 95% confidence interval for the difference in proportions is -5% to +47%. The authors conclude that the new agent is no better than placebo. <span class="ec-prompt">Which of the following best describes the principal flaw in this conclusion?</span> [[Randomization failed to balance the treatment groups->Type II error - Biostat D4]] [[The alpha level was set too conservatively->Type II error - Biostat D1]] [[The confidence interval was calculated incorrectly->Type II error - Biostat D5]] [[The investigators committed a type I error->Type II error - Biostat D2]] [[The outcome measure was not clinically relevant->Type II error - Biostat D3]] [[The study lacked power to detect a real difference->Type II error - Biostat correct]]

<span class="ec-case-marker" hidden data-entry="Type II error. Biostat"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ The study lacked power to detect a real difference</div> With 30 patients per arm, a 21 percentage point difference did not reach significance, and the confidence interval is wide enough to include a large benefit at one end and a small harm at the other. Failing to reject the null hypothesis is not evidence that the null is true. Declaring equivalence from a nonsignificant result in a small trial is a type II error, and the correct statement is that the trial could not resolve whether the drug works. <div class="ec-src"><b>Source:</b> Freiman JA, Chalmers TC, Smith H Jr, Kuebler RR. The importance of beta, the type II error and sample size in the design and interpretation of the randomized control trial. N Engl J Med 1978;299(13):690-694.</div></div> [[Start another case->Hub]] [[Restart this case->Type II error - Biostat]] [[Next case →->Confidence interval interpretation - Biostat]]

<span class="ec-case-marker" hidden data-entry="Type II error. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A threshold of 0.05 is conventional and lowering it would make significance harder to reach, not easier. The problem is sample size, not the threshold. <div class="ec-teach"><div class="th">What the findings point to</div> With 30 patients per arm, a 21 percentage point difference did not reach significance, and the confidence interval is wide enough to include a large benefit at one end and a small harm at the other. Failing to reject the null hypothesis is not evidence that the null is true. Declaring equivalence from a nonsignificant result in a small trial is a type II error, and the correct statement is that the trial could not resolve whether the drug works. <div class="ec-src"><b>Source:</b> Freiman JA, Chalmers TC, Smith H Jr, Kuebler RR. The importance of beta, the type II error and sample size in the design and interpretation of the randomized control trial. N Engl J Med 1978;299(13):690-694.</div></div></div> [[Try this question again->Type II error - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Type II error. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A type I error is rejecting a true null hypothesis. These authors did not reject the null; they accepted it incorrectly. <div class="ec-teach"><div class="th">What the findings point to</div> With 30 patients per arm, a 21 percentage point difference did not reach significance, and the confidence interval is wide enough to include a large benefit at one end and a small harm at the other. Failing to reject the null hypothesis is not evidence that the null is true. Declaring equivalence from a nonsignificant result in a small trial is a type II error, and the correct statement is that the trial could not resolve whether the drug works. <div class="ec-src"><b>Source:</b> Freiman JA, Chalmers TC, Smith H Jr, Kuebler RR. The importance of beta, the type II error and sample size in the design and interpretation of the randomized control trial. N Engl J Med 1978;299(13):690-694.</div></div></div> [[Try this question again->Type II error - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Type II error. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Complete response to an antiemetic is a patient-centered outcome and is an appropriate endpoint. <div class="ec-teach"><div class="th">What the findings point to</div> With 30 patients per arm, a 21 percentage point difference did not reach significance, and the confidence interval is wide enough to include a large benefit at one end and a small harm at the other. Failing to reject the null hypothesis is not evidence that the null is true. Declaring equivalence from a nonsignificant result in a small trial is a type II error, and the correct statement is that the trial could not resolve whether the drug works. <div class="ec-src"><b>Source:</b> Freiman JA, Chalmers TC, Smith H Jr, Kuebler RR. The importance of beta, the type II error and sample size in the design and interpretation of the randomized control trial. N Engl J Med 1978;299(13):690-694.</div></div></div> [[Try this question again->Type II error - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Type II error. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Nothing in the description suggests imbalance, and imbalance would bias the estimate rather than widen the interval. <div class="ec-teach"><div class="th">What the findings point to</div> With 30 patients per arm, a 21 percentage point difference did not reach significance, and the confidence interval is wide enough to include a large benefit at one end and a small harm at the other. Failing to reject the null hypothesis is not evidence that the null is true. Declaring equivalence from a nonsignificant result in a small trial is a type II error, and the correct statement is that the trial could not resolve whether the drug works. <div class="ec-src"><b>Source:</b> Freiman JA, Chalmers TC, Smith H Jr, Kuebler RR. The importance of beta, the type II error and sample size in the design and interpretation of the randomized control trial. N Engl J Med 1978;299(13):690-694.</div></div></div> [[Try this question again->Type II error - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Type II error. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> An interval from -5% to +47% is consistent with a 21 point difference and a small sample. There is no indication of a computational error. <div class="ec-teach"><div class="th">What the findings point to</div> With 30 patients per arm, a 21 percentage point difference did not reach significance, and the confidence interval is wide enough to include a large benefit at one end and a small harm at the other. Failing to reject the null hypothesis is not evidence that the null is true. Declaring equivalence from a nonsignificant result in a small trial is a type II error, and the correct statement is that the trial could not resolve whether the drug works. <div class="ec-src"><b>Source:</b> Freiman JA, Chalmers TC, Smith H Jr, Kuebler RR. The importance of beta, the type II error and sample size in the design and interpretation of the randomized control trial. N Engl J Med 1978;299(13):690-694.</div></div></div> [[Try this question again->Type II error - Biostat]] [[Start another case->Hub]]

<div class="ec-scene">Journal club · 07:45</div> A cohort study of 12,000 adults reports that regular use of a dietary supplement is associated with myocardial infarction with a relative risk of 1.30 and a 95% confidence interval of 0.92 to 1.84. The authors state that the supplement increases cardiac risk and recommend that clinicians advise patients to stop taking it. <span class="ec-prompt">Which of the following best describes the appropriate interpretation of this result?</span> [[A larger sample would necessarily shift the estimate above 1.0->Confidence interval interpretation - Biostat D5]] [[The corresponding P value is below 0.05->Confidence interval interpretation - Biostat D3]] [[The interval indicates that 95% of users have a relative risk in this range->Confidence interval interpretation - Biostat D4]] [[The result is compatible with no association->Confidence interval interpretation - Biostat correct]] [[The result proves the supplement is safe->Confidence interval interpretation - Biostat D2]] [[The supplement raises risk by 30% in the studied population->Confidence interval interpretation - Biostat D1]]

<span class="ec-case-marker" hidden data-entry="Confidence interval interpretation. Biostat"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ The result is compatible with no association</div> The confidence interval includes 1.0, the value indicating no association, so the data are compatible with no effect as well as with a moderate increase and a small decrease in risk. A point estimate of 1.30 without an interval excluding the null does not establish an association. The correct statement is that the study did not demonstrate an effect, not that it demonstrated safety and not that it demonstrated harm. <div class="ec-src"><b>Source:</b> Gardner MJ, Altman DG. Confidence intervals rather than P values: estimation rather than hypothesis testing. Br Med J 1986;292(6522):746-750.</div></div> [[Start another case->Hub]] [[Restart this case->Confidence interval interpretation - Biostat]] [[Next case →->Intention to treat - Biostat]]

<span class="ec-case-marker" hidden data-entry="Confidence interval interpretation. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The 30% figure is a point estimate surrounded by substantial uncertainty. Reporting it as an established effect ignores the interval. <div class="ec-teach"><div class="th">What the findings point to</div> The confidence interval includes 1.0, the value indicating no association, so the data are compatible with no effect as well as with a moderate increase and a small decrease in risk. A point estimate of 1.30 without an interval excluding the null does not establish an association. The correct statement is that the study did not demonstrate an effect, not that it demonstrated safety and not that it demonstrated harm. <div class="ec-src"><b>Source:</b> Gardner MJ, Altman DG. Confidence intervals rather than P values: estimation rather than hypothesis testing. Br Med J 1986;292(6522):746-750.</div></div></div> [[Try this question again->Confidence interval interpretation - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Confidence interval interpretation. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> An interval extending to 1.84 leaves open a substantial increase in risk. Failure to demonstrate harm is not demonstration of safety. <div class="ec-teach"><div class="th">What the findings point to</div> The confidence interval includes 1.0, the value indicating no association, so the data are compatible with no effect as well as with a moderate increase and a small decrease in risk. A point estimate of 1.30 without an interval excluding the null does not establish an association. The correct statement is that the study did not demonstrate an effect, not that it demonstrated safety and not that it demonstrated harm. <div class="ec-src"><b>Source:</b> Gardner MJ, Altman DG. Confidence intervals rather than P values: estimation rather than hypothesis testing. Br Med J 1986;292(6522):746-750.</div></div></div> [[Try this question again->Confidence interval interpretation - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Confidence interval interpretation. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> An interval crossing 1.0 corresponds to a P value above 0.05 by definition. <div class="ec-teach"><div class="th">What the findings point to</div> The confidence interval includes 1.0, the value indicating no association, so the data are compatible with no effect as well as with a moderate increase and a small decrease in risk. A point estimate of 1.30 without an interval excluding the null does not establish an association. The correct statement is that the study did not demonstrate an effect, not that it demonstrated safety and not that it demonstrated harm. <div class="ec-src"><b>Source:</b> Gardner MJ, Altman DG. Confidence intervals rather than P values: estimation rather than hypothesis testing. Br Med J 1986;292(6522):746-750.</div></div></div> [[Try this question again->Confidence interval interpretation - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Confidence interval interpretation. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The interval describes uncertainty about a single population parameter, not the distribution of risk across individuals. <div class="ec-teach"><div class="th">What the findings point to</div> The confidence interval includes 1.0, the value indicating no association, so the data are compatible with no effect as well as with a moderate increase and a small decrease in risk. A point estimate of 1.30 without an interval excluding the null does not establish an association. The correct statement is that the study did not demonstrate an effect, not that it demonstrated safety and not that it demonstrated harm. <div class="ec-src"><b>Source:</b> Gardner MJ, Altman DG. Confidence intervals rather than P values: estimation rather than hypothesis testing. Br Med J 1986;292(6522):746-750.</div></div></div> [[Try this question again->Confidence interval interpretation - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Confidence interval interpretation. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> More data would narrow the interval, but the point estimate could move in either direction. <div class="ec-teach"><div class="th">What the findings point to</div> The confidence interval includes 1.0, the value indicating no association, so the data are compatible with no effect as well as with a moderate increase and a small decrease in risk. A point estimate of 1.30 without an interval excluding the null does not establish an association. The correct statement is that the study did not demonstrate an effect, not that it demonstrated safety and not that it demonstrated harm. <div class="ec-src"><b>Source:</b> Gardner MJ, Altman DG. Confidence intervals rather than P values: estimation rather than hypothesis testing. Br Med J 1986;292(6522):746-750.</div></div></div> [[Try this question again->Confidence interval interpretation - Biostat]] [[Start another case->Hub]]

<div class="ec-scene">Journal club · 07:25</div> In a randomized trial of a demanding 12-week exercise program versus usual care for peripheral artery disease, 220 patients were randomized to each arm. In the exercise arm, 61 patients discontinued the program, most citing pain, and were excluded from the reported analysis. The remaining 159 showed markedly greater improvement in walking distance than the usual care arm, and the authors report a large treatment effect. <span class="ec-prompt">Which of the following best describes the effect of excluding these patients?</span> [[It biases the result toward the null hypothesis->Intention to treat - Biostat D5]] [[It breaks randomization and inflates the apparent benefit->Intention to treat - Biostat correct]] [[It has no effect because dropouts were unrelated to treatment->Intention to treat - Biostat D1]] [[It is acceptable because more than 70% of the arm was retained->Intention to treat - Biostat D4]] [[It provides a valid estimate of efficacy under ideal conditions->Intention to treat - Biostat D3]] [[It reduces type I error by removing noncompliant patients->Intention to treat - Biostat D2]]

<span class="ec-case-marker" hidden data-entry="Intention to treat. Biostat"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ It breaks randomization and inflates the apparent benefit</div> Analyzing only those who completed the program removes patients whose dropout was related to disease severity and to their response to treatment. The remaining group is a selected subset no longer comparable with the control arm, which retained its own less able members. Intention-to-treat analysis preserves the balance randomization created and estimates the effect of offering the intervention, which is the question a clinician faces. <div class="ec-src"><b>Source:</b> Hernán MA, Hernández-Díaz S. Beyond the intention-to-treat in comparative effectiveness research. Clin Trials 2012;9(1):48-55.</div></div> [[Start another case->Hub]] [[Restart this case->Intention to treat - Biostat]] [[Next case →->Study design selection - Biostat]]

<span class="ec-case-marker" hidden data-entry="Intention to treat. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Most discontinued because of pain during exercise, which is directly related both to the intervention and to disease severity. <div class="ec-teach"><div class="th">What the findings point to</div> Analyzing only those who completed the program removes patients whose dropout was related to disease severity and to their response to treatment. The remaining group is a selected subset no longer comparable with the control arm, which retained its own less able members. Intention-to-treat analysis preserves the balance randomization created and estimates the effect of offering the intervention, which is the question a clinician faces. <div class="ec-src"><b>Source:</b> Hernán MA, Hernández-Díaz S. Beyond the intention-to-treat in comparative effectiveness research. Clin Trials 2012;9(1):48-55.</div></div></div> [[Try this question again->Intention to treat - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Intention to treat. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Removing patients selectively introduces bias rather than controlling it, and it makes a spurious positive finding more likely. <div class="ec-teach"><div class="th">What the findings point to</div> Analyzing only those who completed the program removes patients whose dropout was related to disease severity and to their response to treatment. The remaining group is a selected subset no longer comparable with the control arm, which retained its own less able members. Intention-to-treat analysis preserves the balance randomization created and estimates the effect of offering the intervention, which is the question a clinician faces. <div class="ec-src"><b>Source:</b> Hernán MA, Hernández-Díaz S. Beyond the intention-to-treat in comparative effectiveness research. Clin Trials 2012;9(1):48-55.</div></div></div> [[Try this question again->Intention to treat - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Intention to treat. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A per-protocol analysis can address efficacy only when adherence is unrelated to prognosis, which is not the case here. <div class="ec-teach"><div class="th">What the findings point to</div> Analyzing only those who completed the program removes patients whose dropout was related to disease severity and to their response to treatment. The remaining group is a selected subset no longer comparable with the control arm, which retained its own less able members. Intention-to-treat analysis preserves the balance randomization created and estimates the effect of offering the intervention, which is the question a clinician faces. <div class="ec-src"><b>Source:</b> Hernán MA, Hernández-Díaz S. Beyond the intention-to-treat in comparative effectiveness research. Clin Trials 2012;9(1):48-55.</div></div></div> [[Try this question again->Intention to treat - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Intention to treat. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> No retention threshold makes selective exclusion valid when the reason for dropout is linked to outcome. <div class="ec-teach"><div class="th">What the findings point to</div> Analyzing only those who completed the program removes patients whose dropout was related to disease severity and to their response to treatment. The remaining group is a selected subset no longer comparable with the control arm, which retained its own less able members. Intention-to-treat analysis preserves the balance randomization created and estimates the effect of offering the intervention, which is the question a clinician faces. <div class="ec-src"><b>Source:</b> Hernán MA, Hernández-Díaz S. Beyond the intention-to-treat in comparative effectiveness research. Clin Trials 2012;9(1):48-55.</div></div></div> [[Try this question again->Intention to treat - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Intention to treat. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Excluding patients who could not tolerate the intervention removes likely poor responders and biases away from the null. <div class="ec-teach"><div class="th">What the findings point to</div> Analyzing only those who completed the program removes patients whose dropout was related to disease severity and to their response to treatment. The remaining group is a selected subset no longer comparable with the control arm, which retained its own less able members. Intention-to-treat analysis preserves the balance randomization created and estimates the effect of offering the intervention, which is the question a clinician faces. <div class="ec-src"><b>Source:</b> Hernán MA, Hernández-Díaz S. Beyond the intention-to-treat in comparative effectiveness research. Clin Trials 2012;9(1):48-55.</div></div></div> [[Try this question again->Intention to treat - Biostat]] [[Start another case->Hub]]

<div class="ec-scene">Research meeting · 14:30</div> Investigators want to identify risk factors for a rare congenital malformation occurring in approximately 2 per 100,000 live births. They have access to a birth defects registry and to birth records for the surrounding population, and they must complete the work within 18 months with limited funding. Multiple candidate exposures during pregnancy are of interest. <span class="ec-prompt">Which of the following study designs is most appropriate?</span> [[Case series of affected infants->Study design selection - Biostat D4]] [[Case-control study->Study design selection - Biostat correct]] [[Cross-sectional survey->Study design selection - Biostat D2]] [[Ecological study comparing regional rates->Study design selection - Biostat D5]] [[Prospective cohort study->Study design selection - Biostat D1]] [[Randomized controlled trial->Study design selection - Biostat D3]]

<span class="ec-case-marker" hidden data-entry="Study design selection. Biostat"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Case-control study</div> When the outcome is very rare, a cohort would require enrolling hundreds of thousands of pregnancies and following them for years to accumulate enough cases. A case-control design starts from the affected infants in the registry, selects comparable unaffected controls, and looks backward at exposures, which is efficient in time, sample size, and cost. It also accommodates many candidate exposures at once. The measure of association is the odds ratio, which approximates the relative risk when the outcome is rare. <div class="ec-src"><b>Source:</b> Schulz KF, Grimes DA. Case-control studies: research in reverse. Lancet 2002;359(9304):431-434.</div></div> [[Start another case->Hub]] [[Restart this case->Study design selection - Biostat]] [[Next case →->Selection bias - Biostat]]

<span class="ec-case-marker" hidden data-entry="Study design selection. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Following a cohort forward would require an impractically large sample and far more than 18 months to accrue an outcome occurring twice per 100,000 births. <div class="ec-teach"><div class="th">What the findings point to</div> When the outcome is very rare, a cohort would require enrolling hundreds of thousands of pregnancies and following them for years to accumulate enough cases. A case-control design starts from the affected infants in the registry, selects comparable unaffected controls, and looks backward at exposures, which is efficient in time, sample size, and cost. It also accommodates many candidate exposures at once. The measure of association is the odds ratio, which approximates the relative risk when the outcome is rare. <div class="ec-src"><b>Source:</b> Schulz KF, Grimes DA. Case-control studies: research in reverse. Lancet 2002;359(9304):431-434.</div></div></div> [[Try this question again->Study design selection - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Study design selection. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A snapshot measures exposure and outcome simultaneously and cannot establish temporal sequence, which is essential for prenatal exposures. <div class="ec-teach"><div class="th">What the findings point to</div> When the outcome is very rare, a cohort would require enrolling hundreds of thousands of pregnancies and following them for years to accumulate enough cases. A case-control design starts from the affected infants in the registry, selects comparable unaffected controls, and looks backward at exposures, which is efficient in time, sample size, and cost. It also accommodates many candidate exposures at once. The measure of association is the odds ratio, which approximates the relative risk when the outcome is rare. <div class="ec-src"><b>Source:</b> Schulz KF, Grimes DA. Case-control studies: research in reverse. Lancet 2002;359(9304):431-434.</div></div></div> [[Try this question again->Study design selection - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Study design selection. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Randomly assigning pregnant women to suspected teratogenic exposures is unethical and would be impossible to justify. <div class="ec-teach"><div class="th">What the findings point to</div> When the outcome is very rare, a cohort would require enrolling hundreds of thousands of pregnancies and following them for years to accumulate enough cases. A case-control design starts from the affected infants in the registry, selects comparable unaffected controls, and looks backward at exposures, which is efficient in time, sample size, and cost. It also accommodates many candidate exposures at once. The measure of association is the odds ratio, which approximates the relative risk when the outcome is rare. <div class="ec-src"><b>Source:</b> Schulz KF, Grimes DA. Case-control studies: research in reverse. Lancet 2002;359(9304):431-434.</div></div></div> [[Try this question again->Study design selection - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Study design selection. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A series without a comparison group can describe the cases but cannot estimate any association with exposure. <div class="ec-teach"><div class="th">What the findings point to</div> When the outcome is very rare, a cohort would require enrolling hundreds of thousands of pregnancies and following them for years to accumulate enough cases. A case-control design starts from the affected infants in the registry, selects comparable unaffected controls, and looks backward at exposures, which is efficient in time, sample size, and cost. It also accommodates many candidate exposures at once. The measure of association is the odds ratio, which approximates the relative risk when the outcome is rare. <div class="ec-src"><b>Source:</b> Schulz KF, Grimes DA. Case-control studies: research in reverse. Lancet 2002;359(9304):431-434.</div></div></div> [[Try this question again->Study design selection - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Study design selection. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Aggregate comparisons risk the ecological fallacy and cannot link exposure to outcome in individuals. <div class="ec-teach"><div class="th">What the findings point to</div> When the outcome is very rare, a cohort would require enrolling hundreds of thousands of pregnancies and following them for years to accumulate enough cases. A case-control design starts from the affected infants in the registry, selects comparable unaffected controls, and looks backward at exposures, which is efficient in time, sample size, and cost. It also accommodates many candidate exposures at once. The measure of association is the odds ratio, which approximates the relative risk when the outcome is rare. <div class="ec-src"><b>Source:</b> Schulz KF, Grimes DA. Case-control studies: research in reverse. Lancet 2002;359(9304):431-434.</div></div></div> [[Try this question again->Study design selection - Biostat]] [[Start another case->Hub]]

<div class="ec-scene">Journal club · 07:47</div> A hospital-based study compares patients admitted with cholecystitis to patients admitted for other reasons and finds that diabetes mellitus is strongly associated with cholecystitis, with an odds ratio of 2.9. A subsequent population-based study of the same question in the community finds no association. Both studies were adequately powered and used identical diagnostic criteria. <span class="ec-prompt">Which of the following best explains the discrepancy?</span> [[Confounding by body mass index->Selection bias - Biostat D2]] [[Effect modification by hospital admission status->Selection bias - Biostat D5]] [[Misclassification of the outcome in the community study->Selection bias - Biostat D4]] [[Random error in the population-based study->Selection bias - Biostat D3]] [[Recall bias in reporting of diabetes history->Selection bias - Biostat D1]] [[Selection bias from differential probability of admission->Selection bias - Biostat correct]]

<span class="ec-case-marker" hidden data-entry="Selection bias. Biostat"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Selection bias from differential probability of admission</div> When cases and controls are both drawn from hospitalized patients, an association can appear simply because having two conditions raises the likelihood of admission more than having either alone. The hospital population is not representative of the population that generated the cases, and the apparent association is an artifact of who gets through the door. The population-based study, which samples the source population directly, gives the valid estimate. <div class="ec-src"><b>Source:</b> Grimes DA, Schulz KF. Bias and causal associations in observational research. Lancet 2002;359(9302):248-252.</div></div> [[Start another case->Hub]] [[Restart this case->Selection bias - Biostat]] [[Next case →->Confounding and effect modification - Biostat]]

<span class="ec-case-marker" hidden data-entry="Selection bias. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Diabetes is documented in medical records rather than recalled by patients, and recall bias would not differ systematically between hospital and community settings. <div class="ec-teach"><div class="th">What the findings point to</div> When cases and controls are both drawn from hospitalized patients, an association can appear simply because having two conditions raises the likelihood of admission more than having either alone. The hospital population is not representative of the population that generated the cases, and the apparent association is an artifact of who gets through the door. The population-based study, which samples the source population directly, gives the valid estimate. <div class="ec-src"><b>Source:</b> Grimes DA, Schulz KF. Bias and causal associations in observational research. Lancet 2002;359(9302):248-252.</div></div></div> [[Try this question again->Selection bias - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Selection bias. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Obesity is a plausible confounder, but it would be expected to operate in both studies rather than producing an association in only one. <div class="ec-teach"><div class="th">What the findings point to</div> When cases and controls are both drawn from hospitalized patients, an association can appear simply because having two conditions raises the likelihood of admission more than having either alone. The hospital population is not representative of the population that generated the cases, and the apparent association is an artifact of who gets through the door. The population-based study, which samples the source population directly, gives the valid estimate. <div class="ec-src"><b>Source:</b> Grimes DA, Schulz KF. Bias and causal associations in observational research. Lancet 2002;359(9302):248-252.</div></div></div> [[Try this question again->Selection bias - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Selection bias. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Both studies were adequately powered, and chance does not explain a systematic difference between two settings. <div class="ec-teach"><div class="th">What the findings point to</div> When cases and controls are both drawn from hospitalized patients, an association can appear simply because having two conditions raises the likelihood of admission more than having either alone. The hospital population is not representative of the population that generated the cases, and the apparent association is an artifact of who gets through the door. The population-based study, which samples the source population directly, gives the valid estimate. <div class="ec-src"><b>Source:</b> Grimes DA, Schulz KF. Bias and causal associations in observational research. Lancet 2002;359(9302):248-252.</div></div></div> [[Try this question again->Selection bias - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Selection bias. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Both used identical diagnostic criteria, so differential outcome misclassification is not supported. <div class="ec-teach"><div class="th">What the findings point to</div> When cases and controls are both drawn from hospitalized patients, an association can appear simply because having two conditions raises the likelihood of admission more than having either alone. The hospital population is not representative of the population that generated the cases, and the apparent association is an artifact of who gets through the door. The population-based study, which samples the source population directly, gives the valid estimate. <div class="ec-src"><b>Source:</b> Grimes DA, Schulz KF. Bias and causal associations in observational research. Lancet 2002;359(9302):248-252.</div></div></div> [[Try this question again->Selection bias - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Selection bias. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Admission is not a biological modifier of an exposure-disease relationship; it is a mechanism through which subjects were selected. <div class="ec-teach"><div class="th">What the findings point to</div> When cases and controls are both drawn from hospitalized patients, an association can appear simply because having two conditions raises the likelihood of admission more than having either alone. The hospital population is not representative of the population that generated the cases, and the apparent association is an artifact of who gets through the door. The population-based study, which samples the source population directly, gives the valid estimate. <div class="ec-src"><b>Source:</b> Grimes DA, Schulz KF. Bias and causal associations in observational research. Lancet 2002;359(9302):248-252.</div></div></div> [[Try this question again->Selection bias - Biostat]] [[Start another case->Hub]]

<div class="ec-scene">Journal club · 07:55</div> A study reports that a new analgesic is associated with gastrointestinal bleeding with a crude odds ratio of 3.4. When the analysis is stratified by concurrent anticoagulant use, the odds ratio is 3.3 among anticoagulant users and 3.5 among nonusers. When it is stratified by age, the odds ratio is 1.2 in patients younger than 60 years and 6.8 in patients 60 years and older. <span class="ec-prompt">Which of the following best describes the role of age in this analysis?</span> [[Age is a collider that should not be adjusted for->Confounding and effect modification - Biostat D4]] [[Age is a confounder->Confounding and effect modification - Biostat D1]] [[Age is a mediator on the causal pathway->Confounding and effect modification - Biostat D2]] [[Age is a proxy for anticoagulant use->Confounding and effect modification - Biostat D5]] [[Age is a source of information bias->Confounding and effect modification - Biostat D3]] [[Age is an effect modifier->Confounding and effect modification - Biostat correct]]

<span class="ec-case-marker" hidden data-entry="Confounding and effect modification. Biostat"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Age is an effect modifier</div> Stratum-specific estimates that differ substantially from one another indicate that the magnitude of the association depends on the level of that variable, which is effect modification. Because the effect genuinely differs across strata, the correct reporting is separate estimates for each age group rather than a single pooled figure. Anticoagulant use behaves differently: its strata are essentially identical to each other and to the crude estimate, so it is neither a confounder nor a modifier here. <div class="ec-src"><b>Source:</b> Rothman KJ. Epidemiology: An Introduction. 2nd ed. New York: Oxford University Press, 2012.</div></div> [[Start another case->Hub]] [[Restart this case->Confounding and effect modification - Biostat]] [[Next case →->Hazard ratio - Biostat]]

<span class="ec-case-marker" hidden data-entry="Confounding and effect modification. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Confounding is identified when the adjusted estimate differs from the crude estimate, and it is handled by adjustment to produce one summary figure. Here the strata differ from each other, which calls for separate estimates. <div class="ec-teach"><div class="th">What the findings point to</div> Stratum-specific estimates that differ substantially from one another indicate that the magnitude of the association depends on the level of that variable, which is effect modification. Because the effect genuinely differs across strata, the correct reporting is separate estimates for each age group rather than a single pooled figure. Anticoagulant use behaves differently: its strata are essentially identical to each other and to the crude estimate, so it is neither a confounder nor a modifier here. <div class="ec-src"><b>Source:</b> Rothman KJ. Epidemiology: An Introduction. 2nd ed. New York: Oxford University Press, 2012.</div></div></div> [[Try this question again->Confounding and effect modification - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Confounding and effect modification. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A mediator lies between exposure and outcome. Age precedes drug exposure and cannot be caused by it. <div class="ec-teach"><div class="th">What the findings point to</div> Stratum-specific estimates that differ substantially from one another indicate that the magnitude of the association depends on the level of that variable, which is effect modification. Because the effect genuinely differs across strata, the correct reporting is separate estimates for each age group rather than a single pooled figure. Anticoagulant use behaves differently: its strata are essentially identical to each other and to the crude estimate, so it is neither a confounder nor a modifier here. <div class="ec-src"><b>Source:</b> Rothman KJ. Epidemiology: An Introduction. 2nd ed. New York: Oxford University Press, 2012.</div></div></div> [[Try this question again->Confounding and effect modification - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Confounding and effect modification. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Information bias arises from measurement error in exposure or outcome. Nothing here suggests age was measured inaccurately. <div class="ec-teach"><div class="th">What the findings point to</div> Stratum-specific estimates that differ substantially from one another indicate that the magnitude of the association depends on the level of that variable, which is effect modification. Because the effect genuinely differs across strata, the correct reporting is separate estimates for each age group rather than a single pooled figure. Anticoagulant use behaves differently: its strata are essentially identical to each other and to the crude estimate, so it is neither a confounder nor a modifier here. <div class="ec-src"><b>Source:</b> Rothman KJ. Epidemiology: An Introduction. 2nd ed. New York: Oxford University Press, 2012.</div></div></div> [[Try this question again->Confounding and effect modification - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Confounding and effect modification. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A collider is a common effect of exposure and outcome. Age is not caused by either. <div class="ec-teach"><div class="th">What the findings point to</div> Stratum-specific estimates that differ substantially from one another indicate that the magnitude of the association depends on the level of that variable, which is effect modification. Because the effect genuinely differs across strata, the correct reporting is separate estimates for each age group rather than a single pooled figure. Anticoagulant use behaves differently: its strata are essentially identical to each other and to the crude estimate, so it is neither a confounder nor a modifier here. <div class="ec-src"><b>Source:</b> Rothman KJ. Epidemiology: An Introduction. 2nd ed. New York: Oxford University Press, 2012.</div></div></div> [[Try this question again->Confounding and effect modification - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Confounding and effect modification. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The anticoagulant strata show no variation in the estimate, so it cannot account for the pattern seen across age groups. <div class="ec-teach"><div class="th">What the findings point to</div> Stratum-specific estimates that differ substantially from one another indicate that the magnitude of the association depends on the level of that variable, which is effect modification. Because the effect genuinely differs across strata, the correct reporting is separate estimates for each age group rather than a single pooled figure. Anticoagulant use behaves differently: its strata are essentially identical to each other and to the crude estimate, so it is neither a confounder nor a modifier here. <div class="ec-src"><b>Source:</b> Rothman KJ. Epidemiology: An Introduction. 2nd ed. New York: Oxford University Press, 2012.</div></div></div> [[Try this question again->Confounding and effect modification - Biostat]] [[Start another case->Hub]]

<div class="ec-scene">Journal club · 07:20</div> A randomized trial of a targeted agent in advanced malignancy reports a hazard ratio for death of 0.72 with a 95% confidence interval of 0.61 to 0.85. Median overall survival is 14.2 months with the new agent and 11.0 months with standard therapy. The Kaplan-Meier curves separate at 4 months and remain separated throughout follow-up. A resident asks what the hazard ratio means. <span class="ec-prompt">Which of the following is the most accurate interpretation of this hazard ratio?</span> [[28% of patients treated with the new agent are cured->Hazard ratio - Biostat D2]] [[Each patient lives 28% longer with the new agent->Hazard ratio - Biostat D1]] [[The instantaneous rate of death is 28% lower with the new agent->Hazard ratio - Biostat correct]] [[The new agent reduces absolute mortality by 28 percentage points->Hazard ratio - Biostat D4]] [[The probability of surviving to 5 years is 0.72->Hazard ratio - Biostat D3]] [[The result is not statistically significant because it is below 1.0->Hazard ratio - Biostat D5]]

<span class="ec-case-marker" hidden data-entry="Hazard ratio. Biostat"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ The instantaneous rate of death is 28% lower with the new agent</div> A hazard ratio compares the rate at which events occur in the two arms at any given instant, averaged across the follow-up period. A value of 0.72 means that at any moment a patient on the new agent has roughly 72% of the death rate of a patient on standard therapy. It is a rate comparison, not a statement about how many patients survive or by how long any individual's life is extended, and it assumes the ratio is approximately constant over time. <div class="ec-src"><b>Source:</b> Spruance SL, Reid JE, Grace M, Samore M. Hazard ratio in clinical trials. Antimicrob Agents Chemother 2004;48(8):2787-2792.</div></div> [[Start another case->Hub]] [[Restart this case->Hazard ratio - Biostat]] [[Next case →->Recall bias - Biostat]]

<span class="ec-case-marker" hidden data-entry="Hazard ratio. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A hazard ratio does not translate into a proportional gain in survival time for individuals, and the median difference here is 3.2 months on 11.0 months. <div class="ec-teach"><div class="th">What the findings point to</div> A hazard ratio compares the rate at which events occur in the two arms at any given instant, averaged across the follow-up period. A value of 0.72 means that at any moment a patient on the new agent has roughly 72% of the death rate of a patient on standard therapy. It is a rate comparison, not a statement about how many patients survive or by how long any individual's life is extended, and it assumes the ratio is approximately constant over time. <div class="ec-src"><b>Source:</b> Spruance SL, Reid JE, Grace M, Samore M. Hazard ratio in clinical trials. Antimicrob Agents Chemother 2004;48(8):2787-2792.</div></div></div> [[Try this question again->Hazard ratio - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Hazard ratio. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Hazard ratios say nothing about cure, and separation of curves throughout follow-up is consistent with delay rather than cure. <div class="ec-teach"><div class="th">What the findings point to</div> A hazard ratio compares the rate at which events occur in the two arms at any given instant, averaged across the follow-up period. A value of 0.72 means that at any moment a patient on the new agent has roughly 72% of the death rate of a patient on standard therapy. It is a rate comparison, not a statement about how many patients survive or by how long any individual's life is extended, and it assumes the ratio is approximately constant over time. <div class="ec-src"><b>Source:</b> Spruance SL, Reid JE, Grace M, Samore M. Hazard ratio in clinical trials. Antimicrob Agents Chemother 2004;48(8):2787-2792.</div></div></div> [[Try this question again->Hazard ratio - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Hazard ratio. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> That would be a survival proportion at a fixed time point, which is a different quantity entirely. <div class="ec-teach"><div class="th">What the findings point to</div> A hazard ratio compares the rate at which events occur in the two arms at any given instant, averaged across the follow-up period. A value of 0.72 means that at any moment a patient on the new agent has roughly 72% of the death rate of a patient on standard therapy. It is a rate comparison, not a statement about how many patients survive or by how long any individual's life is extended, and it assumes the ratio is approximately constant over time. <div class="ec-src"><b>Source:</b> Spruance SL, Reid JE, Grace M, Samore M. Hazard ratio in clinical trials. Antimicrob Agents Chemother 2004;48(8):2787-2792.</div></div></div> [[Try this question again->Hazard ratio - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Hazard ratio. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Absolute risk difference must be read off the survival curves at a specified time and cannot be inferred from a ratio. <div class="ec-teach"><div class="th">What the findings point to</div> A hazard ratio compares the rate at which events occur in the two arms at any given instant, averaged across the follow-up period. A value of 0.72 means that at any moment a patient on the new agent has roughly 72% of the death rate of a patient on standard therapy. It is a rate comparison, not a statement about how many patients survive or by how long any individual's life is extended, and it assumes the ratio is approximately constant over time. <div class="ec-src"><b>Source:</b> Spruance SL, Reid JE, Grace M, Samore M. Hazard ratio in clinical trials. Antimicrob Agents Chemother 2004;48(8):2787-2792.</div></div></div> [[Try this question again->Hazard ratio - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Hazard ratio. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A confidence interval from 0.61 to 0.85 excludes 1.0, which indicates statistical significance. <div class="ec-teach"><div class="th">What the findings point to</div> A hazard ratio compares the rate at which events occur in the two arms at any given instant, averaged across the follow-up period. A value of 0.72 means that at any moment a patient on the new agent has roughly 72% of the death rate of a patient on standard therapy. It is a rate comparison, not a statement about how many patients survive or by how long any individual's life is extended, and it assumes the ratio is approximately constant over time. <div class="ec-src"><b>Source:</b> Spruance SL, Reid JE, Grace M, Samore M. Hazard ratio in clinical trials. Antimicrob Agents Chemother 2004;48(8):2787-2792.</div></div></div> [[Try this question again->Hazard ratio - Biostat]] [[Start another case->Hub]]

<div class="ec-scene">Research meeting · 15:05</div> A case-control study investigates whether maternal use of a common over-the-counter medication during the first trimester is associated with a birth defect. Mothers of affected infants and mothers of healthy infants are interviewed after delivery about medications taken during pregnancy. Mothers of affected infants report the exposure at nearly three times the rate of control mothers. No prescription records or pharmacy data were used. <span class="ec-prompt">Which of the following most threatens the validity of this finding?</span> [[Confounding by maternal age->Recall bias - Biostat D2]] [[Differential accuracy of exposure reporting between groups->Recall bias - Biostat correct]] [[Inadequate statistical power to detect the association->Recall bias - Biostat D5]] [[Loss to follow-up among control mothers->Recall bias - Biostat D1]] [[Nondifferential misclassification of exposure->Recall bias - Biostat D3]] [[Selection of controls from the same hospital as cases->Recall bias - Biostat D4]]

<span class="ec-case-marker" hidden data-entry="Recall bias. Biostat"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Differential accuracy of exposure reporting between groups</div> Mothers of an affected infant search their pregnancies for explanations and recall exposures more completely and more readily than mothers whose infants are well. This produces systematically better ascertainment of exposure in cases than in controls and can generate an association where none exists. The design feature that permits it is reliance on interview after the outcome is known, and it is addressed by using records generated before the outcome, such as pharmacy dispensing data. <div class="ec-src"><b>Source:</b> Coughlin SS. Recall bias in epidemiologic studies. J Clin Epidemiol 1990;43(1):87-91.</div></div> [[Start another case->Hub]] [[Restart this case->Recall bias - Biostat]] [[Next case →->Publication bias - Biostat]]

<span class="ec-case-marker" hidden data-entry="Recall bias. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A case-control study does not follow subjects forward, so attrition of this kind does not arise. <div class="ec-teach"><div class="th">What the findings point to</div> Mothers of an affected infant search their pregnancies for explanations and recall exposures more completely and more readily than mothers whose infants are well. This produces systematically better ascertainment of exposure in cases than in controls and can generate an association where none exists. The design feature that permits it is reliance on interview after the outcome is known, and it is addressed by using records generated before the outcome, such as pharmacy dispensing data. <div class="ec-src"><b>Source:</b> Coughlin SS. Recall bias in epidemiologic studies. J Clin Epidemiol 1990;43(1):87-91.</div></div></div> [[Try this question again->Recall bias - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Recall bias. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Age is a plausible confounder and can be adjusted for. It does not explain a threefold difference in reported exposure. <div class="ec-teach"><div class="th">What the findings point to</div> Mothers of an affected infant search their pregnancies for explanations and recall exposures more completely and more readily than mothers whose infants are well. This produces systematically better ascertainment of exposure in cases than in controls and can generate an association where none exists. The design feature that permits it is reliance on interview after the outcome is known, and it is addressed by using records generated before the outcome, such as pharmacy dispensing data. <div class="ec-src"><b>Source:</b> Coughlin SS. Recall bias in epidemiologic studies. J Clin Epidemiol 1990;43(1):87-91.</div></div></div> [[Try this question again->Recall bias - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Recall bias. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Misclassification affecting both groups equally would dilute an association toward the null rather than create one. <div class="ec-teach"><div class="th">What the findings point to</div> Mothers of an affected infant search their pregnancies for explanations and recall exposures more completely and more readily than mothers whose infants are well. This produces systematically better ascertainment of exposure in cases than in controls and can generate an association where none exists. The design feature that permits it is reliance on interview after the outcome is known, and it is addressed by using records generated before the outcome, such as pharmacy dispensing data. <div class="ec-src"><b>Source:</b> Coughlin SS. Recall bias in epidemiologic studies. J Clin Epidemiol 1990;43(1):87-91.</div></div></div> [[Try this question again->Recall bias - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Recall bias. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Sampling controls from the source population that produced the cases is generally desirable and is not the flaw here. <div class="ec-teach"><div class="th">What the findings point to</div> Mothers of an affected infant search their pregnancies for explanations and recall exposures more completely and more readily than mothers whose infants are well. This produces systematically better ascertainment of exposure in cases than in controls and can generate an association where none exists. The design feature that permits it is reliance on interview after the outcome is known, and it is addressed by using records generated before the outcome, such as pharmacy dispensing data. <div class="ec-src"><b>Source:</b> Coughlin SS. Recall bias in epidemiologic studies. J Clin Epidemiol 1990;43(1):87-91.</div></div></div> [[Try this question again->Recall bias - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Recall bias. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The study detected a large difference, so lack of power is not the concern. <div class="ec-teach"><div class="th">What the findings point to</div> Mothers of an affected infant search their pregnancies for explanations and recall exposures more completely and more readily than mothers whose infants are well. This produces systematically better ascertainment of exposure in cases than in controls and can generate an association where none exists. The design feature that permits it is reliance on interview after the outcome is known, and it is addressed by using records generated before the outcome, such as pharmacy dispensing data. <div class="ec-src"><b>Source:</b> Coughlin SS. Recall bias in epidemiologic studies. J Clin Epidemiol 1990;43(1):87-91.</div></div></div> [[Try this question again->Recall bias - Biostat]] [[Start another case->Hub]]

<div class="ec-scene">Journal club · 07:50</div> A meta-analysis pools 18 trials of an herbal preparation for migraine prophylaxis and reports a significant benefit. The included trials are predominantly small, and the largest two trials show no effect. A funnel plot of effect size against standard error is markedly asymmetric, with small trials reporting large benefits and an absence of small trials reporting no effect or harm. <span class="ec-prompt">Which of the following best explains the funnel plot asymmetry?</span> [[Differences in migraine definition across the included trials->Publication bias - Biostat D5]] [[Inadequate blinding in the largest two trials->Publication bias - Biostat D3]] [[Random variation expected with a small number of trials->Publication bias - Biostat D2]] [[Selective publication of small positive trials->Publication bias - Biostat correct]] [[True heterogeneity in the underlying treatment effect->Publication bias - Biostat D1]] [[Use of a random-effects rather than a fixed-effect model->Publication bias - Biostat D4]]

<span class="ec-case-marker" hidden data-entry="Publication bias. Biostat"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Selective publication of small positive trials</div> A symmetric funnel is expected when small studies scatter widely around the true effect in both directions. Asymmetry with a missing lower-left region indicates that small studies with null or negative results exist but were never published or indexed. Because meta-analysis can only pool what is retrievable, the summary estimate is inflated. The pattern is reinforced here by the two largest and least publication-prone trials showing no effect. <div class="ec-src"><b>Source:</b> Egger M, Davey Smith G, Schneider M, Minder C. Bias in meta-analysis detected by a simple, graphical test. BMJ 1997;315(7109):629-634.</div></div> [[Start another case->Hub]] [[Restart this case->Publication bias - Biostat]] [[Next case →->Colorectal screening onset - Prevention]]

<span class="ec-case-marker" hidden data-entry="Publication bias. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Genuine heterogeneity widens scatter but does not systematically remove studies from one side of the plot. <div class="ec-teach"><div class="th">What the findings point to</div> A symmetric funnel is expected when small studies scatter widely around the true effect in both directions. Asymmetry with a missing lower-left region indicates that small studies with null or negative results exist but were never published or indexed. Because meta-analysis can only pool what is retrievable, the summary estimate is inflated. The pattern is reinforced here by the two largest and least publication-prone trials showing no effect. <div class="ec-src"><b>Source:</b> Egger M, Davey Smith G, Schneider M, Minder C. Bias in meta-analysis detected by a simple, graphical test. BMJ 1997;315(7109):629-634.</div></div></div> [[Try this question again->Publication bias - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Publication bias. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Eighteen trials with a consistent directional gap is a pattern, not the scatter chance produces. <div class="ec-teach"><div class="th">What the findings point to</div> A symmetric funnel is expected when small studies scatter widely around the true effect in both directions. Asymmetry with a missing lower-left region indicates that small studies with null or negative results exist but were never published or indexed. Because meta-analysis can only pool what is retrievable, the summary estimate is inflated. The pattern is reinforced here by the two largest and least publication-prone trials showing no effect. <div class="ec-src"><b>Source:</b> Egger M, Davey Smith G, Schneider M, Minder C. Bias in meta-analysis detected by a simple, graphical test. BMJ 1997;315(7109):629-634.</div></div></div> [[Try this question again->Publication bias - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Publication bias. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Poor blinding tends to exaggerate apparent benefit, which would push the large trials toward an effect rather than away from one. <div class="ec-teach"><div class="th">What the findings point to</div> A symmetric funnel is expected when small studies scatter widely around the true effect in both directions. Asymmetry with a missing lower-left region indicates that small studies with null or negative results exist but were never published or indexed. Because meta-analysis can only pool what is retrievable, the summary estimate is inflated. The pattern is reinforced here by the two largest and least publication-prone trials showing no effect. <div class="ec-src"><b>Source:</b> Egger M, Davey Smith G, Schneider M, Minder C. Bias in meta-analysis detected by a simple, graphical test. BMJ 1997;315(7109):629-634.</div></div></div> [[Try this question again->Publication bias - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Publication bias. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The choice of model changes weighting and the width of the summary interval but does not create asymmetry in the plot. <div class="ec-teach"><div class="th">What the findings point to</div> A symmetric funnel is expected when small studies scatter widely around the true effect in both directions. Asymmetry with a missing lower-left region indicates that small studies with null or negative results exist but were never published or indexed. Because meta-analysis can only pool what is retrievable, the summary estimate is inflated. The pattern is reinforced here by the two largest and least publication-prone trials showing no effect. <div class="ec-src"><b>Source:</b> Egger M, Davey Smith G, Schneider M, Minder C. Bias in meta-analysis detected by a simple, graphical test. BMJ 1997;315(7109):629-634.</div></div></div> [[Try this question again->Publication bias - Biostat]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Publication bias. Biostat"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Definitional variation contributes to heterogeneity and would scatter effects in both directions rather than in one. <div class="ec-teach"><div class="th">What the findings point to</div> A symmetric funnel is expected when small studies scatter widely around the true effect in both directions. Asymmetry with a missing lower-left region indicates that small studies with null or negative results exist but were never published or indexed. Because meta-analysis can only pool what is retrievable, the summary estimate is inflated. The pattern is reinforced here by the two largest and least publication-prone trials showing no effect. <div class="ec-src"><b>Source:</b> Egger M, Davey Smith G, Schneider M, Minder C. Bias in meta-analysis detected by a simple, graphical test. BMJ 1997;315(7109):629-634.</div></div></div> [[Try this question again->Publication bias - Biostat]] [[Start another case->Hub]]

<div class="ec-scene">Primary care clinic · 09:15</div> A 46-year-old man presents to establish care. He is asymptomatic, has no rectal bleeding or change in bowel habit, and has never had colorectal screening. He has no personal history of adenomatous polyps, no inflammatory bowel disease, and no family history of colorectal cancer or polyposis syndromes. Body mass index is 27 kg/m2. Physical examination including digital rectal examination is normal. <span class="ec-prompt">Which of the following is the most appropriate screening recommendation?</span> [[Begin colorectal cancer screening now->Colorectal screening onset - Prevention correct]] [[Begin screening at age 50->Colorectal screening onset - Prevention D1]] [[Defer screening because he has no family history->Colorectal screening onset - Prevention D5]] [[Order serum carcinoembryonic antigen annually->Colorectal screening onset - Prevention D4]] [[Perform annual digital rectal examination alone->Colorectal screening onset - Prevention D3]] [[Screen only if fecal occult blood testing is positive->Colorectal screening onset - Prevention D2]]

<span class="ec-case-marker" hidden data-entry="Colorectal screening onset. Prevention"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Begin colorectal cancer screening now</div> Screening for average-risk adults begins at age 45, lowered from 50 in the 2021 update in response to rising incidence in younger adults. He is 46 and has never been screened, so screening is indicated today. Several strategies are acceptable, including colonoscopy every 10 years and annual fecal immunochemical testing, and the best test is the one the patient will actually complete. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Screening for Colorectal Cancer: US Preventive Services Task Force Recommendation Statement. JAMA 2021;325(19):1965-1977.</div></div> [[Start another case->Hub]] [[Restart this case->Colorectal screening onset - Prevention]] [[Next case →->Open tibial fracture - Rx]]

<span class="ec-case-marker" hidden data-entry="Colorectal screening onset. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The threshold of 50 was superseded in 2021. Waiting 4 years discards the interval the revision was designed to capture. <div class="ec-teach"><div class="th">What the findings point to</div> Screening for average-risk adults begins at age 45, lowered from 50 in the 2021 update in response to rising incidence in younger adults. He is 46 and has never been screened, so screening is indicated today. Several strategies are acceptable, including colonoscopy every 10 years and annual fecal immunochemical testing, and the best test is the one the patient will actually complete. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Screening for Colorectal Cancer: US Preventive Services Task Force Recommendation Statement. JAMA 2021;325(19):1965-1977.</div></div></div> [[Try this question again->Colorectal screening onset - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Colorectal screening onset. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Guaiac-based occult blood testing performed on a single office specimen is not a validated screening strategy and misses most neoplasia. <div class="ec-teach"><div class="th">What the findings point to</div> Screening for average-risk adults begins at age 45, lowered from 50 in the 2021 update in response to rising incidence in younger adults. He is 46 and has never been screened, so screening is indicated today. Several strategies are acceptable, including colonoscopy every 10 years and annual fecal immunochemical testing, and the best test is the one the patient will actually complete. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Screening for Colorectal Cancer: US Preventive Services Task Force Recommendation Statement. JAMA 2021;325(19):1965-1977.</div></div></div> [[Try this question again->Colorectal screening onset - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Colorectal screening onset. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Digital examination reaches only the distal rectum and has no role as a colorectal cancer screening test. <div class="ec-teach"><div class="th">What the findings point to</div> Screening for average-risk adults begins at age 45, lowered from 50 in the 2021 update in response to rising incidence in younger adults. He is 46 and has never been screened, so screening is indicated today. Several strategies are acceptable, including colonoscopy every 10 years and annual fecal immunochemical testing, and the best test is the one the patient will actually complete. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Screening for Colorectal Cancer: US Preventive Services Task Force Recommendation Statement. JAMA 2021;325(19):1965-1977.</div></div></div> [[Try this question again->Colorectal screening onset - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Colorectal screening onset. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This marker is used to monitor patients with known colorectal cancer. It is neither sensitive nor specific enough to screen. <div class="ec-teach"><div class="th">What the findings point to</div> Screening for average-risk adults begins at age 45, lowered from 50 in the 2021 update in response to rising incidence in younger adults. He is 46 and has never been screened, so screening is indicated today. Several strategies are acceptable, including colonoscopy every 10 years and annual fecal immunochemical testing, and the best test is the one the patient will actually complete. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Screening for Colorectal Cancer: US Preventive Services Task Force Recommendation Statement. JAMA 2021;325(19):1965-1977.</div></div></div> [[Try this question again->Colorectal screening onset - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Colorectal screening onset. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Most colorectal cancers occur in people with no family history, which is why screening is recommended for average-risk adults. <div class="ec-teach"><div class="th">What the findings point to</div> Screening for average-risk adults begins at age 45, lowered from 50 in the 2021 update in response to rising incidence in younger adults. He is 46 and has never been screened, so screening is indicated today. Several strategies are acceptable, including colonoscopy every 10 years and annual fecal immunochemical testing, and the best test is the one the patient will actually complete. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Screening for Colorectal Cancer: US Preventive Services Task Force Recommendation Statement. JAMA 2021;325(19):1965-1977.</div></div></div> [[Try this question again->Colorectal screening onset - Prevention]] [[Start another case->Hub]]

<div class="ec-scene">Primary care clinic · 11:00</div> A 39-year-old woman presents for a routine visit. She has no risk factors she is willing to disclose, no history of injection drug use, no transfusions, and no tattoos. She feels well. Aminotransferase concentrations obtained last year were normal. She has never been tested for hepatitis C virus infection. She asks whether she needs the test her friend mentioned. <span class="ec-prompt">Which of the following is the most appropriate recommendation?</span> [[Annual hepatitis C antibody testing->Hepatitis C screening - Prevention D4]] [[Hepatitis C RNA testing as the initial test->Hepatitis C screening - Prevention D5]] [[One-time hepatitis C antibody testing->Hepatitis C screening - Prevention correct]] [[Testing only adults born between 1945 and 1965->Hepatitis C screening - Prevention D2]] [[Testing only if aminotransferase concentrations become elevated->Hepatitis C screening - Prevention D1]] [[Testing only if she reports injection drug use->Hepatitis C screening - Prevention D3]]

<span class="ec-case-marker" hidden data-entry="Hepatitis C screening. Prevention"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ One-time hepatitis C antibody testing</div> Screening is recommended once for all adults aged 18 to 79 years, regardless of disclosed risk factors. Universal testing replaced risk-based and birth-cohort strategies because risk-based screening misses a large share of infections, disclosure of stigmatized exposures is unreliable, and infection is usually asymptomatic with normal aminotransferases for years. Treatment now cures the great majority of those identified, which is what makes case finding worthwhile. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Screening for Hepatitis C Virus Infection in Adolescents and Adults: US Preventive Services Task Force Recommendation Statement. JAMA 2020;323(10):970-975.</div></div> [[Start another case->Hub]] [[Restart this case->Hepatitis C screening - Prevention]] [[Next case →->HIV preexposure prophylaxis - Prevention]]

<span class="ec-case-marker" hidden data-entry="Hepatitis C screening. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Chronic infection commonly runs with normal enzymes, so waiting for an abnormality misses most cases and allows fibrosis to progress. <div class="ec-teach"><div class="th">What the findings point to</div> Screening is recommended once for all adults aged 18 to 79 years, regardless of disclosed risk factors. Universal testing replaced risk-based and birth-cohort strategies because risk-based screening misses a large share of infections, disclosure of stigmatized exposures is unreliable, and infection is usually asymptomatic with normal aminotransferases for years. Treatment now cures the great majority of those identified, which is what makes case finding worthwhile. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Screening for Hepatitis C Virus Infection in Adolescents and Adults: US Preventive Services Task Force Recommendation Statement. JAMA 2020;323(10):970-975.</div></div></div> [[Try this question again->Hepatitis C screening - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Hepatitis C screening. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The birth cohort strategy was superseded in 2020 by universal adult screening, which captures infections acquired more recently. <div class="ec-teach"><div class="th">What the findings point to</div> Screening is recommended once for all adults aged 18 to 79 years, regardless of disclosed risk factors. Universal testing replaced risk-based and birth-cohort strategies because risk-based screening misses a large share of infections, disclosure of stigmatized exposures is unreliable, and infection is usually asymptomatic with normal aminotransferases for years. Treatment now cures the great majority of those identified, which is what makes case finding worthwhile. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Screening for Hepatitis C Virus Infection in Adolescents and Adults: US Preventive Services Task Force Recommendation Statement. JAMA 2020;323(10):970-975.</div></div></div> [[Try this question again->Hepatitis C screening - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Hepatitis C screening. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Risk-based screening depends on disclosure of stigmatized behavior and misses a substantial proportion of infections. <div class="ec-teach"><div class="th">What the findings point to</div> Screening is recommended once for all adults aged 18 to 79 years, regardless of disclosed risk factors. Universal testing replaced risk-based and birth-cohort strategies because risk-based screening misses a large share of infections, disclosure of stigmatized exposures is unreliable, and infection is usually asymptomatic with normal aminotransferases for years. Treatment now cures the great majority of those identified, which is what makes case finding worthwhile. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Screening for Hepatitis C Virus Infection in Adolescents and Adults: US Preventive Services Task Force Recommendation Statement. JAMA 2020;323(10):970-975.</div></div></div> [[Try this question again->Hepatitis C screening - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Hepatitis C screening. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Repeat testing is reserved for people with ongoing risk. For an adult without continuing exposure, one-time testing suffices. <div class="ec-teach"><div class="th">What the findings point to</div> Screening is recommended once for all adults aged 18 to 79 years, regardless of disclosed risk factors. Universal testing replaced risk-based and birth-cohort strategies because risk-based screening misses a large share of infections, disclosure of stigmatized exposures is unreliable, and infection is usually asymptomatic with normal aminotransferases for years. Treatment now cures the great majority of those identified, which is what makes case finding worthwhile. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Screening for Hepatitis C Virus Infection in Adolescents and Adults: US Preventive Services Task Force Recommendation Statement. JAMA 2020;323(10):970-975.</div></div></div> [[Try this question again->Hepatitis C screening - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Hepatitis C screening. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Antibody testing is the entry point, with RNA reserved to confirm active infection in those who test positive. <div class="ec-teach"><div class="th">What the findings point to</div> Screening is recommended once for all adults aged 18 to 79 years, regardless of disclosed risk factors. Universal testing replaced risk-based and birth-cohort strategies because risk-based screening misses a large share of infections, disclosure of stigmatized exposures is unreliable, and infection is usually asymptomatic with normal aminotransferases for years. Treatment now cures the great majority of those identified, which is what makes case finding worthwhile. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Screening for Hepatitis C Virus Infection in Adolescents and Adults: US Preventive Services Task Force Recommendation Statement. JAMA 2020;323(10):970-975.</div></div></div> [[Try this question again->Hepatitis C screening - Prevention]] [[Start another case->Hub]]

<div class="ec-scene">Primary care clinic · 10:30</div> A 38-year-old woman presents for a wellness visit. Body mass index is 29 kg/m2. She is asymptomatic without polyuria, polydipsia, or weight loss. Blood pressure is 126/80 mm Hg. She has no personal history of gestational diabetes and no family history of diabetes mellitus. She has never had glucose testing. Physical examination shows no acanthosis nigricans. <span class="ec-prompt">Which of the following is the most appropriate screening recommendation?</span> [[Defer screening because blood pressure is normal->Diabetes screening - Prevention D5]] [[Measure random plasma glucose at this visit->Diabetes screening - Prevention D4]] [[Screen beginning at age 45->Diabetes screening - Prevention D1]] [[Screen for diabetes mellitus now->Diabetes screening - Prevention correct]] [[Screen only if a first-degree relative has diabetes->Diabetes screening - Prevention D3]] [[Screen only if she develops symptoms of hyperglycemia->Diabetes screening - Prevention D2]]

<span class="ec-case-marker" hidden data-entry="Diabetes screening. Prevention"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Screen for diabetes mellitus now</div> Screening for prediabetes and type 2 diabetes is recommended in asymptomatic adults aged 35 to 70 years who are overweight or obese, defined as a body mass index of 25 kg/m2 or greater. She is 38 with a body mass index of 29, so she qualifies on age and weight alone, without any additional risk factor. Acceptable tests include fasting plasma glucose, hemoglobin A1c, and an oral glucose tolerance test, repeated at least every 3 years if normal. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Screening for Prediabetes and Type 2 Diabetes: US Preventive Services Task Force Recommendation Statement. JAMA 2021;326(8):736-743.</div></div> [[Start another case->Hub]] [[Restart this case->Diabetes screening - Prevention]] [[Next case →->Refeeding electrolyte shift - Mech]]

<span class="ec-case-marker" hidden data-entry="Diabetes screening. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The age threshold was lowered to 35 in the 2021 statement. Waiting until 45 forfeits 7 years during which prediabetes could be identified and reversed. <div class="ec-teach"><div class="th">What the findings point to</div> Screening for prediabetes and type 2 diabetes is recommended in asymptomatic adults aged 35 to 70 years who are overweight or obese, defined as a body mass index of 25 kg/m2 or greater. She is 38 with a body mass index of 29, so she qualifies on age and weight alone, without any additional risk factor. Acceptable tests include fasting plasma glucose, hemoglobin A1c, and an oral glucose tolerance test, repeated at least every 3 years if normal. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Screening for Prediabetes and Type 2 Diabetes: US Preventive Services Task Force Recommendation Statement. JAMA 2021;326(8):736-743.</div></div></div> [[Try this question again->Diabetes screening - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Diabetes screening. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Polyuria and polydipsia appear late. Screening exists to find disease during the asymptomatic interval when intervention still works. <div class="ec-teach"><div class="th">What the findings point to</div> Screening for prediabetes and type 2 diabetes is recommended in asymptomatic adults aged 35 to 70 years who are overweight or obese, defined as a body mass index of 25 kg/m2 or greater. She is 38 with a body mass index of 29, so she qualifies on age and weight alone, without any additional risk factor. Acceptable tests include fasting plasma glucose, hemoglobin A1c, and an oral glucose tolerance test, repeated at least every 3 years if normal. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Screening for Prediabetes and Type 2 Diabetes: US Preventive Services Task Force Recommendation Statement. JAMA 2021;326(8):736-743.</div></div></div> [[Try this question again->Diabetes screening - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Diabetes screening. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Family history increases risk but is not required. The recommendation is based on age and body mass index. <div class="ec-teach"><div class="th">What the findings point to</div> Screening for prediabetes and type 2 diabetes is recommended in asymptomatic adults aged 35 to 70 years who are overweight or obese, defined as a body mass index of 25 kg/m2 or greater. She is 38 with a body mass index of 29, so she qualifies on age and weight alone, without any additional risk factor. Acceptable tests include fasting plasma glucose, hemoglobin A1c, and an oral glucose tolerance test, repeated at least every 3 years if normal. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Screening for Prediabetes and Type 2 Diabetes: US Preventive Services Task Force Recommendation Statement. JAMA 2021;326(8):736-743.</div></div></div> [[Try this question again->Diabetes screening - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Diabetes screening. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A random value is not a recommended screening test because it is neither standardized nor interpretable against diagnostic thresholds. <div class="ec-teach"><div class="th">What the findings point to</div> Screening for prediabetes and type 2 diabetes is recommended in asymptomatic adults aged 35 to 70 years who are overweight or obese, defined as a body mass index of 25 kg/m2 or greater. She is 38 with a body mass index of 29, so she qualifies on age and weight alone, without any additional risk factor. Acceptable tests include fasting plasma glucose, hemoglobin A1c, and an oral glucose tolerance test, repeated at least every 3 years if normal. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Screening for Prediabetes and Type 2 Diabetes: US Preventive Services Task Force Recommendation Statement. JAMA 2021;326(8):736-743.</div></div></div> [[Try this question again->Diabetes screening - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Diabetes screening. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Hypertension is one of several risk factors that would prompt earlier screening. Its absence does not exempt a patient who already meets criteria. <div class="ec-teach"><div class="th">What the findings point to</div> Screening for prediabetes and type 2 diabetes is recommended in asymptomatic adults aged 35 to 70 years who are overweight or obese, defined as a body mass index of 25 kg/m2 or greater. She is 38 with a body mass index of 29, so she qualifies on age and weight alone, without any additional risk factor. Acceptable tests include fasting plasma glucose, hemoglobin A1c, and an oral glucose tolerance test, repeated at least every 3 years if normal. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Screening for Prediabetes and Type 2 Diabetes: US Preventive Services Task Force Recommendation Statement. JAMA 2021;326(8):736-743.</div></div></div> [[Try this question again->Diabetes screening - Prevention]] [[Start another case->Hub]]

<div class="ec-scene">Sexual health clinic · 16:40</div> A 26-year-old man reports condomless receptive anal intercourse with multiple male partners over the past 6 months and was treated for rectal gonorrhea 2 months ago. He is asymptomatic today. A fourth-generation HIV antigen and antibody assay is negative, HIV RNA is undetectable, serum creatinine is 0.9 mg/dL, and hepatitis B surface antigen is negative with reactive surface antibody. He asks how to reduce his risk. <span class="ec-prompt">Which of the following is the most appropriate recommendation?</span> [[Begin postexposure prophylaxis for 28 days->HIV preexposure prophylaxis - Prevention D2]] [[Defer prophylaxis until hepatitis B immunity is confirmed->HIV preexposure prophylaxis - Prevention D5]] [[Provide condoms and risk reduction counseling alone->HIV preexposure prophylaxis - Prevention D1]] [[Start preexposure prophylaxis with tenofovir and emtricitabine->HIV preexposure prophylaxis - Prevention correct]] [[Start prophylaxis only after a documented HIV exposure->HIV preexposure prophylaxis - Prevention D4]] [[Test for HIV every 3 months without pharmacologic prophylaxis->HIV preexposure prophylaxis - Prevention D3]]

<span class="ec-case-marker" hidden data-entry="HIV preexposure prophylaxis. Prevention"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Start preexposure prophylaxis with tenofovir and emtricitabine</div> He has a recent bacterial sexually transmitted infection and ongoing condomless receptive anal intercourse, both markers of substantial HIV risk, and he is confirmed HIV negative with adequate renal function. Preexposure prophylaxis is recommended for people at increased risk and reduces acquisition markedly when taken consistently. Follow-up includes HIV testing at least every 3 months, renal monitoring, and screening for other sexually transmitted infections. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Preexposure Prophylaxis to Prevent Acquisition of HIV: US Preventive Services Task Force Recommendation Statement. JAMA 2023;330(8):736-745.</div></div> [[Start another case->Hub]] [[Restart this case->HIV preexposure prophylaxis - Prevention]] [[Next case →->Zoster vaccination - Prevention]]

<span class="ec-case-marker" hidden data-entry="HIV preexposure prophylaxis. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Counseling is part of care but has limited effect on incidence by itself, and withholding an effective biomedical intervention from a high-risk patient is not justified. <div class="ec-teach"><div class="th">What the findings point to</div> He has a recent bacterial sexually transmitted infection and ongoing condomless receptive anal intercourse, both markers of substantial HIV risk, and he is confirmed HIV negative with adequate renal function. Preexposure prophylaxis is recommended for people at increased risk and reduces acquisition markedly when taken consistently. Follow-up includes HIV testing at least every 3 months, renal monitoring, and screening for other sexually transmitted infections. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Preexposure Prophylaxis to Prevent Acquisition of HIV: US Preventive Services Task Force Recommendation Statement. JAMA 2023;330(8):736-745.</div></div></div> [[Try this question again->HIV preexposure prophylaxis - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="HIV preexposure prophylaxis. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Postexposure prophylaxis addresses a discrete recent exposure within 72 hours. He describes ongoing risk, which calls for continuous prophylaxis. <div class="ec-teach"><div class="th">What the findings point to</div> He has a recent bacterial sexually transmitted infection and ongoing condomless receptive anal intercourse, both markers of substantial HIV risk, and he is confirmed HIV negative with adequate renal function. Preexposure prophylaxis is recommended for people at increased risk and reduces acquisition markedly when taken consistently. Follow-up includes HIV testing at least every 3 months, renal monitoring, and screening for other sexually transmitted infections. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Preexposure Prophylaxis to Prevent Acquisition of HIV: US Preventive Services Task Force Recommendation Statement. JAMA 2023;330(8):736-745.</div></div></div> [[Try this question again->HIV preexposure prophylaxis - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="HIV preexposure prophylaxis. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Frequent testing detects infection after it occurs. It does not prevent it. <div class="ec-teach"><div class="th">What the findings point to</div> He has a recent bacterial sexually transmitted infection and ongoing condomless receptive anal intercourse, both markers of substantial HIV risk, and he is confirmed HIV negative with adequate renal function. Preexposure prophylaxis is recommended for people at increased risk and reduces acquisition markedly when taken consistently. Follow-up includes HIV testing at least every 3 months, renal monitoring, and screening for other sexually transmitted infections. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Preexposure Prophylaxis to Prevent Acquisition of HIV: US Preventive Services Task Force Recommendation Statement. JAMA 2023;330(8):736-745.</div></div></div> [[Try this question again->HIV preexposure prophylaxis - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="HIV preexposure prophylaxis. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Waiting for a known exposure defeats the purpose of preexposure prophylaxis, since most transmissions occur without an identifiable index event. <div class="ec-teach"><div class="th">What the findings point to</div> He has a recent bacterial sexually transmitted infection and ongoing condomless receptive anal intercourse, both markers of substantial HIV risk, and he is confirmed HIV negative with adequate renal function. Preexposure prophylaxis is recommended for people at increased risk and reduces acquisition markedly when taken consistently. Follow-up includes HIV testing at least every 3 months, renal monitoring, and screening for other sexually transmitted infections. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Preexposure Prophylaxis to Prevent Acquisition of HIV: US Preventive Services Task Force Recommendation Statement. JAMA 2023;330(8):736-745.</div></div></div> [[Try this question again->HIV preexposure prophylaxis - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="HIV preexposure prophylaxis. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> His surface antibody is already reactive and surface antigen negative, so immunity is documented and there is no reason to delay. <div class="ec-teach"><div class="th">What the findings point to</div> He has a recent bacterial sexually transmitted infection and ongoing condomless receptive anal intercourse, both markers of substantial HIV risk, and he is confirmed HIV negative with adequate renal function. Preexposure prophylaxis is recommended for people at increased risk and reduces acquisition markedly when taken consistently. Follow-up includes HIV testing at least every 3 months, renal monitoring, and screening for other sexually transmitted infections. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Preexposure Prophylaxis to Prevent Acquisition of HIV: US Preventive Services Task Force Recommendation Statement. JAMA 2023;330(8):736-745.</div></div></div> [[Try this question again->HIV preexposure prophylaxis - Prevention]] [[Start another case->Hub]]

<div class="ec-scene">Prenatal clinic · 13:50</div> A 29-year-old woman at 29 weeks of gestation presents for routine prenatal care. This is her second pregnancy. She received a tetanus, diphtheria, and acellular pertussis vaccine during her first pregnancy 3 years ago and a tetanus and diphtheria booster 6 years ago. The current pregnancy has been uncomplicated. She asks which vaccines she needs. <span class="ec-prompt">Which of the following is the most appropriate recommendation?</span> [[Administer a tetanus and diphtheria booster without pertussis->Tdap in pregnancy - Prevention D3]] [[Administer the pertussis-containing vaccine during this pregnancy->Tdap in pregnancy - Prevention correct]] [[Administer the vaccine immediately after delivery instead->Tdap in pregnancy - Prevention D2]] [[Defer vaccination because she received it in her last pregnancy->Tdap in pregnancy - Prevention D1]] [[Vaccinate household contacts only->Tdap in pregnancy - Prevention D5]] [[Wait until 37 weeks of gestation to vaccinate->Tdap in pregnancy - Prevention D4]]

<span class="ec-case-marker" hidden data-entry="Tdap in pregnancy. Prevention"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Administer the pertussis-containing vaccine during this pregnancy</div> The vaccine is recommended in every pregnancy, regardless of prior receipt, preferably between 27 and 36 weeks of gestation. The purpose is to generate maternal antibody that crosses the placenta and protects the infant during the first months of life, before the infant series can take effect. Antibody from a prior pregnancy has waned and does not protect this infant. She is at 29 weeks, within the optimal window. <div class="ec-src"><b>Source:</b> Havers FP, Moro PL, Hunter P, Hariri S, Bernstein H. Use of tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis vaccines: updated recommendations of the Advisory Committee on Immunization Practices. United States, 2019. MMWR Morb Mortal Wkly Rep 2020;69(3):77-83.</div></div> [[Start another case->Hub]] [[Restart this case->Tdap in pregnancy - Prevention]] [[Next case →->Preconception folic acid - Prevention]]

<span class="ec-case-marker" hidden data-entry="Tdap in pregnancy. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Antibody wanes substantially between pregnancies, and the recommendation is explicitly for each pregnancy in order to protect each infant. <div class="ec-teach"><div class="th">What the findings point to</div> The vaccine is recommended in every pregnancy, regardless of prior receipt, preferably between 27 and 36 weeks of gestation. The purpose is to generate maternal antibody that crosses the placenta and protects the infant during the first months of life, before the infant series can take effect. Antibody from a prior pregnancy has waned and does not protect this infant. She is at 29 weeks, within the optimal window. <div class="ec-src"><b>Source:</b> Havers FP, Moro PL, Hunter P, Hariri S, Bernstein H. Use of tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis vaccines: updated recommendations of the Advisory Committee on Immunization Practices. United States, 2019. MMWR Morb Mortal Wkly Rep 2020;69(3):77-83.</div></div></div> [[Try this question again->Tdap in pregnancy - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Tdap in pregnancy. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Postpartum vaccination protects the mother but produces no transplacental antibody, leaving the newborn unprotected during the highest-risk months. <div class="ec-teach"><div class="th">What the findings point to</div> The vaccine is recommended in every pregnancy, regardless of prior receipt, preferably between 27 and 36 weeks of gestation. The purpose is to generate maternal antibody that crosses the placenta and protects the infant during the first months of life, before the infant series can take effect. Antibody from a prior pregnancy has waned and does not protect this infant. She is at 29 weeks, within the optimal window. <div class="ec-src"><b>Source:</b> Havers FP, Moro PL, Hunter P, Hariri S, Bernstein H. Use of tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis vaccines: updated recommendations of the Advisory Committee on Immunization Practices. United States, 2019. MMWR Morb Mortal Wkly Rep 2020;69(3):77-83.</div></div></div> [[Try this question again->Tdap in pregnancy - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Tdap in pregnancy. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A booster lacking pertussis antigen does not generate the antibody that protects the infant against the organism of concern. <div class="ec-teach"><div class="th">What the findings point to</div> The vaccine is recommended in every pregnancy, regardless of prior receipt, preferably between 27 and 36 weeks of gestation. The purpose is to generate maternal antibody that crosses the placenta and protects the infant during the first months of life, before the infant series can take effect. Antibody from a prior pregnancy has waned and does not protect this infant. She is at 29 weeks, within the optimal window. <div class="ec-src"><b>Source:</b> Havers FP, Moro PL, Hunter P, Hariri S, Bernstein H. Use of tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis vaccines: updated recommendations of the Advisory Committee on Immunization Practices. United States, 2019. MMWR Morb Mortal Wkly Rep 2020;69(3):77-83.</div></div></div> [[Try this question again->Tdap in pregnancy - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Tdap in pregnancy. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Vaccinating later leaves insufficient time for antibody production and transfer before delivery. <div class="ec-teach"><div class="th">What the findings point to</div> The vaccine is recommended in every pregnancy, regardless of prior receipt, preferably between 27 and 36 weeks of gestation. The purpose is to generate maternal antibody that crosses the placenta and protects the infant during the first months of life, before the infant series can take effect. Antibody from a prior pregnancy has waned and does not protect this infant. She is at 29 weeks, within the optimal window. <div class="ec-src"><b>Source:</b> Havers FP, Moro PL, Hunter P, Hariri S, Bernstein H. Use of tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis vaccines: updated recommendations of the Advisory Committee on Immunization Practices. United States, 2019. MMWR Morb Mortal Wkly Rep 2020;69(3):77-83.</div></div></div> [[Try this question again->Tdap in pregnancy - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Tdap in pregnancy. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Cocooning contacts is a useful adjunct but is less effective than maternal immunization at protecting the newborn directly. <div class="ec-teach"><div class="th">What the findings point to</div> The vaccine is recommended in every pregnancy, regardless of prior receipt, preferably between 27 and 36 weeks of gestation. The purpose is to generate maternal antibody that crosses the placenta and protects the infant during the first months of life, before the infant series can take effect. Antibody from a prior pregnancy has waned and does not protect this infant. She is at 29 weeks, within the optimal window. <div class="ec-src"><b>Source:</b> Havers FP, Moro PL, Hunter P, Hariri S, Bernstein H. Use of tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis vaccines: updated recommendations of the Advisory Committee on Immunization Practices. United States, 2019. MMWR Morb Mortal Wkly Rep 2020;69(3):77-83.</div></div></div> [[Try this question again->Tdap in pregnancy - Prevention]] [[Start another case->Hub]]

<div class="ec-scene">Primary care clinic · 14:20</div> A 63-year-old woman presents for preventive care. She recalls having chickenpox as a child. She received the live attenuated zoster vaccine at age 60. She has no immunocompromising condition and takes no immunosuppressive medication. She had an episode of shingles on the left flank 4 years ago that resolved without postherpetic neuralgia. She asks whether anything further is needed. <span class="ec-prompt">Which of the following is the most appropriate recommendation?</span> [[Administer a single dose of the recombinant vaccine->Zoster vaccination - Prevention D4]] [[Administer two doses of the recombinant zoster vaccine->Zoster vaccination - Prevention correct]] [[Check varicella zoster virus serology before vaccinating->Zoster vaccination - Prevention D5]] [[No further vaccination because she already received a zoster vaccine->Zoster vaccination - Prevention D1]] [[No further vaccination because she has had shingles->Zoster vaccination - Prevention D2]] [[Repeat the live attenuated zoster vaccine->Zoster vaccination - Prevention D3]]

<span class="ec-case-marker" hidden data-entry="Zoster vaccination. Prevention"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Administer two doses of the recombinant zoster vaccine</div> The recombinant adjuvanted vaccine is recommended for all immunocompetent adults 50 years and older, including those who previously received the live attenuated vaccine and those with a prior episode of shingles. It provides substantially higher and more durable efficacy than the live vaccine, and the series is two doses given 2 to 6 months apart. Prior zoster does not confer reliable protection against recurrence. <div class="ec-src"><b>Source:</b> Dooling KL, Guo A, Patel M, et al. Recommendations of the Advisory Committee on Immunization Practices for use of herpes zoster vaccines. MMWR Morb Mortal Wkly Rep 2018;67(3):103-108.</div></div> [[Start another case->Hub]] [[Restart this case->Zoster vaccination - Prevention]] [[Next case →->Rabies postexposure prophylaxis - Prevention]]

<span class="ec-case-marker" hidden data-entry="Zoster vaccination. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Revaccination with the recombinant product is specifically recommended for prior live vaccine recipients, whose protection wanes substantially within a few years. <div class="ec-teach"><div class="th">What the findings point to</div> The recombinant adjuvanted vaccine is recommended for all immunocompetent adults 50 years and older, including those who previously received the live attenuated vaccine and those with a prior episode of shingles. It provides substantially higher and more durable efficacy than the live vaccine, and the series is two doses given 2 to 6 months apart. Prior zoster does not confer reliable protection against recurrence. <div class="ec-src"><b>Source:</b> Dooling KL, Guo A, Patel M, et al. Recommendations of the Advisory Committee on Immunization Practices for use of herpes zoster vaccines. MMWR Morb Mortal Wkly Rep 2018;67(3):103-108.</div></div></div> [[Try this question again->Zoster vaccination - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Zoster vaccination. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A prior episode does not prevent recurrence, and vaccination is recommended regardless of history. <div class="ec-teach"><div class="th">What the findings point to</div> The recombinant adjuvanted vaccine is recommended for all immunocompetent adults 50 years and older, including those who previously received the live attenuated vaccine and those with a prior episode of shingles. It provides substantially higher and more durable efficacy than the live vaccine, and the series is two doses given 2 to 6 months apart. Prior zoster does not confer reliable protection against recurrence. <div class="ec-src"><b>Source:</b> Dooling KL, Guo A, Patel M, et al. Recommendations of the Advisory Committee on Immunization Practices for use of herpes zoster vaccines. MMWR Morb Mortal Wkly Rep 2018;67(3):103-108.</div></div></div> [[Try this question again->Zoster vaccination - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Zoster vaccination. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The live vaccine is no longer available in the United States and was less effective and less durable than the recombinant product. <div class="ec-teach"><div class="th">What the findings point to</div> The recombinant adjuvanted vaccine is recommended for all immunocompetent adults 50 years and older, including those who previously received the live attenuated vaccine and those with a prior episode of shingles. It provides substantially higher and more durable efficacy than the live vaccine, and the series is two doses given 2 to 6 months apart. Prior zoster does not confer reliable protection against recurrence. <div class="ec-src"><b>Source:</b> Dooling KL, Guo A, Patel M, et al. Recommendations of the Advisory Committee on Immunization Practices for use of herpes zoster vaccines. MMWR Morb Mortal Wkly Rep 2018;67(3):103-108.</div></div></div> [[Try this question again->Zoster vaccination - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Zoster vaccination. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A single dose provides incomplete protection. The recommended series is two doses. <div class="ec-teach"><div class="th">What the findings point to</div> The recombinant adjuvanted vaccine is recommended for all immunocompetent adults 50 years and older, including those who previously received the live attenuated vaccine and those with a prior episode of shingles. It provides substantially higher and more durable efficacy than the live vaccine, and the series is two doses given 2 to 6 months apart. Prior zoster does not confer reliable protection against recurrence. <div class="ec-src"><b>Source:</b> Dooling KL, Guo A, Patel M, et al. Recommendations of the Advisory Committee on Immunization Practices for use of herpes zoster vaccines. MMWR Morb Mortal Wkly Rep 2018;67(3):103-108.</div></div></div> [[Try this question again->Zoster vaccination - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Zoster vaccination. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Serologic testing is not recommended before vaccination in this age group, in whom prior infection can be assumed. <div class="ec-teach"><div class="th">What the findings point to</div> The recombinant adjuvanted vaccine is recommended for all immunocompetent adults 50 years and older, including those who previously received the live attenuated vaccine and those with a prior episode of shingles. It provides substantially higher and more durable efficacy than the live vaccine, and the series is two doses given 2 to 6 months apart. Prior zoster does not confer reliable protection against recurrence. <div class="ec-src"><b>Source:</b> Dooling KL, Guo A, Patel M, et al. Recommendations of the Advisory Committee on Immunization Practices for use of herpes zoster vaccines. MMWR Morb Mortal Wkly Rep 2018;67(3):103-108.</div></div></div> [[Try this question again->Zoster vaccination - Prevention]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 21:30</div> A 34-year-old woman awakens to find a bat in her bedroom. She has no visible bite or scratch and cannot be certain whether contact occurred while she slept. The bat flew out of an open window and is unavailable for testing. She has never received rabies vaccine. The wound examination is unremarkable. She is otherwise healthy and takes no medications. <span class="ec-prompt">Which of the following is the most appropriate next step?</span> [[Administer immune globulin alone->Rabies postexposure prophylaxis - Prevention D3]] [[Administer rabies immune globulin and begin the vaccine series->Rabies postexposure prophylaxis - Prevention correct]] [[Administer the vaccine series without immune globulin->Rabies postexposure prophylaxis - Prevention D1]] [[Defer prophylaxis pending capture and testing of the bat->Rabies postexposure prophylaxis - Prevention D5]] [[Observe for symptoms and treat if they develop->Rabies postexposure prophylaxis - Prevention D2]] [[Withhold prophylaxis because no bite is visible->Rabies postexposure prophylaxis - Prevention D4]]

<span class="ec-case-marker" hidden data-entry="Rabies postexposure prophylaxis. Prevention"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Administer rabies immune globulin and begin the vaccine series</div> Bat exposure is treated as an indication for prophylaxis when a bite cannot be reasonably excluded, because bat bites can be small enough to escape notice and the disease is essentially always fatal once symptomatic. A person who was asleep in a room with a bat meets that standard. Because she has never been vaccinated, she requires both passive and active immunization: immune globulin infiltrated around the wound site where identifiable, plus a four-dose vaccine series beginning today. <div class="ec-src"><b>Source:</b> Rupprecht CE, Briggs D, Brown CM, et al. Use of a reduced (4-dose) vaccine schedule for postexposure prophylaxis to prevent human rabies. MMWR Recomm Rep 2010;59(RR-2):1-9.</div></div> [[Start another case->Hub]] [[Restart this case->Rabies postexposure prophylaxis - Prevention]] [[Next case →->Latent tuberculosis - Prevention]]

<span class="ec-case-marker" hidden data-entry="Rabies postexposure prophylaxis. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Immune globulin is omitted only in people previously vaccinated. She has no preexisting immunity and needs passive protection while her own antibody develops. <div class="ec-teach"><div class="th">What the findings point to</div> Bat exposure is treated as an indication for prophylaxis when a bite cannot be reasonably excluded, because bat bites can be small enough to escape notice and the disease is essentially always fatal once symptomatic. A person who was asleep in a room with a bat meets that standard. Because she has never been vaccinated, she requires both passive and active immunization: immune globulin infiltrated around the wound site where identifiable, plus a four-dose vaccine series beginning today. <div class="ec-src"><b>Source:</b> Rupprecht CE, Briggs D, Brown CM, et al. Use of a reduced (4-dose) vaccine schedule for postexposure prophylaxis to prevent human rabies. MMWR Recomm Rep 2010;59(RR-2):1-9.</div></div></div> [[Try this question again->Rabies postexposure prophylaxis - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Rabies postexposure prophylaxis. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Rabies is virtually always fatal once symptoms appear. Prophylaxis has no value at that point. <div class="ec-teach"><div class="th">What the findings point to</div> Bat exposure is treated as an indication for prophylaxis when a bite cannot be reasonably excluded, because bat bites can be small enough to escape notice and the disease is essentially always fatal once symptomatic. A person who was asleep in a room with a bat meets that standard. Because she has never been vaccinated, she requires both passive and active immunization: immune globulin infiltrated around the wound site where identifiable, plus a four-dose vaccine series beginning today. <div class="ec-src"><b>Source:</b> Rupprecht CE, Briggs D, Brown CM, et al. Use of a reduced (4-dose) vaccine schedule for postexposure prophylaxis to prevent human rabies. MMWR Recomm Rep 2010;59(RR-2):1-9.</div></div></div> [[Try this question again->Rabies postexposure prophylaxis - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Rabies postexposure prophylaxis. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Passive antibody wanes within weeks and does not generate lasting immunity. The vaccine series is required. <div class="ec-teach"><div class="th">What the findings point to</div> Bat exposure is treated as an indication for prophylaxis when a bite cannot be reasonably excluded, because bat bites can be small enough to escape notice and the disease is essentially always fatal once symptomatic. A person who was asleep in a room with a bat meets that standard. Because she has never been vaccinated, she requires both passive and active immunization: immune globulin infiltrated around the wound site where identifiable, plus a four-dose vaccine series beginning today. <div class="ec-src"><b>Source:</b> Rupprecht CE, Briggs D, Brown CM, et al. Use of a reduced (4-dose) vaccine schedule for postexposure prophylaxis to prevent human rabies. MMWR Recomm Rep 2010;59(RR-2):1-9.</div></div></div> [[Try this question again->Rabies postexposure prophylaxis - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Rabies postexposure prophylaxis. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The absence of a visible wound is expected with bat exposure and is precisely why this scenario is an accepted indication. <div class="ec-teach"><div class="th">What the findings point to</div> Bat exposure is treated as an indication for prophylaxis when a bite cannot be reasonably excluded, because bat bites can be small enough to escape notice and the disease is essentially always fatal once symptomatic. A person who was asleep in a room with a bat meets that standard. Because she has never been vaccinated, she requires both passive and active immunization: immune globulin infiltrated around the wound site where identifiable, plus a four-dose vaccine series beginning today. <div class="ec-src"><b>Source:</b> Rupprecht CE, Briggs D, Brown CM, et al. Use of a reduced (4-dose) vaccine schedule for postexposure prophylaxis to prevent human rabies. MMWR Recomm Rep 2010;59(RR-2):1-9.</div></div></div> [[Try this question again->Rabies postexposure prophylaxis - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Rabies postexposure prophylaxis. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The animal is gone. Waiting for testing that cannot occur wastes the window in which prophylaxis is effective. <div class="ec-teach"><div class="th">What the findings point to</div> Bat exposure is treated as an indication for prophylaxis when a bite cannot be reasonably excluded, because bat bites can be small enough to escape notice and the disease is essentially always fatal once symptomatic. A person who was asleep in a room with a bat meets that standard. Because she has never been vaccinated, she requires both passive and active immunization: immune globulin infiltrated around the wound site where identifiable, plus a four-dose vaccine series beginning today. <div class="ec-src"><b>Source:</b> Rupprecht CE, Briggs D, Brown CM, et al. Use of a reduced (4-dose) vaccine schedule for postexposure prophylaxis to prevent human rabies. MMWR Recomm Rep 2010;59(RR-2):1-9.</div></div></div> [[Try this question again->Rabies postexposure prophylaxis - Prevention]] [[Start another case->Hub]]

<div class="ec-scene">Occupational health clinic · 08:40</div> A 27-year-old nursing student born in the Philippines has a positive interferon-gamma release assay obtained during preemployment screening. She is asymptomatic without cough, fever, night sweats, or weight loss. Chest radiography is normal. She received bacille Calmette-Guerin vaccination in infancy. She is not pregnant, takes no medications, and has normal aminotransferase concentrations. HIV testing is negative. <span class="ec-prompt">Which of the following is the most appropriate next step?</span> [[Attribute the result to prior bacille Calmette-Guerin vaccination->Latent tuberculosis - Prevention D1]] [[Begin four-drug therapy for active tuberculosis->Latent tuberculosis - Prevention D3]] [[Begin treatment for latent tuberculosis infection->Latent tuberculosis - Prevention correct]] [[Observe with annual chest radiography->Latent tuberculosis - Prevention D5]] [[Obtain sputum cultures before any treatment->Latent tuberculosis - Prevention D4]] [[Repeat the assay in 3 months before deciding->Latent tuberculosis - Prevention D2]]

<span class="ec-case-marker" hidden data-entry="Latent tuberculosis. Prevention"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Begin treatment for latent tuberculosis infection</div> A positive interferon-gamma release assay with a normal chest radiograph and no symptoms indicates latent infection, and treatment is recommended to prevent progression to active disease. The assay is not affected by prior bacille Calmette-Guerin vaccination, which is why it is preferred over the tuberculin skin test in vaccinated people. Preferred regimens are short-course rifamycin-based options, such as 3 months of weekly isoniazid and rifapentine or 4 months of daily rifampin. <div class="ec-src"><b>Source:</b> Sterling TR, Njie G, Zenner D, et al. Guidelines for the treatment of latent tuberculosis infection: recommendations from the National Tuberculosis Controllers Association and CDC, 2020. MMWR Recomm Rep 2020;69(1):1-11.</div></div> [[Start another case->Hub]] [[Restart this case->Latent tuberculosis - Prevention]] [[Next case →->Sepsis risk stratification - Prog]]

<span class="ec-case-marker" hidden data-entry="Latent tuberculosis. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Interferon-gamma release assays use antigens absent from the vaccine strain, so vaccination does not cause a positive result. <div class="ec-teach"><div class="th">What the findings point to</div> A positive interferon-gamma release assay with a normal chest radiograph and no symptoms indicates latent infection, and treatment is recommended to prevent progression to active disease. The assay is not affected by prior bacille Calmette-Guerin vaccination, which is why it is preferred over the tuberculin skin test in vaccinated people. Preferred regimens are short-course rifamycin-based options, such as 3 months of weekly isoniazid and rifapentine or 4 months of daily rifampin. <div class="ec-src"><b>Source:</b> Sterling TR, Njie G, Zenner D, et al. Guidelines for the treatment of latent tuberculosis infection: recommendations from the National Tuberculosis Controllers Association and CDC, 2020. MMWR Recomm Rep 2020;69(1):1-11.</div></div></div> [[Try this question again->Latent tuberculosis - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Latent tuberculosis. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Repeating a positive test in an asymptomatic person with a normal radiograph adds delay and risks a falsely reassuring reversion. <div class="ec-teach"><div class="th">What the findings point to</div> A positive interferon-gamma release assay with a normal chest radiograph and no symptoms indicates latent infection, and treatment is recommended to prevent progression to active disease. The assay is not affected by prior bacille Calmette-Guerin vaccination, which is why it is preferred over the tuberculin skin test in vaccinated people. Preferred regimens are short-course rifamycin-based options, such as 3 months of weekly isoniazid and rifapentine or 4 months of daily rifampin. <div class="ec-src"><b>Source:</b> Sterling TR, Njie G, Zenner D, et al. Guidelines for the treatment of latent tuberculosis infection: recommendations from the National Tuberculosis Controllers Association and CDC, 2020. MMWR Recomm Rep 2020;69(1):1-11.</div></div></div> [[Try this question again->Latent tuberculosis - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Latent tuberculosis. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Multidrug therapy is for active disease. She has no symptoms and a normal radiograph, so treating her as active exposes her to unnecessary toxicity. <div class="ec-teach"><div class="th">What the findings point to</div> A positive interferon-gamma release assay with a normal chest radiograph and no symptoms indicates latent infection, and treatment is recommended to prevent progression to active disease. The assay is not affected by prior bacille Calmette-Guerin vaccination, which is why it is preferred over the tuberculin skin test in vaccinated people. Preferred regimens are short-course rifamycin-based options, such as 3 months of weekly isoniazid and rifapentine or 4 months of daily rifampin. <div class="ec-src"><b>Source:</b> Sterling TR, Njie G, Zenner D, et al. Guidelines for the treatment of latent tuberculosis infection: recommendations from the National Tuberculosis Controllers Association and CDC, 2020. MMWR Recomm Rep 2020;69(1):1-11.</div></div></div> [[Try this question again->Latent tuberculosis - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Latent tuberculosis. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Sputum evaluation is indicated when active disease is suspected. In an asymptomatic patient with a normal radiograph it is not required. <div class="ec-teach"><div class="th">What the findings point to</div> A positive interferon-gamma release assay with a normal chest radiograph and no symptoms indicates latent infection, and treatment is recommended to prevent progression to active disease. The assay is not affected by prior bacille Calmette-Guerin vaccination, which is why it is preferred over the tuberculin skin test in vaccinated people. Preferred regimens are short-course rifamycin-based options, such as 3 months of weekly isoniazid and rifapentine or 4 months of daily rifampin. <div class="ec-src"><b>Source:</b> Sterling TR, Njie G, Zenner D, et al. Guidelines for the treatment of latent tuberculosis infection: recommendations from the National Tuberculosis Controllers Association and CDC, 2020. MMWR Recomm Rep 2020;69(1):1-11.</div></div></div> [[Try this question again->Latent tuberculosis - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Latent tuberculosis. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Radiographic surveillance detects disease after it develops rather than preventing it, and it delivers repeated radiation without benefit. <div class="ec-teach"><div class="th">What the findings point to</div> A positive interferon-gamma release assay with a normal chest radiograph and no symptoms indicates latent infection, and treatment is recommended to prevent progression to active disease. The assay is not affected by prior bacille Calmette-Guerin vaccination, which is why it is preferred over the tuberculin skin test in vaccinated people. Preferred regimens are short-course rifamycin-based options, such as 3 months of weekly isoniazid and rifapentine or 4 months of daily rifampin. <div class="ec-src"><b>Source:</b> Sterling TR, Njie G, Zenner D, et al. Guidelines for the treatment of latent tuberculosis infection: recommendations from the National Tuberculosis Controllers Association and CDC, 2020. MMWR Recomm Rep 2020;69(1):1-11.</div></div></div> [[Try this question again->Latent tuberculosis - Prevention]] [[Start another case->Hub]]

<div class="ec-scene">Primary care clinic · 15:30</div> A 27-year-old woman states that she and her partner plan to begin trying to conceive in about 3 months. She has regular menses, no chronic illness, and takes no medications. She has no personal or family history of neural tube defects. She does not smoke or drink alcohol. Body mass index is 23 kg/m2. She eats a varied diet including fortified cereals and asks what she should do before pregnancy. <span class="ec-prompt">Which of the following is the most appropriate recommendation?</span> [[Begin a prenatal vitamin only in the first trimester->Preconception folic acid - Prevention D5]] [[Begin daily folic acid supplementation now->Preconception folic acid - Prevention correct]] [[Begin supplementation after a positive pregnancy test->Preconception folic acid - Prevention D1]] [[Measure serum folate before deciding on supplementation->Preconception folic acid - Prevention D4]] [[Rely on dietary folate from fortified foods->Preconception folic acid - Prevention D3]] [[Take 4 mg of folic acid daily->Preconception folic acid - Prevention D2]]

<span class="ec-case-marker" hidden data-entry="Preconception folic acid. Prevention"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Begin daily folic acid supplementation now</div> Supplementation with 0.4 to 0.8 mg of folic acid daily is recommended for all people planning or capable of pregnancy, started at least 1 month before conception and continued through the first 2 to 3 months of pregnancy. The neural tube closes by about 28 days after conception, often before pregnancy is recognized, which is why starting after a positive test is too late. Dietary fortification alone does not reliably achieve protective intake. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Folic Acid Supplementation to Prevent Neural Tube Defects: US Preventive Services Task Force Recommendation Statement. JAMA 2023;330(5):454-459.</div></div> [[Start another case->Hub]] [[Restart this case->Preconception folic acid - Prevention]] [[Next case →->Well child visit - Opening]]

<span class="ec-case-marker" hidden data-entry="Preconception folic acid. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Neural tube closure is complete within about 4 weeks of conception, typically around the time a test first turns positive. <div class="ec-teach"><div class="th">What the findings point to</div> Supplementation with 0.4 to 0.8 mg of folic acid daily is recommended for all people planning or capable of pregnancy, started at least 1 month before conception and continued through the first 2 to 3 months of pregnancy. The neural tube closes by about 28 days after conception, often before pregnancy is recognized, which is why starting after a positive test is too late. Dietary fortification alone does not reliably achieve protective intake. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Folic Acid Supplementation to Prevent Neural Tube Defects: US Preventive Services Task Force Recommendation Statement. JAMA 2023;330(5):454-459.</div></div></div> [[Try this question again->Preconception folic acid - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Preconception folic acid. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The high-dose regimen is reserved for women with a previous affected pregnancy. She has no such history, and the higher dose offers no added benefit here. <div class="ec-teach"><div class="th">What the findings point to</div> Supplementation with 0.4 to 0.8 mg of folic acid daily is recommended for all people planning or capable of pregnancy, started at least 1 month before conception and continued through the first 2 to 3 months of pregnancy. The neural tube closes by about 28 days after conception, often before pregnancy is recognized, which is why starting after a positive test is too late. Dietary fortification alone does not reliably achieve protective intake. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Folic Acid Supplementation to Prevent Neural Tube Defects: US Preventive Services Task Force Recommendation Statement. JAMA 2023;330(5):454-459.</div></div></div> [[Try this question again->Preconception folic acid - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Preconception folic acid. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Fortification reduced defect rates at a population level but does not reliably deliver the intake associated with individual protection. <div class="ec-teach"><div class="th">What the findings point to</div> Supplementation with 0.4 to 0.8 mg of folic acid daily is recommended for all people planning or capable of pregnancy, started at least 1 month before conception and continued through the first 2 to 3 months of pregnancy. The neural tube closes by about 28 days after conception, often before pregnancy is recognized, which is why starting after a positive test is too late. Dietary fortification alone does not reliably achieve protective intake. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Folic Acid Supplementation to Prevent Neural Tube Defects: US Preventive Services Task Force Recommendation Statement. JAMA 2023;330(5):454-459.</div></div></div> [[Try this question again->Preconception folic acid - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Preconception folic acid. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Testing is not recommended, because supplementation is safe and inexpensive and the recommendation applies regardless of the baseline concentration. <div class="ec-teach"><div class="th">What the findings point to</div> Supplementation with 0.4 to 0.8 mg of folic acid daily is recommended for all people planning or capable of pregnancy, started at least 1 month before conception and continued through the first 2 to 3 months of pregnancy. The neural tube closes by about 28 days after conception, often before pregnancy is recognized, which is why starting after a positive test is too late. Dietary fortification alone does not reliably achieve protective intake. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Folic Acid Supplementation to Prevent Neural Tube Defects: US Preventive Services Task Force Recommendation Statement. JAMA 2023;330(5):454-459.</div></div></div> [[Try this question again->Preconception folic acid - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Preconception folic acid. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Waiting until pregnancy is established misses the window during which the neural tube forms. <div class="ec-teach"><div class="th">What the findings point to</div> Supplementation with 0.4 to 0.8 mg of folic acid daily is recommended for all people planning or capable of pregnancy, started at least 1 month before conception and continued through the first 2 to 3 months of pregnancy. The neural tube closes by about 28 days after conception, often before pregnancy is recognized, which is why starting after a positive test is too late. Dietary fortification alone does not reliably achieve protective intake. <div class="ec-src"><b>Source:</b> US Preventive Services Task Force. Folic Acid Supplementation to Prevent Neural Tube Defects: US Preventive Services Task Force Recommendation Statement. JAMA 2023;330(5):454-459.</div></div></div> [[Try this question again->Preconception folic acid - Prevention]] [[Start another case->Hub]]

<div class="ec-scene">Primary care clinic · 09:50</div> A 52-year-old man who smokes 20 cigarettes daily wants to quit and has set a quit date in 2 weeks. He has made three prior attempts, twice with nicotine patches and once unaided, relapsing within a month each time. He has a history of well-controlled major depressive disorder on sertraline, with no suicidal ideation and no hospitalizations. He has no seizure history and no eating disorder. He asks which medication gives him the best chance. <span class="ec-prompt">Which of the following is the most appropriate pharmacotherapy?</span> [[Bupropion->Tobacco cessation pharmacotherapy - Prevention D1]] [[Electronic cigarettes as a substitute->Tobacco cessation pharmacotherapy - Prevention D4]] [[Nicotine lozenge as needed without a long-acting agent->Tobacco cessation pharmacotherapy - Prevention D3]] [[Nicotine patch monotherapy->Tobacco cessation pharmacotherapy - Prevention D2]] [[No medication, with behavioral counseling alone->Tobacco cessation pharmacotherapy - Prevention D5]] [[Varenicline->Tobacco cessation pharmacotherapy - Prevention correct]]

<span class="ec-case-marker" hidden data-entry="Tobacco cessation pharmacotherapy. Prevention"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Varenicline</div> In a large randomized trial comparing varenicline, bupropion, nicotine patch, and placebo in smokers with and without psychiatric disorders, varenicline produced the highest abstinence rates, and there was no significant excess of neuropsychiatric adverse events attributable to varenicline or bupropion in either cohort. His stable depression on treatment is not a contraindication, and he has already failed patch monotherapy twice, which makes repeating it the weaker option. <div class="ec-src"><b>Source:</b> Anthenelli RM, Benowitz NL, West R, et al. Neuropsychiatric safety and efficacy of varenicline, bupropion, and nicotine patch in smokers with and without psychiatric disorders (EAGLES): a randomised, double-blind, triple-dummy, placebo-controlled clinical trial. Lancet 2016;387(10037):2507-2520.</div></div> [[Start another case->Hub]] [[Restart this case->Tobacco cessation pharmacotherapy - Prevention]] [[Next case →->Serotonin syndrome mechanism - Mech]]

<span class="ec-case-marker" hidden data-entry="Tobacco cessation pharmacotherapy. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Bupropion is effective and would be reasonable, but it is less effective than varenicline and carries an interaction consideration alongside his serotonergic antidepressant. <div class="ec-teach"><div class="th">What the findings point to</div> In a large randomized trial comparing varenicline, bupropion, nicotine patch, and placebo in smokers with and without psychiatric disorders, varenicline produced the highest abstinence rates, and there was no significant excess of neuropsychiatric adverse events attributable to varenicline or bupropion in either cohort. His stable depression on treatment is not a contraindication, and he has already failed patch monotherapy twice, which makes repeating it the weaker option. <div class="ec-src"><b>Source:</b> Anthenelli RM, Benowitz NL, West R, et al. Neuropsychiatric safety and efficacy of varenicline, bupropion, and nicotine patch in smokers with and without psychiatric disorders (EAGLES): a randomised, double-blind, triple-dummy, placebo-controlled clinical trial. Lancet 2016;387(10037):2507-2520.</div></div></div> [[Try this question again->Tobacco cessation pharmacotherapy - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Tobacco cessation pharmacotherapy. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> He has relapsed twice on patches alone. Repeating a strategy that has already failed him twice is the least promising choice. <div class="ec-teach"><div class="th">What the findings point to</div> In a large randomized trial comparing varenicline, bupropion, nicotine patch, and placebo in smokers with and without psychiatric disorders, varenicline produced the highest abstinence rates, and there was no significant excess of neuropsychiatric adverse events attributable to varenicline or bupropion in either cohort. His stable depression on treatment is not a contraindication, and he has already failed patch monotherapy twice, which makes repeating it the weaker option. <div class="ec-src"><b>Source:</b> Anthenelli RM, Benowitz NL, West R, et al. Neuropsychiatric safety and efficacy of varenicline, bupropion, and nicotine patch in smokers with and without psychiatric disorders (EAGLES): a randomised, double-blind, triple-dummy, placebo-controlled clinical trial. Lancet 2016;387(10037):2507-2520.</div></div></div> [[Try this question again->Tobacco cessation pharmacotherapy - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Tobacco cessation pharmacotherapy. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Short-acting nicotine replacement alone provides less consistent blood concentrations and lower quit rates than combination or first-line pharmacotherapy. <div class="ec-teach"><div class="th">What the findings point to</div> In a large randomized trial comparing varenicline, bupropion, nicotine patch, and placebo in smokers with and without psychiatric disorders, varenicline produced the highest abstinence rates, and there was no significant excess of neuropsychiatric adverse events attributable to varenicline or bupropion in either cohort. His stable depression on treatment is not a contraindication, and he has already failed patch monotherapy twice, which makes repeating it the weaker option. <div class="ec-src"><b>Source:</b> Anthenelli RM, Benowitz NL, West R, et al. Neuropsychiatric safety and efficacy of varenicline, bupropion, and nicotine patch in smokers with and without psychiatric disorders (EAGLES): a randomised, double-blind, triple-dummy, placebo-controlled clinical trial. Lancet 2016;387(10037):2507-2520.</div></div></div> [[Try this question again->Tobacco cessation pharmacotherapy - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Tobacco cessation pharmacotherapy. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> These are not an approved cessation pharmacotherapy, and long-term safety and durable abstinence data remain limited. <div class="ec-teach"><div class="th">What the findings point to</div> In a large randomized trial comparing varenicline, bupropion, nicotine patch, and placebo in smokers with and without psychiatric disorders, varenicline produced the highest abstinence rates, and there was no significant excess of neuropsychiatric adverse events attributable to varenicline or bupropion in either cohort. His stable depression on treatment is not a contraindication, and he has already failed patch monotherapy twice, which makes repeating it the weaker option. <div class="ec-src"><b>Source:</b> Anthenelli RM, Benowitz NL, West R, et al. Neuropsychiatric safety and efficacy of varenicline, bupropion, and nicotine patch in smokers with and without psychiatric disorders (EAGLES): a randomised, double-blind, triple-dummy, placebo-controlled clinical trial. Lancet 2016;387(10037):2507-2520.</div></div></div> [[Try this question again->Tobacco cessation pharmacotherapy - Prevention]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Tobacco cessation pharmacotherapy. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Counseling alone yields substantially lower abstinence than counseling combined with pharmacotherapy in a patient with this relapse history. <div class="ec-teach"><div class="th">What the findings point to</div> In a large randomized trial comparing varenicline, bupropion, nicotine patch, and placebo in smokers with and without psychiatric disorders, varenicline produced the highest abstinence rates, and there was no significant excess of neuropsychiatric adverse events attributable to varenicline or bupropion in either cohort. His stable depression on treatment is not a contraindication, and he has already failed patch monotherapy twice, which makes repeating it the weaker option. <div class="ec-src"><b>Source:</b> Anthenelli RM, Benowitz NL, West R, et al. Neuropsychiatric safety and efficacy of varenicline, bupropion, and nicotine patch in smokers with and without psychiatric disorders (EAGLES): a randomised, double-blind, triple-dummy, placebo-controlled clinical trial. Lancet 2016;387(10037):2507-2520.</div></div></div> [[Try this question again->Tobacco cessation pharmacotherapy - Prevention]] [[Start another case->Hub]]

<div class="ec-scene">Medical ward · 07:15</div> A 58-year-old woman was started on warfarin 10 mg daily 3 days ago for a newly diagnosed deep venous thrombosis, without concurrent parenteral anticoagulation. She now has painful erythematous plaques on both breasts and the right thigh that have progressed over 12 hours to well-demarcated areas with hemorrhagic bullae and central necrosis. Platelet count is 240,000/mm3, international normalized ratio is 3.2, and fibrinogen is 390 mg/dL. The peripheral smear shows no schistocytes. <span class="ec-prompt">Which of the following best explains this patient's presentation?</span> [[Antibody-mediated platelet activation from heparin exposure->Warfarin skin necrosis - Mech D1]] [[Cholesterol embolization from an aortic plaque->Warfarin skin necrosis - Mech D5]] [[Consumptive coagulopathy with widespread fibrin deposition->Warfarin skin necrosis - Mech D2]] [[Direct cytotoxic effect of warfarin on dermal capillaries->Warfarin skin necrosis - Mech D4]] [[Early protein C depletion creating a prothrombotic window->Warfarin skin necrosis - Mech correct]] [[Immune complex vasculitis of dermal vessels->Warfarin skin necrosis - Mech D3]]

<span class="ec-case-marker" hidden data-entry="Warfarin skin necrosis. Mech"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Early protein C depletion creating a prothrombotic window</div> Warfarin inhibits synthesis of factors II, VII, IX, and X and of the anticoagulant proteins C and S. Protein C has a short half-life of about 8 hours, comparable to factor VII and far shorter than factor II, so its activity falls before the procoagulant factors are meaningfully reduced. Loading without bridging anticoagulation creates a window of net hypercoagulability in which dermal microvascular thrombosis produces necrosis in fat-rich areas. Normal platelets, fibrinogen, and smear exclude consumption and microangiopathy. <div class="ec-src"><b>Source:</b> Nazarian RM, Van Cott EM, Zembowicz A, Duncan LM. Warfarin-induced skin necrosis. J Am Acad Dermatol 2009;61(2):325-332.</div></div> [[Start another case->Hub]] [[Restart this case->Warfarin skin necrosis - Mech]] [[Next case →->Tumor lysis syndrome - Mech]]

<span class="ec-case-marker" hidden data-entry="Warfarin skin necrosis. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> She received no heparin, and her platelet count is normal, which excludes heparin-induced thrombocytopenia. <div class="ec-teach"><div class="th">What the findings point to</div> Warfarin inhibits synthesis of factors II, VII, IX, and X and of the anticoagulant proteins C and S. Protein C has a short half-life of about 8 hours, comparable to factor VII and far shorter than factor II, so its activity falls before the procoagulant factors are meaningfully reduced. Loading without bridging anticoagulation creates a window of net hypercoagulability in which dermal microvascular thrombosis produces necrosis in fat-rich areas. Normal platelets, fibrinogen, and smear exclude consumption and microangiopathy. <div class="ec-src"><b>Source:</b> Nazarian RM, Van Cott EM, Zembowicz A, Duncan LM. Warfarin-induced skin necrosis. J Am Acad Dermatol 2009;61(2):325-332.</div></div></div> [[Try this question again->Warfarin skin necrosis - Mech]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Warfarin skin necrosis. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Disseminated intravascular coagulation lowers fibrinogen and platelets and produces schistocytes, none of which is present. <div class="ec-teach"><div class="th">What the findings point to</div> Warfarin inhibits synthesis of factors II, VII, IX, and X and of the anticoagulant proteins C and S. Protein C has a short half-life of about 8 hours, comparable to factor VII and far shorter than factor II, so its activity falls before the procoagulant factors are meaningfully reduced. Loading without bridging anticoagulation creates a window of net hypercoagulability in which dermal microvascular thrombosis produces necrosis in fat-rich areas. Normal platelets, fibrinogen, and smear exclude consumption and microangiopathy. <div class="ec-src"><b>Source:</b> Nazarian RM, Van Cott EM, Zembowicz A, Duncan LM. Warfarin-induced skin necrosis. J Am Acad Dermatol 2009;61(2):325-332.</div></div></div> [[Try this question again->Warfarin skin necrosis - Mech]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Warfarin skin necrosis. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Cutaneous vasculitis produces palpable purpura in dependent areas with an inflammatory infiltrate, not sharply demarcated necrosis over the breasts within 72 hours of starting a drug. <div class="ec-teach"><div class="th">What the findings point to</div> Warfarin inhibits synthesis of factors II, VII, IX, and X and of the anticoagulant proteins C and S. Protein C has a short half-life of about 8 hours, comparable to factor VII and far shorter than factor II, so its activity falls before the procoagulant factors are meaningfully reduced. Loading without bridging anticoagulation creates a window of net hypercoagulability in which dermal microvascular thrombosis produces necrosis in fat-rich areas. Normal platelets, fibrinogen, and smear exclude consumption and microangiopathy. <div class="ec-src"><b>Source:</b> Nazarian RM, Van Cott EM, Zembowicz A, Duncan LM. Warfarin-induced skin necrosis. J Am Acad Dermatol 2009;61(2):325-332.</div></div></div> [[Try this question again->Warfarin skin necrosis - Mech]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Warfarin skin necrosis. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Warfarin has no direct toxicity to vessels. The injury is thrombotic and mediated through the protein C pathway. <div class="ec-teach"><div class="th">What the findings point to</div> Warfarin inhibits synthesis of factors II, VII, IX, and X and of the anticoagulant proteins C and S. Protein C has a short half-life of about 8 hours, comparable to factor VII and far shorter than factor II, so its activity falls before the procoagulant factors are meaningfully reduced. Loading without bridging anticoagulation creates a window of net hypercoagulability in which dermal microvascular thrombosis produces necrosis in fat-rich areas. Normal platelets, fibrinogen, and smear exclude consumption and microangiopathy. <div class="ec-src"><b>Source:</b> Nazarian RM, Van Cott EM, Zembowicz A, Duncan LM. Warfarin-induced skin necrosis. J Am Acad Dermatol 2009;61(2):325-332.</div></div></div> [[Try this question again->Warfarin skin necrosis - Mech]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Warfarin skin necrosis. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Embolic disease follows instrumentation or anticoagulation over weeks and produces livedo and distal digital lesions with eosinophilia. <div class="ec-teach"><div class="th">What the findings point to</div> Warfarin inhibits synthesis of factors II, VII, IX, and X and of the anticoagulant proteins C and S. Protein C has a short half-life of about 8 hours, comparable to factor VII and far shorter than factor II, so its activity falls before the procoagulant factors are meaningfully reduced. Loading without bridging anticoagulation creates a window of net hypercoagulability in which dermal microvascular thrombosis produces necrosis in fat-rich areas. Normal platelets, fibrinogen, and smear exclude consumption and microangiopathy. <div class="ec-src"><b>Source:</b> Nazarian RM, Van Cott EM, Zembowicz A, Duncan LM. Warfarin-induced skin necrosis. J Am Acad Dermatol 2009;61(2):325-332.</div></div></div> [[Try this question again->Warfarin skin necrosis - Mech]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 19:55</div> A 31-year-old man taking sertraline for depression was given tramadol for back pain 8 hours ago. He is agitated and diaphoretic. Temperature is 38.9°C, blood pressure 158/94 mm Hg, and pulse 128/min. Pupils are 6 mm bilaterally. There is inducible clonus at both ankles, hyperreflexia that is more pronounced in the legs than the arms, and intermittent tremor. Bowel sounds are hyperactive. Creatine kinase is 340 U/L. <span class="ec-prompt">Which of the following best explains this patient's presentation?</span> [[Competitive antagonism of central muscarinic receptors->Serotonin syndrome mechanism - Mech D3]] [[Dopamine receptor blockade in the nigrostriatal pathway->Serotonin syndrome mechanism - Mech D1]] [[Excess serotonergic activity at postsynaptic 5-HT2A receptors->Serotonin syndrome mechanism - Mech correct]] [[Excessive central and peripheral cholinergic stimulation->Serotonin syndrome mechanism - Mech D2]] [[Ryanodine receptor calcium release triggered by an anesthetic->Serotonin syndrome mechanism - Mech D5]] [[Uncoupling of oxidative phosphorylation in skeletal muscle->Serotonin syndrome mechanism - Mech D4]]

<span class="ec-case-marker" hidden data-entry="Serotonin syndrome mechanism. Mech"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Excess serotonergic activity at postsynaptic 5-HT2A receptors</div> Combining a selective serotonin reuptake inhibitor with tramadol, which both inhibits reuptake and has serotonergic activity, produces excess synaptic serotonin acting principally at 5-HT2A receptors. The clinical signature is the triad of autonomic instability, altered mental status, and neuromuscular hyperactivity, with clonus and lower-limb predominant hyperreflexia as the most discriminating findings. Onset within hours of adding a serotonergic drug and mydriasis with hyperactive bowel sounds complete the picture. <div class="ec-src"><b>Source:</b> Boyer EW, Shannon M. The serotonin syndrome. N Engl J Med 2005;352(11):1112-1120.</div></div> [[Start another case->Hub]] [[Restart this case->Serotonin syndrome mechanism - Mech]] [[Next case →->Ectopic pregnancy - Dx]]

<span class="ec-case-marker" hidden data-entry="Serotonin syndrome mechanism. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This underlies neuroleptic malignant syndrome, which develops over days, produces lead-pipe rigidity rather than clonus, and is associated with marked creatine kinase elevation and normal or small pupils. <div class="ec-teach"><div class="th">What the findings point to</div> Combining a selective serotonin reuptake inhibitor with tramadol, which both inhibits reuptake and has serotonergic activity, produces excess synaptic serotonin acting principally at 5-HT2A receptors. The clinical signature is the triad of autonomic instability, altered mental status, and neuromuscular hyperactivity, with clonus and lower-limb predominant hyperreflexia as the most discriminating findings. Onset within hours of adding a serotonergic drug and mydriasis with hyperactive bowel sounds complete the picture. <div class="ec-src"><b>Source:</b> Boyer EW, Shannon M. The serotonin syndrome. N Engl J Med 2005;352(11):1112-1120.</div></div></div> [[Try this question again->Serotonin syndrome mechanism - Mech]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Serotonin syndrome mechanism. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A cholinergic toxidrome produces miosis, bronchorrhea, salivation, and bradycardia, essentially the opposite autonomic picture. <div class="ec-teach"><div class="th">What the findings point to</div> Combining a selective serotonin reuptake inhibitor with tramadol, which both inhibits reuptake and has serotonergic activity, produces excess synaptic serotonin acting principally at 5-HT2A receptors. The clinical signature is the triad of autonomic instability, altered mental status, and neuromuscular hyperactivity, with clonus and lower-limb predominant hyperreflexia as the most discriminating findings. Onset within hours of adding a serotonergic drug and mydriasis with hyperactive bowel sounds complete the picture. <div class="ec-src"><b>Source:</b> Boyer EW, Shannon M. The serotonin syndrome. N Engl J Med 2005;352(11):1112-1120.</div></div></div> [[Try this question again->Serotonin syndrome mechanism - Mech]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Serotonin syndrome mechanism. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> An anticholinergic syndrome causes dry skin, absent bowel sounds, and urinary retention. He is diaphoretic with hyperactive bowel sounds. <div class="ec-teach"><div class="th">What the findings point to</div> Combining a selective serotonin reuptake inhibitor with tramadol, which both inhibits reuptake and has serotonergic activity, produces excess synaptic serotonin acting principally at 5-HT2A receptors. The clinical signature is the triad of autonomic instability, altered mental status, and neuromuscular hyperactivity, with clonus and lower-limb predominant hyperreflexia as the most discriminating findings. Onset within hours of adding a serotonergic drug and mydriasis with hyperactive bowel sounds complete the picture. <div class="ec-src"><b>Source:</b> Boyer EW, Shannon M. The serotonin syndrome. N Engl J Med 2005;352(11):1112-1120.</div></div></div> [[Try this question again->Serotonin syndrome mechanism - Mech]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Serotonin syndrome mechanism. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This describes toxins such as salicylates and dinitrophenol, which cause hyperthermia without clonus or hyperreflexia. <div class="ec-teach"><div class="th">What the findings point to</div> Combining a selective serotonin reuptake inhibitor with tramadol, which both inhibits reuptake and has serotonergic activity, produces excess synaptic serotonin acting principally at 5-HT2A receptors. The clinical signature is the triad of autonomic instability, altered mental status, and neuromuscular hyperactivity, with clonus and lower-limb predominant hyperreflexia as the most discriminating findings. Onset within hours of adding a serotonergic drug and mydriasis with hyperactive bowel sounds complete the picture. <div class="ec-src"><b>Source:</b> Boyer EW, Shannon M. The serotonin syndrome. N Engl J Med 2005;352(11):1112-1120.</div></div></div> [[Try this question again->Serotonin syndrome mechanism - Mech]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Serotonin syndrome mechanism. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Malignant hyperthermia follows exposure to volatile agents or succinylcholine and produces rigidity with very high creatine kinase. <div class="ec-teach"><div class="th">What the findings point to</div> Combining a selective serotonin reuptake inhibitor with tramadol, which both inhibits reuptake and has serotonergic activity, produces excess synaptic serotonin acting principally at 5-HT2A receptors. The clinical signature is the triad of autonomic instability, altered mental status, and neuromuscular hyperactivity, with clonus and lower-limb predominant hyperreflexia as the most discriminating findings. Onset within hours of adding a serotonergic drug and mydriasis with hyperactive bowel sounds complete the picture. <div class="ec-src"><b>Source:</b> Boyer EW, Shannon M. The serotonin syndrome. N Engl J Med 2005;352(11):1112-1120.</div></div></div> [[Try this question again->Serotonin syndrome mechanism - Mech]] [[Start another case->Hub]]

<div class="ec-scene">Oncology ward · 05:40</div> A 19-year-old man with newly diagnosed Burkitt lymphoma and bulky abdominal disease received his first cycle of chemotherapy 20 hours ago. He now has muscle cramps and perioral tingling. Serum potassium is 6.4 mEq/L, phosphate 7.9 mg/dL, calcium 6.8 mg/dL, uric acid 13.2 mg/dL, and creatinine has risen from 0.8 to 2.4 mg/dL. Urine output is 15 mL/h. Electrocardiography shows peaked T waves. <span class="ec-prompt">Which of the following best explains the hypocalcemia in this patient?</span> [[Chelation of calcium by released uric acid->Tumor lysis syndrome - Mech D3]] [[Impaired renal hydroxylation of vitamin D->Tumor lysis syndrome - Mech D2]] [[Magnesium depletion causing parathyroid hormone resistance->Tumor lysis syndrome - Mech D5]] [[Precipitation of calcium with released intracellular phosphate->Tumor lysis syndrome - Mech correct]] [[Redistribution of calcium into cells during alkalosis->Tumor lysis syndrome - Mech D4]] [[Suppression of parathyroid hormone secretion by hyperkalemia->Tumor lysis syndrome - Mech D1]]

<span class="ec-case-marker" hidden data-entry="Tumor lysis syndrome. Mech"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Precipitation of calcium with released intracellular phosphate</div> Rapid lysis of a large tumor burden releases potassium, phosphate, and nucleic acids into the circulation. Phosphate concentrations rise sharply, and calcium phosphate precipitates once the solubility product is exceeded, lowering serum calcium and depositing crystals in the renal tubules. This deposition, together with uric acid crystal nephropathy from purine catabolism, drives the acute kidney injury. The hypocalcemia is therefore consumptive rather than a failure of parathyroid or vitamin D physiology. <div class="ec-src"><b>Source:</b> Coiffier B, Altman A, Pui CH, Younes A, Cairo MS. Guidelines for the management of pediatric and adult tumor lysis syndrome: an evidence-based review. J Clin Oncol 2008;26(16):2767-2778.</div></div> [[Start another case->Hub]] [[Restart this case->Tumor lysis syndrome - Mech]] [[Next case →->Sepsis - Ix]]

<span class="ec-case-marker" hidden data-entry="Tumor lysis syndrome. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Potassium does not suppress parathyroid hormone, and the parathyroid response here is appropriately increased rather than suppressed. <div class="ec-teach"><div class="th">What the findings point to</div> Rapid lysis of a large tumor burden releases potassium, phosphate, and nucleic acids into the circulation. Phosphate concentrations rise sharply, and calcium phosphate precipitates once the solubility product is exceeded, lowering serum calcium and depositing crystals in the renal tubules. This deposition, together with uric acid crystal nephropathy from purine catabolism, drives the acute kidney injury. The hypocalcemia is therefore consumptive rather than a failure of parathyroid or vitamin D physiology. <div class="ec-src"><b>Source:</b> Coiffier B, Altman A, Pui CH, Younes A, Cairo MS. Guidelines for the management of pediatric and adult tumor lysis syndrome: an evidence-based review. J Clin Oncol 2008;26(16):2767-2778.</div></div></div> [[Try this question again->Tumor lysis syndrome - Mech]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Tumor lysis syndrome. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Reduced calcitriol production contributes to hypocalcemia in chronic kidney disease over weeks to months, not within 20 hours. <div class="ec-teach"><div class="th">What the findings point to</div> Rapid lysis of a large tumor burden releases potassium, phosphate, and nucleic acids into the circulation. Phosphate concentrations rise sharply, and calcium phosphate precipitates once the solubility product is exceeded, lowering serum calcium and depositing crystals in the renal tubules. This deposition, together with uric acid crystal nephropathy from purine catabolism, drives the acute kidney injury. The hypocalcemia is therefore consumptive rather than a failure of parathyroid or vitamin D physiology. <div class="ec-src"><b>Source:</b> Coiffier B, Altman A, Pui CH, Younes A, Cairo MS. Guidelines for the management of pediatric and adult tumor lysis syndrome: an evidence-based review. J Clin Oncol 2008;26(16):2767-2778.</div></div></div> [[Try this question again->Tumor lysis syndrome - Mech]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Tumor lysis syndrome. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Uric acid causes crystal nephropathy but does not bind calcium in a way that lowers the serum concentration. <div class="ec-teach"><div class="th">What the findings point to</div> Rapid lysis of a large tumor burden releases potassium, phosphate, and nucleic acids into the circulation. Phosphate concentrations rise sharply, and calcium phosphate precipitates once the solubility product is exceeded, lowering serum calcium and depositing crystals in the renal tubules. This deposition, together with uric acid crystal nephropathy from purine catabolism, drives the acute kidney injury. The hypocalcemia is therefore consumptive rather than a failure of parathyroid or vitamin D physiology. <div class="ec-src"><b>Source:</b> Coiffier B, Altman A, Pui CH, Younes A, Cairo MS. Guidelines for the management of pediatric and adult tumor lysis syndrome: an evidence-based review. J Clin Oncol 2008;26(16):2767-2778.</div></div></div> [[Try this question again->Tumor lysis syndrome - Mech]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Tumor lysis syndrome. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Alkalemia lowers ionized calcium by increasing protein binding, but total calcium remains unchanged and there is no alkalosis described. <div class="ec-teach"><div class="th">What the findings point to</div> Rapid lysis of a large tumor burden releases potassium, phosphate, and nucleic acids into the circulation. Phosphate concentrations rise sharply, and calcium phosphate precipitates once the solubility product is exceeded, lowering serum calcium and depositing crystals in the renal tubules. This deposition, together with uric acid crystal nephropathy from purine catabolism, drives the acute kidney injury. The hypocalcemia is therefore consumptive rather than a failure of parathyroid or vitamin D physiology. <div class="ec-src"><b>Source:</b> Coiffier B, Altman A, Pui CH, Younes A, Cairo MS. Guidelines for the management of pediatric and adult tumor lysis syndrome: an evidence-based review. J Clin Oncol 2008;26(16):2767-2778.</div></div></div> [[Try this question again->Tumor lysis syndrome - Mech]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Tumor lysis syndrome. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Severe hypomagnesemia can impair parathyroid hormone secretion and action, but it is not a feature of tumor lysis and no magnesium abnormality is given. <div class="ec-teach"><div class="th">What the findings point to</div> Rapid lysis of a large tumor burden releases potassium, phosphate, and nucleic acids into the circulation. Phosphate concentrations rise sharply, and calcium phosphate precipitates once the solubility product is exceeded, lowering serum calcium and depositing crystals in the renal tubules. This deposition, together with uric acid crystal nephropathy from purine catabolism, drives the acute kidney injury. The hypocalcemia is therefore consumptive rather than a failure of parathyroid or vitamin D physiology. <div class="ec-src"><b>Source:</b> Coiffier B, Altman A, Pui CH, Younes A, Cairo MS. Guidelines for the management of pediatric and adult tumor lysis syndrome: an evidence-based review. J Clin Oncol 2008;26(16):2767-2778.</div></div></div> [[Try this question again->Tumor lysis syndrome - Mech]] [[Start another case->Hub]]

<div class="ec-scene">Medical ward · 06:20</div> A 44-year-old man with alcohol use disorder was admitted after 3 weeks of minimal oral intake, weighing 48 kg. Enteral feeding was started at full caloric goal on admission. On hospital day 3 he becomes confused and weak, with a new oxygen requirement. Serum phosphate is 1.1 mg/dL, potassium 2.9 mEq/L, and magnesium 1.2 mg/dL. Creatine kinase is 900 U/L and echocardiography shows a new left ventricular ejection fraction of 35%. <span class="ec-prompt">Which of the following best explains this patient's deterioration?</span> [[Alcohol-related dilated cardiomyopathy progressing acutely->Refeeding electrolyte shift - Mech D2]] [[Hypocalcemia from vitamin D deficiency impairing contractility->Refeeding electrolyte shift - Mech D5]] [[Insulin-driven intracellular shift of phosphate and other electrolytes->Refeeding electrolyte shift - Mech correct]] [[Renal phosphate wasting from proximal tubular injury->Refeeding electrolyte shift - Mech D3]] [[Sepsis with cytokine-mediated myocardial depression->Refeeding electrolyte shift - Mech D4]] [[Thiamine deficiency causing high-output cardiac failure->Refeeding electrolyte shift - Mech D1]]

<span class="ec-case-marker" hidden data-entry="Refeeding electrolyte shift. Mech"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Insulin-driven intracellular shift of phosphate and other electrolytes</div> Prolonged starvation depletes total body phosphate, potassium, and magnesium while serum concentrations remain deceptively normal. Reintroducing carbohydrate triggers insulin release, which drives glucose, phosphate, potassium, and magnesium into cells and stimulates synthesis of adenosine triphosphate and 2,3-diphosphoglycerate, consuming phosphate further. Severe hypophosphatemia impairs myocardial contractility, respiratory muscle function, and neuronal metabolism. Prevention requires starting at reduced caloric rates with thiamine and aggressive electrolyte repletion. <div class="ec-src"><b>Source:</b> Mehanna HM, Moledina J, Travis J. Refeeding syndrome: what it is, and how to prevent and treat it. BMJ 2008;336(7659):1495-1498.</div></div> [[Start another case->Hub]] [[Restart this case->Refeeding electrolyte shift - Mech]] [[Next case →->Iron deficiency - Rx]]

<span class="ec-case-marker" hidden data-entry="Refeeding electrolyte shift. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Wet beriberi produces a high-output state with warm extremities, not the electrolyte pattern shown, although thiamine deficiency frequently coexists and must be treated. <div class="ec-teach"><div class="th">What the findings point to</div> Prolonged starvation depletes total body phosphate, potassium, and magnesium while serum concentrations remain deceptively normal. Reintroducing carbohydrate triggers insulin release, which drives glucose, phosphate, potassium, and magnesium into cells and stimulates synthesis of adenosine triphosphate and 2,3-diphosphoglycerate, consuming phosphate further. Severe hypophosphatemia impairs myocardial contractility, respiratory muscle function, and neuronal metabolism. Prevention requires starting at reduced caloric rates with thiamine and aggressive electrolyte repletion. <div class="ec-src"><b>Source:</b> Mehanna HM, Moledina J, Travis J. Refeeding syndrome: what it is, and how to prevent and treat it. BMJ 2008;336(7659):1495-1498.</div></div></div> [[Try this question again->Refeeding electrolyte shift - Mech]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Refeeding electrolyte shift. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Alcoholic cardiomyopathy develops over years and does not explain profound hypophosphatemia appearing 3 days after feeding began. <div class="ec-teach"><div class="th">What the findings point to</div> Prolonged starvation depletes total body phosphate, potassium, and magnesium while serum concentrations remain deceptively normal. Reintroducing carbohydrate triggers insulin release, which drives glucose, phosphate, potassium, and magnesium into cells and stimulates synthesis of adenosine triphosphate and 2,3-diphosphoglycerate, consuming phosphate further. Severe hypophosphatemia impairs myocardial contractility, respiratory muscle function, and neuronal metabolism. Prevention requires starting at reduced caloric rates with thiamine and aggressive electrolyte repletion. <div class="ec-src"><b>Source:</b> Mehanna HM, Moledina J, Travis J. Refeeding syndrome: what it is, and how to prevent and treat it. BMJ 2008;336(7659):1495-1498.</div></div></div> [[Try this question again->Refeeding electrolyte shift - Mech]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Refeeding electrolyte shift. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Tubular wasting would produce inappropriately high urinary phosphate excretion, and the temporal link to initiation of feeding points to a shift rather than a loss. <div class="ec-teach"><div class="th">What the findings point to</div> Prolonged starvation depletes total body phosphate, potassium, and magnesium while serum concentrations remain deceptively normal. Reintroducing carbohydrate triggers insulin release, which drives glucose, phosphate, potassium, and magnesium into cells and stimulates synthesis of adenosine triphosphate and 2,3-diphosphoglycerate, consuming phosphate further. Severe hypophosphatemia impairs myocardial contractility, respiratory muscle function, and neuronal metabolism. Prevention requires starting at reduced caloric rates with thiamine and aggressive electrolyte repletion. <div class="ec-src"><b>Source:</b> Mehanna HM, Moledina J, Travis J. Refeeding syndrome: what it is, and how to prevent and treat it. BMJ 2008;336(7659):1495-1498.</div></div></div> [[Try this question again->Refeeding electrolyte shift - Mech]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Refeeding electrolyte shift. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Sepsis is plausible in this population but does not produce this specific triad of phosphate, potassium, and magnesium depletion timed to refeeding. <div class="ec-teach"><div class="th">What the findings point to</div> Prolonged starvation depletes total body phosphate, potassium, and magnesium while serum concentrations remain deceptively normal. Reintroducing carbohydrate triggers insulin release, which drives glucose, phosphate, potassium, and magnesium into cells and stimulates synthesis of adenosine triphosphate and 2,3-diphosphoglycerate, consuming phosphate further. Severe hypophosphatemia impairs myocardial contractility, respiratory muscle function, and neuronal metabolism. Prevention requires starting at reduced caloric rates with thiamine and aggressive electrolyte repletion. <div class="ec-src"><b>Source:</b> Mehanna HM, Moledina J, Travis J. Refeeding syndrome: what it is, and how to prevent and treat it. BMJ 2008;336(7659):1495-1498.</div></div></div> [[Try this question again->Refeeding electrolyte shift - Mech]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Refeeding electrolyte shift. Mech"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Vitamin D deficiency is likely in chronic malnutrition but develops over months and is not the acute driver here. <div class="ec-teach"><div class="th">What the findings point to</div> Prolonged starvation depletes total body phosphate, potassium, and magnesium while serum concentrations remain deceptively normal. Reintroducing carbohydrate triggers insulin release, which drives glucose, phosphate, potassium, and magnesium into cells and stimulates synthesis of adenosine triphosphate and 2,3-diphosphoglycerate, consuming phosphate further. Severe hypophosphatemia impairs myocardial contractility, respiratory muscle function, and neuronal metabolism. Prevention requires starting at reduced caloric rates with thiamine and aggressive electrolyte repletion. <div class="ec-src"><b>Source:</b> Mehanna HM, Moledina J, Travis J. Refeeding syndrome: what it is, and how to prevent and treat it. BMJ 2008;336(7659):1495-1498.</div></div></div> [[Try this question again->Refeeding electrolyte shift - Mech]] [[Start another case->Hub]]

<div class="ec-scene">Cardiology clinic · 11:20</div> A 71-year-old woman is found to have persistent atrial fibrillation on routine electrocardiography. She has hypertension treated with amlodipine, type 2 diabetes mellitus treated with metformin, and no prior stroke or transient ischemic attack. She has no heart failure and no known vascular disease. Blood pressure is 132/78 mm Hg. Echocardiography shows normal left ventricular systolic function and no valvular stenosis. Creatinine clearance is 68 mL/min and hemoglobin is 13.4 g/dL. <span class="ec-prompt">Which of the following best guides the decision about anticoagulation in this patient?</span> [[Her bleeding risk score alone->Stroke risk in atrial fibrillation - Prog D5]] [[Her creatinine clearance->Stroke risk in atrial fibrillation - Prog D3]] [[Her stroke risk score based on clinical comorbidities->Stroke risk in atrial fibrillation - Prog correct]] [[Left atrial size measured on echocardiography->Stroke risk in atrial fibrillation - Prog D1]] [[The presence or absence of palpitations->Stroke risk in atrial fibrillation - Prog D4]] [[The proportion of time spent in atrial fibrillation->Stroke risk in atrial fibrillation - Prog D2]]

<span class="ec-case-marker" hidden data-entry="Stroke risk in atrial fibrillation. Prog"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Her stroke risk score based on clinical comorbidities</div> Anticoagulation in nonvalvular atrial fibrillation is decided by a validated clinical risk score rather than by rhythm pattern, symptom burden, or echocardiographic findings. She accumulates points for age 65 to 74, hypertension, diabetes, and female sex, which places her well above the threshold at which oral anticoagulation is recommended. Paroxysmal, persistent, and permanent atrial fibrillation carry comparable thromboembolic risk, so the pattern of the arrhythmia does not lower the indication. <div class="ec-src"><b>Source:</b> Lip GY, Nieuwlaat R, Pisters R, Lane DA, Crijns HJ. Refining clinical risk stratification for predicting stroke and thromboembolism in atrial fibrillation using a novel risk factor-based approach. Chest 2010;137(2):263-272.</div></div> [[Start another case->Hub]] [[Restart this case->Stroke risk in atrial fibrillation - Prog]] [[Next case →->Hypertrophic cardiomyopathy risk - Prog]]

<span class="ec-case-marker" hidden data-entry="Stroke risk in atrial fibrillation. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Atrial dimensions correlate loosely with the likelihood of maintaining sinus rhythm but are not part of the validated stroke risk assessment. <div class="ec-teach"><div class="th">What the findings point to</div> Anticoagulation in nonvalvular atrial fibrillation is decided by a validated clinical risk score rather than by rhythm pattern, symptom burden, or echocardiographic findings. She accumulates points for age 65 to 74, hypertension, diabetes, and female sex, which places her well above the threshold at which oral anticoagulation is recommended. Paroxysmal, persistent, and permanent atrial fibrillation carry comparable thromboembolic risk, so the pattern of the arrhythmia does not lower the indication. <div class="ec-src"><b>Source:</b> Lip GY, Nieuwlaat R, Pisters R, Lane DA, Crijns HJ. Refining clinical risk stratification for predicting stroke and thromboembolism in atrial fibrillation using a novel risk factor-based approach. Chest 2010;137(2):263-272.</div></div></div> [[Try this question again->Stroke risk in atrial fibrillation - Prog]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Stroke risk in atrial fibrillation. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Burden has been studied but does not replace the clinical score, and persistent and paroxysmal patterns carry similar risk. <div class="ec-teach"><div class="th">What the findings point to</div> Anticoagulation in nonvalvular atrial fibrillation is decided by a validated clinical risk score rather than by rhythm pattern, symptom burden, or echocardiographic findings. She accumulates points for age 65 to 74, hypertension, diabetes, and female sex, which places her well above the threshold at which oral anticoagulation is recommended. Paroxysmal, persistent, and permanent atrial fibrillation carry comparable thromboembolic risk, so the pattern of the arrhythmia does not lower the indication. <div class="ec-src"><b>Source:</b> Lip GY, Nieuwlaat R, Pisters R, Lane DA, Crijns HJ. Refining clinical risk stratification for predicting stroke and thromboembolism in atrial fibrillation using a novel risk factor-based approach. Chest 2010;137(2):263-272.</div></div></div> [[Try this question again->Stroke risk in atrial fibrillation - Prog]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Stroke risk in atrial fibrillation. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Renal function determines the choice and dose of anticoagulant, not whether anticoagulation is indicated. <div class="ec-teach"><div class="th">What the findings point to</div> Anticoagulation in nonvalvular atrial fibrillation is decided by a validated clinical risk score rather than by rhythm pattern, symptom burden, or echocardiographic findings. She accumulates points for age 65 to 74, hypertension, diabetes, and female sex, which places her well above the threshold at which oral anticoagulation is recommended. Paroxysmal, persistent, and permanent atrial fibrillation carry comparable thromboembolic risk, so the pattern of the arrhythmia does not lower the indication. <div class="ec-src"><b>Source:</b> Lip GY, Nieuwlaat R, Pisters R, Lane DA, Crijns HJ. Refining clinical risk stratification for predicting stroke and thromboembolism in atrial fibrillation using a novel risk factor-based approach. Chest 2010;137(2):263-272.</div></div></div> [[Try this question again->Stroke risk in atrial fibrillation - Prog]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Stroke risk in atrial fibrillation. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Symptom burden guides rate and rhythm strategy. It has no relationship to thromboembolic risk. <div class="ec-teach"><div class="th">What the findings point to</div> Anticoagulation in nonvalvular atrial fibrillation is decided by a validated clinical risk score rather than by rhythm pattern, symptom burden, or echocardiographic findings. She accumulates points for age 65 to 74, hypertension, diabetes, and female sex, which places her well above the threshold at which oral anticoagulation is recommended. Paroxysmal, persistent, and permanent atrial fibrillation carry comparable thromboembolic risk, so the pattern of the arrhythmia does not lower the indication. <div class="ec-src"><b>Source:</b> Lip GY, Nieuwlaat R, Pisters R, Lane DA, Crijns HJ. Refining clinical risk stratification for predicting stroke and thromboembolism in atrial fibrillation using a novel risk factor-based approach. Chest 2010;137(2):263-272.</div></div></div> [[Try this question again->Stroke risk in atrial fibrillation - Prog]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Stroke risk in atrial fibrillation. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Bleeding risk is assessed to identify modifiable factors, not as a reason to withhold anticoagulation from a patient with a clear indication. <div class="ec-teach"><div class="th">What the findings point to</div> Anticoagulation in nonvalvular atrial fibrillation is decided by a validated clinical risk score rather than by rhythm pattern, symptom burden, or echocardiographic findings. She accumulates points for age 65 to 74, hypertension, diabetes, and female sex, which places her well above the threshold at which oral anticoagulation is recommended. Paroxysmal, persistent, and permanent atrial fibrillation carry comparable thromboembolic risk, so the pattern of the arrhythmia does not lower the indication. <div class="ec-src"><b>Source:</b> Lip GY, Nieuwlaat R, Pisters R, Lane DA, Crijns HJ. Refining clinical risk stratification for predicting stroke and thromboembolism in atrial fibrillation using a novel risk factor-based approach. Chest 2010;137(2):263-272.</div></div></div> [[Try this question again->Stroke risk in atrial fibrillation - Prog]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 15:45</div> A 46-year-old man with a segmental pulmonary embolism on CT angiography is hemodynamically stable. Blood pressure is 128/76 mm Hg, Pulse 84/min, respirations are 16/min, and oxygen saturation 97% on room air. He has no cancer, no heart failure, no chronic lung disease, and no prior venous thromboembolism. Troponin is undetectable and echocardiography shows a normal right ventricle. He lives with his wife, has reliable transport, and has no bleeding history. Creatinine is 0.9 mg/dL. <span class="ec-prompt">Which of the following is the most appropriate management strategy?</span> [[Admission for 5 days of intravenous unfractionated heparin->Pulmonary embolism risk stratification - Prog D1]] [[Admission for observation without anticoagulation->Pulmonary embolism risk stratification - Prog D5]] [[Catheter-directed thrombolysis->Pulmonary embolism risk stratification - Prog D3]] [[Inferior vena cava filter placement->Pulmonary embolism risk stratification - Prog D4]] [[Outpatient anticoagulation after a short observation period->Pulmonary embolism risk stratification - Prog correct]] [[Systemic thrombolytic therapy->Pulmonary embolism risk stratification - Prog D2]]

<span class="ec-case-marker" hidden data-entry="Pulmonary embolism risk stratification. Prog"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Outpatient anticoagulation after a short observation period</div> Validated severity scores identify a low-risk group with very low short-term mortality, defined by normal hemodynamics, absence of comorbidity, preserved oxygenation, and no evidence of right ventricular strain by troponin or imaging. Randomized data support treating such patients at home with the same outcomes as inpatient care and fewer hospital-acquired complications. He meets every criterion and also has the social supports that outpatient management requires. <div class="ec-src"><b>Source:</b> Aujesky D, Roy PM, Verschuren F, et al. Outpatient versus inpatient treatment for patients with acute pulmonary embolism: an international, open-label, randomised, non-inferiority trial. Lancet 2011;378(9785):41-48.</div></div> [[Start another case->Hub]] [[Restart this case->Pulmonary embolism risk stratification - Prog]] [[Next case →->Acute GI bleed (Sequential - 3 Questions) - Ix]]

<span class="ec-case-marker" hidden data-entry="Pulmonary embolism risk stratification. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Continuous intravenous heparin is reserved for patients who may need rapid reversal or thrombolysis. It commits a low-risk patient to a prolonged admission without benefit. <div class="ec-teach"><div class="th">What the findings point to</div> Validated severity scores identify a low-risk group with very low short-term mortality, defined by normal hemodynamics, absence of comorbidity, preserved oxygenation, and no evidence of right ventricular strain by troponin or imaging. Randomized data support treating such patients at home with the same outcomes as inpatient care and fewer hospital-acquired complications. He meets every criterion and also has the social supports that outpatient management requires. <div class="ec-src"><b>Source:</b> Aujesky D, Roy PM, Verschuren F, et al. Outpatient versus inpatient treatment for patients with acute pulmonary embolism: an international, open-label, randomised, non-inferiority trial. Lancet 2011;378(9785):41-48.</div></div></div> [[Try this question again->Pulmonary embolism risk stratification - Prog]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Pulmonary embolism risk stratification. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Thrombolysis is indicated for hemodynamic instability. Giving it to a normotensive patient with a normal right ventricle adds major bleeding risk for no gain. <div class="ec-teach"><div class="th">What the findings point to</div> Validated severity scores identify a low-risk group with very low short-term mortality, defined by normal hemodynamics, absence of comorbidity, preserved oxygenation, and no evidence of right ventricular strain by troponin or imaging. Randomized data support treating such patients at home with the same outcomes as inpatient care and fewer hospital-acquired complications. He meets every criterion and also has the social supports that outpatient management requires. <div class="ec-src"><b>Source:</b> Aujesky D, Roy PM, Verschuren F, et al. Outpatient versus inpatient treatment for patients with acute pulmonary embolism: an international, open-label, randomised, non-inferiority trial. Lancet 2011;378(9785):41-48.</div></div></div> [[Try this question again->Pulmonary embolism risk stratification - Prog]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Pulmonary embolism risk stratification. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Catheter-based therapy is considered for intermediate-high or high-risk embolism with right ventricular dysfunction, which he does not have. <div class="ec-teach"><div class="th">What the findings point to</div> Validated severity scores identify a low-risk group with very low short-term mortality, defined by normal hemodynamics, absence of comorbidity, preserved oxygenation, and no evidence of right ventricular strain by troponin or imaging. Randomized data support treating such patients at home with the same outcomes as inpatient care and fewer hospital-acquired complications. He meets every criterion and also has the social supports that outpatient management requires. <div class="ec-src"><b>Source:</b> Aujesky D, Roy PM, Verschuren F, et al. Outpatient versus inpatient treatment for patients with acute pulmonary embolism: an international, open-label, randomised, non-inferiority trial. Lancet 2011;378(9785):41-48.</div></div></div> [[Try this question again->Pulmonary embolism risk stratification - Prog]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Pulmonary embolism risk stratification. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Filters are for patients in whom anticoagulation is contraindicated or has failed. He has no bleeding history and can be anticoagulated. <div class="ec-teach"><div class="th">What the findings point to</div> Validated severity scores identify a low-risk group with very low short-term mortality, defined by normal hemodynamics, absence of comorbidity, preserved oxygenation, and no evidence of right ventricular strain by troponin or imaging. Randomized data support treating such patients at home with the same outcomes as inpatient care and fewer hospital-acquired complications. He meets every criterion and also has the social supports that outpatient management requires. <div class="ec-src"><b>Source:</b> Aujesky D, Roy PM, Verschuren F, et al. Outpatient versus inpatient treatment for patients with acute pulmonary embolism: an international, open-label, randomised, non-inferiority trial. Lancet 2011;378(9785):41-48.</div></div></div> [[Try this question again->Pulmonary embolism risk stratification - Prog]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Pulmonary embolism risk stratification. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Withholding anticoagulation from a confirmed pulmonary embolism risks extension and recurrence regardless of where the patient is observed. <div class="ec-teach"><div class="th">What the findings point to</div> Validated severity scores identify a low-risk group with very low short-term mortality, defined by normal hemodynamics, absence of comorbidity, preserved oxygenation, and no evidence of right ventricular strain by troponin or imaging. Randomized data support treating such patients at home with the same outcomes as inpatient care and fewer hospital-acquired complications. He meets every criterion and also has the social supports that outpatient management requires. <div class="ec-src"><b>Source:</b> Aujesky D, Roy PM, Verschuren F, et al. Outpatient versus inpatient treatment for patients with acute pulmonary embolism: an international, open-label, randomised, non-inferiority trial. Lancet 2011;378(9785):41-48.</div></div></div> [[Try this question again->Pulmonary embolism risk stratification - Prog]] [[Start another case->Hub]]

<div class="ec-scene">Emergency department · 12:35</div> A 68-year-old woman with pyelonephritis has a temperature of 38.8°C, blood pressure of 104/64 mm Hg, pulse 106/min, and respirations are 22/min. She is fully oriented. Serum lactate is 3.8 mmol/L, creatinine 1.7 mg/dL from a baseline of 0.9 mg/dL, and leukocyte count 18,200/mm3. The resident notes that her score on a bedside screening tool is only 1 and proposes that she does not have sepsis and can be managed on a general ward without urgent resuscitation. <span class="ec-prompt">Which of the following best describes the appropriate use of this screening tool?</span> [[A score below 2 reliably excludes organ dysfunction->Sepsis risk stratification - Prog D1]] [[It defines septic shock when the score reaches 3->Sepsis risk stratification - Prog D4]] [[It is the preferred single screening tool for sepsis->Sepsis risk stratification - Prog D3]] [[It should be applied only to patients in the intensive care unit->Sepsis risk stratification - Prog D5]] [[It should not be used as a single screen to exclude sepsis->Sepsis risk stratification - Prog correct]] [[It should replace lactate measurement in initial assessment->Sepsis risk stratification - Prog D2]]

<span class="ec-case-marker" hidden data-entry="Sepsis risk stratification. Prog"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ It should not be used as a single screen to exclude sepsis</div> The 2021 guidelines explicitly recommend against using the bedside score as a single screening tool, because its sensitivity is poor and a low score does not rule out sepsis. She has an infection with new organ dysfunction, evidenced by a rising creatinine and a lactate of 3.8 mmol/L, which is what defines sepsis. Management should proceed on the clinical and laboratory findings: cultures, prompt antimicrobials, fluid resuscitation, and repeat lactate measurement. <div class="ec-src"><b>Source:</b> Evans L, Rhodes A, Alhazzani W, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2021. Crit Care Med 2021;49(11):e1063-e1143.</div></div> [[Start another case->Hub]] [[Restart this case->Sepsis risk stratification - Prog]] [[Next case →->Stroke - Ix]]

<span class="ec-case-marker" hidden data-entry="Sepsis risk stratification. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The score is specific but insensitive, and it misses a substantial proportion of patients who go on to deteriorate. <div class="ec-teach"><div class="th">What the findings point to</div> The 2021 guidelines explicitly recommend against using the bedside score as a single screening tool, because its sensitivity is poor and a low score does not rule out sepsis. She has an infection with new organ dysfunction, evidenced by a rising creatinine and a lactate of 3.8 mmol/L, which is what defines sepsis. Management should proceed on the clinical and laboratory findings: cultures, prompt antimicrobials, fluid resuscitation, and repeat lactate measurement. <div class="ec-src"><b>Source:</b> Evans L, Rhodes A, Alhazzani W, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2021. Crit Care Med 2021;49(11):e1063-e1143.</div></div></div> [[Try this question again->Sepsis risk stratification - Prog]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Sepsis risk stratification. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Lactate is a recommended component of initial evaluation and resuscitation and is not superseded by any bedside score. <div class="ec-teach"><div class="th">What the findings point to</div> The 2021 guidelines explicitly recommend against using the bedside score as a single screening tool, because its sensitivity is poor and a low score does not rule out sepsis. She has an infection with new organ dysfunction, evidenced by a rising creatinine and a lactate of 3.8 mmol/L, which is what defines sepsis. Management should proceed on the clinical and laboratory findings: cultures, prompt antimicrobials, fluid resuscitation, and repeat lactate measurement. <div class="ec-src"><b>Source:</b> Evans L, Rhodes A, Alhazzani W, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2021. Crit Care Med 2021;49(11):e1063-e1143.</div></div></div> [[Try this question again->Sepsis risk stratification - Prog]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Sepsis risk stratification. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This position was explicitly reversed in the 2021 update in favor of not relying on it alone. <div class="ec-teach"><div class="th">What the findings point to</div> The 2021 guidelines explicitly recommend against using the bedside score as a single screening tool, because its sensitivity is poor and a low score does not rule out sepsis. She has an infection with new organ dysfunction, evidenced by a rising creatinine and a lactate of 3.8 mmol/L, which is what defines sepsis. Management should proceed on the clinical and laboratory findings: cultures, prompt antimicrobials, fluid resuscitation, and repeat lactate measurement. <div class="ec-src"><b>Source:</b> Evans L, Rhodes A, Alhazzani W, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2021. Crit Care Med 2021;49(11):e1063-e1143.</div></div></div> [[Try this question again->Sepsis risk stratification - Prog]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Sepsis risk stratification. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Septic shock is defined by vasopressor requirement to maintain mean arterial pressure with a lactate above 2 mmol/L after fluid resuscitation. <div class="ec-teach"><div class="th">What the findings point to</div> The 2021 guidelines explicitly recommend against using the bedside score as a single screening tool, because its sensitivity is poor and a low score does not rule out sepsis. She has an infection with new organ dysfunction, evidenced by a rising creatinine and a lactate of 3.8 mmol/L, which is what defines sepsis. Management should proceed on the clinical and laboratory findings: cultures, prompt antimicrobials, fluid resuscitation, and repeat lactate measurement. <div class="ec-src"><b>Source:</b> Evans L, Rhodes A, Alhazzani W, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2021. Crit Care Med 2021;49(11):e1063-e1143.</div></div></div> [[Try this question again->Sepsis risk stratification - Prog]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Sepsis risk stratification. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The tool was developed for use outside intensive care. The problem is its sensitivity, not its setting. <div class="ec-teach"><div class="th">What the findings point to</div> The 2021 guidelines explicitly recommend against using the bedside score as a single screening tool, because its sensitivity is poor and a low score does not rule out sepsis. She has an infection with new organ dysfunction, evidenced by a rising creatinine and a lactate of 3.8 mmol/L, which is what defines sepsis. Management should proceed on the clinical and laboratory findings: cultures, prompt antimicrobials, fluid resuscitation, and repeat lactate measurement. <div class="ec-src"><b>Source:</b> Evans L, Rhodes A, Alhazzani W, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2021. Crit Care Med 2021;49(11):e1063-e1143.</div></div></div> [[Try this question again->Sepsis risk stratification - Prog]] [[Start another case->Hub]]

<div class="ec-scene">Cardiology clinic · 14:50</div> A 22-year-old man is evaluated after his 28-year-old brother died suddenly during exercise. Echocardiography shows asymmetric septal hypertrophy with a maximal wall thickness of 32 mm and no resting outflow gradient. He has had two episodes of unexplained syncope in the past year, one while walking. Ambulatory monitoring records a 9-beat run of nonsustained ventricular tachycardia. Left ventricular ejection fraction is 68% and left atrial diameter is 44 mm. He plays recreational basketball. <span class="ec-prompt">Which of the following findings most strongly indicates a need for an implantable defibrillator?</span> [[His age of 22 years->Hypertrophic cardiomyopathy risk - Prog D5]] [[His participation in recreational basketball->Hypertrophic cardiomyopathy risk - Prog D4]] [[The absence of a resting outflow tract gradient->Hypertrophic cardiomyopathy risk - Prog D2]] [[The left atrial diameter of 44 mm->Hypertrophic cardiomyopathy risk - Prog D3]] [[The left ventricular ejection fraction of 68%->Hypertrophic cardiomyopathy risk - Prog D1]] [[Wall thickness, syncope, and family history together->Hypertrophic cardiomyopathy risk - Prog correct]]

<span class="ec-case-marker" hidden data-entry="Hypertrophic cardiomyopathy risk. Prog"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Wall thickness, syncope, and family history together</div> Risk in hypertrophic cardiomyopathy is assessed by accumulating major markers rather than by any single variable. He carries several of the strongest: a maximal wall thickness of 32 mm, which is well above the 30 mm threshold, unexplained syncope within the past year, nonsustained ventricular tachycardia, and sudden death in a first-degree relative at a young age. This combination places him at high enough risk that primary prevention with a defibrillator is indicated. <div class="ec-src"><b>Source:</b> Ommen SR, Mital S, Burke MA, et al. 2020 AHA/ACC Guideline for the Diagnosis and Treatment of Patients With Hypertrophic Cardiomyopathy. Circulation 2020;142(25):e558-e631.</div></div> [[Start another case->Hub]] [[Restart this case->Hypertrophic cardiomyopathy risk - Prog]] [[Next case →->Pulmonary embolism - Ix]]

<span class="ec-case-marker" hidden data-entry="Hypertrophic cardiomyopathy risk. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Systolic function is typically preserved or hyperdynamic in this disease, and a normal ejection fraction carries no prognostic weight here. <div class="ec-teach"><div class="th">What the findings point to</div> Risk in hypertrophic cardiomyopathy is assessed by accumulating major markers rather than by any single variable. He carries several of the strongest: a maximal wall thickness of 32 mm, which is well above the 30 mm threshold, unexplained syncope within the past year, nonsustained ventricular tachycardia, and sudden death in a first-degree relative at a young age. This combination places him at high enough risk that primary prevention with a defibrillator is indicated. <div class="ec-src"><b>Source:</b> Ommen SR, Mital S, Burke MA, et al. 2020 AHA/ACC Guideline for the Diagnosis and Treatment of Patients With Hypertrophic Cardiomyopathy. Circulation 2020;142(25):e558-e631.</div></div></div> [[Try this question again->Hypertrophic cardiomyopathy risk - Prog]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Hypertrophic cardiomyopathy risk. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Obstruction drives symptoms and guides septal reduction therapy. It is not a primary determinant of arrhythmic risk. <div class="ec-teach"><div class="th">What the findings point to</div> Risk in hypertrophic cardiomyopathy is assessed by accumulating major markers rather than by any single variable. He carries several of the strongest: a maximal wall thickness of 32 mm, which is well above the 30 mm threshold, unexplained syncope within the past year, nonsustained ventricular tachycardia, and sudden death in a first-degree relative at a young age. This combination places him at high enough risk that primary prevention with a defibrillator is indicated. <div class="ec-src"><b>Source:</b> Ommen SR, Mital S, Burke MA, et al. 2020 AHA/ACC Guideline for the Diagnosis and Treatment of Patients With Hypertrophic Cardiomyopathy. Circulation 2020;142(25):e558-e631.</div></div></div> [[Try this question again->Hypertrophic cardiomyopathy risk - Prog]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Hypertrophic cardiomyopathy risk. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Atrial enlargement predicts atrial fibrillation and is a minor risk marker, not a decisive one. <div class="ec-teach"><div class="th">What the findings point to</div> Risk in hypertrophic cardiomyopathy is assessed by accumulating major markers rather than by any single variable. He carries several of the strongest: a maximal wall thickness of 32 mm, which is well above the 30 mm threshold, unexplained syncope within the past year, nonsustained ventricular tachycardia, and sudden death in a first-degree relative at a young age. This combination places him at high enough risk that primary prevention with a defibrillator is indicated. <div class="ec-src"><b>Source:</b> Ommen SR, Mital S, Burke MA, et al. 2020 AHA/ACC Guideline for the Diagnosis and Treatment of Patients With Hypertrophic Cardiomyopathy. Circulation 2020;142(25):e558-e631.</div></div></div> [[Try this question again->Hypertrophic cardiomyopathy risk - Prog]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Hypertrophic cardiomyopathy risk. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Activity recommendations are part of counseling, but exercise participation is not a marker used to determine defibrillator candidacy. <div class="ec-teach"><div class="th">What the findings point to</div> Risk in hypertrophic cardiomyopathy is assessed by accumulating major markers rather than by any single variable. He carries several of the strongest: a maximal wall thickness of 32 mm, which is well above the 30 mm threshold, unexplained syncope within the past year, nonsustained ventricular tachycardia, and sudden death in a first-degree relative at a young age. This combination places him at high enough risk that primary prevention with a defibrillator is indicated. <div class="ec-src"><b>Source:</b> Ommen SR, Mital S, Burke MA, et al. 2020 AHA/ACC Guideline for the Diagnosis and Treatment of Patients With Hypertrophic Cardiomyopathy. Circulation 2020;142(25):e558-e631.</div></div></div> [[Try this question again->Hypertrophic cardiomyopathy risk - Prog]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Hypertrophic cardiomyopathy risk. Prog"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Younger age is associated with higher lifetime risk but is not itself one of the established major risk markers. <div class="ec-teach"><div class="th">What the findings point to</div> Risk in hypertrophic cardiomyopathy is assessed by accumulating major markers rather than by any single variable. He carries several of the strongest: a maximal wall thickness of 32 mm, which is well above the 30 mm threshold, unexplained syncope within the past year, nonsustained ventricular tachycardia, and sudden death in a first-degree relative at a young age. This combination places him at high enough risk that primary prevention with a defibrillator is indicated. <div class="ec-src"><b>Source:</b> Ommen SR, Mital S, Burke MA, et al. 2020 AHA/ACC Guideline for the Diagnosis and Treatment of Patients With Hypertrophic Cardiomyopathy. Circulation 2020;142(25):e558-e631.</div></div></div> [[Try this question again->Hypertrophic cardiomyopathy risk - Prog]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Malnutrition assessment. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Infection is common and must be treated, but antibiotics without a structured feeding plan leave the underlying malnutrition uncorrected and do not prevent the electrolyte shifts that occur once feeding begins. <div class="ec-teach"><div class="th">What the findings point to</div> The correct answer is: Cautious phased refeeding, electrolyte monitoring, treat infection. One begin phased nutritional rehabilitation with micronutrient supplementation, treat intercurrent infection, and monitor electrolytes closely, advancing calories gradually. <div class="ec-src"><b>Source:</b> WHO guideline on the management of severe acute malnutrition; ASPEN refeeding consensus (2020).</div></div></div> [[Try this question again->Malnutrition assessment - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Pneumococcal prevention. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Surveillance imaging detects disease after it develops, delivers repeated radiation, and offers nothing preventive. The question asks how to lower his risk, which vaccination does and imaging does not. <div class="ec-teach"><div class="th">What the findings point to</div> The correct answer is: Administer a pneumococcal conjugate vaccine now. One administer a pneumococcal conjugate vaccine at this visit and document it. <div class="ec-src"><b>Source:</b> Kobayashi M, et al. Expanded Recommendations for Use of Pneumococcal Conjugate Vaccines Among Adults Aged ≥50 Years: ACIP, United States, 2024. MMWR Morb Mortal Wkly Rep 2025.</div></div></div> [[Try this question again->Pneumococcal prevention - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Surgical safety. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Site marking is one element of the protocol but is insufficient alone. The verification that catches errors is the collective pause in which every team member confirms patient, procedure, and site aloud before incision. <div class="ec-teach"><div class="th">What the findings point to</div> The correct answer is: Whole-team time-out: verify patient, procedure, site. The team pauses; everyone actively confirms the correct patient, the correct procedure, and the correct site before the incision is made. <div class="ec-src"><b>Source:</b> The Joint Commission. Universal Protocol for Preventing Wrong Site, Wrong Procedure, Wrong Person Surgery.</div></div></div> [[Try this question again->Surgical safety - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Goals of care. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> He has capacity and has raised the subject himself. Redirecting the decision to relatives removes it from the person entitled to make it and forfeits the opening he has just given one. <div class="ec-teach"><div class="th">What the findings point to</div> The correct answer is: Explore his values, discuss what CPR achieves, and recommend. One explore what he understands and what matters to him, give an honest account of his prognosis and what CPR would and would not achieve, make a clear recommendation, document the resulting order, and involve palliative care. <div class="ec-src"><b>Source:</b> AMA Code of Medical Ethics (withholding or withdrawing life-sustaining treatment); serious illness communication standards.</div></div></div> [[Try this question again->Goals of care - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Suicide risk. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Informal supervision by a relative is not a substitute for evaluation in a patient with a specific plan, firearm access, a prior attempt, and acute alcohol use. It also places an untrained person in an impossible position. <div class="ec-teach"><div class="th">What the findings point to</div> The correct answer is: Hold for psychiatric evaluation and restrict access to means. One keep him in a safe observation area with one-to-one supervision, arrange urgent psychiatric evaluation, initiate an involuntary hold when he tries to leave, and work with his friend and family on removing access to the firearm. <div class="ec-src"><b>Source:</b> APA Practice Guideline for the Assessment and Treatment of Patients With Suicidal Behaviors; SAMHSA suicide prevention guidance.</div></div></div> [[Try this question again->Suicide risk - Opening]] [[Start another case->Hub]]

<span class="ec-case-marker" hidden data-entry="Neonatal meningitis. Opening"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Oral therapy cannot achieve reliable cerebrospinal fluid concentrations and is never appropriate for suspected neonatal meningitis. This infant requires prompt parenteral coverage after cultures are obtained. <div class="ec-teach"><div class="th">What the findings point to</div> The correct answer is: IV ampicillin and cefotaxime, after cultures and LP. Blood cultures and a lumbar puncture are obtained without delay, and ampicillin with cefotaxime goes in immediately afterward. Cerebrospinal fluid shows a raised leukocyte count with neutrophil predominance, low glucose and raised protein. <div class="ec-src"><b>Source:</b> Tunkel AR, et al. IDSA Practice Guidelines for the Management of Bacterial Meningitis. Clin Infect Dis 2004;39(9):1267-1284; AAP Red Book, Meningitis.</div></div></div> [[Try this question again->Neonatal meningitis - Opening]] [[Start another case->Hub]]

<div class="ec-scene">Trauma bay · 21:15</div> A 24-year-old man is brought in after a motorcycle collision. There is a 4-cm wound over the mid-tibia with bone visible at its base. Temperature is 36.8°C, blood pressure is 124/76 mm Hg, pulse is 96/min, and respirations are 18/min. Dorsalis pedis and posterior tibial pulses are 2+ and symmetric. Sensation is intact. Radiography shows a transverse mid-shaft tibial fracture with mild comminution. His last tetanus booster was 4 years ago. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Bedside irrigation and closure in the emergency department->Open tibial fracture - Rx D1]] [[Immediate external fixation without debridement->Open tibial fracture - Rx D2]] [[Intravenous antibiotics and urgent operative irrigation and debridement->Open tibial fracture - Rx correct]] [[Splinting with outpatient orthopedic follow-up in 48 hours->Open tibial fracture - Rx D3]] [[Tetanus immune globulin and observation->Open tibial fracture - Rx D4]] [[Wound culture before starting antibiotics->Open tibial fracture - Rx D5]]

<span class="ec-case-marker" hidden data-entry="Open tibial fracture. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Intravenous antibiotics and urgent operative irrigation and debridement</div> An open fracture is a surgical emergency because the fracture site communicates with the environment. Antibiotics should be given as soon as possible after presentation, with a first-generation cephalosporin for lower-grade injuries, and the wound requires formal operative irrigation and debridement rather than bedside washout. Timing of antibiotics matters more for infection risk than timing of debridement, so the antibiotic should not wait for the operating room. His tetanus status is current at 4 years, so no booster is required. <div class="ec-src"><b>Source:</b> Hoff WS, Bonadies JA, Cachecho R, Dorlac WC. East Practice Management Guidelines Work Group: update to practice management guidelines for prophylactic antibiotic use in open fractures. J Trauma 2011;70(3):751-754.</div></div> [[Next case →->Compartment syndrome fasciotomy - Rx]] [[Start another case->Hub]] [[Restart this case->Open tibial fracture - Rx]]

<span class="ec-case-marker" hidden data-entry="Open tibial fracture. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Emergency department washout does not remove devitalized tissue or foreign material from the fracture site, and primary closure over a contaminated wound traps bacteria in a poorly vascularized bed. <div class="ec-teach"><div class="th">What the findings point to</div> An open fracture is a surgical emergency because the fracture site communicates with the environment. Antibiotics should be given as soon as possible after presentation, with a first-generation cephalosporin for lower-grade injuries, and the wound requires formal operative irrigation and debridement rather than bedside washout. Timing of antibiotics matters more for infection risk than timing of debridement, so the antibiotic should not wait for the operating room. His tetanus status is current at 4 years, so no booster is required. <div class="ec-src"><b>Source:</b> Hoff WS, Bonadies JA, Cachecho R, Dorlac WC. East Practice Management Guidelines Work Group: update to practice management guidelines for prophylactic antibiotic use in open fractures. J Trauma 2011;70(3):751-754.</div></div></div> [[Try this question again->Open tibial fracture - Rx]] [[Next case →->Compartment syndrome fasciotomy - Rx]] [[Start another case->Hub]] [[Restart this case->Open tibial fracture - Rx]]

<span class="ec-case-marker" hidden data-entry="Open tibial fracture. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> External fixation stabilizes the fracture but does nothing about contamination. Stabilization follows debridement rather than replacing it. <div class="ec-teach"><div class="th">What the findings point to</div> An open fracture is a surgical emergency because the fracture site communicates with the environment. Antibiotics should be given as soon as possible after presentation, with a first-generation cephalosporin for lower-grade injuries, and the wound requires formal operative irrigation and debridement rather than bedside washout. Timing of antibiotics matters more for infection risk than timing of debridement, so the antibiotic should not wait for the operating room. His tetanus status is current at 4 years, so no booster is required. <div class="ec-src"><b>Source:</b> Hoff WS, Bonadies JA, Cachecho R, Dorlac WC. East Practice Management Guidelines Work Group: update to practice management guidelines for prophylactic antibiotic use in open fractures. J Trauma 2011;70(3):751-754.</div></div></div> [[Try this question again->Open tibial fracture - Rx]] [[Next case →->Compartment syndrome fasciotomy - Rx]] [[Start another case->Hub]] [[Restart this case->Open tibial fracture - Rx]]

<span class="ec-case-marker" hidden data-entry="Open tibial fracture. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Delay of this magnitude in an open fracture produces deep infection and osteomyelitis rates that are unacceptable. <div class="ec-teach"><div class="th">What the findings point to</div> An open fracture is a surgical emergency because the fracture site communicates with the environment. Antibiotics should be given as soon as possible after presentation, with a first-generation cephalosporin for lower-grade injuries, and the wound requires formal operative irrigation and debridement rather than bedside washout. Timing of antibiotics matters more for infection risk than timing of debridement, so the antibiotic should not wait for the operating room. His tetanus status is current at 4 years, so no booster is required. <div class="ec-src"><b>Source:</b> Hoff WS, Bonadies JA, Cachecho R, Dorlac WC. East Practice Management Guidelines Work Group: update to practice management guidelines for prophylactic antibiotic use in open fractures. J Trauma 2011;70(3):751-754.</div></div></div> [[Try this question again->Open tibial fracture - Rx]] [[Next case →->Compartment syndrome fasciotomy - Rx]] [[Start another case->Hub]] [[Restart this case->Open tibial fracture - Rx]]

<span class="ec-case-marker" hidden data-entry="Open tibial fracture. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Immune globulin is for patients with an uncertain or incomplete primary series. He is 4 years from a booster, and observation ignores the surgical emergency. <div class="ec-teach"><div class="th">What the findings point to</div> An open fracture is a surgical emergency because the fracture site communicates with the environment. Antibiotics should be given as soon as possible after presentation, with a first-generation cephalosporin for lower-grade injuries, and the wound requires formal operative irrigation and debridement rather than bedside washout. Timing of antibiotics matters more for infection risk than timing of debridement, so the antibiotic should not wait for the operating room. His tetanus status is current at 4 years, so no booster is required. <div class="ec-src"><b>Source:</b> Hoff WS, Bonadies JA, Cachecho R, Dorlac WC. East Practice Management Guidelines Work Group: update to practice management guidelines for prophylactic antibiotic use in open fractures. J Trauma 2011;70(3):751-754.</div></div></div> [[Try this question again->Open tibial fracture - Rx]] [[Next case →->Compartment syndrome fasciotomy - Rx]] [[Start another case->Hub]] [[Restart this case->Open tibial fracture - Rx]]

<span class="ec-case-marker" hidden data-entry="Open tibial fracture. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Initial wound cultures correlate poorly with organisms that later cause infection, and waiting for them delays the intervention that most reduces infection risk. <div class="ec-teach"><div class="th">What the findings point to</div> An open fracture is a surgical emergency because the fracture site communicates with the environment. Antibiotics should be given as soon as possible after presentation, with a first-generation cephalosporin for lower-grade injuries, and the wound requires formal operative irrigation and debridement rather than bedside washout. Timing of antibiotics matters more for infection risk than timing of debridement, so the antibiotic should not wait for the operating room. His tetanus status is current at 4 years, so no booster is required. <div class="ec-src"><b>Source:</b> Hoff WS, Bonadies JA, Cachecho R, Dorlac WC. East Practice Management Guidelines Work Group: update to practice management guidelines for prophylactic antibiotic use in open fractures. J Trauma 2011;70(3):751-754.</div></div></div> [[Try this question again->Open tibial fracture - Rx]] [[Next case →->Compartment syndrome fasciotomy - Rx]] [[Start another case->Hub]] [[Restart this case->Open tibial fracture - Rx]]

<div class="ec-scene">Orthopedic ward · 03:40</div> A 19-year-old man is 8 hours post-reduction and casting of a tibial shaft fracture. He reports escalating pain that has required three doses of intravenous morphine. The cast has been split to skin and the padding released. Pain is severe on passive extension of the toes, and the anterior compartment is tense. Pulses remain palpable. Compartment pressures are 52 mm Hg in the anterior compartment; diastolic blood pressure is 68 mm Hg. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Doppler assessment of distal arterial flow->Compartment syndrome fasciotomy - Rx D4]] [[Elevation of the limb above heart level->Compartment syndrome fasciotomy - Rx D1]] [[Emergent four-compartment fasciotomy->Compartment syndrome fasciotomy - Rx correct]] [[Escalation of analgesia and reassessment in 2 hours->Compartment syndrome fasciotomy - Rx D2]] [[Removal of the cast and continued clinical observation->Compartment syndrome fasciotomy - Rx D5]] [[Repeat compartment pressure measurement in 4 hours->Compartment syndrome fasciotomy - Rx D3]]

<span class="ec-case-marker" hidden data-entry="Compartment syndrome fasciotomy. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Emergent four-compartment fasciotomy</div> The delta pressure, diastolic minus compartment pressure, is 16 mm Hg, below the 30 mm Hg threshold at which fasciotomy is indicated. Pain out of proportion and pain on passive stretch are the earliest and most reliable clinical findings. Palpable pulses do not exclude the diagnosis, because compartment pressure rises well above capillary perfusion pressure long before it occludes a major artery. Muscle tolerates roughly 4 to 6 hours of ischemia, so decompression is emergent. <div class="ec-src"><b>Source:</b> McQueen MM, Court-Brown CM. Compartment monitoring in tibial fractures: the pressure threshold for decompression. J Bone Joint Surg Br 1996;78(1):99-104.</div></div> [[Next case →->Septic arthritis drainage - Rx]] [[Start another case->Hub]] [[Restart this case->Compartment syndrome fasciotomy - Rx]]

<span class="ec-case-marker" hidden data-entry="Compartment syndrome fasciotomy. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Elevation reduces arterial inflow and narrows the perfusion gradient further. The limb should be kept at heart level, not raised, and this does not substitute for decompression. <div class="ec-teach"><div class="th">What the findings point to</div> The delta pressure, diastolic minus compartment pressure, is 16 mm Hg, below the 30 mm Hg threshold at which fasciotomy is indicated. Pain out of proportion and pain on passive stretch are the earliest and most reliable clinical findings. Palpable pulses do not exclude the diagnosis, because compartment pressure rises well above capillary perfusion pressure long before it occludes a major artery. Muscle tolerates roughly 4 to 6 hours of ischemia, so decompression is emergent. <div class="ec-src"><b>Source:</b> McQueen MM, Court-Brown CM. Compartment monitoring in tibial fractures: the pressure threshold for decompression. J Bone Joint Surg Br 1996;78(1):99-104.</div></div></div> [[Try this question again->Compartment syndrome fasciotomy - Rx]] [[Next case →->Septic arthritis drainage - Rx]] [[Start another case->Hub]] [[Restart this case->Compartment syndrome fasciotomy - Rx]]

<span class="ec-case-marker" hidden data-entry="Compartment syndrome fasciotomy. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Masking the cardinal symptom while ischemia continues converts a salvageable limb into a contracture or an amputation. <div class="ec-teach"><div class="th">What the findings point to</div> The delta pressure, diastolic minus compartment pressure, is 16 mm Hg, below the 30 mm Hg threshold at which fasciotomy is indicated. Pain out of proportion and pain on passive stretch are the earliest and most reliable clinical findings. Palpable pulses do not exclude the diagnosis, because compartment pressure rises well above capillary perfusion pressure long before it occludes a major artery. Muscle tolerates roughly 4 to 6 hours of ischemia, so decompression is emergent. <div class="ec-src"><b>Source:</b> McQueen MM, Court-Brown CM. Compartment monitoring in tibial fractures: the pressure threshold for decompression. J Bone Joint Surg Br 1996;78(1):99-104.</div></div></div> [[Try this question again->Compartment syndrome fasciotomy - Rx]] [[Next case →->Septic arthritis drainage - Rx]] [[Start another case->Hub]] [[Restart this case->Compartment syndrome fasciotomy - Rx]]

<span class="ec-case-marker" hidden data-entry="Compartment syndrome fasciotomy. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The measurement is already diagnostic. Repeating it wastes the window in which muscle remains viable. <div class="ec-teach"><div class="th">What the findings point to</div> The delta pressure, diastolic minus compartment pressure, is 16 mm Hg, below the 30 mm Hg threshold at which fasciotomy is indicated. Pain out of proportion and pain on passive stretch are the earliest and most reliable clinical findings. Palpable pulses do not exclude the diagnosis, because compartment pressure rises well above capillary perfusion pressure long before it occludes a major artery. Muscle tolerates roughly 4 to 6 hours of ischemia, so decompression is emergent. <div class="ec-src"><b>Source:</b> McQueen MM, Court-Brown CM. Compartment monitoring in tibial fractures: the pressure threshold for decompression. J Bone Joint Surg Br 1996;78(1):99-104.</div></div></div> [[Try this question again->Compartment syndrome fasciotomy - Rx]] [[Next case →->Septic arthritis drainage - Rx]] [[Start another case->Hub]] [[Restart this case->Compartment syndrome fasciotomy - Rx]]

<span class="ec-case-marker" hidden data-entry="Compartment syndrome fasciotomy. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Arterial flow is usually preserved in compartment syndrome. A normal Doppler study is falsely reassuring and has no role in the decision. <div class="ec-teach"><div class="th">What the findings point to</div> The delta pressure, diastolic minus compartment pressure, is 16 mm Hg, below the 30 mm Hg threshold at which fasciotomy is indicated. Pain out of proportion and pain on passive stretch are the earliest and most reliable clinical findings. Palpable pulses do not exclude the diagnosis, because compartment pressure rises well above capillary perfusion pressure long before it occludes a major artery. Muscle tolerates roughly 4 to 6 hours of ischemia, so decompression is emergent. <div class="ec-src"><b>Source:</b> McQueen MM, Court-Brown CM. Compartment monitoring in tibial fractures: the pressure threshold for decompression. J Bone Joint Surg Br 1996;78(1):99-104.</div></div></div> [[Try this question again->Compartment syndrome fasciotomy - Rx]] [[Next case →->Septic arthritis drainage - Rx]] [[Start another case->Hub]] [[Restart this case->Compartment syndrome fasciotomy - Rx]]

<span class="ec-case-marker" hidden data-entry="Compartment syndrome fasciotomy. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The cast has already been split to skin. Further observation once pressures are diagnostic is not an option. <div class="ec-teach"><div class="th">What the findings point to</div> The delta pressure, diastolic minus compartment pressure, is 16 mm Hg, below the 30 mm Hg threshold at which fasciotomy is indicated. Pain out of proportion and pain on passive stretch are the earliest and most reliable clinical findings. Palpable pulses do not exclude the diagnosis, because compartment pressure rises well above capillary perfusion pressure long before it occludes a major artery. Muscle tolerates roughly 4 to 6 hours of ischemia, so decompression is emergent. <div class="ec-src"><b>Source:</b> McQueen MM, Court-Brown CM. Compartment monitoring in tibial fractures: the pressure threshold for decompression. J Bone Joint Surg Br 1996;78(1):99-104.</div></div></div> [[Try this question again->Compartment syndrome fasciotomy - Rx]] [[Next case →->Septic arthritis drainage - Rx]] [[Start another case->Hub]] [[Restart this case->Compartment syndrome fasciotomy - Rx]]

<div class="ec-scene">Emergency department · 14:25</div> A 58-year-old man has 2 days of a hot, swollen, exquisitely painful right knee and is unable to bear weight. Temperature is 38.6°C, blood pressure is 132/78 mm Hg, and pulse is 104/min. Arthrocentesis yields turbid fluid with a leukocyte count of 78,000/mm3, 92% neutrophils, and Gram stain showing gram-positive cocci in clusters. Serum urate is 8.9 mg/dL. Blood cultures have been drawn. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Colchicine and indomethacin for presumed crystal arthropathy->Septic arthritis drainage - Rx D3]] [[Intraarticular corticosteroid injection for symptom control->Septic arthritis drainage - Rx D2]] [[Intravenous vancomycin alone without drainage->Septic arthritis drainage - Rx D1]] [[Magnetic resonance imaging of the knee before treatment->Septic arthritis drainage - Rx D5]] [[Oral cephalexin with outpatient orthopedic follow-up->Septic arthritis drainage - Rx D4]] [[Urgent joint drainage plus intravenous vancomycin->Septic arthritis drainage - Rx correct]]

<span class="ec-case-marker" hidden data-entry="Septic arthritis drainage. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Urgent joint drainage plus intravenous vancomycin</div> Bacterial arthritis destroys articular cartilage within days through leukocyte-derived proteases, so source control is required in addition to antibiotics. The joint must be drained, by arthroscopic or open washout for the knee or by repeated large-bore aspiration, and empiric coverage must include methicillin-resistant Staphylococcus aureus given gram-positive cocci in clusters. Antibiotics alone do not sterilize a closed infected space under pressure. The elevated urate is a distractor; hyperuricemia is common and does not exclude infection. <div class="ec-src"><b>Source:</b> Mathews CJ, Weston VC, Jones A, Field M, Coakley G. Bacterial septic arthritis in adults. Lancet 2010;375(9717):846-855.</div></div> [[Next case →->Necrotizing infection debridement - Rx]] [[Start another case->Hub]] [[Restart this case->Septic arthritis drainage - Rx]]

<span class="ec-case-marker" hidden data-entry="Septic arthritis drainage. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Antibiotic penetration into an infected joint with high bacterial burden and elevated intra-articular pressure is inadequate, and cartilage loss continues while the joint remains undrained. <div class="ec-teach"><div class="th">What the findings point to</div> Bacterial arthritis destroys articular cartilage within days through leukocyte-derived proteases, so source control is required in addition to antibiotics. The joint must be drained, by arthroscopic or open washout for the knee or by repeated large-bore aspiration, and empiric coverage must include methicillin-resistant Staphylococcus aureus given gram-positive cocci in clusters. Antibiotics alone do not sterilize a closed infected space under pressure. The elevated urate is a distractor; hyperuricemia is common and does not exclude infection. <div class="ec-src"><b>Source:</b> Mathews CJ, Weston VC, Jones A, Field M, Coakley G. Bacterial septic arthritis in adults. Lancet 2010;375(9717):846-855.</div></div></div> [[Try this question again->Septic arthritis drainage - Rx]] [[Next case →->Necrotizing infection debridement - Rx]] [[Start another case->Hub]] [[Restart this case->Septic arthritis drainage - Rx]]

<span class="ec-case-marker" hidden data-entry="Septic arthritis drainage. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Injecting steroid into an infected joint suppresses local immunity and accelerates destruction. It is contraindicated. <div class="ec-teach"><div class="th">What the findings point to</div> Bacterial arthritis destroys articular cartilage within days through leukocyte-derived proteases, so source control is required in addition to antibiotics. The joint must be drained, by arthroscopic or open washout for the knee or by repeated large-bore aspiration, and empiric coverage must include methicillin-resistant Staphylococcus aureus given gram-positive cocci in clusters. Antibiotics alone do not sterilize a closed infected space under pressure. The elevated urate is a distractor; hyperuricemia is common and does not exclude infection. <div class="ec-src"><b>Source:</b> Mathews CJ, Weston VC, Jones A, Field M, Coakley G. Bacterial septic arthritis in adults. Lancet 2010;375(9717):846-855.</div></div></div> [[Try this question again->Septic arthritis drainage - Rx]] [[Next case →->Necrotizing infection debridement - Rx]] [[Start another case->Hub]] [[Restart this case->Septic arthritis drainage - Rx]]

<span class="ec-case-marker" hidden data-entry="Septic arthritis drainage. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Gram-positive cocci on Gram stain establish infection. Treating this as gout while bacteria destroy the joint is the most damaging option here. <div class="ec-teach"><div class="th">What the findings point to</div> Bacterial arthritis destroys articular cartilage within days through leukocyte-derived proteases, so source control is required in addition to antibiotics. The joint must be drained, by arthroscopic or open washout for the knee or by repeated large-bore aspiration, and empiric coverage must include methicillin-resistant Staphylococcus aureus given gram-positive cocci in clusters. Antibiotics alone do not sterilize a closed infected space under pressure. The elevated urate is a distractor; hyperuricemia is common and does not exclude infection. <div class="ec-src"><b>Source:</b> Mathews CJ, Weston VC, Jones A, Field M, Coakley G. Bacterial septic arthritis in adults. Lancet 2010;375(9717):846-855.</div></div></div> [[Try this question again->Septic arthritis drainage - Rx]] [[Next case →->Necrotizing infection debridement - Rx]] [[Start another case->Hub]] [[Restart this case->Septic arthritis drainage - Rx]]

<span class="ec-case-marker" hidden data-entry="Septic arthritis drainage. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Oral therapy achieves inadequate synovial concentrations for an established septic joint, and outpatient management forfeits source control. <div class="ec-teach"><div class="th">What the findings point to</div> Bacterial arthritis destroys articular cartilage within days through leukocyte-derived proteases, so source control is required in addition to antibiotics. The joint must be drained, by arthroscopic or open washout for the knee or by repeated large-bore aspiration, and empiric coverage must include methicillin-resistant Staphylococcus aureus given gram-positive cocci in clusters. Antibiotics alone do not sterilize a closed infected space under pressure. The elevated urate is a distractor; hyperuricemia is common and does not exclude infection. <div class="ec-src"><b>Source:</b> Mathews CJ, Weston VC, Jones A, Field M, Coakley G. Bacterial septic arthritis in adults. Lancet 2010;375(9717):846-855.</div></div></div> [[Try this question again->Septic arthritis drainage - Rx]] [[Next case →->Necrotizing infection debridement - Rx]] [[Start another case->Hub]] [[Restart this case->Septic arthritis drainage - Rx]]

<span class="ec-case-marker" hidden data-entry="Septic arthritis drainage. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Imaging may define extent later but adds hours of delay to a diagnosis already made by synovial fluid analysis. <div class="ec-teach"><div class="th">What the findings point to</div> Bacterial arthritis destroys articular cartilage within days through leukocyte-derived proteases, so source control is required in addition to antibiotics. The joint must be drained, by arthroscopic or open washout for the knee or by repeated large-bore aspiration, and empiric coverage must include methicillin-resistant Staphylococcus aureus given gram-positive cocci in clusters. Antibiotics alone do not sterilize a closed infected space under pressure. The elevated urate is a distractor; hyperuricemia is common and does not exclude infection. <div class="ec-src"><b>Source:</b> Mathews CJ, Weston VC, Jones A, Field M, Coakley G. Bacterial septic arthritis in adults. Lancet 2010;375(9717):846-855.</div></div></div> [[Try this question again->Septic arthritis drainage - Rx]] [[Next case →->Necrotizing infection debridement - Rx]] [[Start another case->Hub]] [[Restart this case->Septic arthritis drainage - Rx]]

<div class="ec-scene">Emergency department · 23:33</div> A 61-year-old man with type 2 diabetes mellitus has 18 hours of rapidly worsening left thigh pain. Temperature is 39.1°C, blood pressure is 88/54 mm Hg, pulse is 128/min, and respirations are 26/min. The skin is dusky with a small area of bullae, and the tenderness extends far beyond the visible discoloration. Crepitus is present. Leukocyte count is 24,000/mm3, sodium is 128 mEq/L, creatinine is 2.1 mg/dL, and lactate is 4.6 mmol/L. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Bedside incisional biopsy for frozen section->Necrotizing infection debridement - Rx D3]] [[Broad-spectrum antibiotics and reassessment in 6 hours->Necrotizing infection debridement - Rx D2]] [[Calculation of the LRINEC score to determine disposition->Necrotizing infection debridement - Rx D5]] [[CT of the thigh with contrast before surgical consultation->Necrotizing infection debridement - Rx D1]] [[Hyperbaric oxygen therapy->Necrotizing infection debridement - Rx D4]] [[Immediate surgical exploration and debridement->Necrotizing infection debridement - Rx correct]]

<span class="ec-case-marker" hidden data-entry="Necrotizing infection debridement. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Immediate surgical exploration and debridement</div> Necrotizing soft tissue infection is a surgical diagnosis and a surgical emergency. Pain out of proportion to visible findings, crepitus, bullae, hemodynamic instability, and hyponatremia together make the diagnosis clinically, and time to debridement is the strongest modifiable determinant of survival. Broad-spectrum antibiotics including clindamycin for toxin suppression and fluid resuscitation run in parallel, not before. Imaging is for equivocal cases and this case is not equivocal. <div class="ec-src"><b>Source:</b> Stevens DL, Bryant AE. Necrotizing Soft-Tissue Infections. N Engl J Med 2017;377(23):2253-2265.</div></div> [[Next case →->Hip fracture timing - Rx]] [[Start another case->Hub]] [[Restart this case->Necrotizing infection debridement - Rx]]

<span class="ec-case-marker" hidden data-entry="Necrotizing infection debridement. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Imaging can support an uncertain diagnosis but delays definitive care in a patient who already has crepitus, systemic toxicity, and pain out of proportion. <div class="ec-teach"><div class="th">What the findings point to</div> Necrotizing soft tissue infection is a surgical diagnosis and a surgical emergency. Pain out of proportion to visible findings, crepitus, bullae, hemodynamic instability, and hyponatremia together make the diagnosis clinically, and time to debridement is the strongest modifiable determinant of survival. Broad-spectrum antibiotics including clindamycin for toxin suppression and fluid resuscitation run in parallel, not before. Imaging is for equivocal cases and this case is not equivocal. <div class="ec-src"><b>Source:</b> Stevens DL, Bryant AE. Necrotizing Soft-Tissue Infections. N Engl J Med 2017;377(23):2253-2265.</div></div></div> [[Try this question again->Necrotizing infection debridement - Rx]] [[Next case →->Hip fracture timing - Rx]] [[Start another case->Hub]] [[Restart this case->Necrotizing infection debridement - Rx]]

<span class="ec-case-marker" hidden data-entry="Necrotizing infection debridement. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Antibiotics cannot penetrate necrotic, avascular tissue. 6 hours of observation in a patient with a lactate of 4.6 mmol/L is fatal delay. <div class="ec-teach"><div class="th">What the findings point to</div> Necrotizing soft tissue infection is a surgical diagnosis and a surgical emergency. Pain out of proportion to visible findings, crepitus, bullae, hemodynamic instability, and hyponatremia together make the diagnosis clinically, and time to debridement is the strongest modifiable determinant of survival. Broad-spectrum antibiotics including clindamycin for toxin suppression and fluid resuscitation run in parallel, not before. Imaging is for equivocal cases and this case is not equivocal. <div class="ec-src"><b>Source:</b> Stevens DL, Bryant AE. Necrotizing Soft-Tissue Infections. N Engl J Med 2017;377(23):2253-2265.</div></div></div> [[Try this question again->Necrotizing infection debridement - Rx]] [[Next case →->Hip fracture timing - Rx]] [[Start another case->Hub]] [[Restart this case->Necrotizing infection debridement - Rx]]

<span class="ec-case-marker" hidden data-entry="Necrotizing infection debridement. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Tissue diagnosis is obtained in the operating room during debridement, not as a separate preliminary step. <div class="ec-teach"><div class="th">What the findings point to</div> Necrotizing soft tissue infection is a surgical diagnosis and a surgical emergency. Pain out of proportion to visible findings, crepitus, bullae, hemodynamic instability, and hyponatremia together make the diagnosis clinically, and time to debridement is the strongest modifiable determinant of survival. Broad-spectrum antibiotics including clindamycin for toxin suppression and fluid resuscitation run in parallel, not before. Imaging is for equivocal cases and this case is not equivocal. <div class="ec-src"><b>Source:</b> Stevens DL, Bryant AE. Necrotizing Soft-Tissue Infections. N Engl J Med 2017;377(23):2253-2265.</div></div></div> [[Try this question again->Necrotizing infection debridement - Rx]] [[Next case →->Hip fracture timing - Rx]] [[Start another case->Hub]] [[Restart this case->Necrotizing infection debridement - Rx]]

<span class="ec-case-marker" hidden data-entry="Necrotizing infection debridement. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Hyperbaric oxygen is an adjunct considered after debridement in selected cases. It is never the initial intervention. <div class="ec-teach"><div class="th">What the findings point to</div> Necrotizing soft tissue infection is a surgical diagnosis and a surgical emergency. Pain out of proportion to visible findings, crepitus, bullae, hemodynamic instability, and hyponatremia together make the diagnosis clinically, and time to debridement is the strongest modifiable determinant of survival. Broad-spectrum antibiotics including clindamycin for toxin suppression and fluid resuscitation run in parallel, not before. Imaging is for equivocal cases and this case is not equivocal. <div class="ec-src"><b>Source:</b> Stevens DL, Bryant AE. Necrotizing Soft-Tissue Infections. N Engl J Med 2017;377(23):2253-2265.</div></div></div> [[Try this question again->Necrotizing infection debridement - Rx]] [[Next case →->Hip fracture timing - Rx]] [[Start another case->Hub]] [[Restart this case->Necrotizing infection debridement - Rx]]

<span class="ec-case-marker" hidden data-entry="Necrotizing infection debridement. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Scoring systems were designed to raise suspicion in ambiguous presentations. A low score does not exclude the diagnosis and this presentation needs no score. <div class="ec-teach"><div class="th">What the findings point to</div> Necrotizing soft tissue infection is a surgical diagnosis and a surgical emergency. Pain out of proportion to visible findings, crepitus, bullae, hemodynamic instability, and hyponatremia together make the diagnosis clinically, and time to debridement is the strongest modifiable determinant of survival. Broad-spectrum antibiotics including clindamycin for toxin suppression and fluid resuscitation run in parallel, not before. Imaging is for equivocal cases and this case is not equivocal. <div class="ec-src"><b>Source:</b> Stevens DL, Bryant AE. Necrotizing Soft-Tissue Infections. N Engl J Med 2017;377(23):2253-2265.</div></div></div> [[Try this question again->Necrotizing infection debridement - Rx]] [[Next case →->Hip fracture timing - Rx]] [[Start another case->Hub]] [[Restart this case->Necrotizing infection debridement - Rx]]

<div class="ec-scene">Emergency department · 16:10</div> An 82-year-old woman fell at home and has a displaced femoral neck fracture. She lived independently and walked without aids. Temperature is 36.9°C, blood pressure is 138/80 mm Hg, and pulse is 84/min. She takes amlodipine and atorvastatin. Electrocardiography shows sinus rhythm. Hemoglobin is 12.1 g/dL, creatinine is 0.9 mg/dL, and troponin is undetectable. She has no chest pain and no signs of heart failure. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Delay of surgery for 72 hours of medical optimization->Hip fracture timing - Rx D3]] [[Echocardiography before proceeding to the operating room->Hip fracture timing - Rx D4]] [[Preoperative stress testing before clearance for surgery->Hip fracture timing - Rx D1]] [[Surgical fixation within 24 hours of presentation->Hip fracture timing - Rx correct]] [[Traction and non-operative management with early mobilization->Hip fracture timing - Rx D2]] [[Transfusion to a hemoglobin above 10 g/dL before surgery->Hip fracture timing - Rx D5]]

<span class="ec-case-marker" hidden data-entry="Hip fracture timing. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Surgical fixation within 24 hours of presentation</div> Observational cohort data and a large meta-analysis show that hip fracture surgery performed within about 24 to 48 hours of presentation is associated with lower mortality and fewer major complications, including pneumonia and pressure ulcers, than later surgery. She has no active cardiac, respiratory, or metabolic condition that would be improved by delay, so the correct decision is to proceed within 24 hours rather than to seek further clearance. Preoperative optimization benefits only patients with a specific correctable abnormality. <div class="ec-src"><b>Source:</b> Simunovic N, Devereaux PJ, Sprague S, et al. Effect of early surgery after hip fracture on mortality and complications: systematic review and meta-analysis. CMAJ 2010;182(15):1609-1616.</div></div> [[Next case →->Cauda equina decompression - Rx]] [[Start another case->Hub]] [[Restart this case->Hip fracture timing - Rx]]

<span class="ec-case-marker" hidden data-entry="Hip fracture timing. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Routine noninvasive cardiac testing in a patient with no active cardiac symptoms delays surgery and does not improve outcome. <div class="ec-teach"><div class="th">What the findings point to</div> Observational cohort data and a large meta-analysis show that hip fracture surgery performed within about 24 to 48 hours of presentation is associated with lower mortality and fewer major complications, including pneumonia and pressure ulcers, than later surgery. She has no active cardiac, respiratory, or metabolic condition that would be improved by delay, so the correct decision is to proceed within 24 hours rather than to seek further clearance. Preoperative optimization benefits only patients with a specific correctable abnormality. <div class="ec-src"><b>Source:</b> Simunovic N, Devereaux PJ, Sprague S, et al. Effect of early surgery after hip fracture on mortality and complications: systematic review and meta-analysis. CMAJ 2010;182(15):1609-1616.</div></div></div> [[Try this question again->Hip fracture timing - Rx]] [[Next case →->Cauda equina decompression - Rx]] [[Start another case->Hub]] [[Restart this case->Hip fracture timing - Rx]]

<span class="ec-case-marker" hidden data-entry="Hip fracture timing. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Non-operative management of a displaced femoral neck fracture in an ambulatory patient produces nonunion, chronic pain, and high mortality. <div class="ec-teach"><div class="th">What the findings point to</div> Observational cohort data and a large meta-analysis show that hip fracture surgery performed within about 24 to 48 hours of presentation is associated with lower mortality and fewer major complications, including pneumonia and pressure ulcers, than later surgery. She has no active cardiac, respiratory, or metabolic condition that would be improved by delay, so the correct decision is to proceed within 24 hours rather than to seek further clearance. Preoperative optimization benefits only patients with a specific correctable abnormality. <div class="ec-src"><b>Source:</b> Simunovic N, Devereaux PJ, Sprague S, et al. Effect of early surgery after hip fracture on mortality and complications: systematic review and meta-analysis. CMAJ 2010;182(15):1609-1616.</div></div></div> [[Try this question again->Hip fracture timing - Rx]] [[Next case →->Cauda equina decompression - Rx]] [[Start another case->Hub]] [[Restart this case->Hip fracture timing - Rx]]

<span class="ec-case-marker" hidden data-entry="Hip fracture timing. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Optimization without a defined correctable problem is simply delay, and each day of delay increases mortality. <div class="ec-teach"><div class="th">What the findings point to</div> Observational cohort data and a large meta-analysis show that hip fracture surgery performed within about 24 to 48 hours of presentation is associated with lower mortality and fewer major complications, including pneumonia and pressure ulcers, than later surgery. She has no active cardiac, respiratory, or metabolic condition that would be improved by delay, so the correct decision is to proceed within 24 hours rather than to seek further clearance. Preoperative optimization benefits only patients with a specific correctable abnormality. <div class="ec-src"><b>Source:</b> Simunovic N, Devereaux PJ, Sprague S, et al. Effect of early surgery after hip fracture on mortality and complications: systematic review and meta-analysis. CMAJ 2010;182(15):1609-1616.</div></div></div> [[Try this question again->Hip fracture timing - Rx]] [[Next case →->Cauda equina decompression - Rx]] [[Start another case->Hub]] [[Restart this case->Hip fracture timing - Rx]]

<span class="ec-case-marker" hidden data-entry="Hip fracture timing. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Echocardiography is indicated for a new murmur, unexplained dyspnea, or suspected valvular disease. None is present. <div class="ec-teach"><div class="th">What the findings point to</div> Observational cohort data and a large meta-analysis show that hip fracture surgery performed within about 24 to 48 hours of presentation is associated with lower mortality and fewer major complications, including pneumonia and pressure ulcers, than later surgery. She has no active cardiac, respiratory, or metabolic condition that would be improved by delay, so the correct decision is to proceed within 24 hours rather than to seek further clearance. Preoperative optimization benefits only patients with a specific correctable abnormality. <div class="ec-src"><b>Source:</b> Simunovic N, Devereaux PJ, Sprague S, et al. Effect of early surgery after hip fracture on mortality and complications: systematic review and meta-analysis. CMAJ 2010;182(15):1609-1616.</div></div></div> [[Try this question again->Hip fracture timing - Rx]] [[Next case →->Cauda equina decompression - Rx]] [[Start another case->Hub]] [[Restart this case->Hip fracture timing - Rx]]

<span class="ec-case-marker" hidden data-entry="Hip fracture timing. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A hemoglobin of 12.1 g/dL requires no transfusion, and liberal preoperative transfusion has not improved outcomes in hip fracture. <div class="ec-teach"><div class="th">What the findings point to</div> Observational cohort data and a large meta-analysis show that hip fracture surgery performed within about 24 to 48 hours of presentation is associated with lower mortality and fewer major complications, including pneumonia and pressure ulcers, than later surgery. She has no active cardiac, respiratory, or metabolic condition that would be improved by delay, so the correct decision is to proceed within 24 hours rather than to seek further clearance. Preoperative optimization benefits only patients with a specific correctable abnormality. <div class="ec-src"><b>Source:</b> Simunovic N, Devereaux PJ, Sprague S, et al. Effect of early surgery after hip fracture on mortality and complications: systematic review and meta-analysis. CMAJ 2010;182(15):1609-1616.</div></div></div> [[Try this question again->Hip fracture timing - Rx]] [[Next case →->Cauda equina decompression - Rx]] [[Start another case->Hub]] [[Restart this case->Hip fracture timing - Rx]]

<div class="ec-scene">Emergency department · 05:52</div> A 46-year-old man has 12 hours of severe low back pain radiating down both legs after lifting. He reports numbness in the perineum and has not passed urine since the previous evening. Temperature is 36.7°C, blood pressure is 134/82 mm Hg, and pulse is 88/min. Bladder scan shows 780 mL of retained urine. Perianal sensation is reduced and anal tone is decreased. Strength is 4/5 in both ankles. MRI shows a large central disc herniation at L4-L5 compressing the cauda equina. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Bed rest, analgesia, and repeat examination in 24 hours->Cauda equina decompression - Rx D4]] [[CT-guided epidural steroid injection->Cauda equina decompression - Rx D3]] [[Emergent surgical decompression->Cauda equina decompression - Rx correct]] [[High-dose intravenous dexamethasone and observation->Cauda equina decompression - Rx D2]] [[Repeat MRI with contrast to exclude an infectious cause->Cauda equina decompression - Rx D5]] [[Urinary catheterization and surgery on the next elective list->Cauda equina decompression - Rx D1]]

<span class="ec-case-marker" hidden data-entry="Cauda equina decompression. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Emergent surgical decompression</div> Cauda equina syndrome with urinary retention and saddle anesthesia is a surgical emergency. Recovery of bladder and bowel function correlates strongly with time to decompression, and the presence of established retention marks a transition to a worse prognostic category, which makes further delay more, not less, consequential. Catheterization relieves the bladder but does not address the compression. <div class="ec-src"><b>Source:</b> Todd NV, Dickson RA. Standards of care in cauda equina syndrome. Br J Neurosurg 2016;30(5):518-522.</div></div> [[Next case →->Shoulder dislocation reduction - Rx]] [[Start another case->Hub]] [[Restart this case->Cauda equina decompression - Rx]]

<span class="ec-case-marker" hidden data-entry="Cauda equina decompression. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Catheterization treats a symptom. Deferring decompression to an elective list after retention has developed risks permanent sphincter dysfunction. <div class="ec-teach"><div class="th">What the findings point to</div> Cauda equina syndrome with urinary retention and saddle anesthesia is a surgical emergency. Recovery of bladder and bowel function correlates strongly with time to decompression, and the presence of established retention marks a transition to a worse prognostic category, which makes further delay more, not less, consequential. Catheterization relieves the bladder but does not address the compression. <div class="ec-src"><b>Source:</b> Todd NV, Dickson RA. Standards of care in cauda equina syndrome. Br J Neurosurg 2016;30(5):518-522.</div></div></div> [[Try this question again->Cauda equina decompression - Rx]] [[Next case →->Shoulder dislocation reduction - Rx]] [[Start another case->Hub]] [[Restart this case->Cauda equina decompression - Rx]]

<span class="ec-case-marker" hidden data-entry="Cauda equina decompression. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Corticosteroids have a role in malignant cord compression, not in acute mechanical compression from a disc, and observation forfeits the recovery window. <div class="ec-teach"><div class="th">What the findings point to</div> Cauda equina syndrome with urinary retention and saddle anesthesia is a surgical emergency. Recovery of bladder and bowel function correlates strongly with time to decompression, and the presence of established retention marks a transition to a worse prognostic category, which makes further delay more, not less, consequential. Catheterization relieves the bladder but does not address the compression. <div class="ec-src"><b>Source:</b> Todd NV, Dickson RA. Standards of care in cauda equina syndrome. Br J Neurosurg 2016;30(5):518-522.</div></div></div> [[Try this question again->Cauda equina decompression - Rx]] [[Next case →->Shoulder dislocation reduction - Rx]] [[Start another case->Hub]] [[Restart this case->Cauda equina decompression - Rx]]

<span class="ec-case-marker" hidden data-entry="Cauda equina decompression. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Epidural steroid is for radicular pain without neurologic emergency. It does not decompress the canal. <div class="ec-teach"><div class="th">What the findings point to</div> Cauda equina syndrome with urinary retention and saddle anesthesia is a surgical emergency. Recovery of bladder and bowel function correlates strongly with time to decompression, and the presence of established retention marks a transition to a worse prognostic category, which makes further delay more, not less, consequential. Catheterization relieves the bladder but does not address the compression. <div class="ec-src"><b>Source:</b> Todd NV, Dickson RA. Standards of care in cauda equina syndrome. Br J Neurosurg 2016;30(5):518-522.</div></div></div> [[Try this question again->Cauda equina decompression - Rx]] [[Next case →->Shoulder dislocation reduction - Rx]] [[Start another case->Hub]] [[Restart this case->Cauda equina decompression - Rx]]

<span class="ec-case-marker" hidden data-entry="Cauda equina decompression. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Twenty-4 hours of observation in established cauda equina syndrome is the decision most likely to leave him permanently incontinent. <div class="ec-teach"><div class="th">What the findings point to</div> Cauda equina syndrome with urinary retention and saddle anesthesia is a surgical emergency. Recovery of bladder and bowel function correlates strongly with time to decompression, and the presence of established retention marks a transition to a worse prognostic category, which makes further delay more, not less, consequential. Catheterization relieves the bladder but does not address the compression. <div class="ec-src"><b>Source:</b> Todd NV, Dickson RA. Standards of care in cauda equina syndrome. Br J Neurosurg 2016;30(5):518-522.</div></div></div> [[Try this question again->Cauda equina decompression - Rx]] [[Next case →->Shoulder dislocation reduction - Rx]] [[Start another case->Hub]] [[Restart this case->Cauda equina decompression - Rx]]

<span class="ec-case-marker" hidden data-entry="Cauda equina decompression. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The MRI already demonstrates the compressive lesion. He has no fever or risk factors for epidural abscess. <div class="ec-teach"><div class="th">What the findings point to</div> Cauda equina syndrome with urinary retention and saddle anesthesia is a surgical emergency. Recovery of bladder and bowel function correlates strongly with time to decompression, and the presence of established retention marks a transition to a worse prognostic category, which makes further delay more, not less, consequential. Catheterization relieves the bladder but does not address the compression. <div class="ec-src"><b>Source:</b> Todd NV, Dickson RA. Standards of care in cauda equina syndrome. Br J Neurosurg 2016;30(5):518-522.</div></div></div> [[Try this question again->Cauda equina decompression - Rx]] [[Next case →->Shoulder dislocation reduction - Rx]] [[Start another case->Hub]] [[Restart this case->Cauda equina decompression - Rx]]

<div class="ec-scene">Emergency department · 19:05</div> A 27-year-old man fell on an outstretched arm 40 minutes ago. He holds the right arm slightly abducted and externally rotated and resists all movement. There is loss of the normal deltoid contour. Temperature is 36.8°C, blood pressure is 128/74 mm Hg, and pulse is 92/min. Sensation over the lateral deltoid is intact and the radial pulse is 2+. Radiography confirms an anterior glenohumeral dislocation without fracture. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Closed reduction with procedural sedation->Shoulder dislocation reduction - Rx correct]] [[Immediate open reduction in the operating room->Shoulder dislocation reduction - Rx D3]] [[Intraarticular lidocaine alone without reassessment of the nerve->Shoulder dislocation reduction - Rx D4]] [[MRI of the shoulder before any reduction attempt->Shoulder dislocation reduction - Rx D1]] [[Physical therapy referral for strengthening before reduction->Shoulder dislocation reduction - Rx D5]] [[Sling immobilization and orthopedic follow-up in 1 week->Shoulder dislocation reduction - Rx D2]]

<span class="ec-case-marker" hidden data-entry="Shoulder dislocation reduction. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Closed reduction with procedural sedation</div> An uncomplicated anterior dislocation without associated fracture is reduced promptly, because the longer the humeral head remains dislocated the more muscle spasm develops and the harder reduction becomes. Neurovascular status, in particular axillary nerve sensation over the lateral deltoid, is documented before and after. Post-reduction radiographs confirm position, and the arm is immobilized in a sling. <div class="ec-src"><b>Source:</b> Cunningham NJ. Techniques for reduction of anteroinferior shoulder dislocation. Emerg Med Australas 2005;17(5-6):463-471.</div></div> [[Next case →->Diabetic foot osteomyelitis - Rx]] [[Start another case->Hub]] [[Restart this case->Shoulder dislocation reduction - Rx]]

<span class="ec-case-marker" hidden data-entry="Shoulder dislocation reduction. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Advanced imaging delays reduction for hours and adds nothing when plain films have already excluded fracture. <div class="ec-teach"><div class="th">What the findings point to</div> An uncomplicated anterior dislocation without associated fracture is reduced promptly, because the longer the humeral head remains dislocated the more muscle spasm develops and the harder reduction becomes. Neurovascular status, in particular axillary nerve sensation over the lateral deltoid, is documented before and after. Post-reduction radiographs confirm position, and the arm is immobilized in a sling. <div class="ec-src"><b>Source:</b> Cunningham NJ. Techniques for reduction of anteroinferior shoulder dislocation. Emerg Med Australas 2005;17(5-6):463-471.</div></div></div> [[Try this question again->Shoulder dislocation reduction - Rx]] [[Next case →->Diabetic foot osteomyelitis - Rx]] [[Start another case->Hub]] [[Restart this case->Shoulder dislocation reduction - Rx]]

<span class="ec-case-marker" hidden data-entry="Shoulder dislocation reduction. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Leaving a shoulder dislocated for a week risks axillary nerve injury, cartilage damage, and a reduction that can no longer be achieved closed. <div class="ec-teach"><div class="th">What the findings point to</div> An uncomplicated anterior dislocation without associated fracture is reduced promptly, because the longer the humeral head remains dislocated the more muscle spasm develops and the harder reduction becomes. Neurovascular status, in particular axillary nerve sensation over the lateral deltoid, is documented before and after. Post-reduction radiographs confirm position, and the arm is immobilized in a sling. <div class="ec-src"><b>Source:</b> Cunningham NJ. Techniques for reduction of anteroinferior shoulder dislocation. Emerg Med Australas 2005;17(5-6):463-471.</div></div></div> [[Try this question again->Shoulder dislocation reduction - Rx]] [[Next case →->Diabetic foot osteomyelitis - Rx]] [[Start another case->Hub]] [[Restart this case->Shoulder dislocation reduction - Rx]]

<span class="ec-case-marker" hidden data-entry="Shoulder dislocation reduction. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Open reduction is reserved for irreducible dislocations, associated displaced fractures, or vascular injury, none of which is present. <div class="ec-teach"><div class="th">What the findings point to</div> An uncomplicated anterior dislocation without associated fracture is reduced promptly, because the longer the humeral head remains dislocated the more muscle spasm develops and the harder reduction becomes. Neurovascular status, in particular axillary nerve sensation over the lateral deltoid, is documented before and after. Post-reduction radiographs confirm position, and the arm is immobilized in a sling. <div class="ec-src"><b>Source:</b> Cunningham NJ. Techniques for reduction of anteroinferior shoulder dislocation. Emerg Med Australas 2005;17(5-6):463-471.</div></div></div> [[Try this question again->Shoulder dislocation reduction - Rx]] [[Next case →->Diabetic foot osteomyelitis - Rx]] [[Start another case->Hub]] [[Restart this case->Shoulder dislocation reduction - Rx]]

<span class="ec-case-marker" hidden data-entry="Shoulder dislocation reduction. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Intraarticular anesthesia is a reasonable alternative to sedation, but documenting axillary nerve function before and after reduction is not optional. <div class="ec-teach"><div class="th">What the findings point to</div> An uncomplicated anterior dislocation without associated fracture is reduced promptly, because the longer the humeral head remains dislocated the more muscle spasm develops and the harder reduction becomes. Neurovascular status, in particular axillary nerve sensation over the lateral deltoid, is documented before and after. Post-reduction radiographs confirm position, and the arm is immobilized in a sling. <div class="ec-src"><b>Source:</b> Cunningham NJ. Techniques for reduction of anteroinferior shoulder dislocation. Emerg Med Australas 2005;17(5-6):463-471.</div></div></div> [[Try this question again->Shoulder dislocation reduction - Rx]] [[Next case →->Diabetic foot osteomyelitis - Rx]] [[Start another case->Hub]] [[Restart this case->Shoulder dislocation reduction - Rx]]

<span class="ec-case-marker" hidden data-entry="Shoulder dislocation reduction. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Rehabilitation follows reduction. It has no role in an actively dislocated joint. <div class="ec-teach"><div class="th">What the findings point to</div> An uncomplicated anterior dislocation without associated fracture is reduced promptly, because the longer the humeral head remains dislocated the more muscle spasm develops and the harder reduction becomes. Neurovascular status, in particular axillary nerve sensation over the lateral deltoid, is documented before and after. Post-reduction radiographs confirm position, and the arm is immobilized in a sling. <div class="ec-src"><b>Source:</b> Cunningham NJ. Techniques for reduction of anteroinferior shoulder dislocation. Emerg Med Australas 2005;17(5-6):463-471.</div></div></div> [[Try this question again->Shoulder dislocation reduction - Rx]] [[Next case →->Diabetic foot osteomyelitis - Rx]] [[Start another case->Hub]] [[Restart this case->Shoulder dislocation reduction - Rx]]

<div class="ec-scene">Vascular surgery clinic · 11:20</div> A 64-year-old man with type 2 diabetes mellitus has a plantar ulcer over the third metatarsal head present for 3 months. A sterile probe reaches bone. Temperature is 37.2°C and the foot is warm with palpable pedal pulses and an ankle-brachial index of 1.0. Leukocyte count is 9,800/mm3, erythrocyte sedimentation rate is 82 mm/h, and radiography shows cortical erosion of the third metatarsal head. There is no systemic toxicity and no spreading cellulitis. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[6 weeks of intravenous vancomycin without tissue diagnosis->Diabetic foot osteomyelitis - Rx D3]] [[Bone biopsy for culture before starting antibiotics->Diabetic foot osteomyelitis - Rx correct]] [[Empiric oral antibiotics guided by a superficial wound swab->Diabetic foot osteomyelitis - Rx D1]] [[Hyperbaric oxygen therapy as primary treatment->Diabetic foot osteomyelitis - Rx D5]] [[Immediate transmetatarsal amputation->Diabetic foot osteomyelitis - Rx D2]] [[Revascularization of the affected limb->Diabetic foot osteomyelitis - Rx D4]]

<span class="ec-case-marker" hidden data-entry="Diabetic foot osteomyelitis. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Bone biopsy for culture before starting antibiotics</div> A positive probe-to-bone test with radiographic erosion and an erythrocyte sedimentation rate above 70 mm/h makes osteomyelitis very likely, but the organism determines a prolonged and toxic antibiotic course. Because he has no systemic toxicity and no spreading infection, there is time to obtain bone for culture before treatment, and doing so substantially improves the accuracy of therapy. Superficial wound swabs reflect colonization and should not guide treatment. <div class="ec-src"><b>Source:</b> Lipsky BA, Senneville É, Abbas ZG, et al. Guidelines on the diagnosis and treatment of foot infection in persons with diabetes (IWGDF 2019 update). Diabetes Metab Res Rev 2020;36(S1):e3280.</div></div> [[Next case →->Spinal epidural abscess - Rx]] [[Start another case->Hub]] [[Restart this case->Diabetic foot osteomyelitis - Rx]]

<span class="ec-case-marker" hidden data-entry="Diabetic foot osteomyelitis. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Surface swabs grow colonizing flora that correlate poorly with bone pathogens, and empiric therapy chosen this way is frequently wrong for weeks. <div class="ec-teach"><div class="th">What the findings point to</div> A positive probe-to-bone test with radiographic erosion and an erythrocyte sedimentation rate above 70 mm/h makes osteomyelitis very likely, but the organism determines a prolonged and toxic antibiotic course. Because he has no systemic toxicity and no spreading infection, there is time to obtain bone for culture before treatment, and doing so substantially improves the accuracy of therapy. Superficial wound swabs reflect colonization and should not guide treatment. <div class="ec-src"><b>Source:</b> Lipsky BA, Senneville É, Abbas ZG, et al. Guidelines on the diagnosis and treatment of foot infection in persons with diabetes (IWGDF 2019 update). Diabetes Metab Res Rev 2020;36(S1):e3280.</div></div></div> [[Try this question again->Diabetic foot osteomyelitis - Rx]] [[Next case →->Spinal epidural abscess - Rx]] [[Start another case->Hub]] [[Restart this case->Diabetic foot osteomyelitis - Rx]]

<span class="ec-case-marker" hidden data-entry="Diabetic foot osteomyelitis. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Amputation is considered for uncontrolled infection, critical ischemia, or failure of medical therapy. He is perfused, systemically well, and untreated. <div class="ec-teach"><div class="th">What the findings point to</div> A positive probe-to-bone test with radiographic erosion and an erythrocyte sedimentation rate above 70 mm/h makes osteomyelitis very likely, but the organism determines a prolonged and toxic antibiotic course. Because he has no systemic toxicity and no spreading infection, there is time to obtain bone for culture before treatment, and doing so substantially improves the accuracy of therapy. Superficial wound swabs reflect colonization and should not guide treatment. <div class="ec-src"><b>Source:</b> Lipsky BA, Senneville É, Abbas ZG, et al. Guidelines on the diagnosis and treatment of foot infection in persons with diabetes (IWGDF 2019 update). Diabetes Metab Res Rev 2020;36(S1):e3280.</div></div></div> [[Try this question again->Diabetic foot osteomyelitis - Rx]] [[Next case →->Spinal epidural abscess - Rx]] [[Start another case->Hub]] [[Restart this case->Diabetic foot osteomyelitis - Rx]]

<span class="ec-case-marker" hidden data-entry="Diabetic foot osteomyelitis. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Committing to 6 weeks of parenteral therapy without an organism risks both undertreatment and unnecessary toxicity. <div class="ec-teach"><div class="th">What the findings point to</div> A positive probe-to-bone test with radiographic erosion and an erythrocyte sedimentation rate above 70 mm/h makes osteomyelitis very likely, but the organism determines a prolonged and toxic antibiotic course. Because he has no systemic toxicity and no spreading infection, there is time to obtain bone for culture before treatment, and doing so substantially improves the accuracy of therapy. Superficial wound swabs reflect colonization and should not guide treatment. <div class="ec-src"><b>Source:</b> Lipsky BA, Senneville É, Abbas ZG, et al. Guidelines on the diagnosis and treatment of foot infection in persons with diabetes (IWGDF 2019 update). Diabetes Metab Res Rev 2020;36(S1):e3280.</div></div></div> [[Try this question again->Diabetic foot osteomyelitis - Rx]] [[Next case →->Spinal epidural abscess - Rx]] [[Start another case->Hub]] [[Restart this case->Diabetic foot osteomyelitis - Rx]]

<span class="ec-case-marker" hidden data-entry="Diabetic foot osteomyelitis. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> His ankle-brachial index is 1.0 and pulses are palpable, so there is no ischemia to correct. <div class="ec-teach"><div class="th">What the findings point to</div> A positive probe-to-bone test with radiographic erosion and an erythrocyte sedimentation rate above 70 mm/h makes osteomyelitis very likely, but the organism determines a prolonged and toxic antibiotic course. Because he has no systemic toxicity and no spreading infection, there is time to obtain bone for culture before treatment, and doing so substantially improves the accuracy of therapy. Superficial wound swabs reflect colonization and should not guide treatment. <div class="ec-src"><b>Source:</b> Lipsky BA, Senneville É, Abbas ZG, et al. Guidelines on the diagnosis and treatment of foot infection in persons with diabetes (IWGDF 2019 update). Diabetes Metab Res Rev 2020;36(S1):e3280.</div></div></div> [[Try this question again->Diabetic foot osteomyelitis - Rx]] [[Next case →->Spinal epidural abscess - Rx]] [[Start another case->Hub]] [[Restart this case->Diabetic foot osteomyelitis - Rx]]

<span class="ec-case-marker" hidden data-entry="Diabetic foot osteomyelitis. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Hyperbaric oxygen is an adjunct in selected refractory cases and is not primary therapy for a newly diagnosed bone infection. <div class="ec-teach"><div class="th">What the findings point to</div> A positive probe-to-bone test with radiographic erosion and an erythrocyte sedimentation rate above 70 mm/h makes osteomyelitis very likely, but the organism determines a prolonged and toxic antibiotic course. Because he has no systemic toxicity and no spreading infection, there is time to obtain bone for culture before treatment, and doing so substantially improves the accuracy of therapy. Superficial wound swabs reflect colonization and should not guide treatment. <div class="ec-src"><b>Source:</b> Lipsky BA, Senneville É, Abbas ZG, et al. Guidelines on the diagnosis and treatment of foot infection in persons with diabetes (IWGDF 2019 update). Diabetes Metab Res Rev 2020;36(S1):e3280.</div></div></div> [[Try this question again->Diabetic foot osteomyelitis - Rx]] [[Next case →->Spinal epidural abscess - Rx]] [[Start another case->Hub]] [[Restart this case->Diabetic foot osteomyelitis - Rx]]

<div class="ec-scene">Emergency department · 02:15</div> A 55-year-old man who injects drugs has 5 days of worsening mid-back pain and 1 day of leg weakness. Temperature is 38.9°C, blood pressure is 118/70 mm Hg, and pulse is 112/min. Strength is 3/5 in both legs with a T8 sensory level. Leukocyte count is 19,600/mm3, erythrocyte sedimentation rate is 96 mm/h, and C-reactive protein is 214 mg/L. MRI of the spine shows a posterior epidural collection from T7 to T9 with cord compression. Blood cultures are drawn. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[CT-guided aspiration of the collection for culture->Spinal epidural abscess - Rx D2]] [[Dexamethasone and admission for observation->Spinal epidural abscess - Rx D3]] [[Emergent surgical decompression with intravenous antibiotics->Spinal epidural abscess - Rx correct]] [[Empiric antituberculous therapy pending culture->Spinal epidural abscess - Rx D4]] [[Intravenous vancomycin alone with serial neurologic checks->Spinal epidural abscess - Rx D1]] [[Repeat MRI in 24 hours to assess progression->Spinal epidural abscess - Rx D5]]

<span class="ec-case-marker" hidden data-entry="Spinal epidural abscess. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Emergent surgical decompression with intravenous antibiotics</div> Epidural abscess with a neurologic deficit is a surgical emergency. Neurologic recovery correlates with the degree of deficit at the time of decompression, and a patient who is already weak deteriorates quickly to paraplegia. Antibiotics run concurrently after cultures, covering methicillin-resistant Staphylococcus aureus, but medical therapy alone is reserved for patients without deficit and without instability. <div class="ec-src"><b>Source:</b> Darouiche RO. Spinal epidural abscess. N Engl J Med 2006;355(19):2012-2020.</div></div> [[Next case →->Achilles tendon rupture - Rx]] [[Start another case->Hub]] [[Restart this case->Spinal epidural abscess - Rx]]

<span class="ec-case-marker" hidden data-entry="Spinal epidural abscess. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Medical management alone is an option only when there is no neurologic deficit. He is already 3/5 with a sensory level. <div class="ec-teach"><div class="th">What the findings point to</div> Epidural abscess with a neurologic deficit is a surgical emergency. Neurologic recovery correlates with the degree of deficit at the time of decompression, and a patient who is already weak deteriorates quickly to paraplegia. Antibiotics run concurrently after cultures, covering methicillin-resistant Staphylococcus aureus, but medical therapy alone is reserved for patients without deficit and without instability. <div class="ec-src"><b>Source:</b> Darouiche RO. Spinal epidural abscess. N Engl J Med 2006;355(19):2012-2020.</div></div></div> [[Try this question again->Spinal epidural abscess - Rx]] [[Next case →->Achilles tendon rupture - Rx]] [[Start another case->Hub]] [[Restart this case->Spinal epidural abscess - Rx]]

<span class="ec-case-marker" hidden data-entry="Spinal epidural abscess. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Needle aspiration may yield an organism but does not decompress the cord, and the organism can be obtained at operation. <div class="ec-teach"><div class="th">What the findings point to</div> Epidural abscess with a neurologic deficit is a surgical emergency. Neurologic recovery correlates with the degree of deficit at the time of decompression, and a patient who is already weak deteriorates quickly to paraplegia. Antibiotics run concurrently after cultures, covering methicillin-resistant Staphylococcus aureus, but medical therapy alone is reserved for patients without deficit and without instability. <div class="ec-src"><b>Source:</b> Darouiche RO. Spinal epidural abscess. N Engl J Med 2006;355(19):2012-2020.</div></div></div> [[Try this question again->Spinal epidural abscess - Rx]] [[Next case →->Achilles tendon rupture - Rx]] [[Start another case->Hub]] [[Restart this case->Spinal epidural abscess - Rx]]

<span class="ec-case-marker" hidden data-entry="Spinal epidural abscess. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Steroids have no established role here and observation wastes the interval during which function is recoverable. <div class="ec-teach"><div class="th">What the findings point to</div> Epidural abscess with a neurologic deficit is a surgical emergency. Neurologic recovery correlates with the degree of deficit at the time of decompression, and a patient who is already weak deteriorates quickly to paraplegia. Antibiotics run concurrently after cultures, covering methicillin-resistant Staphylococcus aureus, but medical therapy alone is reserved for patients without deficit and without instability. <div class="ec-src"><b>Source:</b> Darouiche RO. Spinal epidural abscess. N Engl J Med 2006;355(19):2012-2020.</div></div></div> [[Try this question again->Spinal epidural abscess - Rx]] [[Next case →->Achilles tendon rupture - Rx]] [[Start another case->Hub]] [[Restart this case->Spinal epidural abscess - Rx]]

<span class="ec-case-marker" hidden data-entry="Spinal epidural abscess. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Tuberculous spondylitis is typically indolent over months with vertebral destruction. This is an acute pyogenic presentation. <div class="ec-teach"><div class="th">What the findings point to</div> Epidural abscess with a neurologic deficit is a surgical emergency. Neurologic recovery correlates with the degree of deficit at the time of decompression, and a patient who is already weak deteriorates quickly to paraplegia. Antibiotics run concurrently after cultures, covering methicillin-resistant Staphylococcus aureus, but medical therapy alone is reserved for patients without deficit and without instability. <div class="ec-src"><b>Source:</b> Darouiche RO. Spinal epidural abscess. N Engl J Med 2006;355(19):2012-2020.</div></div></div> [[Try this question again->Spinal epidural abscess - Rx]] [[Next case →->Achilles tendon rupture - Rx]] [[Start another case->Hub]] [[Restart this case->Spinal epidural abscess - Rx]]

<span class="ec-case-marker" hidden data-entry="Spinal epidural abscess. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The MRI has already established compression. Serial imaging documents deterioration rather than preventing it. <div class="ec-teach"><div class="th">What the findings point to</div> Epidural abscess with a neurologic deficit is a surgical emergency. Neurologic recovery correlates with the degree of deficit at the time of decompression, and a patient who is already weak deteriorates quickly to paraplegia. Antibiotics run concurrently after cultures, covering methicillin-resistant Staphylococcus aureus, but medical therapy alone is reserved for patients without deficit and without instability. <div class="ec-src"><b>Source:</b> Darouiche RO. Spinal epidural abscess. N Engl J Med 2006;355(19):2012-2020.</div></div></div> [[Try this question again->Spinal epidural abscess - Rx]] [[Next case →->Achilles tendon rupture - Rx]] [[Start another case->Hub]] [[Restart this case->Spinal epidural abscess - Rx]]

<div class="ec-scene">Sports medicine clinic · 10:45</div> A 41-year-old recreational tennis player felt a sudden snap in the back of the ankle 2 days ago and could not push off. He is otherwise healthy and takes no medications. Temperature is 36.7°C. There is a palpable gap 4 cm above the calcaneal insertion, and squeezing the calf produces no plantar flexion. Ultrasonography confirms a complete midsubstance rupture with a 2-cm gap in neutral position that approximates in plantarflexion. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Corticosteroid injection around the tendon for pain->Achilles tendon rupture - Rx D5]] [[Functional rehabilitation in a plantarflexion orthosis->Achilles tendon rupture - Rx correct]] [[Open surgical repair within 1 week for all complete ruptures->Achilles tendon rupture - Rx D1]] [[Platelet-rich plasma injection into the tendon gap->Achilles tendon rupture - Rx D3]] [[Rigid below-knee cast in neutral for 8 weeks->Achilles tendon rupture - Rx D2]] [[Weight bearing as tolerated without any orthosis->Achilles tendon rupture - Rx D4]]

<span class="ec-case-marker" hidden data-entry="Achilles tendon rupture. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Functional rehabilitation in a plantarflexion orthosis</div> For an acute midsubstance rupture that approximates in plantarflexion, modern functional rehabilitation with early weight bearing in a graduated orthosis achieves re-rupture rates comparable to operative repair while avoiding wound complications and infection. Operative repair is reserved for large irreducible gaps, delayed presentation, re-rupture, or high-demand athletes who accept the surgical risk. Rigid casting without early motion has worse functional outcomes than either. <div class="ec-src"><b>Source:</b> Willits K, Amendola A, Bryant D, et al. Operative versus nonoperative treatment of acute Achilles tendon ruptures: a multicenter randomized trial. J Bone Joint Surg Am 2010;92(17):2767-2775.</div></div> [[Next case →->Gout flare therapy - Rx]] [[Start another case->Hub]] [[Restart this case->Achilles tendon rupture - Rx]]

<span class="ec-case-marker" hidden data-entry="Achilles tendon rupture. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Routine operative repair does not reduce re-rupture meaningfully once functional rehabilitation is used and adds wound infection and sural nerve injury risk. <div class="ec-teach"><div class="th">What the findings point to</div> For an acute midsubstance rupture that approximates in plantarflexion, modern functional rehabilitation with early weight bearing in a graduated orthosis achieves re-rupture rates comparable to operative repair while avoiding wound complications and infection. Operative repair is reserved for large irreducible gaps, delayed presentation, re-rupture, or high-demand athletes who accept the surgical risk. Rigid casting without early motion has worse functional outcomes than either. <div class="ec-src"><b>Source:</b> Willits K, Amendola A, Bryant D, et al. Operative versus nonoperative treatment of acute Achilles tendon ruptures: a multicenter randomized trial. J Bone Joint Surg Am 2010;92(17):2767-2775.</div></div></div> [[Try this question again->Achilles tendon rupture - Rx]] [[Next case →->Gout flare therapy - Rx]] [[Start another case->Hub]] [[Restart this case->Achilles tendon rupture - Rx]]

<span class="ec-case-marker" hidden data-entry="Achilles tendon rupture. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Immobilization in neutral without early controlled motion produces stiffness, muscle atrophy, and inferior functional recovery. <div class="ec-teach"><div class="th">What the findings point to</div> For an acute midsubstance rupture that approximates in plantarflexion, modern functional rehabilitation with early weight bearing in a graduated orthosis achieves re-rupture rates comparable to operative repair while avoiding wound complications and infection. Operative repair is reserved for large irreducible gaps, delayed presentation, re-rupture, or high-demand athletes who accept the surgical risk. Rigid casting without early motion has worse functional outcomes than either. <div class="ec-src"><b>Source:</b> Willits K, Amendola A, Bryant D, et al. Operative versus nonoperative treatment of acute Achilles tendon ruptures: a multicenter randomized trial. J Bone Joint Surg Am 2010;92(17):2767-2775.</div></div></div> [[Try this question again->Achilles tendon rupture - Rx]] [[Next case →->Gout flare therapy - Rx]] [[Start another case->Hub]] [[Restart this case->Achilles tendon rupture - Rx]]

<span class="ec-case-marker" hidden data-entry="Achilles tendon rupture. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Randomized data do not show benefit for acute rupture, and it does not restore tendon continuity. <div class="ec-teach"><div class="th">What the findings point to</div> For an acute midsubstance rupture that approximates in plantarflexion, modern functional rehabilitation with early weight bearing in a graduated orthosis achieves re-rupture rates comparable to operative repair while avoiding wound complications and infection. Operative repair is reserved for large irreducible gaps, delayed presentation, re-rupture, or high-demand athletes who accept the surgical risk. Rigid casting without early motion has worse functional outcomes than either. <div class="ec-src"><b>Source:</b> Willits K, Amendola A, Bryant D, et al. Operative versus nonoperative treatment of acute Achilles tendon ruptures: a multicenter randomized trial. J Bone Joint Surg Am 2010;92(17):2767-2775.</div></div></div> [[Try this question again->Achilles tendon rupture - Rx]] [[Next case →->Gout flare therapy - Rx]] [[Start another case->Hub]] [[Restart this case->Achilles tendon rupture - Rx]]

<span class="ec-case-marker" hidden data-entry="Achilles tendon rupture. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Unprotected weight bearing allows the tendon ends to separate and predicts elongation and poor push-off strength. <div class="ec-teach"><div class="th">What the findings point to</div> For an acute midsubstance rupture that approximates in plantarflexion, modern functional rehabilitation with early weight bearing in a graduated orthosis achieves re-rupture rates comparable to operative repair while avoiding wound complications and infection. Operative repair is reserved for large irreducible gaps, delayed presentation, re-rupture, or high-demand athletes who accept the surgical risk. Rigid casting without early motion has worse functional outcomes than either. <div class="ec-src"><b>Source:</b> Willits K, Amendola A, Bryant D, et al. Operative versus nonoperative treatment of acute Achilles tendon ruptures: a multicenter randomized trial. J Bone Joint Surg Am 2010;92(17):2767-2775.</div></div></div> [[Try this question again->Achilles tendon rupture - Rx]] [[Next case →->Gout flare therapy - Rx]] [[Start another case->Hub]] [[Restart this case->Achilles tendon rupture - Rx]]

<span class="ec-case-marker" hidden data-entry="Achilles tendon rupture. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Peritendinous steroid weakens collagen and is contraindicated in an acute rupture. <div class="ec-teach"><div class="th">What the findings point to</div> For an acute midsubstance rupture that approximates in plantarflexion, modern functional rehabilitation with early weight bearing in a graduated orthosis achieves re-rupture rates comparable to operative repair while avoiding wound complications and infection. Operative repair is reserved for large irreducible gaps, delayed presentation, re-rupture, or high-demand athletes who accept the surgical risk. Rigid casting without early motion has worse functional outcomes than either. <div class="ec-src"><b>Source:</b> Willits K, Amendola A, Bryant D, et al. Operative versus nonoperative treatment of acute Achilles tendon ruptures: a multicenter randomized trial. J Bone Joint Surg Am 2010;92(17):2767-2775.</div></div></div> [[Try this question again->Achilles tendon rupture - Rx]] [[Next case →->Gout flare therapy - Rx]] [[Start another case->Hub]] [[Restart this case->Achilles tendon rupture - Rx]]

<div class="ec-scene">Primary care clinic · 09:47</div> A 62-year-old man has 18 hours of an exquisitely painful, swollen, erythematous first metatarsophalangeal joint. This is his third episode. Temperature is 37.3°C and blood pressure is 142/86 mm Hg. He has stage 3b chronic kidney disease with an estimated glomerular filtration rate of 34 mL/min/1.73 m2, and heart failure with an ejection fraction of 35% on furosemide. Arthrocentesis shows negatively birefringent needle-shaped crystals and no organisms. <span class="ec-prompt">Which of the following is the most appropriate pharmacotherapy?</span> [[Full-dose oral colchicine 0.6 mg three times daily->Gout flare therapy - Rx D2]] [[High-dose indomethacin for 5 days->Gout flare therapy - Rx D1]] [[Initiation of allopurinol at 300 mg daily during the flare->Gout flare therapy - Rx D3]] [[Intraarticular corticosteroid injection->Gout flare therapy - Rx correct]] [[Intravenous ketorolac->Gout flare therapy - Rx D4]] [[Pegloticase infusion->Gout flare therapy - Rx D5]]

<span class="ec-case-marker" hidden data-entry="Gout flare therapy. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Intraarticular corticosteroid injection</div> Nonsteroidal anti-inflammatory drugs are contraindicated by his chronic kidney disease and heart failure, and colchicine requires substantial dose reduction below an estimated glomerular filtration rate of 30 to 45 mL/min with meaningful toxicity risk. For a flare limited to one accessible joint with infection excluded by arthrocentesis, intraarticular corticosteroid gives rapid relief with negligible systemic exposure, avoiding both the renal and the fluid-retention problems. Systemic steroid is the alternative when several joints are involved. <div class="ec-src"><b>Source:</b> FitzGerald JD, Dalbeth N, Mikuls T, et al. 2020 American College of Rheumatology Guideline for the Management of Gout. Arthritis Rheumatol 2020;72(6):879-895.</div></div> [[Next case →->Rheumatoid arthritis initial DMARD - Rx]] [[Start another case->Hub]] [[Restart this case->Gout flare therapy - Rx]]

<span class="ec-case-marker" hidden data-entry="Gout flare therapy. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Nonsteroidal agents reduce renal perfusion and promote sodium retention, which is hazardous with an eGFR of 34 mL/min and an ejection fraction of 35%. <div class="ec-teach"><div class="th">What the findings point to</div> Nonsteroidal anti-inflammatory drugs are contraindicated by his chronic kidney disease and heart failure, and colchicine requires substantial dose reduction below an estimated glomerular filtration rate of 30 to 45 mL/min with meaningful toxicity risk. For a flare limited to one accessible joint with infection excluded by arthrocentesis, intraarticular corticosteroid gives rapid relief with negligible systemic exposure, avoiding both the renal and the fluid-retention problems. Systemic steroid is the alternative when several joints are involved. <div class="ec-src"><b>Source:</b> FitzGerald JD, Dalbeth N, Mikuls T, et al. 2020 American College of Rheumatology Guideline for the Management of Gout. Arthritis Rheumatol 2020;72(6):879-895.</div></div></div> [[Try this question again->Gout flare therapy - Rx]] [[Next case →->Rheumatoid arthritis initial DMARD - Rx]] [[Start another case->Hub]] [[Restart this case->Gout flare therapy - Rx]]

<span class="ec-case-marker" hidden data-entry="Gout flare therapy. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Colchicine is renally cleared and accumulates at this level of function, producing neuromyopathy and marrow suppression. Any use requires substantial dose reduction. <div class="ec-teach"><div class="th">What the findings point to</div> Nonsteroidal anti-inflammatory drugs are contraindicated by his chronic kidney disease and heart failure, and colchicine requires substantial dose reduction below an estimated glomerular filtration rate of 30 to 45 mL/min with meaningful toxicity risk. For a flare limited to one accessible joint with infection excluded by arthrocentesis, intraarticular corticosteroid gives rapid relief with negligible systemic exposure, avoiding both the renal and the fluid-retention problems. Systemic steroid is the alternative when several joints are involved. <div class="ec-src"><b>Source:</b> FitzGerald JD, Dalbeth N, Mikuls T, et al. 2020 American College of Rheumatology Guideline for the Management of Gout. Arthritis Rheumatol 2020;72(6):879-895.</div></div></div> [[Try this question again->Gout flare therapy - Rx]] [[Next case →->Rheumatoid arthritis initial DMARD - Rx]] [[Start another case->Hub]] [[Restart this case->Gout flare therapy - Rx]]

<span class="ec-case-marker" hidden data-entry="Gout flare therapy. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Starting urate-lowering therapy is appropriate after or alongside anti-inflammatory cover, but allopurinol alone does not treat an acute flare and the starting dose in chronic kidney disease should be 100 mg or less. <div class="ec-teach"><div class="th">What the findings point to</div> Nonsteroidal anti-inflammatory drugs are contraindicated by his chronic kidney disease and heart failure, and colchicine requires substantial dose reduction below an estimated glomerular filtration rate of 30 to 45 mL/min with meaningful toxicity risk. For a flare limited to one accessible joint with infection excluded by arthrocentesis, intraarticular corticosteroid gives rapid relief with negligible systemic exposure, avoiding both the renal and the fluid-retention problems. Systemic steroid is the alternative when several joints are involved. <div class="ec-src"><b>Source:</b> FitzGerald JD, Dalbeth N, Mikuls T, et al. 2020 American College of Rheumatology Guideline for the Management of Gout. Arthritis Rheumatol 2020;72(6):879-895.</div></div></div> [[Try this question again->Gout flare therapy - Rx]] [[Next case →->Rheumatoid arthritis initial DMARD - Rx]] [[Start another case->Hub]] [[Restart this case->Gout flare therapy - Rx]]

<span class="ec-case-marker" hidden data-entry="Gout flare therapy. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Parenteral administration does not avoid the renal and cardiac effects of nonsteroidal inhibition. <div class="ec-teach"><div class="th">What the findings point to</div> Nonsteroidal anti-inflammatory drugs are contraindicated by his chronic kidney disease and heart failure, and colchicine requires substantial dose reduction below an estimated glomerular filtration rate of 30 to 45 mL/min with meaningful toxicity risk. For a flare limited to one accessible joint with infection excluded by arthrocentesis, intraarticular corticosteroid gives rapid relief with negligible systemic exposure, avoiding both the renal and the fluid-retention problems. Systemic steroid is the alternative when several joints are involved. <div class="ec-src"><b>Source:</b> FitzGerald JD, Dalbeth N, Mikuls T, et al. 2020 American College of Rheumatology Guideline for the Management of Gout. Arthritis Rheumatol 2020;72(6):879-895.</div></div></div> [[Try this question again->Gout flare therapy - Rx]] [[Next case →->Rheumatoid arthritis initial DMARD - Rx]] [[Start another case->Hub]] [[Restart this case->Gout flare therapy - Rx]]

<span class="ec-case-marker" hidden data-entry="Gout flare therapy. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Pegloticase is for refractory tophaceous gout after failure of oral urate-lowering therapy, not for an acute flare. <div class="ec-teach"><div class="th">What the findings point to</div> Nonsteroidal anti-inflammatory drugs are contraindicated by his chronic kidney disease and heart failure, and colchicine requires substantial dose reduction below an estimated glomerular filtration rate of 30 to 45 mL/min with meaningful toxicity risk. For a flare limited to one accessible joint with infection excluded by arthrocentesis, intraarticular corticosteroid gives rapid relief with negligible systemic exposure, avoiding both the renal and the fluid-retention problems. Systemic steroid is the alternative when several joints are involved. <div class="ec-src"><b>Source:</b> FitzGerald JD, Dalbeth N, Mikuls T, et al. 2020 American College of Rheumatology Guideline for the Management of Gout. Arthritis Rheumatol 2020;72(6):879-895.</div></div></div> [[Try this question again->Gout flare therapy - Rx]] [[Next case →->Rheumatoid arthritis initial DMARD - Rx]] [[Start another case->Hub]] [[Restart this case->Gout flare therapy - Rx]]

<div class="ec-scene">Rheumatology clinic · 13:30</div> A 43-year-old woman has 4 months of symmetric pain and swelling in the metacarpophalangeal and proximal interphalangeal joints with 90 minutes of morning stiffness. Rheumatoid factor and anti-cyclic citrullinated peptide antibodies are positive, and erythrocyte sedimentation rate is 54 mm/h. Radiographs show periarticular osteopenia without erosions. She has no liver disease, drinks no alcohol, and is not pregnant and is using reliable contraception. Hepatitis B and C serologies and a tuberculin test are negative. <span class="ec-prompt">Which of the following is the most appropriate initial pharmacotherapy?</span> [[Adalimumab as initial monotherapy->Rheumatoid arthritis initial DMARD - Rx D1]] [[Hydroxychloroquine monotherapy->Rheumatoid arthritis initial DMARD - Rx D3]] [[Long-term prednisone 10 mg daily alone->Rheumatoid arthritis initial DMARD - Rx D2]] [[Methotrexate with folic acid supplementation->Rheumatoid arthritis initial DMARD - Rx correct]] [[Naproxen with as-needed analgesia->Rheumatoid arthritis initial DMARD - Rx D4]] [[Tofacitinib as initial therapy->Rheumatoid arthritis initial DMARD - Rx D5]]

<span class="ec-case-marker" hidden data-entry="Rheumatoid arthritis initial DMARD. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Methotrexate with folic acid supplementation</div> Methotrexate is the recommended first-line disease-modifying agent for moderate to severe rheumatoid arthritis, including in patients who are seropositive and have high disease activity. It is started early because irreversible joint damage occurs within the first 2 years, and folic acid reduces mucosal and hematologic toxicity without compromising efficacy. Biologic therapy is added if the response to methotrexate is inadequate. Reliable contraception is required, which she has. <div class="ec-src"><b>Source:</b> Fraenkel L, Bathon JM, England BR, et al. 2021 American College of Rheumatology Guideline for the Treatment of Rheumatoid Arthritis. Arthritis Rheumatol 2021;73(7):1108-1123.</div></div> [[Next case →->Osteoporosis pharmacotherapy - Rx]] [[Start another case->Hub]] [[Restart this case->Rheumatoid arthritis initial DMARD - Rx]]

<span class="ec-case-marker" hidden data-entry="Rheumatoid arthritis initial DMARD. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Tumor necrosis factor inhibitors are reserved for inadequate response to methotrexate. Using one first adds cost and infection risk without superior outcomes. <div class="ec-teach"><div class="th">What the findings point to</div> Methotrexate is the recommended first-line disease-modifying agent for moderate to severe rheumatoid arthritis, including in patients who are seropositive and have high disease activity. It is started early because irreversible joint damage occurs within the first 2 years, and folic acid reduces mucosal and hematologic toxicity without compromising efficacy. Biologic therapy is added if the response to methotrexate is inadequate. Reliable contraception is required, which she has. <div class="ec-src"><b>Source:</b> Fraenkel L, Bathon JM, England BR, et al. 2021 American College of Rheumatology Guideline for the Treatment of Rheumatoid Arthritis. Arthritis Rheumatol 2021;73(7):1108-1123.</div></div></div> [[Try this question again->Rheumatoid arthritis initial DMARD - Rx]] [[Next case →->Osteoporosis pharmacotherapy - Rx]] [[Start another case->Hub]] [[Restart this case->Rheumatoid arthritis initial DMARD - Rx]]

<span class="ec-case-marker" hidden data-entry="Rheumatoid arthritis initial DMARD. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Glucocorticoids control symptoms and are used as a bridge, but as monotherapy they do not prevent erosion and carry cumulative toxicity. <div class="ec-teach"><div class="th">What the findings point to</div> Methotrexate is the recommended first-line disease-modifying agent for moderate to severe rheumatoid arthritis, including in patients who are seropositive and have high disease activity. It is started early because irreversible joint damage occurs within the first 2 years, and folic acid reduces mucosal and hematologic toxicity without compromising efficacy. Biologic therapy is added if the response to methotrexate is inadequate. Reliable contraception is required, which she has. <div class="ec-src"><b>Source:</b> Fraenkel L, Bathon JM, England BR, et al. 2021 American College of Rheumatology Guideline for the Treatment of Rheumatoid Arthritis. Arthritis Rheumatol 2021;73(7):1108-1123.</div></div></div> [[Try this question again->Rheumatoid arthritis initial DMARD - Rx]] [[Next case →->Osteoporosis pharmacotherapy - Rx]] [[Start another case->Hub]] [[Restart this case->Rheumatoid arthritis initial DMARD - Rx]]

<span class="ec-case-marker" hidden data-entry="Rheumatoid arthritis initial DMARD. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Hydroxychloroquine is appropriate for mild disease. With seropositivity, an elevated sedimentation rate, and polyarticular involvement, it is insufficient. <div class="ec-teach"><div class="th">What the findings point to</div> Methotrexate is the recommended first-line disease-modifying agent for moderate to severe rheumatoid arthritis, including in patients who are seropositive and have high disease activity. It is started early because irreversible joint damage occurs within the first 2 years, and folic acid reduces mucosal and hematologic toxicity without compromising efficacy. Biologic therapy is added if the response to methotrexate is inadequate. Reliable contraception is required, which she has. <div class="ec-src"><b>Source:</b> Fraenkel L, Bathon JM, England BR, et al. 2021 American College of Rheumatology Guideline for the Treatment of Rheumatoid Arthritis. Arthritis Rheumatol 2021;73(7):1108-1123.</div></div></div> [[Try this question again->Rheumatoid arthritis initial DMARD - Rx]] [[Next case →->Osteoporosis pharmacotherapy - Rx]] [[Start another case->Hub]] [[Restart this case->Rheumatoid arthritis initial DMARD - Rx]]

<span class="ec-case-marker" hidden data-entry="Rheumatoid arthritis initial DMARD. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Nonsteroidal agents relieve symptoms and modify nothing. Relying on them allows erosions to develop. <div class="ec-teach"><div class="th">What the findings point to</div> Methotrexate is the recommended first-line disease-modifying agent for moderate to severe rheumatoid arthritis, including in patients who are seropositive and have high disease activity. It is started early because irreversible joint damage occurs within the first 2 years, and folic acid reduces mucosal and hematologic toxicity without compromising efficacy. Biologic therapy is added if the response to methotrexate is inadequate. Reliable contraception is required, which she has. <div class="ec-src"><b>Source:</b> Fraenkel L, Bathon JM, England BR, et al. 2021 American College of Rheumatology Guideline for the Treatment of Rheumatoid Arthritis. Arthritis Rheumatol 2021;73(7):1108-1123.</div></div></div> [[Try this question again->Rheumatoid arthritis initial DMARD - Rx]] [[Next case →->Osteoporosis pharmacotherapy - Rx]] [[Start another case->Hub]] [[Restart this case->Rheumatoid arthritis initial DMARD - Rx]]

<span class="ec-case-marker" hidden data-entry="Rheumatoid arthritis initial DMARD. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Janus kinase inhibitors follow methotrexate failure and carry thrombotic and cardiovascular warnings that make them inappropriate first-line. <div class="ec-teach"><div class="th">What the findings point to</div> Methotrexate is the recommended first-line disease-modifying agent for moderate to severe rheumatoid arthritis, including in patients who are seropositive and have high disease activity. It is started early because irreversible joint damage occurs within the first 2 years, and folic acid reduces mucosal and hematologic toxicity without compromising efficacy. Biologic therapy is added if the response to methotrexate is inadequate. Reliable contraception is required, which she has. <div class="ec-src"><b>Source:</b> Fraenkel L, Bathon JM, England BR, et al. 2021 American College of Rheumatology Guideline for the Treatment of Rheumatoid Arthritis. Arthritis Rheumatol 2021;73(7):1108-1123.</div></div></div> [[Try this question again->Rheumatoid arthritis initial DMARD - Rx]] [[Next case →->Osteoporosis pharmacotherapy - Rx]] [[Start another case->Hub]] [[Restart this case->Rheumatoid arthritis initial DMARD - Rx]]

<div class="ec-scene">Primary care clinic · 14:40</div> A 71-year-old woman sustained a vertebral compression fracture after minimal trauma. Bone densitometry shows a lumbar spine T-score of −3.1. Serum calcium is 9.2 mg/dL, 25-hydroxyvitamin D is 34 ng/mL, creatinine is 0.8 mg/dL with an estimated glomerular filtration rate of 72 mL/min/1.73 m2, and parathyroid hormone is normal. She has gastroesophageal reflux disease requiring daily therapy and cannot remain upright for 30 minutes after waking because of orthostatic dizziness. <span class="ec-prompt">Which of the following is the most appropriate pharmacotherapy?</span> [[Calcitonin nasal spray->Osteoporosis pharmacotherapy - Rx D5]] [[Calcium and vitamin D supplementation alone->Osteoporosis pharmacotherapy - Rx D2]] [[Conjugated estrogen therapy->Osteoporosis pharmacotherapy - Rx D3]] [[Intravenous zoledronic acid once yearly->Osteoporosis pharmacotherapy - Rx correct]] [[Oral alendronate weekly->Osteoporosis pharmacotherapy - Rx D1]] [[Raloxifene->Osteoporosis pharmacotherapy - Rx D4]]

<span class="ec-case-marker" hidden data-entry="Osteoporosis pharmacotherapy. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Intravenous zoledronic acid once yearly</div> She has established severe osteoporosis with a fragility fracture and requires antiresorptive therapy. Oral bisphosphonates demand that the patient remain upright and fasting for at least 30 minutes, which she cannot do, and they worsen reflux. Annual intravenous zoledronic acid bypasses both problems, and her renal function is well above the threshold at which it is contraindicated. Calcium and vitamin D are continued alongside. <div class="ec-src"><b>Source:</b> Eastell R, Rosen CJ, Black DM, et al. Pharmacological Management of Osteoporosis in Postmenopausal Women: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2019;104(5):1595-1622.</div></div> [[Next case →->Cellulitis antibiotic choice - Rx]] [[Start another case->Hub]] [[Restart this case->Osteoporosis pharmacotherapy - Rx]]

<span class="ec-case-marker" hidden data-entry="Osteoporosis pharmacotherapy. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Oral bisphosphonates require upright fasting dosing she cannot comply with and aggravate her esophageal disease. <div class="ec-teach"><div class="th">What the findings point to</div> She has established severe osteoporosis with a fragility fracture and requires antiresorptive therapy. Oral bisphosphonates demand that the patient remain upright and fasting for at least 30 minutes, which she cannot do, and they worsen reflux. Annual intravenous zoledronic acid bypasses both problems, and her renal function is well above the threshold at which it is contraindicated. Calcium and vitamin D are continued alongside. <div class="ec-src"><b>Source:</b> Eastell R, Rosen CJ, Black DM, et al. Pharmacological Management of Osteoporosis in Postmenopausal Women: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2019;104(5):1595-1622.</div></div></div> [[Try this question again->Osteoporosis pharmacotherapy - Rx]] [[Next case →->Cellulitis antibiotic choice - Rx]] [[Start another case->Hub]] [[Restart this case->Osteoporosis pharmacotherapy - Rx]]

<span class="ec-case-marker" hidden data-entry="Osteoporosis pharmacotherapy. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Supplementation is adjunctive. It does not reduce fracture risk adequately in someone who has already fractured with a T-score of −3.1. <div class="ec-teach"><div class="th">What the findings point to</div> She has established severe osteoporosis with a fragility fracture and requires antiresorptive therapy. Oral bisphosphonates demand that the patient remain upright and fasting for at least 30 minutes, which she cannot do, and they worsen reflux. Annual intravenous zoledronic acid bypasses both problems, and her renal function is well above the threshold at which it is contraindicated. Calcium and vitamin D are continued alongside. <div class="ec-src"><b>Source:</b> Eastell R, Rosen CJ, Black DM, et al. Pharmacological Management of Osteoporosis in Postmenopausal Women: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2019;104(5):1595-1622.</div></div></div> [[Try this question again->Osteoporosis pharmacotherapy - Rx]] [[Next case →->Cellulitis antibiotic choice - Rx]] [[Start another case->Hub]] [[Restart this case->Osteoporosis pharmacotherapy - Rx]]

<span class="ec-case-marker" hidden data-entry="Osteoporosis pharmacotherapy. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Estrogen is used for prevention in selected younger postmenopausal women with vasomotor symptoms, not as treatment for established fracture at age 71. <div class="ec-teach"><div class="th">What the findings point to</div> She has established severe osteoporosis with a fragility fracture and requires antiresorptive therapy. Oral bisphosphonates demand that the patient remain upright and fasting for at least 30 minutes, which she cannot do, and they worsen reflux. Annual intravenous zoledronic acid bypasses both problems, and her renal function is well above the threshold at which it is contraindicated. Calcium and vitamin D are continued alongside. <div class="ec-src"><b>Source:</b> Eastell R, Rosen CJ, Black DM, et al. Pharmacological Management of Osteoporosis in Postmenopausal Women: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2019;104(5):1595-1622.</div></div></div> [[Try this question again->Osteoporosis pharmacotherapy - Rx]] [[Next case →->Cellulitis antibiotic choice - Rx]] [[Start another case->Hub]] [[Restart this case->Osteoporosis pharmacotherapy - Rx]]

<span class="ec-case-marker" hidden data-entry="Osteoporosis pharmacotherapy. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Raloxifene reduces vertebral but not hip fracture risk and increases thromboembolic risk. It is a second-line choice here. <div class="ec-teach"><div class="th">What the findings point to</div> She has established severe osteoporosis with a fragility fracture and requires antiresorptive therapy. Oral bisphosphonates demand that the patient remain upright and fasting for at least 30 minutes, which she cannot do, and they worsen reflux. Annual intravenous zoledronic acid bypasses both problems, and her renal function is well above the threshold at which it is contraindicated. Calcium and vitamin D are continued alongside. <div class="ec-src"><b>Source:</b> Eastell R, Rosen CJ, Black DM, et al. Pharmacological Management of Osteoporosis in Postmenopausal Women: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2019;104(5):1595-1622.</div></div></div> [[Try this question again->Osteoporosis pharmacotherapy - Rx]] [[Next case →->Cellulitis antibiotic choice - Rx]] [[Start another case->Hub]] [[Restart this case->Osteoporosis pharmacotherapy - Rx]]

<span class="ec-case-marker" hidden data-entry="Osteoporosis pharmacotherapy. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Calcitonin has weak antifracture efficacy and a malignancy signal on long-term use. It is not a first-line agent. <div class="ec-teach"><div class="th">What the findings point to</div> She has established severe osteoporosis with a fragility fracture and requires antiresorptive therapy. Oral bisphosphonates demand that the patient remain upright and fasting for at least 30 minutes, which she cannot do, and they worsen reflux. Annual intravenous zoledronic acid bypasses both problems, and her renal function is well above the threshold at which it is contraindicated. Calcium and vitamin D are continued alongside. <div class="ec-src"><b>Source:</b> Eastell R, Rosen CJ, Black DM, et al. Pharmacological Management of Osteoporosis in Postmenopausal Women: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2019;104(5):1595-1622.</div></div></div> [[Try this question again->Osteoporosis pharmacotherapy - Rx]] [[Next case →->Cellulitis antibiotic choice - Rx]] [[Start another case->Hub]] [[Restart this case->Osteoporosis pharmacotherapy - Rx]]

<div class="ec-scene">Urgent care · 17:20</div> A 38-year-old woman has 3 days of a spreading, warm, tender, non-purulent erythematous area on the left shin with a sharply demarcated border. There is no abscess, no drainage, and no crepitus. Temperature is 37.9°C, blood pressure is 122/74 mm Hg, and pulse is 92/min. She is otherwise healthy, has no immunocompromise, and has no history of methicillin-resistant Staphylococcus aureus infection. She can take oral medication and tolerates penicillins. <span class="ec-prompt">Which of the following is the most appropriate pharmacotherapy?</span> [[Intravenous vancomycin->Cellulitis antibiotic choice - Rx D3]] [[Oral cephalexin->Cellulitis antibiotic choice - Rx correct]] [[Oral cephalexin plus trimethoprim-sulfamethoxazole->Cellulitis antibiotic choice - Rx D2]] [[Oral linezolid->Cellulitis antibiotic choice - Rx D4]] [[Oral trimethoprim-sulfamethoxazole->Cellulitis antibiotic choice - Rx D1]] [[Topical mupirocin to the affected area->Cellulitis antibiotic choice - Rx D5]]

<span class="ec-case-marker" hidden data-entry="Cellulitis antibiotic choice. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Oral cephalexin</div> Non-purulent cellulitis without drainage or abscess is overwhelmingly streptococcal, so coverage should target beta-hemolytic streptococci with a beta-lactam such as cephalexin or dicloxacillin. Routine coverage for methicillin-resistant Staphylococcus aureus is added only when purulence, penetrating trauma, injection drug use, known colonization, or failure of beta-lactam therapy is present. She is systemically well and can take oral therapy, so admission is unnecessary. <div class="ec-src"><b>Source:</b> Stevens DL, Bisno AL, Chambers HF, et al. Practice Guidelines for the Diagnosis and Management of Skin and Soft Tissue Infections: 2014 Update by the Infectious Diseases Society of America. Clin Infect Dis 2014;59(2):e10-e52.</div></div> [[Next case →->SJS causative drug withdrawal - Rx]] [[Start another case->Hub]] [[Restart this case->Cellulitis antibiotic choice - Rx]]

<span class="ec-case-marker" hidden data-entry="Cellulitis antibiotic choice. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This covers methicillin-resistant staphylococci but has poor streptococcal activity, which makes it a worse choice for non-purulent cellulitis. <div class="ec-teach"><div class="th">What the findings point to</div> Non-purulent cellulitis without drainage or abscess is overwhelmingly streptococcal, so coverage should target beta-hemolytic streptococci with a beta-lactam such as cephalexin or dicloxacillin. Routine coverage for methicillin-resistant Staphylococcus aureus is added only when purulence, penetrating trauma, injection drug use, known colonization, or failure of beta-lactam therapy is present. She is systemically well and can take oral therapy, so admission is unnecessary. <div class="ec-src"><b>Source:</b> Stevens DL, Bisno AL, Chambers HF, et al. Practice Guidelines for the Diagnosis and Management of Skin and Soft Tissue Infections: 2014 Update by the Infectious Diseases Society of America. Clin Infect Dis 2014;59(2):e10-e52.</div></div></div> [[Try this question again->Cellulitis antibiotic choice - Rx]] [[Next case →->SJS causative drug withdrawal - Rx]] [[Start another case->Hub]] [[Restart this case->Cellulitis antibiotic choice - Rx]]

<span class="ec-case-marker" hidden data-entry="Cellulitis antibiotic choice. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Adding coverage for resistant staphylococci to non-purulent cellulitis has not improved cure rates and doubles adverse effects. <div class="ec-teach"><div class="th">What the findings point to</div> Non-purulent cellulitis without drainage or abscess is overwhelmingly streptococcal, so coverage should target beta-hemolytic streptococci with a beta-lactam such as cephalexin or dicloxacillin. Routine coverage for methicillin-resistant Staphylococcus aureus is added only when purulence, penetrating trauma, injection drug use, known colonization, or failure of beta-lactam therapy is present. She is systemically well and can take oral therapy, so admission is unnecessary. <div class="ec-src"><b>Source:</b> Stevens DL, Bisno AL, Chambers HF, et al. Practice Guidelines for the Diagnosis and Management of Skin and Soft Tissue Infections: 2014 Update by the Infectious Diseases Society of America. Clin Infect Dis 2014;59(2):e10-e52.</div></div></div> [[Try this question again->Cellulitis antibiotic choice - Rx]] [[Next case →->SJS causative drug withdrawal - Rx]] [[Start another case->Hub]] [[Restart this case->Cellulitis antibiotic choice - Rx]]

<span class="ec-case-marker" hidden data-entry="Cellulitis antibiotic choice. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Parenteral therapy is for systemic toxicity, rapid progression, or failed oral therapy. She has none of these. <div class="ec-teach"><div class="th">What the findings point to</div> Non-purulent cellulitis without drainage or abscess is overwhelmingly streptococcal, so coverage should target beta-hemolytic streptococci with a beta-lactam such as cephalexin or dicloxacillin. Routine coverage for methicillin-resistant Staphylococcus aureus is added only when purulence, penetrating trauma, injection drug use, known colonization, or failure of beta-lactam therapy is present. She is systemically well and can take oral therapy, so admission is unnecessary. <div class="ec-src"><b>Source:</b> Stevens DL, Bisno AL, Chambers HF, et al. Practice Guidelines for the Diagnosis and Management of Skin and Soft Tissue Infections: 2014 Update by the Infectious Diseases Society of America. Clin Infect Dis 2014;59(2):e10-e52.</div></div></div> [[Try this question again->Cellulitis antibiotic choice - Rx]] [[Next case →->SJS causative drug withdrawal - Rx]] [[Start another case->Hub]] [[Restart this case->Cellulitis antibiotic choice - Rx]]

<span class="ec-case-marker" hidden data-entry="Cellulitis antibiotic choice. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Linezolid is reserved for resistant organisms or treatment failure and carries myelosuppression and serotonergic interaction risk. <div class="ec-teach"><div class="th">What the findings point to</div> Non-purulent cellulitis without drainage or abscess is overwhelmingly streptococcal, so coverage should target beta-hemolytic streptococci with a beta-lactam such as cephalexin or dicloxacillin. Routine coverage for methicillin-resistant Staphylococcus aureus is added only when purulence, penetrating trauma, injection drug use, known colonization, or failure of beta-lactam therapy is present. She is systemically well and can take oral therapy, so admission is unnecessary. <div class="ec-src"><b>Source:</b> Stevens DL, Bisno AL, Chambers HF, et al. Practice Guidelines for the Diagnosis and Management of Skin and Soft Tissue Infections: 2014 Update by the Infectious Diseases Society of America. Clin Infect Dis 2014;59(2):e10-e52.</div></div></div> [[Try this question again->Cellulitis antibiotic choice - Rx]] [[Next case →->SJS causative drug withdrawal - Rx]] [[Start another case->Hub]] [[Restart this case->Cellulitis antibiotic choice - Rx]]

<span class="ec-case-marker" hidden data-entry="Cellulitis antibiotic choice. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Topical therapy treats impetigo and decolonizes nares. It cannot treat dermal and subcutaneous infection. <div class="ec-teach"><div class="th">What the findings point to</div> Non-purulent cellulitis without drainage or abscess is overwhelmingly streptococcal, so coverage should target beta-hemolytic streptococci with a beta-lactam such as cephalexin or dicloxacillin. Routine coverage for methicillin-resistant Staphylococcus aureus is added only when purulence, penetrating trauma, injection drug use, known colonization, or failure of beta-lactam therapy is present. She is systemically well and can take oral therapy, so admission is unnecessary. <div class="ec-src"><b>Source:</b> Stevens DL, Bisno AL, Chambers HF, et al. Practice Guidelines for the Diagnosis and Management of Skin and Soft Tissue Infections: 2014 Update by the Infectious Diseases Society of America. Clin Infect Dis 2014;59(2):e10-e52.</div></div></div> [[Try this question again->Cellulitis antibiotic choice - Rx]] [[Next case →->SJS causative drug withdrawal - Rx]] [[Start another case->Hub]] [[Restart this case->Cellulitis antibiotic choice - Rx]]

<div class="ec-scene">Emergency department · 12:10</div> A 34-year-old woman started lamotrigine 18 days ago. She now has fever, a painful dusky rash covering about 12% of her body surface with sheets of epidermis separating on gentle lateral pressure, and erosions of the oral and conjunctival mucosa. Temperature is 38.7°C, blood pressure is 106/64 mm Hg, pulse is 118/min, and respirations are 22/min. She also takes sertraline, which she has taken for 3 years, and a daily multivitamin. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Discontinuation of all medications including sertraline->SJS causative drug withdrawal - Rx D1]] [[Empiric broad-spectrum antibiotics for all patients->SJS causative drug withdrawal - Rx D4]] [[High-dose systemic corticosteroids as definitive therapy->SJS causative drug withdrawal - Rx D2]] [[Immediate discontinuation of lamotrigine and transfer to a burn unit->SJS causative drug withdrawal - Rx correct]] [[Intravenous immune globulin without stopping lamotrigine->SJS causative drug withdrawal - Rx D3]] [[Silver sulfadiazine dressings to the denuded areas->SJS causative drug withdrawal - Rx D5]]

<span class="ec-case-marker" hidden data-entry="SJS causative drug withdrawal. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Immediate discontinuation of lamotrigine and transfer to a burn unit</div> The single intervention with the clearest mortality benefit in Stevens-Johnson syndrome and toxic epidermal necrolysis is early withdrawal of the causative drug, and lamotrigine started 18 days ago fits the classic latency. Care then mirrors major burn management: fluid resuscitation, temperature control, wound care, ophthalmologic involvement for the conjunctival erosions, and nutritional support, which is why transfer to a burn unit improves survival. Sertraline at 3 years is not a plausible culprit. <div class="ec-src"><b>Source:</b> Schneider JA, Cohen PR. Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis: A Concise Review with a Comprehensive Summary of Therapeutic Interventions. Adv Ther 2017;34(6):1235-1244.</div></div> [[Next case →->Psoriasis escalation - Rx]] [[Start another case->Hub]] [[Restart this case->SJS causative drug withdrawal - Rx]]

<span class="ec-case-marker" hidden data-entry="SJS causative drug withdrawal. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Stopping a drug taken uneventfully for 3 years is unnecessary and risks serotonin discontinuation symptoms. The recently introduced agent is the culprit. <div class="ec-teach"><div class="th">What the findings point to</div> The single intervention with the clearest mortality benefit in Stevens-Johnson syndrome and toxic epidermal necrolysis is early withdrawal of the causative drug, and lamotrigine started 18 days ago fits the classic latency. Care then mirrors major burn management: fluid resuscitation, temperature control, wound care, ophthalmologic involvement for the conjunctival erosions, and nutritional support, which is why transfer to a burn unit improves survival. Sertraline at 3 years is not a plausible culprit. <div class="ec-src"><b>Source:</b> Schneider JA, Cohen PR. Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis: A Concise Review with a Comprehensive Summary of Therapeutic Interventions. Adv Ther 2017;34(6):1235-1244.</div></div></div> [[Try this question again->SJS causative drug withdrawal - Rx]] [[Next case →->Psoriasis escalation - Rx]] [[Start another case->Hub]] [[Restart this case->SJS causative drug withdrawal - Rx]]

<span class="ec-case-marker" hidden data-entry="SJS causative drug withdrawal. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Corticosteroid use remains controversial, with conflicting outcome data and infection risk. It is not the intervention that changes survival. <div class="ec-teach"><div class="th">What the findings point to</div> The single intervention with the clearest mortality benefit in Stevens-Johnson syndrome and toxic epidermal necrolysis is early withdrawal of the causative drug, and lamotrigine started 18 days ago fits the classic latency. Care then mirrors major burn management: fluid resuscitation, temperature control, wound care, ophthalmologic involvement for the conjunctival erosions, and nutritional support, which is why transfer to a burn unit improves survival. Sertraline at 3 years is not a plausible culprit. <div class="ec-src"><b>Source:</b> Schneider JA, Cohen PR. Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis: A Concise Review with a Comprehensive Summary of Therapeutic Interventions. Adv Ther 2017;34(6):1235-1244.</div></div></div> [[Try this question again->SJS causative drug withdrawal - Rx]] [[Next case →->Psoriasis escalation - Rx]] [[Start another case->Hub]] [[Restart this case->SJS causative drug withdrawal - Rx]]

<span class="ec-case-marker" hidden data-entry="SJS causative drug withdrawal. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Continuing the offending drug while giving immune globulin leaves the driver of epidermal necrosis in place. Withdrawal comes first. <div class="ec-teach"><div class="th">What the findings point to</div> The single intervention with the clearest mortality benefit in Stevens-Johnson syndrome and toxic epidermal necrolysis is early withdrawal of the causative drug, and lamotrigine started 18 days ago fits the classic latency. Care then mirrors major burn management: fluid resuscitation, temperature control, wound care, ophthalmologic involvement for the conjunctival erosions, and nutritional support, which is why transfer to a burn unit improves survival. Sertraline at 3 years is not a plausible culprit. <div class="ec-src"><b>Source:</b> Schneider JA, Cohen PR. Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis: A Concise Review with a Comprehensive Summary of Therapeutic Interventions. Adv Ther 2017;34(6):1235-1244.</div></div></div> [[Try this question again->SJS causative drug withdrawal - Rx]] [[Next case →->Psoriasis escalation - Rx]] [[Start another case->Hub]] [[Restart this case->SJS causative drug withdrawal - Rx]]

<span class="ec-case-marker" hidden data-entry="SJS causative drug withdrawal. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Prophylactic antibiotics are not recommended and select resistant organisms. Antibiotics are given for documented infection. <div class="ec-teach"><div class="th">What the findings point to</div> The single intervention with the clearest mortality benefit in Stevens-Johnson syndrome and toxic epidermal necrolysis is early withdrawal of the causative drug, and lamotrigine started 18 days ago fits the classic latency. Care then mirrors major burn management: fluid resuscitation, temperature control, wound care, ophthalmologic involvement for the conjunctival erosions, and nutritional support, which is why transfer to a burn unit improves survival. Sertraline at 3 years is not a plausible culprit. <div class="ec-src"><b>Source:</b> Schneider JA, Cohen PR. Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis: A Concise Review with a Comprehensive Summary of Therapeutic Interventions. Adv Ther 2017;34(6):1235-1244.</div></div></div> [[Try this question again->SJS causative drug withdrawal - Rx]] [[Next case →->Psoriasis escalation - Rx]] [[Start another case->Hub]] [[Restart this case->SJS causative drug withdrawal - Rx]]

<span class="ec-case-marker" hidden data-entry="SJS causative drug withdrawal. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Sulfonamide-containing topicals are avoided because sulfonamides are themselves a common cause of this reaction. <div class="ec-teach"><div class="th">What the findings point to</div> The single intervention with the clearest mortality benefit in Stevens-Johnson syndrome and toxic epidermal necrolysis is early withdrawal of the causative drug, and lamotrigine started 18 days ago fits the classic latency. Care then mirrors major burn management: fluid resuscitation, temperature control, wound care, ophthalmologic involvement for the conjunctival erosions, and nutritional support, which is why transfer to a burn unit improves survival. Sertraline at 3 years is not a plausible culprit. <div class="ec-src"><b>Source:</b> Schneider JA, Cohen PR. Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis: A Concise Review with a Comprehensive Summary of Therapeutic Interventions. Adv Ther 2017;34(6):1235-1244.</div></div></div> [[Try this question again->SJS causative drug withdrawal - Rx]] [[Next case →->Psoriasis escalation - Rx]] [[Start another case->Hub]] [[Restart this case->SJS causative drug withdrawal - Rx]]

<div class="ec-scene">Dermatology clinic · 15:15</div> A 45-year-old man has plaque psoriasis covering roughly 18% of his body surface with involvement of the scalp, elbows, and knees, plus dactylitis and morning stiffness in three fingers. He has used potent topical corticosteroids and calcipotriene for 8 months and phototherapy for 4 months with minimal improvement. He has no history of tuberculosis, and interferon-gamma release assay, hepatitis serologies, and liver enzymes are normal. He has no heart failure and no demyelinating disease. <span class="ec-prompt">Which of the following is the most appropriate pharmacotherapy?</span> [[Acitretin monotherapy->Psoriasis escalation - Rx D3]] [[Addition of more phototherapy sessions weekly->Psoriasis escalation - Rx D5]] [[Continued topical corticosteroids at higher potency->Psoriasis escalation - Rx D1]] [[Cyclosporine for long-term maintenance->Psoriasis escalation - Rx D4]] [[Oral prednisone taper->Psoriasis escalation - Rx D2]] [[Tumor necrosis factor inhibitor such as adalimumab->Psoriasis escalation - Rx correct]]

<span class="ec-case-marker" hidden data-entry="Psoriasis escalation. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Tumor necrosis factor inhibitor such as adalimumab</div> He has moderate to severe psoriasis by body surface area that has failed topical therapy and phototherapy, and he has coexisting psoriatic arthritis evidenced by dactylitis and inflammatory stiffness. A biologic agent that treats both skin and joint disease is indicated, and his screening for tuberculosis, hepatitis, heart failure, and demyelinating disease is clear. Interleukin-17 and interleukin-23 inhibitors are also reasonable and treat both domains. <div class="ec-src"><b>Source:</b> Menter A, Strober BE, Kaplan DH, et al. Joint AAD-NPF guidelines of care for the management of psoriasis with biologics. J Am Acad Dermatol 2019;80(4):1029-1072.</div></div> [[Next case →->Dialysis initiation - Rx]] [[Start another case->Hub]] [[Restart this case->Psoriasis escalation - Rx]]

<span class="ec-case-marker" hidden data-entry="Psoriasis escalation. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> 8 months of potent topical therapy has already failed, and escalating potency over 18% of body surface risks skin atrophy and adrenal suppression. <div class="ec-teach"><div class="th">What the findings point to</div> He has moderate to severe psoriasis by body surface area that has failed topical therapy and phototherapy, and he has coexisting psoriatic arthritis evidenced by dactylitis and inflammatory stiffness. A biologic agent that treats both skin and joint disease is indicated, and his screening for tuberculosis, hepatitis, heart failure, and demyelinating disease is clear. Interleukin-17 and interleukin-23 inhibitors are also reasonable and treat both domains. <div class="ec-src"><b>Source:</b> Menter A, Strober BE, Kaplan DH, et al. Joint AAD-NPF guidelines of care for the management of psoriasis with biologics. J Am Acad Dermatol 2019;80(4):1029-1072.</div></div></div> [[Try this question again->Psoriasis escalation - Rx]] [[Next case →->Dialysis initiation - Rx]] [[Start another case->Hub]] [[Restart this case->Psoriasis escalation - Rx]]

<span class="ec-case-marker" hidden data-entry="Psoriasis escalation. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Systemic corticosteroids are avoided in psoriasis because withdrawal can precipitate pustular flares. <div class="ec-teach"><div class="th">What the findings point to</div> He has moderate to severe psoriasis by body surface area that has failed topical therapy and phototherapy, and he has coexisting psoriatic arthritis evidenced by dactylitis and inflammatory stiffness. A biologic agent that treats both skin and joint disease is indicated, and his screening for tuberculosis, hepatitis, heart failure, and demyelinating disease is clear. Interleukin-17 and interleukin-23 inhibitors are also reasonable and treat both domains. <div class="ec-src"><b>Source:</b> Menter A, Strober BE, Kaplan DH, et al. Joint AAD-NPF guidelines of care for the management of psoriasis with biologics. J Am Acad Dermatol 2019;80(4):1029-1072.</div></div></div> [[Try this question again->Psoriasis escalation - Rx]] [[Next case →->Dialysis initiation - Rx]] [[Start another case->Hub]] [[Restart this case->Psoriasis escalation - Rx]]

<span class="ec-case-marker" hidden data-entry="Psoriasis escalation. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Acitretin is modestly effective as monotherapy, is teratogenic for 3 years after stopping, and does not treat the joint disease. <div class="ec-teach"><div class="th">What the findings point to</div> He has moderate to severe psoriasis by body surface area that has failed topical therapy and phototherapy, and he has coexisting psoriatic arthritis evidenced by dactylitis and inflammatory stiffness. A biologic agent that treats both skin and joint disease is indicated, and his screening for tuberculosis, hepatitis, heart failure, and demyelinating disease is clear. Interleukin-17 and interleukin-23 inhibitors are also reasonable and treat both domains. <div class="ec-src"><b>Source:</b> Menter A, Strober BE, Kaplan DH, et al. Joint AAD-NPF guidelines of care for the management of psoriasis with biologics. J Am Acad Dermatol 2019;80(4):1029-1072.</div></div></div> [[Try this question again->Psoriasis escalation - Rx]] [[Next case →->Dialysis initiation - Rx]] [[Start another case->Hub]] [[Restart this case->Psoriasis escalation - Rx]]

<span class="ec-case-marker" hidden data-entry="Psoriasis escalation. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Cyclosporine works quickly but nephrotoxicity and hypertension limit it to short courses, not maintenance. <div class="ec-teach"><div class="th">What the findings point to</div> He has moderate to severe psoriasis by body surface area that has failed topical therapy and phototherapy, and he has coexisting psoriatic arthritis evidenced by dactylitis and inflammatory stiffness. A biologic agent that treats both skin and joint disease is indicated, and his screening for tuberculosis, hepatitis, heart failure, and demyelinating disease is clear. Interleukin-17 and interleukin-23 inhibitors are also reasonable and treat both domains. <div class="ec-src"><b>Source:</b> Menter A, Strober BE, Kaplan DH, et al. Joint AAD-NPF guidelines of care for the management of psoriasis with biologics. J Am Acad Dermatol 2019;80(4):1029-1072.</div></div></div> [[Try this question again->Psoriasis escalation - Rx]] [[Next case →->Dialysis initiation - Rx]] [[Start another case->Hub]] [[Restart this case->Psoriasis escalation - Rx]]

<span class="ec-case-marker" hidden data-entry="Psoriasis escalation. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> 4 months of phototherapy has failed. More of a failed modality delays effective treatment. <div class="ec-teach"><div class="th">What the findings point to</div> He has moderate to severe psoriasis by body surface area that has failed topical therapy and phototherapy, and he has coexisting psoriatic arthritis evidenced by dactylitis and inflammatory stiffness. A biologic agent that treats both skin and joint disease is indicated, and his screening for tuberculosis, hepatitis, heart failure, and demyelinating disease is clear. Interleukin-17 and interleukin-23 inhibitors are also reasonable and treat both domains. <div class="ec-src"><b>Source:</b> Menter A, Strober BE, Kaplan DH, et al. Joint AAD-NPF guidelines of care for the management of psoriasis with biologics. J Am Acad Dermatol 2019;80(4):1029-1072.</div></div></div> [[Try this question again->Psoriasis escalation - Rx]] [[Next case →->Dialysis initiation - Rx]] [[Start another case->Hub]] [[Restart this case->Psoriasis escalation - Rx]]

<div class="ec-scene">Nephrology consult · 06:20</div> A 58-year-old man with diabetic nephropathy is admitted with 4 days of nausea, hiccups, and confusion. Temperature is 36.9°C, blood pressure is 168/94 mm Hg, pulse is 96/min, and respirations are 24/min. Examination shows a pericardial friction rub and asterixis. Creatinine is 8.4 mg/dL, blood urea nitrogen is 142 mg/dL, potassium is 5.4 mEq/L, and bicarbonate is 16 mEq/L. He is producing 400 mL of urine daily and is euvolemic Examination shows. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Initiation of hemodialysis->Dialysis initiation - Rx correct]] [[Intensified blood pressure control with intravenous labetalol->Dialysis initiation - Rx D3]] [[Protein restriction and outpatient nephrology follow-up->Dialysis initiation - Rx D4]] [[Repeat laboratory studies in 24 hours to confirm the trend->Dialysis initiation - Rx D5]] [[Sodium bicarbonate infusion for the acidosis->Dialysis initiation - Rx D2]] [[Sodium polystyrene sulfonate for the potassium->Dialysis initiation - Rx D1]]

<span class="ec-case-marker" hidden data-entry="Dialysis initiation. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Initiation of hemodialysis</div> Uremic pericarditis and uremic encephalopathy are absolute indications for dialysis regardless of the creatinine value. The mnemonic indications are acidosis, electrolyte derangement, intoxication, volume overload and uremia, and he has two uremic complications with a friction rub and asterixis. Trials of early versus delayed initiation address asymptomatic patients based on numbers alone; they do not apply once a uremic complication has appeared. <div class="ec-src"><b>Source:</b> Bagshaw SM, Wald R, Adhikari NKJ, et al. Timing of Initiation of Renal-Replacement Therapy in Acutely Ill Critically Ill Patients (STARRT-AKI). N Engl J Med 2020;383(3):240-251.</div></div> [[Next case →->Obstructive uropathy decompression - Rx]] [[Start another case->Hub]] [[Restart this case->Dialysis initiation - Rx]]

<span class="ec-case-marker" hidden data-entry="Dialysis initiation. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A potassium of 5.4 mEq/L is not the indication here, and binders do not treat pericarditis or encephalopathy. <div class="ec-teach"><div class="th">What the findings point to</div> Uremic pericarditis and uremic encephalopathy are absolute indications for dialysis regardless of the creatinine value. The mnemonic indications are acidosis, electrolyte derangement, intoxication, volume overload and uremia, and he has two uremic complications with a friction rub and asterixis. Trials of early versus delayed initiation address asymptomatic patients based on numbers alone; they do not apply once a uremic complication has appeared. <div class="ec-src"><b>Source:</b> Bagshaw SM, Wald R, Adhikari NKJ, et al. Timing of Initiation of Renal-Replacement Therapy in Acutely Ill Critically Ill Patients (STARRT-AKI). N Engl J Med 2020;383(3):240-251.</div></div></div> [[Try this question again->Dialysis initiation - Rx]] [[Next case →->Obstructive uropathy decompression - Rx]] [[Start another case->Hub]] [[Restart this case->Dialysis initiation - Rx]]

<span class="ec-case-marker" hidden data-entry="Dialysis initiation. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Bicarbonate partially corrects one abnormality while the uremic complications that threaten him continue. <div class="ec-teach"><div class="th">What the findings point to</div> Uremic pericarditis and uremic encephalopathy are absolute indications for dialysis regardless of the creatinine value. The mnemonic indications are acidosis, electrolyte derangement, intoxication, volume overload and uremia, and he has two uremic complications with a friction rub and asterixis. Trials of early versus delayed initiation address asymptomatic patients based on numbers alone; they do not apply once a uremic complication has appeared. <div class="ec-src"><b>Source:</b> Bagshaw SM, Wald R, Adhikari NKJ, et al. Timing of Initiation of Renal-Replacement Therapy in Acutely Ill Critically Ill Patients (STARRT-AKI). N Engl J Med 2020;383(3):240-251.</div></div></div> [[Try this question again->Dialysis initiation - Rx]] [[Next case →->Obstructive uropathy decompression - Rx]] [[Start another case->Hub]] [[Restart this case->Dialysis initiation - Rx]]

<span class="ec-case-marker" hidden data-entry="Dialysis initiation. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> His hypertension is a consequence, not the problem. Lowering pressure does not address uremia. <div class="ec-teach"><div class="th">What the findings point to</div> Uremic pericarditis and uremic encephalopathy are absolute indications for dialysis regardless of the creatinine value. The mnemonic indications are acidosis, electrolyte derangement, intoxication, volume overload and uremia, and he has two uremic complications with a friction rub and asterixis. Trials of early versus delayed initiation address asymptomatic patients based on numbers alone; they do not apply once a uremic complication has appeared. <div class="ec-src"><b>Source:</b> Bagshaw SM, Wald R, Adhikari NKJ, et al. Timing of Initiation of Renal-Replacement Therapy in Acutely Ill Critically Ill Patients (STARRT-AKI). N Engl J Med 2020;383(3):240-251.</div></div></div> [[Try this question again->Dialysis initiation - Rx]] [[Next case →->Obstructive uropathy decompression - Rx]] [[Start another case->Hub]] [[Restart this case->Dialysis initiation - Rx]]

<span class="ec-case-marker" hidden data-entry="Dialysis initiation. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Dietary measures slow progression in stable outpatients. They have no role once uremic pericarditis is present. <div class="ec-teach"><div class="th">What the findings point to</div> Uremic pericarditis and uremic encephalopathy are absolute indications for dialysis regardless of the creatinine value. The mnemonic indications are acidosis, electrolyte derangement, intoxication, volume overload and uremia, and he has two uremic complications with a friction rub and asterixis. Trials of early versus delayed initiation address asymptomatic patients based on numbers alone; they do not apply once a uremic complication has appeared. <div class="ec-src"><b>Source:</b> Bagshaw SM, Wald R, Adhikari NKJ, et al. Timing of Initiation of Renal-Replacement Therapy in Acutely Ill Critically Ill Patients (STARRT-AKI). N Engl J Med 2020;383(3):240-251.</div></div></div> [[Try this question again->Dialysis initiation - Rx]] [[Next case →->Obstructive uropathy decompression - Rx]] [[Start another case->Hub]] [[Restart this case->Dialysis initiation - Rx]]

<span class="ec-case-marker" hidden data-entry="Dialysis initiation. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Uremic pericarditis can progress to tamponade. Waiting a day for confirmation of an established diagnosis is not defensible. <div class="ec-teach"><div class="th">What the findings point to</div> Uremic pericarditis and uremic encephalopathy are absolute indications for dialysis regardless of the creatinine value. The mnemonic indications are acidosis, electrolyte derangement, intoxication, volume overload and uremia, and he has two uremic complications with a friction rub and asterixis. Trials of early versus delayed initiation address asymptomatic patients based on numbers alone; they do not apply once a uremic complication has appeared. <div class="ec-src"><b>Source:</b> Bagshaw SM, Wald R, Adhikari NKJ, et al. Timing of Initiation of Renal-Replacement Therapy in Acutely Ill Critically Ill Patients (STARRT-AKI). N Engl J Med 2020;383(3):240-251.</div></div></div> [[Try this question again->Dialysis initiation - Rx]] [[Next case →->Obstructive uropathy decompression - Rx]] [[Start another case->Hub]] [[Restart this case->Dialysis initiation - Rx]]

<div class="ec-scene">Emergency department · 20:40</div> A 67-year-old man with known prostate cancer has 2 days of anuria and rising creatinine. Temperature is 38.4°C, blood pressure is 96/58 mm Hg, pulse is 118/min, and respirations are 22/min. Creatinine is 5.8 mg/dL from a baseline of 1.2 mg/dL, and potassium is 6.1 mEq/L. Bladder scan shows 40 mL. CT shows bilateral hydronephrosis with distal ureteral obstruction from pelvic nodal disease. Urinalysis shows pyuria and blood cultures are drawn. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Emergent hemodialysis for the hyperkalemia->Obstructive uropathy decompression - Rx D3]] [[High-dose intravenous furosemide to restore urine output->Obstructive uropathy decompression - Rx D4]] [[Intravenous antibiotics alone with fluid resuscitation->Obstructive uropathy decompression - Rx D2]] [[Palliative care consultation given metastatic disease->Obstructive uropathy decompression - Rx D5]] [[Urethral catheterization->Obstructive uropathy decompression - Rx D1]] [[Urgent percutaneous nephrostomy with antibiotics->Obstructive uropathy decompression - Rx correct]]

<span class="ec-case-marker" hidden data-entry="Obstructive uropathy decompression. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Urgent percutaneous nephrostomy with antibiotics</div> An obstructed, infected upper tract is a urologic emergency. Infection behind an obstruction does not respond to antibiotics alone because the drug cannot reach the closed, infected collecting system, and sepsis progresses. Decompression by percutaneous nephrostomy or retrograde stenting must accompany antimicrobial therapy, and it simultaneously relieves the postrenal failure and the hyperkalemia driving it. <div class="ec-src"><b>Source:</b> Wagenlehner FME, Pilatz A, Weidner W, Naber KG. Urosepsis: Overview of the diagnostic and treatment challenges. Microbiol Spectr 2015;3(5).</div></div> [[Next case →->Hyperkalemia intervention - Rx]] [[Start another case->Hub]] [[Restart this case->Obstructive uropathy decompression - Rx]]

<span class="ec-case-marker" hidden data-entry="Obstructive uropathy decompression. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The bladder contains 40 mL, so the obstruction is above the bladder. A urethral catheter drains nothing. <div class="ec-teach"><div class="th">What the findings point to</div> An obstructed, infected upper tract is a urologic emergency. Infection behind an obstruction does not respond to antibiotics alone because the drug cannot reach the closed, infected collecting system, and sepsis progresses. Decompression by percutaneous nephrostomy or retrograde stenting must accompany antimicrobial therapy, and it simultaneously relieves the postrenal failure and the hyperkalemia driving it. <div class="ec-src"><b>Source:</b> Wagenlehner FME, Pilatz A, Weidner W, Naber KG. Urosepsis: Overview of the diagnostic and treatment challenges. Microbiol Spectr 2015;3(5).</div></div></div> [[Try this question again->Obstructive uropathy decompression - Rx]] [[Next case →->Hyperkalemia intervention - Rx]] [[Start another case->Hub]] [[Restart this case->Obstructive uropathy decompression - Rx]]

<span class="ec-case-marker" hidden data-entry="Obstructive uropathy decompression. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Antibiotics cannot sterilize an obstructed system. Without decompression, septic shock progresses. <div class="ec-teach"><div class="th">What the findings point to</div> An obstructed, infected upper tract is a urologic emergency. Infection behind an obstruction does not respond to antibiotics alone because the drug cannot reach the closed, infected collecting system, and sepsis progresses. Decompression by percutaneous nephrostomy or retrograde stenting must accompany antimicrobial therapy, and it simultaneously relieves the postrenal failure and the hyperkalemia driving it. <div class="ec-src"><b>Source:</b> Wagenlehner FME, Pilatz A, Weidner W, Naber KG. Urosepsis: Overview of the diagnostic and treatment challenges. Microbiol Spectr 2015;3(5).</div></div></div> [[Try this question again->Obstructive uropathy decompression - Rx]] [[Next case →->Hyperkalemia intervention - Rx]] [[Start another case->Hub]] [[Restart this case->Obstructive uropathy decompression - Rx]]

<span class="ec-case-marker" hidden data-entry="Obstructive uropathy decompression. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Dialysis treats a consequence. Relieving the obstruction corrects the renal failure and the potassium at their source. <div class="ec-teach"><div class="th">What the findings point to</div> An obstructed, infected upper tract is a urologic emergency. Infection behind an obstruction does not respond to antibiotics alone because the drug cannot reach the closed, infected collecting system, and sepsis progresses. Decompression by percutaneous nephrostomy or retrograde stenting must accompany antimicrobial therapy, and it simultaneously relieves the postrenal failure and the hyperkalemia driving it. <div class="ec-src"><b>Source:</b> Wagenlehner FME, Pilatz A, Weidner W, Naber KG. Urosepsis: Overview of the diagnostic and treatment challenges. Microbiol Spectr 2015;3(5).</div></div></div> [[Try this question again->Obstructive uropathy decompression - Rx]] [[Next case →->Hyperkalemia intervention - Rx]] [[Start another case->Hub]] [[Restart this case->Obstructive uropathy decompression - Rx]]

<span class="ec-case-marker" hidden data-entry="Obstructive uropathy decompression. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Diuretics do not overcome mechanical obstruction and worsen volume depletion in a hypotensive patient. <div class="ec-teach"><div class="th">What the findings point to</div> An obstructed, infected upper tract is a urologic emergency. Infection behind an obstruction does not respond to antibiotics alone because the drug cannot reach the closed, infected collecting system, and sepsis progresses. Decompression by percutaneous nephrostomy or retrograde stenting must accompany antimicrobial therapy, and it simultaneously relieves the postrenal failure and the hyperkalemia driving it. <div class="ec-src"><b>Source:</b> Wagenlehner FME, Pilatz A, Weidner W, Naber KG. Urosepsis: Overview of the diagnostic and treatment challenges. Microbiol Spectr 2015;3(5).</div></div></div> [[Try this question again->Obstructive uropathy decompression - Rx]] [[Next case →->Hyperkalemia intervention - Rx]] [[Start another case->Hub]] [[Restart this case->Obstructive uropathy decompression - Rx]]

<span class="ec-case-marker" hidden data-entry="Obstructive uropathy decompression. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Obstruction from nodal disease is often reversible, and this is a treatable acute emergency regardless of the underlying cancer stage. <div class="ec-teach"><div class="th">What the findings point to</div> An obstructed, infected upper tract is a urologic emergency. Infection behind an obstruction does not respond to antibiotics alone because the drug cannot reach the closed, infected collecting system, and sepsis progresses. Decompression by percutaneous nephrostomy or retrograde stenting must accompany antimicrobial therapy, and it simultaneously relieves the postrenal failure and the hyperkalemia driving it. <div class="ec-src"><b>Source:</b> Wagenlehner FME, Pilatz A, Weidner W, Naber KG. Urosepsis: Overview of the diagnostic and treatment challenges. Microbiol Spectr 2015;3(5).</div></div></div> [[Try this question again->Obstructive uropathy decompression - Rx]] [[Next case →->Hyperkalemia intervention - Rx]] [[Start another case->Hub]] [[Restart this case->Obstructive uropathy decompression - Rx]]

<div class="ec-scene">Emergency department · 09:35</div> A 72-year-old woman with chronic kidney disease presents with weakness. Temperature is 36.6°C, blood pressure is 108/64 mm Hg, pulse is 46/min, and respirations are 16/min. Serum potassium is 7.4 mEq/L, creatinine is 3.6 mg/dL, and bicarbonate is 18 mEq/L. Electrocardiography shows a widened QRS at 148 milliseconds with a sine-wave pattern beginning to emerge and absent P waves. She takes lisinopril and spironolactone. <span class="ec-prompt">Which of the following is the most appropriate immediate intervention?</span> [[Intravenous calcium gluconate->Hyperkalemia intervention - Rx correct]] [[Intravenous regular insulin with dextrose->Hyperkalemia intervention - Rx D1]] [[Intravenous sodium bicarbonate->Hyperkalemia intervention - Rx D5]] [[Nebulized albuterol at high dose->Hyperkalemia intervention - Rx D2]] [[Sodium zirconium cyclosilicate orally->Hyperkalemia intervention - Rx D3]] [[Urgent hemodialysis->Hyperkalemia intervention - Rx D4]]

<span class="ec-case-marker" hidden data-entry="Hyperkalemia intervention. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Intravenous calcium gluconate</div> With a sine-wave pattern the patient is minutes from cardiac arrest. Calcium does not lower potassium; it antagonizes the effect of hyperkalemia at the myocyte membrane and restores the transmembrane threshold potential within minutes. It is therefore always the first intervention when electrocardiographic changes are present. Insulin with glucose, beta-agonist, and definitive removal by dialysis follow immediately afterward, and the offending drugs are stopped. <div class="ec-src"><b>Source:</b> Lindner G, Burdmann EA, Clase CM, et al. Acute hyperkalemia in the emergency department: a summary from a Kidney Disease: Improving Global Outcomes conference. Eur J Emerg Med 2020;27(5):329-337.</div></div> [[Next case →->Urinary retention decompression - Rx]] [[Start another case->Hub]] [[Restart this case->Hyperkalemia intervention - Rx]]

<span class="ec-case-marker" hidden data-entry="Hyperkalemia intervention. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Insulin shifts potassium intracellularly and is essential, but it takes 15 to 30 minutes to act. Membrane stabilization must come first. <div class="ec-teach"><div class="th">What the findings point to</div> With a sine-wave pattern the patient is minutes from cardiac arrest. Calcium does not lower potassium; it antagonizes the effect of hyperkalemia at the myocyte membrane and restores the transmembrane threshold potential within minutes. It is therefore always the first intervention when electrocardiographic changes are present. Insulin with glucose, beta-agonist, and definitive removal by dialysis follow immediately afterward, and the offending drugs are stopped. <div class="ec-src"><b>Source:</b> Lindner G, Burdmann EA, Clase CM, et al. Acute hyperkalemia in the emergency department: a summary from a Kidney Disease: Improving Global Outcomes conference. Eur J Emerg Med 2020;27(5):329-337.</div></div></div> [[Try this question again->Hyperkalemia intervention - Rx]] [[Next case →->Urinary retention decompression - Rx]] [[Start another case->Hub]] [[Restart this case->Hyperkalemia intervention - Rx]]

<span class="ec-case-marker" hidden data-entry="Hyperkalemia intervention. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Beta-agonists shift potassium but act over 30 minutes and lower it modestly. They do not protect the myocardium now. <div class="ec-teach"><div class="th">What the findings point to</div> With a sine-wave pattern the patient is minutes from cardiac arrest. Calcium does not lower potassium; it antagonizes the effect of hyperkalemia at the myocyte membrane and restores the transmembrane threshold potential within minutes. It is therefore always the first intervention when electrocardiographic changes are present. Insulin with glucose, beta-agonist, and definitive removal by dialysis follow immediately afterward, and the offending drugs are stopped. <div class="ec-src"><b>Source:</b> Lindner G, Burdmann EA, Clase CM, et al. Acute hyperkalemia in the emergency department: a summary from a Kidney Disease: Improving Global Outcomes conference. Eur J Emerg Med 2020;27(5):329-337.</div></div></div> [[Try this question again->Hyperkalemia intervention - Rx]] [[Next case →->Urinary retention decompression - Rx]] [[Start another case->Hub]] [[Restart this case->Hyperkalemia intervention - Rx]]

<span class="ec-case-marker" hidden data-entry="Hyperkalemia intervention. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Gastrointestinal binders remove potassium over hours and have no role as the immediate intervention in an unstable patient. <div class="ec-teach"><div class="th">What the findings point to</div> With a sine-wave pattern the patient is minutes from cardiac arrest. Calcium does not lower potassium; it antagonizes the effect of hyperkalemia at the myocyte membrane and restores the transmembrane threshold potential within minutes. It is therefore always the first intervention when electrocardiographic changes are present. Insulin with glucose, beta-agonist, and definitive removal by dialysis follow immediately afterward, and the offending drugs are stopped. <div class="ec-src"><b>Source:</b> Lindner G, Burdmann EA, Clase CM, et al. Acute hyperkalemia in the emergency department: a summary from a Kidney Disease: Improving Global Outcomes conference. Eur J Emerg Med 2020;27(5):329-337.</div></div></div> [[Try this question again->Hyperkalemia intervention - Rx]] [[Next case →->Urinary retention decompression - Rx]] [[Start another case->Hub]] [[Restart this case->Hyperkalemia intervention - Rx]]

<span class="ec-case-marker" hidden data-entry="Hyperkalemia intervention. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Dialysis is the definitive removal step and should be arranged, but it cannot be initiated within the minutes this rhythm allows. <div class="ec-teach"><div class="th">What the findings point to</div> With a sine-wave pattern the patient is minutes from cardiac arrest. Calcium does not lower potassium; it antagonizes the effect of hyperkalemia at the myocyte membrane and restores the transmembrane threshold potential within minutes. It is therefore always the first intervention when electrocardiographic changes are present. Insulin with glucose, beta-agonist, and definitive removal by dialysis follow immediately afterward, and the offending drugs are stopped. <div class="ec-src"><b>Source:</b> Lindner G, Burdmann EA, Clase CM, et al. Acute hyperkalemia in the emergency department: a summary from a Kidney Disease: Improving Global Outcomes conference. Eur J Emerg Med 2020;27(5):329-337.</div></div></div> [[Try this question again->Hyperkalemia intervention - Rx]] [[Next case →->Urinary retention decompression - Rx]] [[Start another case->Hub]] [[Restart this case->Hyperkalemia intervention - Rx]]

<span class="ec-case-marker" hidden data-entry="Hyperkalemia intervention. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Bicarbonate has an unreliable and modest potassium-lowering effect, particularly in patients with kidney failure, and does not stabilize the membrane. <div class="ec-teach"><div class="th">What the findings point to</div> With a sine-wave pattern the patient is minutes from cardiac arrest. Calcium does not lower potassium; it antagonizes the effect of hyperkalemia at the myocyte membrane and restores the transmembrane threshold potential within minutes. It is therefore always the first intervention when electrocardiographic changes are present. Insulin with glucose, beta-agonist, and definitive removal by dialysis follow immediately afterward, and the offending drugs are stopped. <div class="ec-src"><b>Source:</b> Lindner G, Burdmann EA, Clase CM, et al. Acute hyperkalemia in the emergency department: a summary from a Kidney Disease: Improving Global Outcomes conference. Eur J Emerg Med 2020;27(5):329-337.</div></div></div> [[Try this question again->Hyperkalemia intervention - Rx]] [[Next case →->Urinary retention decompression - Rx]] [[Start another case->Hub]] [[Restart this case->Hyperkalemia intervention - Rx]]

<div class="ec-scene">Emergency department · 02:05</div> A 74-year-old man has been unable to void for 14 hours and has suprapubic pain. Temperature is 36.8°C, blood pressure is 152/88 mm Hg, and pulse is 96/min. The bladder is palpable to the umbilicus and bladder scan shows 1,150 mL. Creatinine is 2.4 mg/dL from a baseline of 1.1 mg/dL. He was started on diphenhydramine and pseudoephedrine 2 days ago for a cold. Digital rectal examination shows a smoothly enlarged prostate without nodules. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Finasteride to reduce prostate volume->Urinary retention decompression - Rx D4]] [[Intermittent clamping of the catheter every 500 mL->Urinary retention decompression - Rx D3]] [[Intravenous fluids and observation for spontaneous voiding->Urinary retention decompression - Rx D5]] [[Suprapubic catheter placement as first-line->Urinary retention decompression - Rx D2]] [[Tamsulosin alone with outpatient urology follow-up->Urinary retention decompression - Rx D1]] [[Urethral catheterization with complete bladder drainage->Urinary retention decompression - Rx correct]]

<span class="ec-case-marker" hidden data-entry="Urinary retention decompression. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Urethral catheterization with complete bladder drainage</div> Acute retention with postrenal azotemia requires immediate decompression, and catheterization both relieves the obstruction and corrects the kidney injury. Older teaching to clamp intermittently to avoid decompression hematuria is not supported; complete drainage is appropriate. Post-obstructive diuresis must then be anticipated and urine output replaced. The anticholinergic and alpha-agonist he started 2 days ago are the precipitant and should be stopped. <div class="ec-src"><b>Source:</b> Selius BA, Subedi R. Urinary retention in adults: diagnosis and initial management. Am Fam Physician 2008;77(5):643-650.</div></div> [[Next case →->BPH pharmacotherapy - Rx]] [[Start another case->Hub]] [[Restart this case->Urinary retention decompression - Rx]]

<span class="ec-case-marker" hidden data-entry="Urinary retention decompression. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Alpha blockade improves the chance of a successful voiding trial later. It does not empty a bladder holding 1,150 mL tonight. <div class="ec-teach"><div class="th">What the findings point to</div> Acute retention with postrenal azotemia requires immediate decompression, and catheterization both relieves the obstruction and corrects the kidney injury. Older teaching to clamp intermittently to avoid decompression hematuria is not supported; complete drainage is appropriate. Post-obstructive diuresis must then be anticipated and urine output replaced. The anticholinergic and alpha-agonist he started 2 days ago are the precipitant and should be stopped. <div class="ec-src"><b>Source:</b> Selius BA, Subedi R. Urinary retention in adults: diagnosis and initial management. Am Fam Physician 2008;77(5):643-650.</div></div></div> [[Try this question again->Urinary retention decompression - Rx]] [[Next case →->BPH pharmacotherapy - Rx]] [[Start another case->Hub]] [[Restart this case->Urinary retention decompression - Rx]]

<span class="ec-case-marker" hidden data-entry="Urinary retention decompression. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Suprapubic drainage is reserved for failed or contraindicated urethral catheterization, such as urethral stricture or trauma. <div class="ec-teach"><div class="th">What the findings point to</div> Acute retention with postrenal azotemia requires immediate decompression, and catheterization both relieves the obstruction and corrects the kidney injury. Older teaching to clamp intermittently to avoid decompression hematuria is not supported; complete drainage is appropriate. Post-obstructive diuresis must then be anticipated and urine output replaced. The anticholinergic and alpha-agonist he started 2 days ago are the precipitant and should be stopped. <div class="ec-src"><b>Source:</b> Selius BA, Subedi R. Urinary retention in adults: diagnosis and initial management. Am Fam Physician 2008;77(5):643-650.</div></div></div> [[Try this question again->Urinary retention decompression - Rx]] [[Next case →->BPH pharmacotherapy - Rx]] [[Start another case->Hub]] [[Restart this case->Urinary retention decompression - Rx]]

<span class="ec-case-marker" hidden data-entry="Urinary retention decompression. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Gradual decompression has not been shown to prevent hematuria or hypotension and delays relief. <div class="ec-teach"><div class="th">What the findings point to</div> Acute retention with postrenal azotemia requires immediate decompression, and catheterization both relieves the obstruction and corrects the kidney injury. Older teaching to clamp intermittently to avoid decompression hematuria is not supported; complete drainage is appropriate. Post-obstructive diuresis must then be anticipated and urine output replaced. The anticholinergic and alpha-agonist he started 2 days ago are the precipitant and should be stopped. <div class="ec-src"><b>Source:</b> Selius BA, Subedi R. Urinary retention in adults: diagnosis and initial management. Am Fam Physician 2008;77(5):643-650.</div></div></div> [[Try this question again->Urinary retention decompression - Rx]] [[Next case →->BPH pharmacotherapy - Rx]] [[Start another case->Hub]] [[Restart this case->Urinary retention decompression - Rx]]

<span class="ec-case-marker" hidden data-entry="Urinary retention decompression. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Five-alpha reductase inhibitors take months to shrink the prostate and are irrelevant to an acute obstruction. <div class="ec-teach"><div class="th">What the findings point to</div> Acute retention with postrenal azotemia requires immediate decompression, and catheterization both relieves the obstruction and corrects the kidney injury. Older teaching to clamp intermittently to avoid decompression hematuria is not supported; complete drainage is appropriate. Post-obstructive diuresis must then be anticipated and urine output replaced. The anticholinergic and alpha-agonist he started 2 days ago are the precipitant and should be stopped. <div class="ec-src"><b>Source:</b> Selius BA, Subedi R. Urinary retention in adults: diagnosis and initial management. Am Fam Physician 2008;77(5):643-650.</div></div></div> [[Try this question again->Urinary retention decompression - Rx]] [[Next case →->BPH pharmacotherapy - Rx]] [[Start another case->Hub]] [[Restart this case->Urinary retention decompression - Rx]]

<span class="ec-case-marker" hidden data-entry="Urinary retention decompression. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Giving fluid to an obstructed bladder increases pressure and risks rupture without addressing the obstruction. <div class="ec-teach"><div class="th">What the findings point to</div> Acute retention with postrenal azotemia requires immediate decompression, and catheterization both relieves the obstruction and corrects the kidney injury. Older teaching to clamp intermittently to avoid decompression hematuria is not supported; complete drainage is appropriate. Post-obstructive diuresis must then be anticipated and urine output replaced. The anticholinergic and alpha-agonist he started 2 days ago are the precipitant and should be stopped. <div class="ec-src"><b>Source:</b> Selius BA, Subedi R. Urinary retention in adults: diagnosis and initial management. Am Fam Physician 2008;77(5):643-650.</div></div></div> [[Try this question again->Urinary retention decompression - Rx]] [[Next case →->BPH pharmacotherapy - Rx]] [[Start another case->Hub]] [[Restart this case->Urinary retention decompression - Rx]]

<div class="ec-scene">Primary care clinic · 11:05</div> A 66-year-old man reports 2 years of progressive nocturia four times nightly, weak stream, hesitancy, and incomplete emptying. Blood pressure is 118/72 mm Hg and pulse is 72/min. Digital rectal examination shows a markedly enlarged, smooth prostate estimated at 65 g. Prostate-specific antigen is 3.8 ng/mL. Postvoid residual is 110 mL and creatinine is 1.0 mg/dL. He has no orthostatic symptoms and is scheduled for cataract surgery in 6 weeks. <span class="ec-prompt">Which of the following is the most appropriate pharmacotherapy?</span> [[5-alpha reductase inhibitor such as finasteride->BPH pharmacotherapy - Rx correct]] [[Desmopressin at bedtime->BPH pharmacotherapy - Rx D4]] [[Immediate referral for transurethral resection->BPH pharmacotherapy - Rx D5]] [[Oxybutynin for the nocturia->BPH pharmacotherapy - Rx D2]] [[Tadalafil 5 mg daily->BPH pharmacotherapy - Rx D3]] [[Tamsulosin started today->BPH pharmacotherapy - Rx D1]]

<span class="ec-case-marker" hidden data-entry="BPH pharmacotherapy. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ 5-alpha reductase inhibitor such as finasteride</div> With a prostate estimated at 65 g, gland volume above roughly 30 to 40 g predicts benefit from 5-alpha reductase inhibition, which shrinks the prostate over 6 to 12 months and reduces the risk of acute retention and the need for surgery. Alpha blockers act faster but carry intraoperative floppy iris syndrome risk, which matters because he has cataract surgery scheduled in 6 weeks. Starting the reductase inhibitor now and deferring any alpha blocker until after the operation avoids that complication. <div class="ec-src"><b>Source:</b> Lerner LB, McVary KT, Barry MJ, et al. Management of Lower Urinary Tract Symptoms Attributed to Benign Prostatic Hyperplasia: AUA Guideline. J Urol 2021;206(4):806-817.</div></div> [[Next case →->Contrast nephropathy prevention - Prevention]] [[Start another case->Hub]] [[Restart this case->BPH pharmacotherapy - Rx]]

<span class="ec-case-marker" hidden data-entry="BPH pharmacotherapy. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Alpha blockers precipitate intraoperative floppy iris syndrome, and starting one 6 weeks before cataract surgery is the specific situation in which this is avoided. <div class="ec-teach"><div class="th">What the findings point to</div> With a prostate estimated at 65 g, gland volume above roughly 30 to 40 g predicts benefit from 5-alpha reductase inhibition, which shrinks the prostate over 6 to 12 months and reduces the risk of acute retention and the need for surgery. Alpha blockers act faster but carry intraoperative floppy iris syndrome risk, which matters because he has cataract surgery scheduled in 6 weeks. Starting the reductase inhibitor now and deferring any alpha blocker until after the operation avoids that complication. <div class="ec-src"><b>Source:</b> Lerner LB, McVary KT, Barry MJ, et al. Management of Lower Urinary Tract Symptoms Attributed to Benign Prostatic Hyperplasia: AUA Guideline. J Urol 2021;206(4):806-817.</div></div></div> [[Try this question again->BPH pharmacotherapy - Rx]] [[Next case →->Contrast nephropathy prevention - Prevention]] [[Start another case->Hub]] [[Restart this case->BPH pharmacotherapy - Rx]]

<span class="ec-case-marker" hidden data-entry="BPH pharmacotherapy. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Anticholinergics worsen emptying and risk precipitating retention in a man with a postvoid residual of 110 mL and obstruction. <div class="ec-teach"><div class="th">What the findings point to</div> With a prostate estimated at 65 g, gland volume above roughly 30 to 40 g predicts benefit from 5-alpha reductase inhibition, which shrinks the prostate over 6 to 12 months and reduces the risk of acute retention and the need for surgery. Alpha blockers act faster but carry intraoperative floppy iris syndrome risk, which matters because he has cataract surgery scheduled in 6 weeks. Starting the reductase inhibitor now and deferring any alpha blocker until after the operation avoids that complication. <div class="ec-src"><b>Source:</b> Lerner LB, McVary KT, Barry MJ, et al. Management of Lower Urinary Tract Symptoms Attributed to Benign Prostatic Hyperplasia: AUA Guideline. J Urol 2021;206(4):806-817.</div></div></div> [[Try this question again->BPH pharmacotherapy - Rx]] [[Next case →->Contrast nephropathy prevention - Prevention]] [[Start another case->Hub]] [[Restart this case->BPH pharmacotherapy - Rx]]

<span class="ec-case-marker" hidden data-entry="BPH pharmacotherapy. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Daily tadalafil improves symptoms modestly and is an option, but it does not reduce gland volume or retention risk in a 65 g prostate. <div class="ec-teach"><div class="th">What the findings point to</div> With a prostate estimated at 65 g, gland volume above roughly 30 to 40 g predicts benefit from 5-alpha reductase inhibition, which shrinks the prostate over 6 to 12 months and reduces the risk of acute retention and the need for surgery. Alpha blockers act faster but carry intraoperative floppy iris syndrome risk, which matters because he has cataract surgery scheduled in 6 weeks. Starting the reductase inhibitor now and deferring any alpha blocker until after the operation avoids that complication. <div class="ec-src"><b>Source:</b> Lerner LB, McVary KT, Barry MJ, et al. Management of Lower Urinary Tract Symptoms Attributed to Benign Prostatic Hyperplasia: AUA Guideline. J Urol 2021;206(4):806-817.</div></div></div> [[Try this question again->BPH pharmacotherapy - Rx]] [[Next case →->Contrast nephropathy prevention - Prevention]] [[Start another case->Hub]] [[Restart this case->BPH pharmacotherapy - Rx]]

<span class="ec-case-marker" hidden data-entry="BPH pharmacotherapy. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Desmopressin targets nocturnal polyuria and carries serious hyponatremia risk in older men. His nocturia is obstructive. <div class="ec-teach"><div class="th">What the findings point to</div> With a prostate estimated at 65 g, gland volume above roughly 30 to 40 g predicts benefit from 5-alpha reductase inhibition, which shrinks the prostate over 6 to 12 months and reduces the risk of acute retention and the need for surgery. Alpha blockers act faster but carry intraoperative floppy iris syndrome risk, which matters because he has cataract surgery scheduled in 6 weeks. Starting the reductase inhibitor now and deferring any alpha blocker until after the operation avoids that complication. <div class="ec-src"><b>Source:</b> Lerner LB, McVary KT, Barry MJ, et al. Management of Lower Urinary Tract Symptoms Attributed to Benign Prostatic Hyperplasia: AUA Guideline. J Urol 2021;206(4):806-817.</div></div></div> [[Try this question again->BPH pharmacotherapy - Rx]] [[Next case →->Contrast nephropathy prevention - Prevention]] [[Start another case->Hub]] [[Restart this case->BPH pharmacotherapy - Rx]]

<span class="ec-case-marker" hidden data-entry="BPH pharmacotherapy. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Surgery is appropriate after failed medical therapy or for refractory retention, recurrent infection, stones, or renal impairment, none of which he has. <div class="ec-teach"><div class="th">What the findings point to</div> With a prostate estimated at 65 g, gland volume above roughly 30 to 40 g predicts benefit from 5-alpha reductase inhibition, which shrinks the prostate over 6 to 12 months and reduces the risk of acute retention and the need for surgery. Alpha blockers act faster but carry intraoperative floppy iris syndrome risk, which matters because he has cataract surgery scheduled in 6 weeks. Starting the reductase inhibitor now and deferring any alpha blocker until after the operation avoids that complication. <div class="ec-src"><b>Source:</b> Lerner LB, McVary KT, Barry MJ, et al. Management of Lower Urinary Tract Symptoms Attributed to Benign Prostatic Hyperplasia: AUA Guideline. J Urol 2021;206(4):806-817.</div></div></div> [[Try this question again->BPH pharmacotherapy - Rx]] [[Next case →->Contrast nephropathy prevention - Prevention]] [[Start another case->Hub]] [[Restart this case->BPH pharmacotherapy - Rx]]

<div class="ec-scene">Preprocedure area · 07:45</div> A 69-year-old man with type 2 diabetes mellitus is scheduled for coronary angiography. Creatinine is 1.9 mg/dL with an estimated glomerular filtration rate of 36 mL/min/1.73 m2. Blood pressure is 128/76 mm Hg, pulse is 74/min, and he is euvolemic with no jugular venous distention and clear lungs. He takes metformin, lisinopril, and furosemide. Ejection fraction is 55%. <span class="ec-prompt">Which of the following is the most appropriate step to reduce his risk of contrast-associated kidney injury?</span> [[High-dose furosemide to maintain urine output->Contrast nephropathy prevention - Prevention D4]] [[Intravenous isotonic saline before and after the procedure->Contrast nephropathy prevention - Prevention correct]] [[Intravenous sodium bicarbonate instead of saline->Contrast nephropathy prevention - Prevention D2]] [[Oral N-acetylcysteine before and after contrast->Contrast nephropathy prevention - Prevention D1]] [[Prophylactic hemodialysis after the procedure->Contrast nephropathy prevention - Prevention D3]] [[Substituting gadolinium contrast for iodinated contrast->Contrast nephropathy prevention - Prevention D5]]

<span class="ec-case-marker" hidden data-entry="Contrast nephropathy prevention. Prevention"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Intravenous isotonic saline before and after the procedure</div> Volume expansion with isotonic crystalloid is the only intervention with consistent supporting evidence for reducing contrast-associated acute kidney injury in patients with reduced glomerular filtration rate. Minimizing contrast volume and holding nephrotoxins are also appropriate. Metformin is held not to protect the kidney but because kidney injury would predispose to lactic acidosis, and it is restarted after renal function is confirmed stable. <div class="ec-src"><b>Source:</b> Weisbord SD, Gallagher M, Jneid H, et al. Outcomes after Angiography with Sodium Bicarbonate and Acetylcysteine (PRESERVE). N Engl J Med 2018;378(7):603-614.</div></div> [[Next case →->Transplant rejection - Dx]] [[Start another case->Hub]] [[Restart this case->Contrast nephropathy prevention - Prevention]]

<span class="ec-case-marker" hidden data-entry="Contrast nephropathy prevention. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A large randomized trial found no benefit from acetylcysteine for contrast-associated kidney injury or for death and dialysis. <div class="ec-teach"><div class="th">What the findings point to</div> Volume expansion with isotonic crystalloid is the only intervention with consistent supporting evidence for reducing contrast-associated acute kidney injury in patients with reduced glomerular filtration rate. Minimizing contrast volume and holding nephrotoxins are also appropriate. Metformin is held not to protect the kidney but because kidney injury would predispose to lactic acidosis, and it is restarted after renal function is confirmed stable. <div class="ec-src"><b>Source:</b> Weisbord SD, Gallagher M, Jneid H, et al. Outcomes after Angiography with Sodium Bicarbonate and Acetylcysteine (PRESERVE). N Engl J Med 2018;378(7):603-614.</div></div></div> [[Try this question again->Contrast nephropathy prevention - Prevention]] [[Next case →->Transplant rejection - Dx]] [[Start another case->Hub]] [[Restart this case->Contrast nephropathy prevention - Prevention]]

<span class="ec-case-marker" hidden data-entry="Contrast nephropathy prevention. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The same trial found bicarbonate no better than isotonic saline, so there is no reason to prefer it. <div class="ec-teach"><div class="th">What the findings point to</div> Volume expansion with isotonic crystalloid is the only intervention with consistent supporting evidence for reducing contrast-associated acute kidney injury in patients with reduced glomerular filtration rate. Minimizing contrast volume and holding nephrotoxins are also appropriate. Metformin is held not to protect the kidney but because kidney injury would predispose to lactic acidosis, and it is restarted after renal function is confirmed stable. <div class="ec-src"><b>Source:</b> Weisbord SD, Gallagher M, Jneid H, et al. Outcomes after Angiography with Sodium Bicarbonate and Acetylcysteine (PRESERVE). N Engl J Med 2018;378(7):603-614.</div></div></div> [[Try this question again->Contrast nephropathy prevention - Prevention]] [[Next case →->Transplant rejection - Dx]] [[Start another case->Hub]] [[Restart this case->Contrast nephropathy prevention - Prevention]]

<span class="ec-case-marker" hidden data-entry="Contrast nephropathy prevention. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Post-procedure dialysis does not prevent injury and exposes the patient to the risks of vascular access. <div class="ec-teach"><div class="th">What the findings point to</div> Volume expansion with isotonic crystalloid is the only intervention with consistent supporting evidence for reducing contrast-associated acute kidney injury in patients with reduced glomerular filtration rate. Minimizing contrast volume and holding nephrotoxins are also appropriate. Metformin is held not to protect the kidney but because kidney injury would predispose to lactic acidosis, and it is restarted after renal function is confirmed stable. <div class="ec-src"><b>Source:</b> Weisbord SD, Gallagher M, Jneid H, et al. Outcomes after Angiography with Sodium Bicarbonate and Acetylcysteine (PRESERVE). N Engl J Med 2018;378(7):603-614.</div></div></div> [[Try this question again->Contrast nephropathy prevention - Prevention]] [[Next case →->Transplant rejection - Dx]] [[Start another case->Hub]] [[Restart this case->Contrast nephropathy prevention - Prevention]]

<span class="ec-case-marker" hidden data-entry="Contrast nephropathy prevention. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Forced diuresis worsens volume depletion and increases the risk of injury rather than reducing it. <div class="ec-teach"><div class="th">What the findings point to</div> Volume expansion with isotonic crystalloid is the only intervention with consistent supporting evidence for reducing contrast-associated acute kidney injury in patients with reduced glomerular filtration rate. Minimizing contrast volume and holding nephrotoxins are also appropriate. Metformin is held not to protect the kidney but because kidney injury would predispose to lactic acidosis, and it is restarted after renal function is confirmed stable. <div class="ec-src"><b>Source:</b> Weisbord SD, Gallagher M, Jneid H, et al. Outcomes after Angiography with Sodium Bicarbonate and Acetylcysteine (PRESERVE). N Engl J Med 2018;378(7):603-614.</div></div></div> [[Try this question again->Contrast nephropathy prevention - Prevention]] [[Next case →->Transplant rejection - Dx]] [[Start another case->Hub]] [[Restart this case->Contrast nephropathy prevention - Prevention]]

<span class="ec-case-marker" hidden data-entry="Contrast nephropathy prevention. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Gadolinium is not a substitute for coronary angiography and carries nephrogenic systemic fibrosis risk at reduced glomerular filtration rate. <div class="ec-teach"><div class="th">What the findings point to</div> Volume expansion with isotonic crystalloid is the only intervention with consistent supporting evidence for reducing contrast-associated acute kidney injury in patients with reduced glomerular filtration rate. Minimizing contrast volume and holding nephrotoxins are also appropriate. Metformin is held not to protect the kidney but because kidney injury would predispose to lactic acidosis, and it is restarted after renal function is confirmed stable. <div class="ec-src"><b>Source:</b> Weisbord SD, Gallagher M, Jneid H, et al. Outcomes after Angiography with Sodium Bicarbonate and Acetylcysteine (PRESERVE). N Engl J Med 2018;378(7):603-614.</div></div></div> [[Try this question again->Contrast nephropathy prevention - Prevention]] [[Next case →->Transplant rejection - Dx]] [[Start another case->Hub]] [[Restart this case->Contrast nephropathy prevention - Prevention]]

<div class="ec-scene">Transplant clinic · 10:15</div> A 41-year-old woman is 5 weeks after a deceased-donor kidney transplant on tacrolimus, mycophenolate, and prednisone. Creatinine has risen from 1.2 to 2.3 mg/dL over 6 days. Temperature is 37.4°C, blood pressure is 148/90 mm Hg, and pulse is 84/min. There is mild graft tenderness and urine output has fallen. Tacrolimus trough is 6 ng/mL, within target. Ultrasonography shows no hydronephrosis and normal arterial and venous flow. Urinalysis shows no casts and BK virus PCR is negative. <span class="ec-prompt">Which of the following is the most appropriate next step in evaluation?</span> [[Empiric pulse methylprednisolone without biopsy->Transplant rejection - Dx D1]] [[Increase the tacrolimus dose->Transplant rejection - Dx D2]] [[Percutaneous allograft biopsy->Transplant rejection - Dx correct]] [[Reduce immunosuppression and observe->Transplant rejection - Dx D3]] [[Repeat ultrasonography with resistive indices in 1 week->Transplant rejection - Dx D4]] [[Start valganciclovir for presumed cytomegalovirus disease->Transplant rejection - Dx D5]]

<span class="ec-case-marker" hidden data-entry="Transplant rejection. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Percutaneous allograft biopsy</div> Rising creatinine in the early post-transplant period with obstruction, vascular compromise, BK nephropathy, and calcineurin inhibitor toxicity all excluded points to rejection, but the distinction between cell-mediated and antibody-mediated rejection changes treatment completely. Only histology makes that distinction, and treating empirically with pulse steroid would be wrong if the process is antibody mediated. Biopsy is the standard of care before treating a rejection episode. <div class="ec-src"><b>Source:</b> Kidney Disease: Improving Global Outcomes (KDIGO) Transplant Work Group. KDIGO clinical practice guideline for the care of kidney transplant recipients. Am J Transplant 2009;9(S3):S1-S155.</div></div> [[Next case →->Nephrolithiasis intervention - Rx]] [[Start another case->Hub]] [[Restart this case->Transplant rejection - Dx]]

<span class="ec-case-marker" hidden data-entry="Transplant rejection. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Steroid pulse treats cell-mediated rejection and is ineffective for antibody-mediated rejection, which requires plasmapheresis and immune globulin. <div class="ec-teach"><div class="th">What the findings point to</div> Rising creatinine in the early post-transplant period with obstruction, vascular compromise, BK nephropathy, and calcineurin inhibitor toxicity all excluded points to rejection, but the distinction between cell-mediated and antibody-mediated rejection changes treatment completely. Only histology makes that distinction, and treating empirically with pulse steroid would be wrong if the process is antibody mediated. Biopsy is the standard of care before treating a rejection episode. <div class="ec-src"><b>Source:</b> Kidney Disease: Improving Global Outcomes (KDIGO) Transplant Work Group. KDIGO clinical practice guideline for the care of kidney transplant recipients. Am J Transplant 2009;9(S3):S1-S155.</div></div></div> [[Try this question again->Transplant rejection - Dx]] [[Next case →->Nephrolithiasis intervention - Rx]] [[Start another case->Hub]] [[Restart this case->Transplant rejection - Dx]]

<span class="ec-case-marker" hidden data-entry="Transplant rejection. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The trough is already in target. Raising it risks calcineurin inhibitor nephrotoxicity, which produces the same rising creatinine. <div class="ec-teach"><div class="th">What the findings point to</div> Rising creatinine in the early post-transplant period with obstruction, vascular compromise, BK nephropathy, and calcineurin inhibitor toxicity all excluded points to rejection, but the distinction between cell-mediated and antibody-mediated rejection changes treatment completely. Only histology makes that distinction, and treating empirically with pulse steroid would be wrong if the process is antibody mediated. Biopsy is the standard of care before treating a rejection episode. <div class="ec-src"><b>Source:</b> Kidney Disease: Improving Global Outcomes (KDIGO) Transplant Work Group. KDIGO clinical practice guideline for the care of kidney transplant recipients. Am J Transplant 2009;9(S3):S1-S155.</div></div></div> [[Try this question again->Transplant rejection - Dx]] [[Next case →->Nephrolithiasis intervention - Rx]] [[Start another case->Hub]] [[Restart this case->Transplant rejection - Dx]]

<span class="ec-case-marker" hidden data-entry="Transplant rejection. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Reducing immunosuppression during a suspected rejection episode accelerates graft loss. <div class="ec-teach"><div class="th">What the findings point to</div> Rising creatinine in the early post-transplant period with obstruction, vascular compromise, BK nephropathy, and calcineurin inhibitor toxicity all excluded points to rejection, but the distinction between cell-mediated and antibody-mediated rejection changes treatment completely. Only histology makes that distinction, and treating empirically with pulse steroid would be wrong if the process is antibody mediated. Biopsy is the standard of care before treating a rejection episode. <div class="ec-src"><b>Source:</b> Kidney Disease: Improving Global Outcomes (KDIGO) Transplant Work Group. KDIGO clinical practice guideline for the care of kidney transplant recipients. Am J Transplant 2009;9(S3):S1-S155.</div></div></div> [[Try this question again->Transplant rejection - Dx]] [[Next case →->Nephrolithiasis intervention - Rx]] [[Start another case->Hub]] [[Restart this case->Transplant rejection - Dx]]

<span class="ec-case-marker" hidden data-entry="Transplant rejection. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Resistive indices are nonspecific, and a week of observation during acute rejection risks irreversible damage. <div class="ec-teach"><div class="th">What the findings point to</div> Rising creatinine in the early post-transplant period with obstruction, vascular compromise, BK nephropathy, and calcineurin inhibitor toxicity all excluded points to rejection, but the distinction between cell-mediated and antibody-mediated rejection changes treatment completely. Only histology makes that distinction, and treating empirically with pulse steroid would be wrong if the process is antibody mediated. Biopsy is the standard of care before treating a rejection episode. <div class="ec-src"><b>Source:</b> Kidney Disease: Improving Global Outcomes (KDIGO) Transplant Work Group. KDIGO clinical practice guideline for the care of kidney transplant recipients. Am J Transplant 2009;9(S3):S1-S155.</div></div></div> [[Try this question again->Transplant rejection - Dx]] [[Next case →->Nephrolithiasis intervention - Rx]] [[Start another case->Hub]] [[Restart this case->Transplant rejection - Dx]]

<span class="ec-case-marker" hidden data-entry="Transplant rejection. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Cytomegalovirus can cause graft dysfunction but usually with systemic features and a positive viral load, which has not been obtained or suggested. <div class="ec-teach"><div class="th">What the findings point to</div> Rising creatinine in the early post-transplant period with obstruction, vascular compromise, BK nephropathy, and calcineurin inhibitor toxicity all excluded points to rejection, but the distinction between cell-mediated and antibody-mediated rejection changes treatment completely. Only histology makes that distinction, and treating empirically with pulse steroid would be wrong if the process is antibody mediated. Biopsy is the standard of care before treating a rejection episode. <div class="ec-src"><b>Source:</b> Kidney Disease: Improving Global Outcomes (KDIGO) Transplant Work Group. KDIGO clinical practice guideline for the care of kidney transplant recipients. Am J Transplant 2009;9(S3):S1-S155.</div></div></div> [[Try this question again->Transplant rejection - Dx]] [[Next case →->Nephrolithiasis intervention - Rx]] [[Start another case->Hub]] [[Restart this case->Transplant rejection - Dx]]

<div class="ec-scene">Emergency department · 04:25</div> A 44-year-old man has 6 hours of severe right flank pain radiating to the groin with vomiting. Temperature is 38.9°C, blood pressure is 94/56 mm Hg, pulse is 124/min, and respirations are 24/min. Leukocyte count is 21,000/mm3 and lactate is 3.4 mmol/L. Urinalysis shows pyuria, bacteriuria, and nitrites. Creatinine is 1.8 mg/dL. Noncontrast CT shows an 8-mm stone at the right ureteropelvic junction with moderate hydronephrosis and perinephric stranding. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Aggressive intravenous fluids to flush the stone through->Nephrolithiasis intervention - Rx D5]] [[Emergent decompression by ureteral stent or nephrostomy with antibiotics->Nephrolithiasis intervention - Rx correct]] [[Emergent ureteroscopy with stone extraction->Nephrolithiasis intervention - Rx D2]] [[Extracorporeal shock wave lithotripsy->Nephrolithiasis intervention - Rx D4]] [[Intravenous antibiotics and analgesia with admission for observation->Nephrolithiasis intervention - Rx D1]] [[Tamsulosin as medical expulsive therapy->Nephrolithiasis intervention - Rx D3]]

<span class="ec-case-marker" hidden data-entry="Nephrolithiasis intervention. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Emergent decompression by ureteral stent or nephrostomy with antibiotics</div> An obstructing stone with infection above it is an emergency. The infected, obstructed system is a closed abscess that antibiotics cannot reach, and mortality is high without drainage. Decompression is achieved by retrograde stent or percutaneous nephrostomy; definitive stone removal is deferred until the infection is treated. Attempting primary stone extraction in an infected system can precipitate septic shock. <div class="ec-src"><b>Source:</b> Assimos D, Krambeck A, Miller NL, et al. Surgical Management of Stones: AUA/Endourology Society Guideline. J Urol 2016;196(4):1153-1160.</div></div> [[Next case →->Rhabdomyolysis intervention - Rx]] [[Start another case->Hub]] [[Restart this case->Nephrolithiasis intervention - Rx]]

<span class="ec-case-marker" hidden data-entry="Nephrolithiasis intervention. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Antibiotics alone cannot sterilize an obstructed collecting system, and observation in a hypotensive septic patient is fatal delay. <div class="ec-teach"><div class="th">What the findings point to</div> An obstructing stone with infection above it is an emergency. The infected, obstructed system is a closed abscess that antibiotics cannot reach, and mortality is high without drainage. Decompression is achieved by retrograde stent or percutaneous nephrostomy; definitive stone removal is deferred until the infection is treated. Attempting primary stone extraction in an infected system can precipitate septic shock. <div class="ec-src"><b>Source:</b> Assimos D, Krambeck A, Miller NL, et al. Surgical Management of Stones: AUA/Endourology Society Guideline. J Urol 2016;196(4):1153-1160.</div></div></div> [[Try this question again->Nephrolithiasis intervention - Rx]] [[Next case →->Rhabdomyolysis intervention - Rx]] [[Start another case->Hub]] [[Restart this case->Nephrolithiasis intervention - Rx]]

<span class="ec-case-marker" hidden data-entry="Nephrolithiasis intervention. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Manipulating an infected stone raises intrarenal pressure and can produce fulminant sepsis. Drainage first, definitive treatment later. <div class="ec-teach"><div class="th">What the findings point to</div> An obstructing stone with infection above it is an emergency. The infected, obstructed system is a closed abscess that antibiotics cannot reach, and mortality is high without drainage. Decompression is achieved by retrograde stent or percutaneous nephrostomy; definitive stone removal is deferred until the infection is treated. Attempting primary stone extraction in an infected system can precipitate septic shock. <div class="ec-src"><b>Source:</b> Assimos D, Krambeck A, Miller NL, et al. Surgical Management of Stones: AUA/Endourology Society Guideline. J Urol 2016;196(4):1153-1160.</div></div></div> [[Try this question again->Nephrolithiasis intervention - Rx]] [[Next case →->Rhabdomyolysis intervention - Rx]] [[Start another case->Hub]] [[Restart this case->Nephrolithiasis intervention - Rx]]

<span class="ec-case-marker" hidden data-entry="Nephrolithiasis intervention. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Expulsive therapy is for uncomplicated distal stones in a well patient. It has no role in infected obstruction. <div class="ec-teach"><div class="th">What the findings point to</div> An obstructing stone with infection above it is an emergency. The infected, obstructed system is a closed abscess that antibiotics cannot reach, and mortality is high without drainage. Decompression is achieved by retrograde stent or percutaneous nephrostomy; definitive stone removal is deferred until the infection is treated. Attempting primary stone extraction in an infected system can precipitate septic shock. <div class="ec-src"><b>Source:</b> Assimos D, Krambeck A, Miller NL, et al. Surgical Management of Stones: AUA/Endourology Society Guideline. J Urol 2016;196(4):1153-1160.</div></div></div> [[Try this question again->Nephrolithiasis intervention - Rx]] [[Next case →->Rhabdomyolysis intervention - Rx]] [[Start another case->Hub]] [[Restart this case->Nephrolithiasis intervention - Rx]]

<span class="ec-case-marker" hidden data-entry="Nephrolithiasis intervention. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Lithotripsy is contraindicated in active infection and does not provide immediate decompression. <div class="ec-teach"><div class="th">What the findings point to</div> An obstructing stone with infection above it is an emergency. The infected, obstructed system is a closed abscess that antibiotics cannot reach, and mortality is high without drainage. Decompression is achieved by retrograde stent or percutaneous nephrostomy; definitive stone removal is deferred until the infection is treated. Attempting primary stone extraction in an infected system can precipitate septic shock. <div class="ec-src"><b>Source:</b> Assimos D, Krambeck A, Miller NL, et al. Surgical Management of Stones: AUA/Endourology Society Guideline. J Urol 2016;196(4):1153-1160.</div></div></div> [[Try this question again->Nephrolithiasis intervention - Rx]] [[Next case →->Rhabdomyolysis intervention - Rx]] [[Start another case->Hub]] [[Restart this case->Nephrolithiasis intervention - Rx]]

<span class="ec-case-marker" hidden data-entry="Nephrolithiasis intervention. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Fluid loading does not move an 8-mm obstructing stone and increases pressure in an infected system. <div class="ec-teach"><div class="th">What the findings point to</div> An obstructing stone with infection above it is an emergency. The infected, obstructed system is a closed abscess that antibiotics cannot reach, and mortality is high without drainage. Decompression is achieved by retrograde stent or percutaneous nephrostomy; definitive stone removal is deferred until the infection is treated. Attempting primary stone extraction in an infected system can precipitate septic shock. <div class="ec-src"><b>Source:</b> Assimos D, Krambeck A, Miller NL, et al. Surgical Management of Stones: AUA/Endourology Society Guideline. J Urol 2016;196(4):1153-1160.</div></div></div> [[Try this question again->Nephrolithiasis intervention - Rx]] [[Next case →->Rhabdomyolysis intervention - Rx]] [[Start another case->Hub]] [[Restart this case->Nephrolithiasis intervention - Rx]]

<div class="ec-scene">Emergency department · 13:55</div> A 23-year-old man collapsed during a military training run in hot weather and was found down for an unknown period. Temperature is 39.4°C, blood pressure is 102/58 mm Hg, pulse is 126/min, and respirations are 24/min. Urine is dark brown and dipstick is strongly positive for blood with no erythrocytes on microscopy. Creatine kinase is 78,000 U/L, creatinine is 2.2 mg/dL, potassium is 5.8 mEq/L, calcium is 7.2 mg/dL, and phosphate is 6.9 mg/dL. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Aggressive intravenous isotonic crystalloid->Rhabdomyolysis intervention - Rx correct]] [[Immediate hemodialysis->Rhabdomyolysis intervention - Rx D2]] [[Intravenous calcium gluconate to correct the hypocalcemia->Rhabdomyolysis intervention - Rx D1]] [[Intravenous mannitol as the primary intervention->Rhabdomyolysis intervention - Rx D3]] [[Loop diuretic to force urine output->Rhabdomyolysis intervention - Rx D5]] [[Urinary alkalinization with bicarbonate as the primary intervention->Rhabdomyolysis intervention - Rx D4]]

<span class="ec-case-marker" hidden data-entry="Rhabdomyolysis intervention. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Aggressive intravenous isotonic crystalloid</div> Early and aggressive volume expansion is the intervention that most reduces the risk of myoglobinuric acute kidney injury, by restoring renal perfusion and diluting and flushing tubular myoglobin. Rates of 1 to 2 L per hour initially, titrated to a urine output target of 200 to 300 mL per hour, are standard. Hypocalcemia is not corrected unless symptomatic or accompanied by dangerous hyperkalemia, because calcium precipitates with the elevated phosphate and rebound hypercalcemia occurs during recovery. <div class="ec-src"><b>Source:</b> Bosch X, Poch E, Grau JM. Rhabdomyolysis and acute kidney injury. N Engl J Med 2009;361(1):62-72.</div></div> [[Next case →->Hyponatremia correction rate - Rx]] [[Start another case->Hub]] [[Restart this case->Rhabdomyolysis intervention - Rx]]

<span class="ec-case-marker" hidden data-entry="Rhabdomyolysis intervention. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Calcium is withheld in rhabdomyolysis unless there is symptomatic hypocalcemia or cardiotoxic hyperkalemia, because it precipitates with phosphate and causes rebound hypercalcemia. <div class="ec-teach"><div class="th">What the findings point to</div> Early and aggressive volume expansion is the intervention that most reduces the risk of myoglobinuric acute kidney injury, by restoring renal perfusion and diluting and flushing tubular myoglobin. Rates of 1 to 2 L per hour initially, titrated to a urine output target of 200 to 300 mL per hour, are standard. Hypocalcemia is not corrected unless symptomatic or accompanied by dangerous hyperkalemia, because calcium precipitates with the elevated phosphate and rebound hypercalcemia occurs during recovery. <div class="ec-src"><b>Source:</b> Bosch X, Poch E, Grau JM. Rhabdomyolysis and acute kidney injury. N Engl J Med 2009;361(1):62-72.</div></div></div> [[Try this question again->Rhabdomyolysis intervention - Rx]] [[Next case →->Hyponatremia correction rate - Rx]] [[Start another case->Hub]] [[Restart this case->Rhabdomyolysis intervention - Rx]]

<span class="ec-case-marker" hidden data-entry="Rhabdomyolysis intervention. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Dialysis is reserved for refractory hyperkalemia, acidosis, or volume overload. Myoglobin is poorly dialyzed and dialysis does not prevent injury. <div class="ec-teach"><div class="th">What the findings point to</div> Early and aggressive volume expansion is the intervention that most reduces the risk of myoglobinuric acute kidney injury, by restoring renal perfusion and diluting and flushing tubular myoglobin. Rates of 1 to 2 L per hour initially, titrated to a urine output target of 200 to 300 mL per hour, are standard. Hypocalcemia is not corrected unless symptomatic or accompanied by dangerous hyperkalemia, because calcium precipitates with the elevated phosphate and rebound hypercalcemia occurs during recovery. <div class="ec-src"><b>Source:</b> Bosch X, Poch E, Grau JM. Rhabdomyolysis and acute kidney injury. N Engl J Med 2009;361(1):62-72.</div></div></div> [[Try this question again->Rhabdomyolysis intervention - Rx]] [[Next case →->Hyponatremia correction rate - Rx]] [[Start another case->Hub]] [[Restart this case->Rhabdomyolysis intervention - Rx]]

<span class="ec-case-marker" hidden data-entry="Rhabdomyolysis intervention. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Mannitol has not been shown to add benefit over crystalloid alone and risks volume depletion and hyperosmolality. <div class="ec-teach"><div class="th">What the findings point to</div> Early and aggressive volume expansion is the intervention that most reduces the risk of myoglobinuric acute kidney injury, by restoring renal perfusion and diluting and flushing tubular myoglobin. Rates of 1 to 2 L per hour initially, titrated to a urine output target of 200 to 300 mL per hour, are standard. Hypocalcemia is not corrected unless symptomatic or accompanied by dangerous hyperkalemia, because calcium precipitates with the elevated phosphate and rebound hypercalcemia occurs during recovery. <div class="ec-src"><b>Source:</b> Bosch X, Poch E, Grau JM. Rhabdomyolysis and acute kidney injury. N Engl J Med 2009;361(1):62-72.</div></div></div> [[Try this question again->Rhabdomyolysis intervention - Rx]] [[Next case →->Hyponatremia correction rate - Rx]] [[Start another case->Hub]] [[Restart this case->Rhabdomyolysis intervention - Rx]]

<span class="ec-case-marker" hidden data-entry="Rhabdomyolysis intervention. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Alkalinization is a debated adjunct. It does not substitute for volume expansion and can worsen hypocalcemia. <div class="ec-teach"><div class="th">What the findings point to</div> Early and aggressive volume expansion is the intervention that most reduces the risk of myoglobinuric acute kidney injury, by restoring renal perfusion and diluting and flushing tubular myoglobin. Rates of 1 to 2 L per hour initially, titrated to a urine output target of 200 to 300 mL per hour, are standard. Hypocalcemia is not corrected unless symptomatic or accompanied by dangerous hyperkalemia, because calcium precipitates with the elevated phosphate and rebound hypercalcemia occurs during recovery. <div class="ec-src"><b>Source:</b> Bosch X, Poch E, Grau JM. Rhabdomyolysis and acute kidney injury. N Engl J Med 2009;361(1):62-72.</div></div></div> [[Try this question again->Rhabdomyolysis intervention - Rx]] [[Next case →->Hyponatremia correction rate - Rx]] [[Start another case->Hub]] [[Restart this case->Rhabdomyolysis intervention - Rx]]

<span class="ec-case-marker" hidden data-entry="Rhabdomyolysis intervention. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Diuretics reduce intravascular volume and renal perfusion, which is the opposite of what is required. <div class="ec-teach"><div class="th">What the findings point to</div> Early and aggressive volume expansion is the intervention that most reduces the risk of myoglobinuric acute kidney injury, by restoring renal perfusion and diluting and flushing tubular myoglobin. Rates of 1 to 2 L per hour initially, titrated to a urine output target of 200 to 300 mL per hour, are standard. Hypocalcemia is not corrected unless symptomatic or accompanied by dangerous hyperkalemia, because calcium precipitates with the elevated phosphate and rebound hypercalcemia occurs during recovery. <div class="ec-src"><b>Source:</b> Bosch X, Poch E, Grau JM. Rhabdomyolysis and acute kidney injury. N Engl J Med 2009;361(1):62-72.</div></div></div> [[Try this question again->Rhabdomyolysis intervention - Rx]] [[Next case →->Hyponatremia correction rate - Rx]] [[Start another case->Hub]] [[Restart this case->Rhabdomyolysis intervention - Rx]]

<div class="ec-scene">Intensive care unit · 22:30</div> A 52-year-old woman with chronic alcohol use and poor intake is admitted with a serum sodium of 106 mEq/L, confusion, and a witnessed generalized seizure. Temperature is 36.4°C, blood pressure is 104/62 mm Hg, and pulse is 98/min. She appears volume depleted. Serum osmolality is 228 mOsm/kg, urine osmolality is 180 mOsm/kg, and urine sodium is 12 mEq/L. Her sodium is presumed chronic given weeks of poor intake. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Fluid restriction to 800 mL daily->Hyponatremia correction rate - Rx D3]] [[Hypertonic 3% saline bolus with a correction limit of 8 mEq/L in 24 hours->Hyponatremia correction rate - Rx correct]] [[Intravenous lorazepam alone with observation of the sodium->Hyponatremia correction rate - Rx D5]] [[Isotonic saline alone at 100 mL per hour->Hyponatremia correction rate - Rx D1]] [[Rapid correction to a sodium above 125 mEq/L within 12 hours->Hyponatremia correction rate - Rx D2]] [[Tolvaptan->Hyponatremia correction rate - Rx D4]]

<span class="ec-case-marker" hidden data-entry="Hyponatremia correction rate. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Hypertonic 3% saline bolus with a correction limit of 8 mEq/L in 24 hours</div> A seizure from hyponatremia is a neurologic emergency requiring immediate hypertonic saline to raise the sodium by 4 to 6 mEq/L quickly and stop the seizure. Chronic hyponatremia at 106 mEq/L carries a high risk of osmotic demyelination, so the total rise must be capped at 8 mEq/L over 24 hours with frequent measurement, and overcorrection is actively reversed with dextrose in water and desmopressin if it occurs. Both halves of this, urgent partial correction and a strict ceiling, are required. <div class="ec-src"><b>Source:</b> Verbalis JG, Goldsmith SR, Greenberg A, et al. Diagnosis, evaluation, and treatment of hyponatremia: expert panel recommendations. Am J Med 2013;126(10 Suppl 1):S1-S42.</div></div> [[Next case →->Intubation timing - Rx]] [[Start another case->Hub]] [[Restart this case->Hyponatremia correction rate - Rx]]

<span class="ec-case-marker" hidden data-entry="Hyponatremia correction rate. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Isotonic saline corrects volume depletion but raises sodium too slowly to stop an active seizure from cerebral edema. <div class="ec-teach"><div class="th">What the findings point to</div> A seizure from hyponatremia is a neurologic emergency requiring immediate hypertonic saline to raise the sodium by 4 to 6 mEq/L quickly and stop the seizure. Chronic hyponatremia at 106 mEq/L carries a high risk of osmotic demyelination, so the total rise must be capped at 8 mEq/L over 24 hours with frequent measurement, and overcorrection is actively reversed with dextrose in water and desmopressin if it occurs. Both halves of this, urgent partial correction and a strict ceiling, are required. <div class="ec-src"><b>Source:</b> Verbalis JG, Goldsmith SR, Greenberg A, et al. Diagnosis, evaluation, and treatment of hyponatremia: expert panel recommendations. Am J Med 2013;126(10 Suppl 1):S1-S42.</div></div></div> [[Try this question again->Hyponatremia correction rate - Rx]] [[Next case →->Intubation timing - Rx]] [[Start another case->Hub]] [[Restart this case->Hyponatremia correction rate - Rx]]

<span class="ec-case-marker" hidden data-entry="Hyponatremia correction rate. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Raising the sodium by nearly 20 mEq/L in a chronically hyponatremic patient is the classic cause of osmotic demyelination syndrome. <div class="ec-teach"><div class="th">What the findings point to</div> A seizure from hyponatremia is a neurologic emergency requiring immediate hypertonic saline to raise the sodium by 4 to 6 mEq/L quickly and stop the seizure. Chronic hyponatremia at 106 mEq/L carries a high risk of osmotic demyelination, so the total rise must be capped at 8 mEq/L over 24 hours with frequent measurement, and overcorrection is actively reversed with dextrose in water and desmopressin if it occurs. Both halves of this, urgent partial correction and a strict ceiling, are required. <div class="ec-src"><b>Source:</b> Verbalis JG, Goldsmith SR, Greenberg A, et al. Diagnosis, evaluation, and treatment of hyponatremia: expert panel recommendations. Am J Med 2013;126(10 Suppl 1):S1-S42.</div></div></div> [[Try this question again->Hyponatremia correction rate - Rx]] [[Next case →->Intubation timing - Rx]] [[Start another case->Hub]] [[Restart this case->Hyponatremia correction rate - Rx]]

<span class="ec-case-marker" hidden data-entry="Hyponatremia correction rate. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Restriction is used in euvolemic hyponatremia from inappropriate antidiuresis. She is volume depleted and seizing. <div class="ec-teach"><div class="th">What the findings point to</div> A seizure from hyponatremia is a neurologic emergency requiring immediate hypertonic saline to raise the sodium by 4 to 6 mEq/L quickly and stop the seizure. Chronic hyponatremia at 106 mEq/L carries a high risk of osmotic demyelination, so the total rise must be capped at 8 mEq/L over 24 hours with frequent measurement, and overcorrection is actively reversed with dextrose in water and desmopressin if it occurs. Both halves of this, urgent partial correction and a strict ceiling, are required. <div class="ec-src"><b>Source:</b> Verbalis JG, Goldsmith SR, Greenberg A, et al. Diagnosis, evaluation, and treatment of hyponatremia: expert panel recommendations. Am J Med 2013;126(10 Suppl 1):S1-S42.</div></div></div> [[Try this question again->Hyponatremia correction rate - Rx]] [[Next case →->Intubation timing - Rx]] [[Start another case->Hub]] [[Restart this case->Hyponatremia correction rate - Rx]]

<span class="ec-case-marker" hidden data-entry="Hyponatremia correction rate. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Vasopressin receptor antagonists are contraindicated in severe symptomatic hyponatremia because the rate of correction cannot be controlled. <div class="ec-teach"><div class="th">What the findings point to</div> A seizure from hyponatremia is a neurologic emergency requiring immediate hypertonic saline to raise the sodium by 4 to 6 mEq/L quickly and stop the seizure. Chronic hyponatremia at 106 mEq/L carries a high risk of osmotic demyelination, so the total rise must be capped at 8 mEq/L over 24 hours with frequent measurement, and overcorrection is actively reversed with dextrose in water and desmopressin if it occurs. Both halves of this, urgent partial correction and a strict ceiling, are required. <div class="ec-src"><b>Source:</b> Verbalis JG, Goldsmith SR, Greenberg A, et al. Diagnosis, evaluation, and treatment of hyponatremia: expert panel recommendations. Am J Med 2013;126(10 Suppl 1):S1-S42.</div></div></div> [[Try this question again->Hyponatremia correction rate - Rx]] [[Next case →->Intubation timing - Rx]] [[Start another case->Hub]] [[Restart this case->Hyponatremia correction rate - Rx]]

<span class="ec-case-marker" hidden data-entry="Hyponatremia correction rate. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Benzodiazepine may terminate the seizure transiently, but the cerebral edema driving it persists until the sodium rises. <div class="ec-teach"><div class="th">What the findings point to</div> A seizure from hyponatremia is a neurologic emergency requiring immediate hypertonic saline to raise the sodium by 4 to 6 mEq/L quickly and stop the seizure. Chronic hyponatremia at 106 mEq/L carries a high risk of osmotic demyelination, so the total rise must be capped at 8 mEq/L over 24 hours with frequent measurement, and overcorrection is actively reversed with dextrose in water and desmopressin if it occurs. Both halves of this, urgent partial correction and a strict ceiling, are required. <div class="ec-src"><b>Source:</b> Verbalis JG, Goldsmith SR, Greenberg A, et al. Diagnosis, evaluation, and treatment of hyponatremia: expert panel recommendations. Am J Med 2013;126(10 Suppl 1):S1-S42.</div></div></div> [[Try this question again->Hyponatremia correction rate - Rx]] [[Next case →->Intubation timing - Rx]] [[Start another case->Hub]] [[Restart this case->Hyponatremia correction rate - Rx]]

<div class="ec-scene">Emergency department · 18:20</div> A 58-year-old man with severe asthma has been receiving continuous nebulized albuterol, ipratropium, intravenous methylprednisolone, and magnesium for 90 minutes. He is now drowsy and answering in single words. Temperature is 37.1°C, blood pressure is 138/84 mm Hg, pulse is 132/min, and respirations are 34/min. Breath sounds are markedly diminished with minimal wheeze. Arterial blood gas analysis shows pH 7.24, PaCO2 58 mm Hg, and PaO2 64 mm Hg on 100% oxygen. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Endotracheal intubation and mechanical ventilation->Intubation timing - Rx correct]] [[Heliox and reassessment in 30 minutes->Intubation timing - Rx D3]] [[Increase the oxygen and repeat the blood gas in 1 hour->Intubation timing - Rx D4]] [[Intravenous epinephrine and continued observation->Intubation timing - Rx D2]] [[Intravenous ketamine for bronchodilation without airway control->Intubation timing - Rx D5]] [[Noninvasive positive pressure ventilation->Intubation timing - Rx D1]]

<span class="ec-case-marker" hidden data-entry="Intubation timing. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Endotracheal intubation and mechanical ventilation</div> A rising carbon dioxide in acute asthma signals that the patient can no longer sustain the work of breathing, and a quiet chest with drowsiness indicates impending arrest. Waiting for further deterioration converts a controlled intubation into a crash airway in a patient with severe bronchospasm. Ventilation afterward uses low rates and prolonged expiratory time with permissive hypercapnia to avoid dynamic hyperinflation. <div class="ec-src"><b>Source:</b> Brenner B, Corbridge T, Kazzi A. Intubation and mechanical ventilation of the asthmatic patient in respiratory failure. Proc Am Thorac Soc 2009;6(4):371-379.</div></div> [[Next case →->Chest tube indication - Rx]] [[Start another case->Hub]] [[Restart this case->Intubation timing - Rx]]

<span class="ec-case-marker" hidden data-entry="Intubation timing. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Noninvasive support may help selected cooperative asthmatics earlier in the course. A drowsy patient who cannot protect the airway is not a candidate. <div class="ec-teach"><div class="th">What the findings point to</div> A rising carbon dioxide in acute asthma signals that the patient can no longer sustain the work of breathing, and a quiet chest with drowsiness indicates impending arrest. Waiting for further deterioration converts a controlled intubation into a crash airway in a patient with severe bronchospasm. Ventilation afterward uses low rates and prolonged expiratory time with permissive hypercapnia to avoid dynamic hyperinflation. <div class="ec-src"><b>Source:</b> Brenner B, Corbridge T, Kazzi A. Intubation and mechanical ventilation of the asthmatic patient in respiratory failure. Proc Am Thorac Soc 2009;6(4):371-379.</div></div></div> [[Try this question again->Intubation timing - Rx]] [[Next case →->Chest tube indication - Rx]] [[Start another case->Hub]] [[Restart this case->Intubation timing - Rx]]

<span class="ec-case-marker" hidden data-entry="Intubation timing. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Parenteral epinephrine is a reasonable adjunct but does not address the immediate failure of ventilation in an obtunded patient. <div class="ec-teach"><div class="th">What the findings point to</div> A rising carbon dioxide in acute asthma signals that the patient can no longer sustain the work of breathing, and a quiet chest with drowsiness indicates impending arrest. Waiting for further deterioration converts a controlled intubation into a crash airway in a patient with severe bronchospasm. Ventilation afterward uses low rates and prolonged expiratory time with permissive hypercapnia to avoid dynamic hyperinflation. <div class="ec-src"><b>Source:</b> Brenner B, Corbridge T, Kazzi A. Intubation and mechanical ventilation of the asthmatic patient in respiratory failure. Proc Am Thorac Soc 2009;6(4):371-379.</div></div></div> [[Try this question again->Intubation timing - Rx]] [[Next case →->Chest tube indication - Rx]] [[Start another case->Hub]] [[Restart this case->Intubation timing - Rx]]

<span class="ec-case-marker" hidden data-entry="Intubation timing. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Heliox may reduce work of breathing transiently but has no mortality benefit and buying 30 minutes here risks arrest. <div class="ec-teach"><div class="th">What the findings point to</div> A rising carbon dioxide in acute asthma signals that the patient can no longer sustain the work of breathing, and a quiet chest with drowsiness indicates impending arrest. Waiting for further deterioration converts a controlled intubation into a crash airway in a patient with severe bronchospasm. Ventilation afterward uses low rates and prolonged expiratory time with permissive hypercapnia to avoid dynamic hyperinflation. <div class="ec-src"><b>Source:</b> Brenner B, Corbridge T, Kazzi A. Intubation and mechanical ventilation of the asthmatic patient in respiratory failure. Proc Am Thorac Soc 2009;6(4):371-379.</div></div></div> [[Try this question again->Intubation timing - Rx]] [[Next case →->Chest tube indication - Rx]] [[Start another case->Hub]] [[Restart this case->Intubation timing - Rx]]

<span class="ec-case-marker" hidden data-entry="Intubation timing. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> He is already on 100% oxygen. The problem is ventilation, not oxygenation, and an hour is far too long. <div class="ec-teach"><div class="th">What the findings point to</div> A rising carbon dioxide in acute asthma signals that the patient can no longer sustain the work of breathing, and a quiet chest with drowsiness indicates impending arrest. Waiting for further deterioration converts a controlled intubation into a crash airway in a patient with severe bronchospasm. Ventilation afterward uses low rates and prolonged expiratory time with permissive hypercapnia to avoid dynamic hyperinflation. <div class="ec-src"><b>Source:</b> Brenner B, Corbridge T, Kazzi A. Intubation and mechanical ventilation of the asthmatic patient in respiratory failure. Proc Am Thorac Soc 2009;6(4):371-379.</div></div></div> [[Try this question again->Intubation timing - Rx]] [[Next case →->Chest tube indication - Rx]] [[Start another case->Hub]] [[Restart this case->Intubation timing - Rx]]

<span class="ec-case-marker" hidden data-entry="Intubation timing. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Ketamine is often chosen as the induction agent for intubation, but sedating an obtunded hypercapnic patient without securing the airway is dangerous. <div class="ec-teach"><div class="th">What the findings point to</div> A rising carbon dioxide in acute asthma signals that the patient can no longer sustain the work of breathing, and a quiet chest with drowsiness indicates impending arrest. Waiting for further deterioration converts a controlled intubation into a crash airway in a patient with severe bronchospasm. Ventilation afterward uses low rates and prolonged expiratory time with permissive hypercapnia to avoid dynamic hyperinflation. <div class="ec-src"><b>Source:</b> Brenner B, Corbridge T, Kazzi A. Intubation and mechanical ventilation of the asthmatic patient in respiratory failure. Proc Am Thorac Soc 2009;6(4):371-379.</div></div></div> [[Try this question again->Intubation timing - Rx]] [[Next case →->Chest tube indication - Rx]] [[Start another case->Hub]] [[Restart this case->Intubation timing - Rx]]

<div class="ec-scene">Emergency department · 23:05</div> A 26-year-old tall thin man has sudden right pleuritic chest pain and dyspnea. Temperature is 36.8°C, blood pressure is 126/76 mm Hg, pulse is 96/min, respirations are 22/min, and oxygen saturation is 95% on room air. Breath sounds are reduced on the right with hyperresonance. The trachea is midline and there is no jugular venous distention. Chest radiography shows a right pneumothorax with a 4-cm rim between the lung margin and the chest wall at the level of the hilum. This is his first episode. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[CT of the chest before any intervention->Chest tube indication - Rx D5]] [[Immediate needle decompression in the second intercostal space->Chest tube indication - Rx D2]] [[Large-bore chest tube placement->Chest tube indication - Rx D3]] [[Needle aspiration or small-bore catheter drainage->Chest tube indication - Rx correct]] [[Observation with high-flow oxygen and repeat film in 6 hours->Chest tube indication - Rx D1]] [[Video-assisted thoracoscopic pleurodesis->Chest tube indication - Rx D4]]

<span class="ec-case-marker" hidden data-entry="Chest tube indication. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Needle aspiration or small-bore catheter drainage</div> This is a large primary spontaneous pneumothorax, defined by a rim of 2 cm or more, in a stable patient. The 2023 British Thoracic Society guideline update, informed by a randomized trial showing conservative management is noninferior to drainage, now allows conservative management with ambulatory follow-up for a minimally symptomatic or asymptomatic primary spontaneous pneumothorax of any size, not only those under 2 cm. Given his ongoing pleuritic pain and dyspnea, active drainage is still reasonable here, and if drainage is chosen a large-bore chest tube is not needed: simple aspiration or a small-bore catheter achieves resolution with less pain and shorter stay, and is the preferred first intervention when active treatment is selected. Tension physiology is absent, so there is no indication for immediate decompression. <div class="ec-src"><b>Source:</b> Roberts ME, Rahman NM, Maskell NA, et al. British Thoracic Society Guideline for pleural disease. Thorax 2023;78(Suppl 3):s1-s42.</div></div> [[Next case →->Cardioversion versus rate control - Rx]] [[Start another case->Hub]] [[Restart this case->Chest tube indication - Rx]]

<span class="ec-case-marker" hidden data-entry="Chest tube indication. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Observation is now an accepted option for a pneumothorax this size when the patient is minimally symptomatic, but he has ongoing pleuritic pain and dyspnea, not minimal symptoms, so proceeding to aspiration or small-bore catheter drainage rather than watching is still the better choice. <div class="ec-teach"><div class="th">What the findings point to</div> This is a large primary spontaneous pneumothorax, defined by a rim of 2 cm or more, in a stable patient. The 2023 British Thoracic Society guideline update, informed by a randomized trial showing conservative management is noninferior to drainage, now allows conservative management with ambulatory follow-up for a minimally symptomatic or asymptomatic primary spontaneous pneumothorax of any size, not only those under 2 cm. Given his ongoing pleuritic pain and dyspnea, active drainage is still reasonable here, and if drainage is chosen a large-bore chest tube is not needed: simple aspiration or a small-bore catheter achieves resolution with less pain and shorter stay, and is the preferred first intervention when active treatment is selected. Tension physiology is absent, so there is no indication for immediate decompression. <div class="ec-src"><b>Source:</b> Roberts ME, Rahman NM, Maskell NA, et al. British Thoracic Society Guideline for pleural disease. Thorax 2023;78(Suppl 3):s1-s42.</div></div></div> [[Try this question again->Chest tube indication - Rx]] [[Next case →->Cardioversion versus rate control - Rx]] [[Start another case->Hub]] [[Restart this case->Chest tube indication - Rx]]

<span class="ec-case-marker" hidden data-entry="Chest tube indication. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Needle decompression is for tension pneumothorax. He is normotensive with a midline trachea and no distended neck veins. <div class="ec-teach"><div class="th">What the findings point to</div> This is a large primary spontaneous pneumothorax, defined by a rim of 2 cm or more, in a stable patient. The 2023 British Thoracic Society guideline update, informed by a randomized trial showing conservative management is noninferior to drainage, now allows conservative management with ambulatory follow-up for a minimally symptomatic or asymptomatic primary spontaneous pneumothorax of any size, not only those under 2 cm. Given his ongoing pleuritic pain and dyspnea, active drainage is still reasonable here, and if drainage is chosen a large-bore chest tube is not needed: simple aspiration or a small-bore catheter achieves resolution with less pain and shorter stay, and is the preferred first intervention when active treatment is selected. Tension physiology is absent, so there is no indication for immediate decompression. <div class="ec-src"><b>Source:</b> Roberts ME, Rahman NM, Maskell NA, et al. British Thoracic Society Guideline for pleural disease. Thorax 2023;78(Suppl 3):s1-s42.</div></div></div> [[Try this question again->Chest tube indication - Rx]] [[Next case →->Cardioversion versus rate control - Rx]] [[Start another case->Hub]] [[Restart this case->Chest tube indication - Rx]]

<span class="ec-case-marker" hidden data-entry="Chest tube indication. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A large tube provides no advantage over small-bore drainage for a primary spontaneous pneumothorax and causes more pain. <div class="ec-teach"><div class="th">What the findings point to</div> This is a large primary spontaneous pneumothorax, defined by a rim of 2 cm or more, in a stable patient. The 2023 British Thoracic Society guideline update, informed by a randomized trial showing conservative management is noninferior to drainage, now allows conservative management with ambulatory follow-up for a minimally symptomatic or asymptomatic primary spontaneous pneumothorax of any size, not only those under 2 cm. Given his ongoing pleuritic pain and dyspnea, active drainage is still reasonable here, and if drainage is chosen a large-bore chest tube is not needed: simple aspiration or a small-bore catheter achieves resolution with less pain and shorter stay, and is the preferred first intervention when active treatment is selected. Tension physiology is absent, so there is no indication for immediate decompression. <div class="ec-src"><b>Source:</b> Roberts ME, Rahman NM, Maskell NA, et al. British Thoracic Society Guideline for pleural disease. Thorax 2023;78(Suppl 3):s1-s42.</div></div></div> [[Try this question again->Chest tube indication - Rx]] [[Next case →->Cardioversion versus rate control - Rx]] [[Start another case->Hub]] [[Restart this case->Chest tube indication - Rx]]

<span class="ec-case-marker" hidden data-entry="Chest tube indication. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Surgical pleurodesis is considered for recurrence, persistent air leak, or high-risk occupations. This is a first episode. <div class="ec-teach"><div class="th">What the findings point to</div> This is a large primary spontaneous pneumothorax, defined by a rim of 2 cm or more, in a stable patient. The 2023 British Thoracic Society guideline update, informed by a randomized trial showing conservative management is noninferior to drainage, now allows conservative management with ambulatory follow-up for a minimally symptomatic or asymptomatic primary spontaneous pneumothorax of any size, not only those under 2 cm. Given his ongoing pleuritic pain and dyspnea, active drainage is still reasonable here, and if drainage is chosen a large-bore chest tube is not needed: simple aspiration or a small-bore catheter achieves resolution with less pain and shorter stay, and is the preferred first intervention when active treatment is selected. Tension physiology is absent, so there is no indication for immediate decompression. <div class="ec-src"><b>Source:</b> Roberts ME, Rahman NM, Maskell NA, et al. British Thoracic Society Guideline for pleural disease. Thorax 2023;78(Suppl 3):s1-s42.</div></div></div> [[Try this question again->Chest tube indication - Rx]] [[Next case →->Cardioversion versus rate control - Rx]] [[Start another case->Hub]] [[Restart this case->Chest tube indication - Rx]]

<span class="ec-case-marker" hidden data-entry="Chest tube indication. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The diagnosis and size are established on plain film. CT adds radiation and delay without changing management. <div class="ec-teach"><div class="th">What the findings point to</div> This is a large primary spontaneous pneumothorax, defined by a rim of 2 cm or more, in a stable patient. The 2023 British Thoracic Society guideline update, informed by a randomized trial showing conservative management is noninferior to drainage, now allows conservative management with ambulatory follow-up for a minimally symptomatic or asymptomatic primary spontaneous pneumothorax of any size, not only those under 2 cm. Given his ongoing pleuritic pain and dyspnea, active drainage is still reasonable here, and if drainage is chosen a large-bore chest tube is not needed: simple aspiration or a small-bore catheter achieves resolution with less pain and shorter stay, and is the preferred first intervention when active treatment is selected. Tension physiology is absent, so there is no indication for immediate decompression. <div class="ec-src"><b>Source:</b> Roberts ME, Rahman NM, Maskell NA, et al. British Thoracic Society Guideline for pleural disease. Thorax 2023;78(Suppl 3):s1-s42.</div></div></div> [[Try this question again->Chest tube indication - Rx]] [[Next case →->Cardioversion versus rate control - Rx]] [[Start another case->Hub]] [[Restart this case->Chest tube indication - Rx]]

<div class="ec-scene">Emergency department · 15:58</div> A 64-year-old man has palpitations that began 3 hours ago. Blood pressure is 78/48 mm Hg, pulse is 168/min and irregularly irregular, and respirations are 26/min. He is diaphoretic, cool peripherally, and has new crackles at both lung bases with an oxygen saturation of 90% on room air. Electrocardiography shows atrial fibrillation with a rapid ventricular response and no pre-excitation. He has had no prior anticoagulation. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Heparin infusion followed by cardioversion in 3 weeks->Cardioversion versus rate control - Rx D4]] [[Immediate synchronized electrical cardioversion->Cardioversion versus rate control - Rx correct]] [[Intravenous amiodarone loading->Cardioversion versus rate control - Rx D5]] [[Intravenous diltiazem for rate control->Cardioversion versus rate control - Rx D1]] [[Intravenous metoprolol for rate control->Cardioversion versus rate control - Rx D2]] [[Transesophageal echocardiography before cardioversion to exclude thrombus->Cardioversion versus rate control - Rx D3]]

<span class="ec-case-marker" hidden data-entry="Cardioversion versus rate control. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Immediate synchronized electrical cardioversion</div> Atrial fibrillation with hemodynamic instability, defined by hypotension, pulmonary edema, or ongoing ischemia, requires immediate synchronized cardioversion regardless of the duration of the arrhythmia or the anticoagulation status. The thromboembolic risk of cardioverting without anticoagulation is accepted because the alternative is cardiogenic collapse. Anticoagulation is started afterward, and synchronization is essential to avoid inducing ventricular fibrillation. <div class="ec-src"><b>Source:</b> January CT, Wann LS, Calkins H, et al. 2019 AHA/ACC/HRS Focused Update of the 2014 Guideline for the Management of Patients With Atrial Fibrillation. Circulation 2019;140(2):e125-e151.</div></div> [[Next case →->Pericardiocentesis indication - Rx]] [[Start another case->Hub]] [[Restart this case->Cardioversion versus rate control - Rx]]

<span class="ec-case-marker" hidden data-entry="Cardioversion versus rate control. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Calcium channel blockade has negative inotropic effects and will worsen hypotension and pulmonary edema in a patient who is already in shock. <div class="ec-teach"><div class="th">What the findings point to</div> Atrial fibrillation with hemodynamic instability, defined by hypotension, pulmonary edema, or ongoing ischemia, requires immediate synchronized cardioversion regardless of the duration of the arrhythmia or the anticoagulation status. The thromboembolic risk of cardioverting without anticoagulation is accepted because the alternative is cardiogenic collapse. Anticoagulation is started afterward, and synchronization is essential to avoid inducing ventricular fibrillation. <div class="ec-src"><b>Source:</b> January CT, Wann LS, Calkins H, et al. 2019 AHA/ACC/HRS Focused Update of the 2014 Guideline for the Management of Patients With Atrial Fibrillation. Circulation 2019;140(2):e125-e151.</div></div></div> [[Try this question again->Cardioversion versus rate control - Rx]] [[Next case →->Pericardiocentesis indication - Rx]] [[Start another case->Hub]] [[Restart this case->Cardioversion versus rate control - Rx]]

<span class="ec-case-marker" hidden data-entry="Cardioversion versus rate control. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Beta blockade in decompensated heart failure with hypotension precipitates further collapse. <div class="ec-teach"><div class="th">What the findings point to</div> Atrial fibrillation with hemodynamic instability, defined by hypotension, pulmonary edema, or ongoing ischemia, requires immediate synchronized cardioversion regardless of the duration of the arrhythmia or the anticoagulation status. The thromboembolic risk of cardioverting without anticoagulation is accepted because the alternative is cardiogenic collapse. Anticoagulation is started afterward, and synchronization is essential to avoid inducing ventricular fibrillation. <div class="ec-src"><b>Source:</b> January CT, Wann LS, Calkins H, et al. 2019 AHA/ACC/HRS Focused Update of the 2014 Guideline for the Management of Patients With Atrial Fibrillation. Circulation 2019;140(2):e125-e151.</div></div></div> [[Try this question again->Cardioversion versus rate control - Rx]] [[Next case →->Pericardiocentesis indication - Rx]] [[Start another case->Hub]] [[Restart this case->Cardioversion versus rate control - Rx]]

<span class="ec-case-marker" hidden data-entry="Cardioversion versus rate control. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The transesophageal-guided strategy applies to stable patients. An unstable patient is cardioverted immediately. <div class="ec-teach"><div class="th">What the findings point to</div> Atrial fibrillation with hemodynamic instability, defined by hypotension, pulmonary edema, or ongoing ischemia, requires immediate synchronized cardioversion regardless of the duration of the arrhythmia or the anticoagulation status. The thromboembolic risk of cardioverting without anticoagulation is accepted because the alternative is cardiogenic collapse. Anticoagulation is started afterward, and synchronization is essential to avoid inducing ventricular fibrillation. <div class="ec-src"><b>Source:</b> January CT, Wann LS, Calkins H, et al. 2019 AHA/ACC/HRS Focused Update of the 2014 Guideline for the Management of Patients With Atrial Fibrillation. Circulation 2019;140(2):e125-e151.</div></div></div> [[Try this question again->Cardioversion versus rate control - Rx]] [[Next case →->Pericardiocentesis indication - Rx]] [[Start another case->Hub]] [[Restart this case->Cardioversion versus rate control - Rx]]

<span class="ec-case-marker" hidden data-entry="Cardioversion versus rate control. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> 3 weeks of anticoagulation before cardioversion is the elective pathway for stable patients. He will not survive the wait. <div class="ec-teach"><div class="th">What the findings point to</div> Atrial fibrillation with hemodynamic instability, defined by hypotension, pulmonary edema, or ongoing ischemia, requires immediate synchronized cardioversion regardless of the duration of the arrhythmia or the anticoagulation status. The thromboembolic risk of cardioverting without anticoagulation is accepted because the alternative is cardiogenic collapse. Anticoagulation is started afterward, and synchronization is essential to avoid inducing ventricular fibrillation. <div class="ec-src"><b>Source:</b> January CT, Wann LS, Calkins H, et al. 2019 AHA/ACC/HRS Focused Update of the 2014 Guideline for the Management of Patients With Atrial Fibrillation. Circulation 2019;140(2):e125-e151.</div></div></div> [[Try this question again->Cardioversion versus rate control - Rx]] [[Next case →->Pericardiocentesis indication - Rx]] [[Start another case->Hub]] [[Restart this case->Cardioversion versus rate control - Rx]]

<span class="ec-case-marker" hidden data-entry="Cardioversion versus rate control. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Chemical cardioversion is slower and less reliable than electrical, and it is inappropriate as the first step in shock. <div class="ec-teach"><div class="th">What the findings point to</div> Atrial fibrillation with hemodynamic instability, defined by hypotension, pulmonary edema, or ongoing ischemia, requires immediate synchronized cardioversion regardless of the duration of the arrhythmia or the anticoagulation status. The thromboembolic risk of cardioverting without anticoagulation is accepted because the alternative is cardiogenic collapse. Anticoagulation is started afterward, and synchronization is essential to avoid inducing ventricular fibrillation. <div class="ec-src"><b>Source:</b> January CT, Wann LS, Calkins H, et al. 2019 AHA/ACC/HRS Focused Update of the 2014 Guideline for the Management of Patients With Atrial Fibrillation. Circulation 2019;140(2):e125-e151.</div></div></div> [[Try this question again->Cardioversion versus rate control - Rx]] [[Next case →->Pericardiocentesis indication - Rx]] [[Start another case->Hub]] [[Restart this case->Cardioversion versus rate control - Rx]]

<div class="ec-scene">Emergency department · 11:50</div> A 57-year-old woman with metastatic breast cancer has 2 days of progressive dyspnea. Blood pressure is 84/62 mm Hg with a 16 mm Hg inspiratory fall in systolic pressure, pulse is 128/min, and respirations are 28/min. Jugular venous pressure is elevated, heart sounds are muffled, and the lungs are clear. Electrocardiography shows low voltage with electrical alternans. Echocardiography shows a large circumferential effusion with right atrial systolic collapse and right ventricular diastolic collapse. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Anticoagulation for presumed pulmonary embolism->Pericardiocentesis indication - Rx D4]] [[CT of the chest to characterize the effusion->Pericardiocentesis indication - Rx D3]] [[Intravenous fluid bolus alone with observation->Pericardiocentesis indication - Rx D2]] [[Intravenous furosemide for the elevated venous pressure->Pericardiocentesis indication - Rx D1]] [[Pericardial window under general anesthesia as the first step->Pericardiocentesis indication - Rx D5]] [[Urgent echocardiographically guided pericardiocentesis->Pericardiocentesis indication - Rx correct]]

<span class="ec-case-marker" hidden data-entry="Pericardiocentesis indication. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Urgent echocardiographically guided pericardiocentesis</div> Cardiac tamponade is a mechanical obstruction to ventricular filling, and the only effective treatment is removal of the fluid. Hypotension, elevated jugular venous pressure with clear lungs, pulsus paradoxus above 10 mm Hg, electrical alternans, and chamber collapse on echocardiography establish the diagnosis. Intravenous fluid is a temporizing measure while drainage is arranged, not a treatment. Diuretics and vasodilators reduce preload and are actively harmful. <div class="ec-src"><b>Source:</b> Adler Y, Charron P, Imazio M, et al. 2015 ESC Guidelines for the diagnosis and management of pericardial diseases. Eur Heart J 2015;36(42):2921-2964.</div></div> [[Next case →->Massive transfusion protocol - Rx]] [[Start another case->Hub]] [[Restart this case->Pericardiocentesis indication - Rx]]

<span class="ec-case-marker" hidden data-entry="Pericardiocentesis indication. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Diuresis reduces the filling pressure that is maintaining cardiac output against the effusion and can precipitate arrest. <div class="ec-teach"><div class="th">What the findings point to</div> Cardiac tamponade is a mechanical obstruction to ventricular filling, and the only effective treatment is removal of the fluid. Hypotension, elevated jugular venous pressure with clear lungs, pulsus paradoxus above 10 mm Hg, electrical alternans, and chamber collapse on echocardiography establish the diagnosis. Intravenous fluid is a temporizing measure while drainage is arranged, not a treatment. Diuretics and vasodilators reduce preload and are actively harmful. <div class="ec-src"><b>Source:</b> Adler Y, Charron P, Imazio M, et al. 2015 ESC Guidelines for the diagnosis and management of pericardial diseases. Eur Heart J 2015;36(42):2921-2964.</div></div></div> [[Try this question again->Pericardiocentesis indication - Rx]] [[Next case →->Massive transfusion protocol - Rx]] [[Start another case->Hub]] [[Restart this case->Pericardiocentesis indication - Rx]]

<span class="ec-case-marker" hidden data-entry="Pericardiocentesis indication. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A fluid bolus can temporarily augment filling while drainage is prepared, but relying on it alone leaves the obstruction in place. <div class="ec-teach"><div class="th">What the findings point to</div> Cardiac tamponade is a mechanical obstruction to ventricular filling, and the only effective treatment is removal of the fluid. Hypotension, elevated jugular venous pressure with clear lungs, pulsus paradoxus above 10 mm Hg, electrical alternans, and chamber collapse on echocardiography establish the diagnosis. Intravenous fluid is a temporizing measure while drainage is arranged, not a treatment. Diuretics and vasodilators reduce preload and are actively harmful. <div class="ec-src"><b>Source:</b> Adler Y, Charron P, Imazio M, et al. 2015 ESC Guidelines for the diagnosis and management of pericardial diseases. Eur Heart J 2015;36(42):2921-2964.</div></div></div> [[Try this question again->Pericardiocentesis indication - Rx]] [[Next case →->Massive transfusion protocol - Rx]] [[Start another case->Hub]] [[Restart this case->Pericardiocentesis indication - Rx]]

<span class="ec-case-marker" hidden data-entry="Pericardiocentesis indication. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Imaging beyond the echocardiogram adds nothing and moves an unstable patient away from resuscitation capability. <div class="ec-teach"><div class="th">What the findings point to</div> Cardiac tamponade is a mechanical obstruction to ventricular filling, and the only effective treatment is removal of the fluid. Hypotension, elevated jugular venous pressure with clear lungs, pulsus paradoxus above 10 mm Hg, electrical alternans, and chamber collapse on echocardiography establish the diagnosis. Intravenous fluid is a temporizing measure while drainage is arranged, not a treatment. Diuretics and vasodilators reduce preload and are actively harmful. <div class="ec-src"><b>Source:</b> Adler Y, Charron P, Imazio M, et al. 2015 ESC Guidelines for the diagnosis and management of pericardial diseases. Eur Heart J 2015;36(42):2921-2964.</div></div></div> [[Try this question again->Pericardiocentesis indication - Rx]] [[Next case →->Massive transfusion protocol - Rx]] [[Start another case->Hub]] [[Restart this case->Pericardiocentesis indication - Rx]]

<span class="ec-case-marker" hidden data-entry="Pericardiocentesis indication. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Clear lungs with elevated venous pressure can suggest embolism, but the echocardiogram has already shown the cause, and anticoagulation would convert the effusion to hemopericardium. <div class="ec-teach"><div class="th">What the findings point to</div> Cardiac tamponade is a mechanical obstruction to ventricular filling, and the only effective treatment is removal of the fluid. Hypotension, elevated jugular venous pressure with clear lungs, pulsus paradoxus above 10 mm Hg, electrical alternans, and chamber collapse on echocardiography establish the diagnosis. Intravenous fluid is a temporizing measure while drainage is arranged, not a treatment. Diuretics and vasodilators reduce preload and are actively harmful. <div class="ec-src"><b>Source:</b> Adler Y, Charron P, Imazio M, et al. 2015 ESC Guidelines for the diagnosis and management of pericardial diseases. Eur Heart J 2015;36(42):2921-2964.</div></div></div> [[Try this question again->Pericardiocentesis indication - Rx]] [[Next case →->Massive transfusion protocol - Rx]] [[Start another case->Hub]] [[Restart this case->Pericardiocentesis indication - Rx]]

<span class="ec-case-marker" hidden data-entry="Pericardiocentesis indication. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Surgical drainage is appropriate for recurrent or loculated effusions. General anesthesia with positive pressure in untreated tamponade can cause cardiovascular collapse. <div class="ec-teach"><div class="th">What the findings point to</div> Cardiac tamponade is a mechanical obstruction to ventricular filling, and the only effective treatment is removal of the fluid. Hypotension, elevated jugular venous pressure with clear lungs, pulsus paradoxus above 10 mm Hg, electrical alternans, and chamber collapse on echocardiography establish the diagnosis. Intravenous fluid is a temporizing measure while drainage is arranged, not a treatment. Diuretics and vasodilators reduce preload and are actively harmful. <div class="ec-src"><b>Source:</b> Adler Y, Charron P, Imazio M, et al. 2015 ESC Guidelines for the diagnosis and management of pericardial diseases. Eur Heart J 2015;36(42):2921-2964.</div></div></div> [[Try this question again->Pericardiocentesis indication - Rx]] [[Next case →->Massive transfusion protocol - Rx]] [[Start another case->Hub]] [[Restart this case->Pericardiocentesis indication - Rx]]

<div class="ec-scene">Trauma bay · 00:40</div> A 31-year-old woman arrives after a high-speed collision. Blood pressure is 72/40 mm Hg, pulse is 142/min, and respirations are 30/min. She is cool and mottled. Focused ultrasonography shows free fluid in the abdomen. Two liters of crystalloid have been given with a transient response. Hemoglobin is 7.1 g/dL, INR is 1.6, fibrinogen is 118 mg/dL, and platelet count is 94,000/mm3. She is being taken to the operating room. The injury occurred 45 minutes ago. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Balanced transfusion of red cells, plasma, and platelets plus tranexamic acid->Massive transfusion protocol - Rx correct]] [[Continued crystalloid resuscitation to a mean arterial pressure above 65 mm Hg->Massive transfusion protocol - Rx D1]] [[Delay transfusion until type-specific blood is available->Massive transfusion protocol - Rx D5]] [[Recombinant factor VIIa->Massive transfusion protocol - Rx D4]] [[Red cells alone until the hemoglobin exceeds 10 g/dL->Massive transfusion protocol - Rx D2]] [[Vasopressor infusion to support the blood pressure->Massive transfusion protocol - Rx D3]]

<span class="ec-case-marker" hidden data-entry="Massive transfusion protocol. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Balanced transfusion of red cells, plasma, and platelets plus tranexamic acid</div> Hemorrhagic shock with an established coagulopathy is treated with balanced component therapy approximating whole blood, in roughly equal ratios of red cells, plasma, and platelets, rather than with further crystalloid, which dilutes clotting factors and worsens acidosis. Tranexamic acid reduces mortality when given within 3 hours of injury, and she is at 45 minutes. Definitive surgical control of the bleeding proceeds in parallel. <div class="ec-src"><b>Source:</b> CRASH-2 trial collaborators. Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage. Lancet 2010;376(9734):23-32.</div></div> [[Next case →->Variceal band ligation - Rx]] [[Start another case->Hub]] [[Restart this case->Massive transfusion protocol - Rx]]

<span class="ec-case-marker" hidden data-entry="Massive transfusion protocol. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Large-volume crystalloid dilutes clotting factors, worsens acidosis and hypothermia, and dislodges formed clot. <div class="ec-teach"><div class="th">What the findings point to</div> Hemorrhagic shock with an established coagulopathy is treated with balanced component therapy approximating whole blood, in roughly equal ratios of red cells, plasma, and platelets, rather than with further crystalloid, which dilutes clotting factors and worsens acidosis. Tranexamic acid reduces mortality when given within 3 hours of injury, and she is at 45 minutes. Definitive surgical control of the bleeding proceeds in parallel. <div class="ec-src"><b>Source:</b> CRASH-2 trial collaborators. Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage. Lancet 2010;376(9734):23-32.</div></div></div> [[Try this question again->Massive transfusion protocol - Rx]] [[Next case →->Variceal band ligation - Rx]] [[Start another case->Hub]] [[Restart this case->Massive transfusion protocol - Rx]]

<span class="ec-case-marker" hidden data-entry="Massive transfusion protocol. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Red cells alone worsen dilutional coagulopathy in a patient who already has an INR of 1.6 and a fibrinogen of 118 mg/dL. <div class="ec-teach"><div class="th">What the findings point to</div> Hemorrhagic shock with an established coagulopathy is treated with balanced component therapy approximating whole blood, in roughly equal ratios of red cells, plasma, and platelets, rather than with further crystalloid, which dilutes clotting factors and worsens acidosis. Tranexamic acid reduces mortality when given within 3 hours of injury, and she is at 45 minutes. Definitive surgical control of the bleeding proceeds in parallel. <div class="ec-src"><b>Source:</b> CRASH-2 trial collaborators. Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage. Lancet 2010;376(9734):23-32.</div></div></div> [[Try this question again->Massive transfusion protocol - Rx]] [[Next case →->Variceal band ligation - Rx]] [[Start another case->Hub]] [[Restart this case->Massive transfusion protocol - Rx]]

<span class="ec-case-marker" hidden data-entry="Massive transfusion protocol. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Vasopressors in uncontrolled hemorrhage raise pressure by vasoconstriction while tissue perfusion falls further. Volume and surgical control are what she needs. <div class="ec-teach"><div class="th">What the findings point to</div> Hemorrhagic shock with an established coagulopathy is treated with balanced component therapy approximating whole blood, in roughly equal ratios of red cells, plasma, and platelets, rather than with further crystalloid, which dilutes clotting factors and worsens acidosis. Tranexamic acid reduces mortality when given within 3 hours of injury, and she is at 45 minutes. Definitive surgical control of the bleeding proceeds in parallel. <div class="ec-src"><b>Source:</b> CRASH-2 trial collaborators. Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage. Lancet 2010;376(9734):23-32.</div></div></div> [[Try this question again->Massive transfusion protocol - Rx]] [[Next case →->Variceal band ligation - Rx]] [[Start another case->Hub]] [[Restart this case->Massive transfusion protocol - Rx]]

<span class="ec-case-marker" hidden data-entry="Massive transfusion protocol. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Factor VIIa has not improved survival in trauma and increases thrombotic events. It is not part of initial resuscitation. <div class="ec-teach"><div class="th">What the findings point to</div> Hemorrhagic shock with an established coagulopathy is treated with balanced component therapy approximating whole blood, in roughly equal ratios of red cells, plasma, and platelets, rather than with further crystalloid, which dilutes clotting factors and worsens acidosis. Tranexamic acid reduces mortality when given within 3 hours of injury, and she is at 45 minutes. Definitive surgical control of the bleeding proceeds in parallel. <div class="ec-src"><b>Source:</b> CRASH-2 trial collaborators. Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage. Lancet 2010;376(9734):23-32.</div></div></div> [[Try this question again->Massive transfusion protocol - Rx]] [[Next case →->Variceal band ligation - Rx]] [[Start another case->Hub]] [[Restart this case->Massive transfusion protocol - Rx]]

<span class="ec-case-marker" hidden data-entry="Massive transfusion protocol. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Uncrossmatched group O red cells are given immediately in exsanguinating hemorrhage. Waiting for typing costs lives. <div class="ec-teach"><div class="th">What the findings point to</div> Hemorrhagic shock with an established coagulopathy is treated with balanced component therapy approximating whole blood, in roughly equal ratios of red cells, plasma, and platelets, rather than with further crystalloid, which dilutes clotting factors and worsens acidosis. Tranexamic acid reduces mortality when given within 3 hours of injury, and she is at 45 minutes. Definitive surgical control of the bleeding proceeds in parallel. <div class="ec-src"><b>Source:</b> CRASH-2 trial collaborators. Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage. Lancet 2010;376(9734):23-32.</div></div></div> [[Try this question again->Massive transfusion protocol - Rx]] [[Next case →->Variceal band ligation - Rx]] [[Start another case->Hub]] [[Restart this case->Massive transfusion protocol - Rx]]

<div class="ec-scene">Intensive care unit · 03:15</div> A 54-year-old man with cirrhosis presents with hematemesis. Blood pressure is 88/54 mm Hg, pulse is 118/min, and respirations are 22/min. Hemoglobin is 6.8 g/dL, INR is 1.8, and platelet count is 62,000/mm3. He has received two units of red cells, intravenous octreotide, and ceftriaxone, and airway protection has been secured. He is now hemodynamically stabilized. Endoscopy is available. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Balloon tamponade with a Sengstaken-Blakemore tube->Variceal band ligation - Rx D1]] [[Endoscopic variceal band ligation->Variceal band ligation - Rx correct]] [[Fresh frozen plasma to correct the INR before endoscopy->Variceal band ligation - Rx D4]] [[Proton pump infusion and observation for 24 hours->Variceal band ligation - Rx D5]] [[Transfusion to a hemoglobin above 10 g/dL->Variceal band ligation - Rx D3]] [[Transjugular intrahepatic portosystemic shunt as the first intervention->Variceal band ligation - Rx D2]]

<span class="ec-case-marker" hidden data-entry="Variceal band ligation. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Endoscopic variceal band ligation</div> Once the patient is resuscitated and the airway is protected, urgent endoscopy within 12 hours provides both diagnosis and definitive hemostasis, and band ligation is preferred over sclerotherapy for esophageal varices because it has lower rates of rebleeding and complications. Vasoactive therapy and antibiotic prophylaxis, both already given, are adjuncts that reduce bleeding and mortality but do not stop an actively bleeding varix. <div class="ec-src"><b>Source:</b> Garcia-Tsao G, Abraldes JG, Berzigotti A, Bosch J. Portal hypertensive bleeding in cirrhosis: Risk stratification, diagnosis, and management: 2016 practice guidance by the AASLD. Hepatology 2017;65(1):310-335.</div></div> [[Next case →->ERCP in cholangitis - Rx]] [[Start another case->Hub]] [[Restart this case->Variceal band ligation - Rx]]

<span class="ec-case-marker" hidden data-entry="Variceal band ligation. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Balloon tamponade is a temporizing bridge for uncontrollable bleeding when endoscopy has failed or is unavailable, and carries esophageal perforation risk. <div class="ec-teach"><div class="th">What the findings point to</div> Once the patient is resuscitated and the airway is protected, urgent endoscopy within 12 hours provides both diagnosis and definitive hemostasis, and band ligation is preferred over sclerotherapy for esophageal varices because it has lower rates of rebleeding and complications. Vasoactive therapy and antibiotic prophylaxis, both already given, are adjuncts that reduce bleeding and mortality but do not stop an actively bleeding varix. <div class="ec-src"><b>Source:</b> Garcia-Tsao G, Abraldes JG, Berzigotti A, Bosch J. Portal hypertensive bleeding in cirrhosis: Risk stratification, diagnosis, and management: 2016 practice guidance by the AASLD. Hepatology 2017;65(1):310-335.</div></div></div> [[Try this question again->Variceal band ligation - Rx]] [[Next case →->ERCP in cholangitis - Rx]] [[Start another case->Hub]] [[Restart this case->Variceal band ligation - Rx]]

<span class="ec-case-marker" hidden data-entry="Variceal band ligation. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Early shunting benefits selected high-risk patients after endoscopic therapy. It is not the first-line hemostatic intervention. <div class="ec-teach"><div class="th">What the findings point to</div> Once the patient is resuscitated and the airway is protected, urgent endoscopy within 12 hours provides both diagnosis and definitive hemostasis, and band ligation is preferred over sclerotherapy for esophageal varices because it has lower rates of rebleeding and complications. Vasoactive therapy and antibiotic prophylaxis, both already given, are adjuncts that reduce bleeding and mortality but do not stop an actively bleeding varix. <div class="ec-src"><b>Source:</b> Garcia-Tsao G, Abraldes JG, Berzigotti A, Bosch J. Portal hypertensive bleeding in cirrhosis: Risk stratification, diagnosis, and management: 2016 practice guidance by the AASLD. Hepatology 2017;65(1):310-335.</div></div></div> [[Try this question again->Variceal band ligation - Rx]] [[Next case →->ERCP in cholangitis - Rx]] [[Start another case->Hub]] [[Restart this case->Variceal band ligation - Rx]]

<span class="ec-case-marker" hidden data-entry="Variceal band ligation. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Liberal transfusion raises portal pressure and increases rebleeding and mortality. A restrictive target near 7 g/dL is preferred. <div class="ec-teach"><div class="th">What the findings point to</div> Once the patient is resuscitated and the airway is protected, urgent endoscopy within 12 hours provides both diagnosis and definitive hemostasis, and band ligation is preferred over sclerotherapy for esophageal varices because it has lower rates of rebleeding and complications. Vasoactive therapy and antibiotic prophylaxis, both already given, are adjuncts that reduce bleeding and mortality but do not stop an actively bleeding varix. <div class="ec-src"><b>Source:</b> Garcia-Tsao G, Abraldes JG, Berzigotti A, Bosch J. Portal hypertensive bleeding in cirrhosis: Risk stratification, diagnosis, and management: 2016 practice guidance by the AASLD. Hepatology 2017;65(1):310-335.</div></div></div> [[Try this question again->Variceal band ligation - Rx]] [[Next case →->ERCP in cholangitis - Rx]] [[Start another case->Hub]] [[Restart this case->Variceal band ligation - Rx]]

<span class="ec-case-marker" hidden data-entry="Variceal band ligation. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The INR in cirrhosis does not reflect bleeding risk, and plasma expands volume and raises portal pressure without improving hemostasis. <div class="ec-teach"><div class="th">What the findings point to</div> Once the patient is resuscitated and the airway is protected, urgent endoscopy within 12 hours provides both diagnosis and definitive hemostasis, and band ligation is preferred over sclerotherapy for esophageal varices because it has lower rates of rebleeding and complications. Vasoactive therapy and antibiotic prophylaxis, both already given, are adjuncts that reduce bleeding and mortality but do not stop an actively bleeding varix. <div class="ec-src"><b>Source:</b> Garcia-Tsao G, Abraldes JG, Berzigotti A, Bosch J. Portal hypertensive bleeding in cirrhosis: Risk stratification, diagnosis, and management: 2016 practice guidance by the AASLD. Hepatology 2017;65(1):310-335.</div></div></div> [[Try this question again->Variceal band ligation - Rx]] [[Next case →->ERCP in cholangitis - Rx]] [[Start another case->Hub]] [[Restart this case->Variceal band ligation - Rx]]

<span class="ec-case-marker" hidden data-entry="Variceal band ligation. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Acid suppression treats peptic ulcer bleeding. It does not control variceal hemorrhage. <div class="ec-teach"><div class="th">What the findings point to</div> Once the patient is resuscitated and the airway is protected, urgent endoscopy within 12 hours provides both diagnosis and definitive hemostasis, and band ligation is preferred over sclerotherapy for esophageal varices because it has lower rates of rebleeding and complications. Vasoactive therapy and antibiotic prophylaxis, both already given, are adjuncts that reduce bleeding and mortality but do not stop an actively bleeding varix. <div class="ec-src"><b>Source:</b> Garcia-Tsao G, Abraldes JG, Berzigotti A, Bosch J. Portal hypertensive bleeding in cirrhosis: Risk stratification, diagnosis, and management: 2016 practice guidance by the AASLD. Hepatology 2017;65(1):310-335.</div></div></div> [[Try this question again->Variceal band ligation - Rx]] [[Next case →->ERCP in cholangitis - Rx]] [[Start another case->Hub]] [[Restart this case->Variceal band ligation - Rx]]

<div class="ec-scene">Intensive care unit · 05:50</div> A 70-year-old woman has fever, right upper quadrant pain, and jaundice. Temperature is 39.2°C, blood pressure is 82/50 mm Hg despite 2 L of crystalloid, pulse is 126/min, and she is confused. Total bilirubin is 6.8 mg/dL, alkaline phosphatase is 420 U/L, leukocyte count is 22,000/mm3, and lactate is 4.2 mmol/L. Ultrasonography shows a dilated common bile duct at 12 mm with stones. Piperacillin-tazobactam has been given and norepinephrine started. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Continued antibiotics and vasopressors with reassessment in 12 hours->ERCP in cholangitis - Rx D1]] [[Emergency open cholecystectomy->ERCP in cholangitis - Rx D2]] [[Escalation to meropenem and observation->ERCP in cholangitis - Rx D5]] [[Magnetic resonance cholangiopancreatography to confirm the stones->ERCP in cholangitis - Rx D3]] [[Percutaneous cholecystostomy->ERCP in cholangitis - Rx D4]] [[Urgent endoscopic retrograde cholangiopancreatography for biliary drainage->ERCP in cholangitis - Rx correct]]

<span class="ec-case-marker" hidden data-entry="ERCP in cholangitis. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Urgent endoscopic retrograde cholangiopancreatography for biliary drainage</div> Cholangitis with hypotension and confusion is suppurative cholangitis, and the obstructed infected biliary tree is a closed abscess. Antibiotics and vasopressors support the patient but do not achieve source control, and mortality without drainage is very high. Urgent endoscopic drainage within hours is the definitive intervention, with percutaneous transhepatic drainage as the alternative where endoscopy is not feasible. Cholecystectomy follows after recovery. <div class="ec-src"><b>Source:</b> Miura F, Okamoto K, Takada T, et al. Tokyo Guidelines 2018: initial management of acute biliary infection and flowchart for acute cholangitis. J Hepatobiliary Pancreat Sci 2018;25(1):31-40.</div></div> [[Next case →->Central line indication - Rx]] [[Start another case->Hub]] [[Restart this case->ERCP in cholangitis - Rx]]

<span class="ec-case-marker" hidden data-entry="ERCP in cholangitis. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> 12 hours without drainage in suppurative cholangitis has a very high mortality. Source control cannot wait. <div class="ec-teach"><div class="th">What the findings point to</div> Cholangitis with hypotension and confusion is suppurative cholangitis, and the obstructed infected biliary tree is a closed abscess. Antibiotics and vasopressors support the patient but do not achieve source control, and mortality without drainage is very high. Urgent endoscopic drainage within hours is the definitive intervention, with percutaneous transhepatic drainage as the alternative where endoscopy is not feasible. Cholecystectomy follows after recovery. <div class="ec-src"><b>Source:</b> Miura F, Okamoto K, Takada T, et al. Tokyo Guidelines 2018: initial management of acute biliary infection and flowchart for acute cholangitis. J Hepatobiliary Pancreat Sci 2018;25(1):31-40.</div></div></div> [[Try this question again->ERCP in cholangitis - Rx]] [[Next case →->Central line indication - Rx]] [[Start another case->Hub]] [[Restart this case->ERCP in cholangitis - Rx]]

<span class="ec-case-marker" hidden data-entry="ERCP in cholangitis. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Cholecystectomy addresses the gallbladder, not the obstructed common duct, and major surgery in septic shock carries prohibitive risk. <div class="ec-teach"><div class="th">What the findings point to</div> Cholangitis with hypotension and confusion is suppurative cholangitis, and the obstructed infected biliary tree is a closed abscess. Antibiotics and vasopressors support the patient but do not achieve source control, and mortality without drainage is very high. Urgent endoscopic drainage within hours is the definitive intervention, with percutaneous transhepatic drainage as the alternative where endoscopy is not feasible. Cholecystectomy follows after recovery. <div class="ec-src"><b>Source:</b> Miura F, Okamoto K, Takada T, et al. Tokyo Guidelines 2018: initial management of acute biliary infection and flowchart for acute cholangitis. J Hepatobiliary Pancreat Sci 2018;25(1):31-40.</div></div></div> [[Try this question again->ERCP in cholangitis - Rx]] [[Next case →->Central line indication - Rx]] [[Start another case->Hub]] [[Restart this case->ERCP in cholangitis - Rx]]

<span class="ec-case-marker" hidden data-entry="ERCP in cholangitis. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> The ultrasound has already shown a dilated duct with stones in a patient with the classic triad plus shock. Further imaging is delay. <div class="ec-teach"><div class="th">What the findings point to</div> Cholangitis with hypotension and confusion is suppurative cholangitis, and the obstructed infected biliary tree is a closed abscess. Antibiotics and vasopressors support the patient but do not achieve source control, and mortality without drainage is very high. Urgent endoscopic drainage within hours is the definitive intervention, with percutaneous transhepatic drainage as the alternative where endoscopy is not feasible. Cholecystectomy follows after recovery. <div class="ec-src"><b>Source:</b> Miura F, Okamoto K, Takada T, et al. Tokyo Guidelines 2018: initial management of acute biliary infection and flowchart for acute cholangitis. J Hepatobiliary Pancreat Sci 2018;25(1):31-40.</div></div></div> [[Try this question again->ERCP in cholangitis - Rx]] [[Next case →->Central line indication - Rx]] [[Start another case->Hub]] [[Restart this case->ERCP in cholangitis - Rx]]

<span class="ec-case-marker" hidden data-entry="ERCP in cholangitis. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Gallbladder drainage is for acute cholecystitis in poor surgical candidates. It does not decompress the common bile duct. <div class="ec-teach"><div class="th">What the findings point to</div> Cholangitis with hypotension and confusion is suppurative cholangitis, and the obstructed infected biliary tree is a closed abscess. Antibiotics and vasopressors support the patient but do not achieve source control, and mortality without drainage is very high. Urgent endoscopic drainage within hours is the definitive intervention, with percutaneous transhepatic drainage as the alternative where endoscopy is not feasible. Cholecystectomy follows after recovery. <div class="ec-src"><b>Source:</b> Miura F, Okamoto K, Takada T, et al. Tokyo Guidelines 2018: initial management of acute biliary infection and flowchart for acute cholangitis. J Hepatobiliary Pancreat Sci 2018;25(1):31-40.</div></div></div> [[Try this question again->ERCP in cholangitis - Rx]] [[Next case →->Central line indication - Rx]] [[Start another case->Hub]] [[Restart this case->ERCP in cholangitis - Rx]]

<span class="ec-case-marker" hidden data-entry="ERCP in cholangitis. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Changing the antibiotic does not achieve source control in an obstructed system. <div class="ec-teach"><div class="th">What the findings point to</div> Cholangitis with hypotension and confusion is suppurative cholangitis, and the obstructed infected biliary tree is a closed abscess. Antibiotics and vasopressors support the patient but do not achieve source control, and mortality without drainage is very high. Urgent endoscopic drainage within hours is the definitive intervention, with percutaneous transhepatic drainage as the alternative where endoscopy is not feasible. Cholecystectomy follows after recovery. <div class="ec-src"><b>Source:</b> Miura F, Okamoto K, Takada T, et al. Tokyo Guidelines 2018: initial management of acute biliary infection and flowchart for acute cholangitis. J Hepatobiliary Pancreat Sci 2018;25(1):31-40.</div></div></div> [[Try this question again->ERCP in cholangitis - Rx]] [[Next case →->Central line indication - Rx]] [[Start another case->Hub]] [[Restart this case->ERCP in cholangitis - Rx]]

<div class="ec-scene">Emergency department · 08:10</div> A 66-year-old man with septic shock from pneumonia has received 30 mL/kg of crystalloid. Blood pressure remains 76/44 mm Hg with a mean arterial pressure of 55 mm Hg, pulse is 118/min, and lactate is 4.8 mmol/L. He has two functioning 18-gauge peripheral intravenous catheters. Norepinephrine has been started peripherally and is being titrated upward. The intensive care unit has a bed available in 30 minutes. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Continue peripheral norepinephrine while arranging central access->Central line indication - Rx correct]] [[Give a further 30 mL/kg of crystalloid before any vasopressor->Central line indication - Rx D2]] [[Place a pulmonary artery catheter to guide therapy->Central line indication - Rx D3]] [[Start dopamine instead to avoid the need for central access->Central line indication - Rx D4]] [[Stop the norepinephrine until central access is obtained->Central line indication - Rx D1]] [[Transfuse red cells to improve oxygen delivery->Central line indication - Rx D5]]

<span class="ec-case-marker" hidden data-entry="Central line indication. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Continue peripheral norepinephrine while arranging central access</div> Vasopressor initiation should not be delayed for central access, and short-term peripheral administration of norepinephrine through a well-sited proximal catheter is safe with monitoring for extravasation. Central venous access is still appropriate for a patient likely to need prolonged or escalating vasopressor support, but it is arranged in parallel rather than as a prerequisite. The priority is maintaining perfusion pressure without interruption. <div class="ec-src"><b>Source:</b> Evans L, Rhodes A, Alhazzani W, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2021. Crit Care Med 2021;49(11):e1063-e1143.</div></div> [[Next case →->Tension pneumothorax decompression - Rx]] [[Start another case->Hub]] [[Restart this case->Central line indication - Rx]]

<span class="ec-case-marker" hidden data-entry="Central line indication. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Interrupting vasopressor support in a patient with a mean arterial pressure of 55 mm Hg to await a procedure causes avoidable hypoperfusion. <div class="ec-teach"><div class="th">What the findings point to</div> Vasopressor initiation should not be delayed for central access, and short-term peripheral administration of norepinephrine through a well-sited proximal catheter is safe with monitoring for extravasation. Central venous access is still appropriate for a patient likely to need prolonged or escalating vasopressor support, but it is arranged in parallel rather than as a prerequisite. The priority is maintaining perfusion pressure without interruption. <div class="ec-src"><b>Source:</b> Evans L, Rhodes A, Alhazzani W, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2021. Crit Care Med 2021;49(11):e1063-e1143.</div></div></div> [[Try this question again->Central line indication - Rx]] [[Next case →->Tension pneumothorax decompression - Rx]] [[Start another case->Hub]] [[Restart this case->Central line indication - Rx]]

<span class="ec-case-marker" hidden data-entry="Central line indication. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> He has already received the recommended initial volume and remains hypotensive. Continued large-volume loading in a patient with pneumonia risks worsening oxygenation. <div class="ec-teach"><div class="th">What the findings point to</div> Vasopressor initiation should not be delayed for central access, and short-term peripheral administration of norepinephrine through a well-sited proximal catheter is safe with monitoring for extravasation. Central venous access is still appropriate for a patient likely to need prolonged or escalating vasopressor support, but it is arranged in parallel rather than as a prerequisite. The priority is maintaining perfusion pressure without interruption. <div class="ec-src"><b>Source:</b> Evans L, Rhodes A, Alhazzani W, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2021. Crit Care Med 2021;49(11):e1063-e1143.</div></div></div> [[Try this question again->Central line indication - Rx]] [[Next case →->Tension pneumothorax decompression - Rx]] [[Start another case->Hub]] [[Restart this case->Central line indication - Rx]]

<span class="ec-case-marker" hidden data-entry="Central line indication. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Pulmonary artery catheterization has not improved outcomes in septic shock and is not part of routine management. <div class="ec-teach"><div class="th">What the findings point to</div> Vasopressor initiation should not be delayed for central access, and short-term peripheral administration of norepinephrine through a well-sited proximal catheter is safe with monitoring for extravasation. Central venous access is still appropriate for a patient likely to need prolonged or escalating vasopressor support, but it is arranged in parallel rather than as a prerequisite. The priority is maintaining perfusion pressure without interruption. <div class="ec-src"><b>Source:</b> Evans L, Rhodes A, Alhazzani W, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2021. Crit Care Med 2021;49(11):e1063-e1143.</div></div></div> [[Try this question again->Central line indication - Rx]] [[Next case →->Tension pneumothorax decompression - Rx]] [[Start another case->Hub]] [[Restart this case->Central line indication - Rx]]

<span class="ec-case-marker" hidden data-entry="Central line indication. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Dopamine causes more arrhythmias than norepinephrine and is not preferred, and it carries the same extravasation concerns. <div class="ec-teach"><div class="th">What the findings point to</div> Vasopressor initiation should not be delayed for central access, and short-term peripheral administration of norepinephrine through a well-sited proximal catheter is safe with monitoring for extravasation. Central venous access is still appropriate for a patient likely to need prolonged or escalating vasopressor support, but it is arranged in parallel rather than as a prerequisite. The priority is maintaining perfusion pressure without interruption. <div class="ec-src"><b>Source:</b> Evans L, Rhodes A, Alhazzani W, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2021. Crit Care Med 2021;49(11):e1063-e1143.</div></div></div> [[Try this question again->Central line indication - Rx]] [[Next case →->Tension pneumothorax decompression - Rx]] [[Start another case->Hub]] [[Restart this case->Central line indication - Rx]]

<span class="ec-case-marker" hidden data-entry="Central line indication. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Transfusion is guided by hemoglobin thresholds, and no anemia is described. It does not address vasoplegia. <div class="ec-teach"><div class="th">What the findings point to</div> Vasopressor initiation should not be delayed for central access, and short-term peripheral administration of norepinephrine through a well-sited proximal catheter is safe with monitoring for extravasation. Central venous access is still appropriate for a patient likely to need prolonged or escalating vasopressor support, but it is arranged in parallel rather than as a prerequisite. The priority is maintaining perfusion pressure without interruption. <div class="ec-src"><b>Source:</b> Evans L, Rhodes A, Alhazzani W, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2021. Crit Care Med 2021;49(11):e1063-e1143.</div></div></div> [[Try this question again->Central line indication - Rx]] [[Next case →->Tension pneumothorax decompression - Rx]] [[Start another case->Hub]] [[Restart this case->Central line indication - Rx]]

<div class="ec-scene">Trauma bay · 19:30</div> A 34-year-old man arrives after a fall from height. He is agitated and cyanotic. Blood pressure is 68/40 mm Hg, pulse is 138/min, respirations are 36/min, and oxygen saturation is 82% on a non-rebreather mask. Breath sounds are absent on the left with hyperresonance, the trachea is deviated to the right, and the neck veins are distended. He is being bag-mask ventilated with increasing resistance. <span class="ec-prompt">Which of the following is the most appropriate immediate intervention?</span> [[Bedside ultrasonography to assess for lung sliding->Tension pneumothorax decompression - Rx D3]] [[Chest radiography to confirm the diagnosis->Tension pneumothorax decompression - Rx D1]] [[Endotracheal intubation first->Tension pneumothorax decompression - Rx D2]] [[Immediate needle or finger thoracostomy->Tension pneumothorax decompression - Rx correct]] [[Large-volume fluid resuscitation for the hypotension->Tension pneumothorax decompression - Rx D4]] [[Placement of a definitive chest tube in the operating room->Tension pneumothorax decompression - Rx D5]]

<span class="ec-case-marker" hidden data-entry="Tension pneumothorax decompression. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Immediate needle or finger thoracostomy</div> Tension pneumothorax is a clinical diagnosis and a treat-first emergency. Air trapped under pressure shifts the mediastinum and obstructs venous return, producing obstructive shock that kills within minutes. Decompression must precede any imaging. Finger thoracostomy in the fifth intercostal space at the anterior axillary line is more reliable than needle decompression in adults because a standard needle frequently fails to reach the pleural space, and a definitive chest tube follows. <div class="ec-src"><b>Source:</b> Leigh-Smith S, Harris T. Tension pneumothorax, time for a re-think? Emerg Med J 2005;22(1):8-16.</div></div> [[Next case →->Developmental milestones - Dx]] [[Start another case->Hub]] [[Restart this case->Tension pneumothorax decompression - Rx]]

<span class="ec-case-marker" hidden data-entry="Tension pneumothorax decompression. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Imaging in suspected tension pneumothorax is a fatal delay. The diagnosis is made at the bedside and treated immediately. <div class="ec-teach"><div class="th">What the findings point to</div> Tension pneumothorax is a clinical diagnosis and a treat-first emergency. Air trapped under pressure shifts the mediastinum and obstructs venous return, producing obstructive shock that kills within minutes. Decompression must precede any imaging. Finger thoracostomy in the fifth intercostal space at the anterior axillary line is more reliable than needle decompression in adults because a standard needle frequently fails to reach the pleural space, and a definitive chest tube follows. <div class="ec-src"><b>Source:</b> Leigh-Smith S, Harris T. Tension pneumothorax, time for a re-think? Emerg Med J 2005;22(1):8-16.</div></div></div> [[Try this question again->Tension pneumothorax decompression - Rx]] [[Next case →->Developmental milestones - Dx]] [[Start another case->Hub]] [[Restart this case->Tension pneumothorax decompression - Rx]]

<span class="ec-case-marker" hidden data-entry="Tension pneumothorax decompression. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Positive pressure ventilation forces more air into the pleural space under tension and accelerates cardiovascular collapse. Decompress first. <div class="ec-teach"><div class="th">What the findings point to</div> Tension pneumothorax is a clinical diagnosis and a treat-first emergency. Air trapped under pressure shifts the mediastinum and obstructs venous return, producing obstructive shock that kills within minutes. Decompression must precede any imaging. Finger thoracostomy in the fifth intercostal space at the anterior axillary line is more reliable than needle decompression in adults because a standard needle frequently fails to reach the pleural space, and a definitive chest tube follows. <div class="ec-src"><b>Source:</b> Leigh-Smith S, Harris T. Tension pneumothorax, time for a re-think? Emerg Med J 2005;22(1):8-16.</div></div></div> [[Try this question again->Tension pneumothorax decompression - Rx]] [[Next case →->Developmental milestones - Dx]] [[Start another case->Hub]] [[Restart this case->Tension pneumothorax decompression - Rx]]

<span class="ec-case-marker" hidden data-entry="Tension pneumothorax decompression. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Ultrasound is useful in equivocal cases. With tracheal deviation and distended neck veins the diagnosis is not equivocal. <div class="ec-teach"><div class="th">What the findings point to</div> Tension pneumothorax is a clinical diagnosis and a treat-first emergency. Air trapped under pressure shifts the mediastinum and obstructs venous return, producing obstructive shock that kills within minutes. Decompression must precede any imaging. Finger thoracostomy in the fifth intercostal space at the anterior axillary line is more reliable than needle decompression in adults because a standard needle frequently fails to reach the pleural space, and a definitive chest tube follows. <div class="ec-src"><b>Source:</b> Leigh-Smith S, Harris T. Tension pneumothorax, time for a re-think? Emerg Med J 2005;22(1):8-16.</div></div></div> [[Try this question again->Tension pneumothorax decompression - Rx]] [[Next case →->Developmental milestones - Dx]] [[Start another case->Hub]] [[Restart this case->Tension pneumothorax decompression - Rx]]

<span class="ec-case-marker" hidden data-entry="Tension pneumothorax decompression. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Fluid cannot overcome a mechanical obstruction to venous return and delays the only effective treatment. <div class="ec-teach"><div class="th">What the findings point to</div> Tension pneumothorax is a clinical diagnosis and a treat-first emergency. Air trapped under pressure shifts the mediastinum and obstructs venous return, producing obstructive shock that kills within minutes. Decompression must precede any imaging. Finger thoracostomy in the fifth intercostal space at the anterior axillary line is more reliable than needle decompression in adults because a standard needle frequently fails to reach the pleural space, and a definitive chest tube follows. <div class="ec-src"><b>Source:</b> Leigh-Smith S, Harris T. Tension pneumothorax, time for a re-think? Emerg Med J 2005;22(1):8-16.</div></div></div> [[Try this question again->Tension pneumothorax decompression - Rx]] [[Next case →->Developmental milestones - Dx]] [[Start another case->Hub]] [[Restart this case->Tension pneumothorax decompression - Rx]]

<span class="ec-case-marker" hidden data-entry="Tension pneumothorax decompression. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Moving the patient wastes the minutes available. Immediate decompression at the bedside, then a tube. <div class="ec-teach"><div class="th">What the findings point to</div> Tension pneumothorax is a clinical diagnosis and a treat-first emergency. Air trapped under pressure shifts the mediastinum and obstructs venous return, producing obstructive shock that kills within minutes. Decompression must precede any imaging. Finger thoracostomy in the fifth intercostal space at the anterior axillary line is more reliable than needle decompression in adults because a standard needle frequently fails to reach the pleural space, and a definitive chest tube follows. <div class="ec-src"><b>Source:</b> Leigh-Smith S, Harris T. Tension pneumothorax, time for a re-think? Emerg Med J 2005;22(1):8-16.</div></div></div> [[Try this question again->Tension pneumothorax decompression - Rx]] [[Next case →->Developmental milestones - Dx]] [[Start another case->Hub]] [[Restart this case->Tension pneumothorax decompression - Rx]]

<div class="ec-scene">Pediatric clinic · 09:20</div> A 20-month-old boy is brought for a routine visit. He walks well and climbs stairs holding a rail. He uses 6 words consistently, does not combine words, follows a one-step command, and points to indicate what he wants. He makes eye contact, shares enjoyment by looking at his mother, and plays reciprocal games. Hearing screening at birth was normal and he had recurrent otitis media with three episodes in the past year. Growth parameters are at the 50th percentile. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Chromosomal microarray testing->Developmental milestones - Dx D5]] [[Formal audiologic evaluation and referral for speech evaluation->Developmental milestones - Dx correct]] [[Reassurance that late talking is common in boys->Developmental milestones - Dx D1]] [[Referral for autism spectrum evaluation as the priority->Developmental milestones - Dx D2]] [[Repeat assessment at the 24-month visit->Developmental milestones - Dx D3]] [[Tympanostomy tube placement now->Developmental milestones - Dx D4]]

<span class="ec-case-marker" hidden data-entry="Developmental milestones. Dx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Formal audiologic evaluation and referral for speech evaluation</div> At 20 months a child is expected to have roughly 50 words and to be beginning two-word combinations, so 6 words is a meaningful expressive language delay. His social milestones, joint attention, eye contact, and reciprocal play are intact, which argues against autism spectrum disorder and points toward an isolated expressive delay. Recurrent otitis media with effusion is a common and correctable contributor, so formal audiology precedes or accompanies speech-language referral even with a normal newborn screen. <div class="ec-src"><b>Source:</b> Council on Children With Disabilities, Section on Developmental Behavioral Pediatrics. Identifying Infants and Young Children With Developmental Disorders in the Medical Home. Pediatrics 2006;118(1):405-420.</div></div> [[Next case →->Geriatric falls assessment - Prevention]] [[Start another case->Hub]] [[Restart this case->Developmental milestones - Dx]]

<span class="ec-case-marker" hidden data-entry="Developmental milestones. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Attributing a delay of this magnitude to sex delays intervention during the period when it is most effective. <div class="ec-teach"><div class="th">What the findings point to</div> At 20 months a child is expected to have roughly 50 words and to be beginning two-word combinations, so 6 words is a meaningful expressive language delay. His social milestones, joint attention, eye contact, and reciprocal play are intact, which argues against autism spectrum disorder and points toward an isolated expressive delay. Recurrent otitis media with effusion is a common and correctable contributor, so formal audiology precedes or accompanies speech-language referral even with a normal newborn screen. <div class="ec-src"><b>Source:</b> Council on Children With Disabilities, Section on Developmental Behavioral Pediatrics. Identifying Infants and Young Children With Developmental Disorders in the Medical Home. Pediatrics 2006;118(1):405-420.</div></div></div> [[Try this question again->Developmental milestones - Dx]] [[Next case →->Geriatric falls assessment - Prevention]] [[Start another case->Hub]] [[Restart this case->Developmental milestones - Dx]]

<span class="ec-case-marker" hidden data-entry="Developmental milestones. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Preserved joint attention, eye contact, shared enjoyment, and reciprocal play make autism much less likely. The deficit is confined to expressive language. <div class="ec-teach"><div class="th">What the findings point to</div> At 20 months a child is expected to have roughly 50 words and to be beginning two-word combinations, so 6 words is a meaningful expressive language delay. His social milestones, joint attention, eye contact, and reciprocal play are intact, which argues against autism spectrum disorder and points toward an isolated expressive delay. Recurrent otitis media with effusion is a common and correctable contributor, so formal audiology precedes or accompanies speech-language referral even with a normal newborn screen. <div class="ec-src"><b>Source:</b> Council on Children With Disabilities, Section on Developmental Behavioral Pediatrics. Identifying Infants and Young Children With Developmental Disorders in the Medical Home. Pediatrics 2006;118(1):405-420.</div></div></div> [[Try this question again->Developmental milestones - Dx]] [[Next case →->Geriatric falls assessment - Prevention]] [[Start another case->Hub]] [[Restart this case->Developmental milestones - Dx]]

<span class="ec-case-marker" hidden data-entry="Developmental milestones. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> 4 months of watchful waiting in a child with a clear expressive delay and a treatable hearing risk factor wastes the intervention window. <div class="ec-teach"><div class="th">What the findings point to</div> At 20 months a child is expected to have roughly 50 words and to be beginning two-word combinations, so 6 words is a meaningful expressive language delay. His social milestones, joint attention, eye contact, and reciprocal play are intact, which argues against autism spectrum disorder and points toward an isolated expressive delay. Recurrent otitis media with effusion is a common and correctable contributor, so formal audiology precedes or accompanies speech-language referral even with a normal newborn screen. <div class="ec-src"><b>Source:</b> Council on Children With Disabilities, Section on Developmental Behavioral Pediatrics. Identifying Infants and Young Children With Developmental Disorders in the Medical Home. Pediatrics 2006;118(1):405-420.</div></div></div> [[Try this question again->Developmental milestones - Dx]] [[Next case →->Geriatric falls assessment - Prevention]] [[Start another case->Hub]] [[Restart this case->Developmental milestones - Dx]]

<span class="ec-case-marker" hidden data-entry="Developmental milestones. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Tubes are considered for persistent effusion with documented hearing loss. Audiology is required before the decision. <div class="ec-teach"><div class="th">What the findings point to</div> At 20 months a child is expected to have roughly 50 words and to be beginning two-word combinations, so 6 words is a meaningful expressive language delay. His social milestones, joint attention, eye contact, and reciprocal play are intact, which argues against autism spectrum disorder and points toward an isolated expressive delay. Recurrent otitis media with effusion is a common and correctable contributor, so formal audiology precedes or accompanies speech-language referral even with a normal newborn screen. <div class="ec-src"><b>Source:</b> Council on Children With Disabilities, Section on Developmental Behavioral Pediatrics. Identifying Infants and Young Children With Developmental Disorders in the Medical Home. Pediatrics 2006;118(1):405-420.</div></div></div> [[Try this question again->Developmental milestones - Dx]] [[Next case →->Geriatric falls assessment - Prevention]] [[Start another case->Hub]] [[Restart this case->Developmental milestones - Dx]]

<span class="ec-case-marker" hidden data-entry="Developmental milestones. Dx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Genetic testing is appropriate for global developmental delay or dysmorphic features. He has isolated expressive delay with normal motor and social milestones. <div class="ec-teach"><div class="th">What the findings point to</div> At 20 months a child is expected to have roughly 50 words and to be beginning two-word combinations, so 6 words is a meaningful expressive language delay. His social milestones, joint attention, eye contact, and reciprocal play are intact, which argues against autism spectrum disorder and points toward an isolated expressive delay. Recurrent otitis media with effusion is a common and correctable contributor, so formal audiology precedes or accompanies speech-language referral even with a normal newborn screen. <div class="ec-src"><b>Source:</b> Council on Children With Disabilities, Section on Developmental Behavioral Pediatrics. Identifying Infants and Young Children With Developmental Disorders in the Medical Home. Pediatrics 2006;118(1):405-420.</div></div></div> [[Try this question again->Developmental milestones - Dx]] [[Next case →->Geriatric falls assessment - Prevention]] [[Start another case->Hub]] [[Restart this case->Developmental milestones - Dx]]

<div class="ec-scene">Primary care clinic · 10:50</div> An 81-year-old woman reports two falls in the past 6 months, one with a wrist fracture. She lives alone. Blood pressure is 142/78 mm Hg supine and 118/64 mm Hg standing, with no symptoms. Pulse is 72/min. She takes amitriptyline for insomnia, lorazepam as needed, hydrochlorothiazide, and omeprazole. Timed Up and Go test takes 18 seconds. Vision was last checked 4 years ago. Cognitive screening is normal. <span class="ec-prompt">Which of the following interventions is most likely to reduce her risk of further falls?</span> [[Adding vitamin D 800 IU daily as the primary intervention->Geriatric falls assessment - Prevention D2]] [[Deprescribing the amitriptyline and lorazepam->Geriatric falls assessment - Prevention correct]] [[Increasing the hydrochlorothiazide to control the hypertension->Geriatric falls assessment - Prevention D4]] [[Prescribing a bed alarm and a personal emergency response device->Geriatric falls assessment - Prevention D1]] [[Recommending she use a wheelchair for mobility outside the home->Geriatric falls assessment - Prevention D3]] [[Referral for hip protector fitting->Geriatric falls assessment - Prevention D5]]

<span class="ec-case-marker" hidden data-entry="Geriatric falls assessment. Prevention"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Deprescribing the amitriptyline and lorazepam</div> Medication review with withdrawal of fall-risk-increasing drugs is among the most effective single interventions, and she is taking two of the highest-risk classes. Amitriptyline is anticholinergic, sedating, and orthostatic, and benzodiazepines impair balance and reaction time; both appear on the Beers criteria as medications to avoid in older adults. Exercise with balance training, vision assessment, and vitamin D are all appropriate additions, but removing the offending drugs addresses the largest modifiable contributor here. <div class="ec-src"><b>Source:</b> By the 2023 American Geriatrics Society Beers Criteria Update Expert Panel. American Geriatrics Society 2023 updated AGS Beers Criteria for potentially inappropriate medication use in older adults. J Am Geriatr Soc 2023;71(7):2052-2081.</div></div> [[Next case →->Childhood immunization catch-up - Prevention]] [[Start another case->Hub]] [[Restart this case->Geriatric falls assessment - Prevention]]

<span class="ec-case-marker" hidden data-entry="Geriatric falls assessment. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Alarms and alert devices shorten the time lying on the floor after a fall. They do not prevent falls. <div class="ec-teach"><div class="th">What the findings point to</div> Medication review with withdrawal of fall-risk-increasing drugs is among the most effective single interventions, and she is taking two of the highest-risk classes. Amitriptyline is anticholinergic, sedating, and orthostatic, and benzodiazepines impair balance and reaction time; both appear on the Beers criteria as medications to avoid in older adults. Exercise with balance training, vision assessment, and vitamin D are all appropriate additions, but removing the offending drugs addresses the largest modifiable contributor here. <div class="ec-src"><b>Source:</b> By the 2023 American Geriatrics Society Beers Criteria Update Expert Panel. American Geriatrics Society 2023 updated AGS Beers Criteria for potentially inappropriate medication use in older adults. J Am Geriatr Soc 2023;71(7):2052-2081.</div></div></div> [[Try this question again->Geriatric falls assessment - Prevention]] [[Next case →->Childhood immunization catch-up - Prevention]] [[Start another case->Hub]] [[Restart this case->Geriatric falls assessment - Prevention]]

<span class="ec-case-marker" hidden data-entry="Geriatric falls assessment. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Vitamin D is reasonable adjunctive care but has modest effect on fall rates and does not address two high-risk sedating medications. <div class="ec-teach"><div class="th">What the findings point to</div> Medication review with withdrawal of fall-risk-increasing drugs is among the most effective single interventions, and she is taking two of the highest-risk classes. Amitriptyline is anticholinergic, sedating, and orthostatic, and benzodiazepines impair balance and reaction time; both appear on the Beers criteria as medications to avoid in older adults. Exercise with balance training, vision assessment, and vitamin D are all appropriate additions, but removing the offending drugs addresses the largest modifiable contributor here. <div class="ec-src"><b>Source:</b> By the 2023 American Geriatrics Society Beers Criteria Update Expert Panel. American Geriatrics Society 2023 updated AGS Beers Criteria for potentially inappropriate medication use in older adults. J Am Geriatr Soc 2023;71(7):2052-2081.</div></div></div> [[Try this question again->Geriatric falls assessment - Prevention]] [[Next case →->Childhood immunization catch-up - Prevention]] [[Start another case->Hub]] [[Restart this case->Geriatric falls assessment - Prevention]]

<span class="ec-case-marker" hidden data-entry="Geriatric falls assessment. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Reducing ambulation accelerates deconditioning and increases long-term fall and mortality risk. <div class="ec-teach"><div class="th">What the findings point to</div> Medication review with withdrawal of fall-risk-increasing drugs is among the most effective single interventions, and she is taking two of the highest-risk classes. Amitriptyline is anticholinergic, sedating, and orthostatic, and benzodiazepines impair balance and reaction time; both appear on the Beers criteria as medications to avoid in older adults. Exercise with balance training, vision assessment, and vitamin D are all appropriate additions, but removing the offending drugs addresses the largest modifiable contributor here. <div class="ec-src"><b>Source:</b> By the 2023 American Geriatrics Society Beers Criteria Update Expert Panel. American Geriatrics Society 2023 updated AGS Beers Criteria for potentially inappropriate medication use in older adults. J Am Geriatr Soc 2023;71(7):2052-2081.</div></div></div> [[Try this question again->Geriatric falls assessment - Prevention]] [[Next case →->Childhood immunization catch-up - Prevention]] [[Start another case->Hub]] [[Restart this case->Geriatric falls assessment - Prevention]]

<span class="ec-case-marker" hidden data-entry="Geriatric falls assessment. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Her standing pressure is already 118/64 mm Hg. More diuretic worsens orthostasis and falls. <div class="ec-teach"><div class="th">What the findings point to</div> Medication review with withdrawal of fall-risk-increasing drugs is among the most effective single interventions, and she is taking two of the highest-risk classes. Amitriptyline is anticholinergic, sedating, and orthostatic, and benzodiazepines impair balance and reaction time; both appear on the Beers criteria as medications to avoid in older adults. Exercise with balance training, vision assessment, and vitamin D are all appropriate additions, but removing the offending drugs addresses the largest modifiable contributor here. <div class="ec-src"><b>Source:</b> By the 2023 American Geriatrics Society Beers Criteria Update Expert Panel. American Geriatrics Society 2023 updated AGS Beers Criteria for potentially inappropriate medication use in older adults. J Am Geriatr Soc 2023;71(7):2052-2081.</div></div></div> [[Try this question again->Geriatric falls assessment - Prevention]] [[Next case →->Childhood immunization catch-up - Prevention]] [[Start another case->Hub]] [[Restart this case->Geriatric falls assessment - Prevention]]

<span class="ec-case-marker" hidden data-entry="Geriatric falls assessment. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Hip protectors may reduce fracture in institutional settings with good adherence. They do not reduce falls and adherence at home is poor. <div class="ec-teach"><div class="th">What the findings point to</div> Medication review with withdrawal of fall-risk-increasing drugs is among the most effective single interventions, and she is taking two of the highest-risk classes. Amitriptyline is anticholinergic, sedating, and orthostatic, and benzodiazepines impair balance and reaction time; both appear on the Beers criteria as medications to avoid in older adults. Exercise with balance training, vision assessment, and vitamin D are all appropriate additions, but removing the offending drugs addresses the largest modifiable contributor here. <div class="ec-src"><b>Source:</b> By the 2023 American Geriatrics Society Beers Criteria Update Expert Panel. American Geriatrics Society 2023 updated AGS Beers Criteria for potentially inappropriate medication use in older adults. J Am Geriatr Soc 2023;71(7):2052-2081.</div></div></div> [[Try this question again->Geriatric falls assessment - Prevention]] [[Next case →->Childhood immunization catch-up - Prevention]] [[Start another case->Hub]] [[Restart this case->Geriatric falls assessment - Prevention]]

<div class="ec-scene">Pediatric clinic · 13:45</div> A 5-year-old girl who recently arrived from abroad is brought for school entry. Written records show three doses of diphtheria-tetanus-pertussis, three doses of inactivated poliovirus, and one dose of measles-mumps-rubella given at 11 months of age. There is no record of varicella. She is well, afebrile, growing normally, and has no immunocompromising condition. Her mother reports no history of chickenpox. <span class="ec-prompt">Which of the following is the most appropriate next step?</span> [[Accept the 11-month measles dose and give only the second dose->Childhood immunization catch-up - Prevention D1]] [[Administer a second measles-mumps-rubella dose and begin varicella series->Childhood immunization catch-up - Prevention correct]] [[Check serology for measles and varicella before vaccinating->Childhood immunization catch-up - Prevention D3]] [[Defer vaccination until a complete original record is obtained from abroad->Childhood immunization catch-up - Prevention D4]] [[Give varicella vaccine only and defer measles-mumps-rubella->Childhood immunization catch-up - Prevention D5]] [[Restart all vaccine series from the beginning->Childhood immunization catch-up - Prevention D2]]

<span class="ec-case-marker" hidden data-entry="Childhood immunization catch-up. Prevention"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Administer a second measles-mumps-rubella dose and begin varicella series</div> Two doses of measles-containing vaccine are required, and a dose given before 12 months of age does not count toward the series because maternal antibody may blunt the response. She therefore needs a valid first dose now and the second at the routine interval, and she requires the varicella series since there is no record and no reliable history of disease. Written records from abroad are accepted as valid if they document date, vaccine, and appropriate age and interval. <div class="ec-src"><b>Source:</b> Wodi AP, Murthy N, Bernstein H, et al. Advisory Committee on Immunization Practices Recommended Immunization Schedule for Children and Adolescents Aged 18 Years or Younger. MMWR Morb Mortal Wkly Rep 2024;73(1):6-10.</div></div> [[Next case →->Newborn hyperbilirubinemia threshold - Rx]] [[Start another case->Hub]] [[Restart this case->Childhood immunization catch-up - Prevention]]

<span class="ec-case-marker" hidden data-entry="Childhood immunization catch-up. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A measles-containing dose given before the first birthday is invalid and does not count toward the two-dose requirement. <div class="ec-teach"><div class="th">What the findings point to</div> Two doses of measles-containing vaccine are required, and a dose given before 12 months of age does not count toward the series because maternal antibody may blunt the response. She therefore needs a valid first dose now and the second at the routine interval, and she requires the varicella series since there is no record and no reliable history of disease. Written records from abroad are accepted as valid if they document date, vaccine, and appropriate age and interval. <div class="ec-src"><b>Source:</b> Wodi AP, Murthy N, Bernstein H, et al. Advisory Committee on Immunization Practices Recommended Immunization Schedule for Children and Adolescents Aged 18 Years or Younger. MMWR Morb Mortal Wkly Rep 2024;73(1):6-10.</div></div></div> [[Try this question again->Childhood immunization catch-up - Prevention]] [[Next case →->Newborn hyperbilirubinemia threshold - Rx]] [[Start another case->Hub]] [[Restart this case->Childhood immunization catch-up - Prevention]]

<span class="ec-case-marker" hidden data-entry="Childhood immunization catch-up. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Valid doses documented in writing are counted. Restarting exposes the child to unnecessary injections without benefit. <div class="ec-teach"><div class="th">What the findings point to</div> Two doses of measles-containing vaccine are required, and a dose given before 12 months of age does not count toward the series because maternal antibody may blunt the response. She therefore needs a valid first dose now and the second at the routine interval, and she requires the varicella series since there is no record and no reliable history of disease. Written records from abroad are accepted as valid if they document date, vaccine, and appropriate age and interval. <div class="ec-src"><b>Source:</b> Wodi AP, Murthy N, Bernstein H, et al. Advisory Committee on Immunization Practices Recommended Immunization Schedule for Children and Adolescents Aged 18 Years or Younger. MMWR Morb Mortal Wkly Rep 2024;73(1):6-10.</div></div></div> [[Try this question again->Childhood immunization catch-up - Prevention]] [[Next case →->Newborn hyperbilirubinemia threshold - Rx]] [[Start another case->Hub]] [[Restart this case->Childhood immunization catch-up - Prevention]]

<span class="ec-case-marker" hidden data-entry="Childhood immunization catch-up. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Serologic testing is not required before catch-up vaccination and adds cost and a return visit. Vaccinating a person who is already immune is safe. <div class="ec-teach"><div class="th">What the findings point to</div> Two doses of measles-containing vaccine are required, and a dose given before 12 months of age does not count toward the series because maternal antibody may blunt the response. She therefore needs a valid first dose now and the second at the routine interval, and she requires the varicella series since there is no record and no reliable history of disease. Written records from abroad are accepted as valid if they document date, vaccine, and appropriate age and interval. <div class="ec-src"><b>Source:</b> Wodi AP, Murthy N, Bernstein H, et al. Advisory Committee on Immunization Practices Recommended Immunization Schedule for Children and Adolescents Aged 18 Years or Younger. MMWR Morb Mortal Wkly Rep 2024;73(1):6-10.</div></div></div> [[Try this question again->Childhood immunization catch-up - Prevention]] [[Next case →->Newborn hyperbilirubinemia threshold - Rx]] [[Start another case->Hub]] [[Restart this case->Childhood immunization catch-up - Prevention]]

<span class="ec-case-marker" hidden data-entry="Childhood immunization catch-up. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Waiting for records that may never arrive leaves her unprotected and unable to enter school. <div class="ec-teach"><div class="th">What the findings point to</div> Two doses of measles-containing vaccine are required, and a dose given before 12 months of age does not count toward the series because maternal antibody may blunt the response. She therefore needs a valid first dose now and the second at the routine interval, and she requires the varicella series since there is no record and no reliable history of disease. Written records from abroad are accepted as valid if they document date, vaccine, and appropriate age and interval. <div class="ec-src"><b>Source:</b> Wodi AP, Murthy N, Bernstein H, et al. Advisory Committee on Immunization Practices Recommended Immunization Schedule for Children and Adolescents Aged 18 Years or Younger. MMWR Morb Mortal Wkly Rep 2024;73(1):6-10.</div></div></div> [[Try this question again->Childhood immunization catch-up - Prevention]] [[Next case →->Newborn hyperbilirubinemia threshold - Rx]] [[Start another case->Hub]] [[Restart this case->Childhood immunization catch-up - Prevention]]

<span class="ec-case-marker" hidden data-entry="Childhood immunization catch-up. Prevention"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Both are due now and can be administered at the same visit at different sites. <div class="ec-teach"><div class="th">What the findings point to</div> Two doses of measles-containing vaccine are required, and a dose given before 12 months of age does not count toward the series because maternal antibody may blunt the response. She therefore needs a valid first dose now and the second at the routine interval, and she requires the varicella series since there is no record and no reliable history of disease. Written records from abroad are accepted as valid if they document date, vaccine, and appropriate age and interval. <div class="ec-src"><b>Source:</b> Wodi AP, Murthy N, Bernstein H, et al. Advisory Committee on Immunization Practices Recommended Immunization Schedule for Children and Adolescents Aged 18 Years or Younger. MMWR Morb Mortal Wkly Rep 2024;73(1):6-10.</div></div></div> [[Try this question again->Childhood immunization catch-up - Prevention]] [[Next case →->Newborn hyperbilirubinemia threshold - Rx]] [[Start another case->Hub]] [[Restart this case->Childhood immunization catch-up - Prevention]]

<div class="ec-scene">Postnatal ward · 07:30</div> A term newborn at 38 weeks gestational age is 52 hours old and appears jaundiced to the mid-abdomen. Birth weight was 3,280 g and current weight is 3,050 g. Feeding is exclusively breast milk and has been difficult. Total serum bilirubin is 17.2 mg/dL and direct bilirubin is 0.6 mg/dL. Mother is blood group O positive and the infant is A positive. Direct antiglobulin test is positive. Hemoglobin is 14.8 g/dL and reticulocyte count is elevated. The infant is alert with normal tone. <span class="ec-prompt">Which of the following is the most appropriate next step in management?</span> [[Discontinue breastfeeding and substitute formula for 48 hours->Newborn hyperbilirubinemia threshold - Rx D2]] [[Immediate exchange transfusion->Newborn hyperbilirubinemia threshold - Rx D1]] [[Intensive phototherapy and support of feeding->Newborn hyperbilirubinemia threshold - Rx correct]] [[Intravenous immune globulin as the initial intervention->Newborn hyperbilirubinemia threshold - Rx D4]] [[Observation with repeat bilirubin in 12 hours->Newborn hyperbilirubinemia threshold - Rx D3]] [[Phenobarbital to induce hepatic conjugation->Newborn hyperbilirubinemia threshold - Rx D5]]

<span class="ec-case-marker" hidden data-entry="Newborn hyperbilirubinemia threshold. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Intensive phototherapy and support of feeding</div> He has ABO incompatibility with a positive direct antiglobulin test, which is a recognized neurotoxicity risk factor and lowers the phototherapy threshold. At 52 hours with a bilirubin of 17.2 mg/dL and a hemolytic risk factor, intensive phototherapy is indicated. Feeding support matters because the 7% weight loss reflects inadequate intake, which reduces enteral elimination of bilirubin. Exchange transfusion is reserved for much higher levels or for signs of acute bilirubin encephalopathy, which he does not have. <div class="ec-src"><b>Source:</b> Kemper AR, Newman TB, Slaughter JL, et al. Clinical Practice Guideline Revision: Management of Hyperbilirubinemia in the Newborn Infant 35 or More Weeks of Gestation. Pediatrics 2022;150(3):e2022058859.</div></div> [[Next case →->Malignant hyperthermia - Rx]] [[Start another case->Hub]] [[Restart this case->Newborn hyperbilirubinemia threshold - Rx]]

<span class="ec-case-marker" hidden data-entry="Newborn hyperbilirubinemia threshold. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Exchange transfusion is reserved for bilirubin concentrations well above the phototherapy threshold or for signs of acute bilirubin encephalopathy. He is alert with normal tone. <div class="ec-teach"><div class="th">What the findings point to</div> He has ABO incompatibility with a positive direct antiglobulin test, which is a recognized neurotoxicity risk factor and lowers the phototherapy threshold. At 52 hours with a bilirubin of 17.2 mg/dL and a hemolytic risk factor, intensive phototherapy is indicated. Feeding support matters because the 7% weight loss reflects inadequate intake, which reduces enteral elimination of bilirubin. Exchange transfusion is reserved for much higher levels or for signs of acute bilirubin encephalopathy, which he does not have. <div class="ec-src"><b>Source:</b> Kemper AR, Newman TB, Slaughter JL, et al. Clinical Practice Guideline Revision: Management of Hyperbilirubinemia in the Newborn Infant 35 or More Weeks of Gestation. Pediatrics 2022;150(3):e2022058859.</div></div></div> [[Try this question again->Newborn hyperbilirubinemia threshold - Rx]] [[Next case →->Malignant hyperthermia - Rx]] [[Start another case->Hub]] [[Restart this case->Newborn hyperbilirubinemia threshold - Rx]]

<span class="ec-case-marker" hidden data-entry="Newborn hyperbilirubinemia threshold. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Interrupting breastfeeding is not recommended. Supporting and increasing effective feeding achieves the same goal without undermining lactation. <div class="ec-teach"><div class="th">What the findings point to</div> He has ABO incompatibility with a positive direct antiglobulin test, which is a recognized neurotoxicity risk factor and lowers the phototherapy threshold. At 52 hours with a bilirubin of 17.2 mg/dL and a hemolytic risk factor, intensive phototherapy is indicated. Feeding support matters because the 7% weight loss reflects inadequate intake, which reduces enteral elimination of bilirubin. Exchange transfusion is reserved for much higher levels or for signs of acute bilirubin encephalopathy, which he does not have. <div class="ec-src"><b>Source:</b> Kemper AR, Newman TB, Slaughter JL, et al. Clinical Practice Guideline Revision: Management of Hyperbilirubinemia in the Newborn Infant 35 or More Weeks of Gestation. Pediatrics 2022;150(3):e2022058859.</div></div></div> [[Try this question again->Newborn hyperbilirubinemia threshold - Rx]] [[Next case →->Malignant hyperthermia - Rx]] [[Start another case->Hub]] [[Restart this case->Newborn hyperbilirubinemia threshold - Rx]]

<span class="ec-case-marker" hidden data-entry="Newborn hyperbilirubinemia threshold. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> With a positive antiglobulin test and a rising bilirubin, waiting 12 hours risks crossing the exchange threshold. <div class="ec-teach"><div class="th">What the findings point to</div> He has ABO incompatibility with a positive direct antiglobulin test, which is a recognized neurotoxicity risk factor and lowers the phototherapy threshold. At 52 hours with a bilirubin of 17.2 mg/dL and a hemolytic risk factor, intensive phototherapy is indicated. Feeding support matters because the 7% weight loss reflects inadequate intake, which reduces enteral elimination of bilirubin. Exchange transfusion is reserved for much higher levels or for signs of acute bilirubin encephalopathy, which he does not have. <div class="ec-src"><b>Source:</b> Kemper AR, Newman TB, Slaughter JL, et al. Clinical Practice Guideline Revision: Management of Hyperbilirubinemia in the Newborn Infant 35 or More Weeks of Gestation. Pediatrics 2022;150(3):e2022058859.</div></div></div> [[Try this question again->Newborn hyperbilirubinemia threshold - Rx]] [[Next case →->Malignant hyperthermia - Rx]] [[Start another case->Hub]] [[Restart this case->Newborn hyperbilirubinemia threshold - Rx]]

<span class="ec-case-marker" hidden data-entry="Newborn hyperbilirubinemia threshold. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Immune globulin is considered in isoimmune hemolytic disease when bilirubin continues rising despite intensive phototherapy, not as the first step. <div class="ec-teach"><div class="th">What the findings point to</div> He has ABO incompatibility with a positive direct antiglobulin test, which is a recognized neurotoxicity risk factor and lowers the phototherapy threshold. At 52 hours with a bilirubin of 17.2 mg/dL and a hemolytic risk factor, intensive phototherapy is indicated. Feeding support matters because the 7% weight loss reflects inadequate intake, which reduces enteral elimination of bilirubin. Exchange transfusion is reserved for much higher levels or for signs of acute bilirubin encephalopathy, which he does not have. <div class="ec-src"><b>Source:</b> Kemper AR, Newman TB, Slaughter JL, et al. Clinical Practice Guideline Revision: Management of Hyperbilirubinemia in the Newborn Infant 35 or More Weeks of Gestation. Pediatrics 2022;150(3):e2022058859.</div></div></div> [[Try this question again->Newborn hyperbilirubinemia threshold - Rx]] [[Next case →->Malignant hyperthermia - Rx]] [[Start another case->Hub]] [[Restart this case->Newborn hyperbilirubinemia threshold - Rx]]

<span class="ec-case-marker" hidden data-entry="Newborn hyperbilirubinemia threshold. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Phenobarbital acts too slowly to be useful in acute neonatal hyperbilirubinemia and carries sedative risk. <div class="ec-teach"><div class="th">What the findings point to</div> He has ABO incompatibility with a positive direct antiglobulin test, which is a recognized neurotoxicity risk factor and lowers the phototherapy threshold. At 52 hours with a bilirubin of 17.2 mg/dL and a hemolytic risk factor, intensive phototherapy is indicated. Feeding support matters because the 7% weight loss reflects inadequate intake, which reduces enteral elimination of bilirubin. Exchange transfusion is reserved for much higher levels or for signs of acute bilirubin encephalopathy, which he does not have. <div class="ec-src"><b>Source:</b> Kemper AR, Newman TB, Slaughter JL, et al. Clinical Practice Guideline Revision: Management of Hyperbilirubinemia in the Newborn Infant 35 or More Weeks of Gestation. Pediatrics 2022;150(3):e2022058859.</div></div></div> [[Try this question again->Newborn hyperbilirubinemia threshold - Rx]] [[Next case →->Malignant hyperthermia - Rx]] [[Start another case->Hub]] [[Restart this case->Newborn hyperbilirubinemia threshold - Rx]]

<div class="ec-scene">Operating room · 10:40</div> A 24-year-old man is 40 minutes into an open appendectomy under sevoflurane and a succinylcholine induction. The circulating nurse reports the end-tidal carbon dioxide has risen from 38 to 66 mm Hg despite an increase in minute ventilation, and the anesthesiologist now feels rigidity in the jaw and both forearms. Temperature has climbed from 36.9°C to 38.9°C over 10 minutes, pulse is 142/min, and blood pressure is 146/92 mm Hg. Arterial blood gas shows pH 7.21, PaCO2 61 mm Hg, and potassium 5.8 mEq/L. <span class="ec-prompt">Which of the following is the most appropriate immediate management?</span> [[Apply external cooling and give intravenous calcium gluconate for the potassium->Malignant hyperthermia - Rx D5]] [[Discontinue sevoflurane and succinylcholine and give intravenous dantrolene sodium->Malignant hyperthermia - Rx correct]] [[Give a second dose of succinylcholine to control the rigidity and secure the airway->Malignant hyperthermia - Rx D3]] [[Increase minute ventilation further and continue the operation under the same anesthetic->Malignant hyperthermia - Rx D1]] [[Order a stat serum creatine kinase level and wait for the result before treating->Malignant hyperthermia - Rx D4]] [[Switch from sevoflurane to desflurane and continue the case->Malignant hyperthermia - Rx D2]]

<span class="ec-case-marker" hidden data-entry="Malignant hyperthermia. Rx"></span><div class="ec-verdict good"><div class="ec-vhead good">✓ Discontinue sevoflurane and succinylcholine and give intravenous dantrolene sodium</div> The end-tidal carbon dioxide climbing despite increased ventilation, the jaw and limb rigidity, and the rising temperature after sevoflurane and succinylcholine mark malignant hyperthermia. Dantrolene binds the ryanodine receptor and halts the uncontrolled sarcoplasmic calcium release driving the hypermetabolic state; every triggering agent must be stopped in the same moment, since dantrolene given alongside a continuing trigger cannot outpace ongoing calcium release. Active cooling, correction of hyperkalemia and acidosis, and monitoring for recrudescence over the following 24 to 48 hours follow once dantrolene is running. <div class="ec-src"><b>Source:</b> Larach MG, Gronert GA, Allen GC, Brandom BW, Lehman EB. Clinical presentation, treatment, and complications of malignant hyperthermia in North America from 1987 to 2006: a report from the North American Malignant Hyperthermia Registry of MHAUS. Anesth Analg 2010;110(2):498-507.</div></div> [[Next case →->Hub]] [[Start another case->Hub]] [[Restart this case->Malignant hyperthermia - Rx]]

<span class="ec-case-marker" hidden data-entry="Malignant hyperthermia. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Increasing ventilation lowers carbon dioxide only marginally when production is this deranged, and continuing the trigger allows the hypermetabolic process to accelerate. <div class="ec-teach"><div class="th">What the findings point to</div> Rising end-tidal carbon dioxide out of proportion to minute ventilation, masseter and generalized muscle rigidity, tachycardia, and climbing temperature after exposure to a volatile anesthetic or succinylcholine define malignant hyperthermia, a pharmacogenetic disorder of the skeletal muscle ryanodine receptor that causes uncontrolled calcium release and hypermetabolism. Every triggering agent must be stopped immediately, and dantrolene, which blocks calcium release at the ryanodine receptor, is the only drug that reverses the process; delaying it while pursuing other measures allows rhabdomyolysis, hyperkalemic arrest, and DIC to develop. <div class="ec-src"><b>Source:</b> Larach MG, Gronert GA, Allen GC, Brandom BW, Lehman EB. Clinical presentation, treatment, and complications of malignant hyperthermia in North America from 1987 to 2006: a report from the North American Malignant Hyperthermia Registry of MHAUS. Anesth Analg 2010;110(2):498-507.</div></div></div> [[Try this question again->Malignant hyperthermia - Rx]] [[Next case →->Hub]] [[Start another case->Hub]] [[Restart this case->Malignant hyperthermia - Rx]]

<span class="ec-case-marker" hidden data-entry="Malignant hyperthermia. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> All volatile anesthetics, not only sevoflurane, trigger malignant hyperthermia. Substituting another volatile agent does not remove the trigger. <div class="ec-teach"><div class="th">What the findings point to</div> Rising end-tidal carbon dioxide out of proportion to minute ventilation, masseter and generalized muscle rigidity, tachycardia, and climbing temperature after exposure to a volatile anesthetic or succinylcholine define malignant hyperthermia, a pharmacogenetic disorder of the skeletal muscle ryanodine receptor that causes uncontrolled calcium release and hypermetabolism. Every triggering agent must be stopped immediately, and dantrolene, which blocks calcium release at the ryanodine receptor, is the only drug that reverses the process; delaying it while pursuing other measures allows rhabdomyolysis, hyperkalemic arrest, and DIC to develop. <div class="ec-src"><b>Source:</b> Larach MG, Gronert GA, Allen GC, Brandom BW, Lehman EB. Clinical presentation, treatment, and complications of malignant hyperthermia in North America from 1987 to 2006: a report from the North American Malignant Hyperthermia Registry of MHAUS. Anesth Analg 2010;110(2):498-507.</div></div></div> [[Try this question again->Malignant hyperthermia - Rx]] [[Next case →->Hub]] [[Start another case->Hub]] [[Restart this case->Malignant hyperthermia - Rx]]

<span class="ec-case-marker" hidden data-entry="Malignant hyperthermia. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Succinylcholine is itself a triggering agent. A second dose would worsen the calcium release rather than control the rigidity. <div class="ec-teach"><div class="th">What the findings point to</div> Rising end-tidal carbon dioxide out of proportion to minute ventilation, masseter and generalized muscle rigidity, tachycardia, and climbing temperature after exposure to a volatile anesthetic or succinylcholine define malignant hyperthermia, a pharmacogenetic disorder of the skeletal muscle ryanodine receptor that causes uncontrolled calcium release and hypermetabolism. Every triggering agent must be stopped immediately, and dantrolene, which blocks calcium release at the ryanodine receptor, is the only drug that reverses the process; delaying it while pursuing other measures allows rhabdomyolysis, hyperkalemic arrest, and DIC to develop. <div class="ec-src"><b>Source:</b> Larach MG, Gronert GA, Allen GC, Brandom BW, Lehman EB. Clinical presentation, treatment, and complications of malignant hyperthermia in North America from 1987 to 2006: a report from the North American Malignant Hyperthermia Registry of MHAUS. Anesth Analg 2010;110(2):498-507.</div></div></div> [[Try this question again->Malignant hyperthermia - Rx]] [[Next case →->Hub]] [[Start another case->Hub]] [[Restart this case->Malignant hyperthermia - Rx]]

<span class="ec-case-marker" hidden data-entry="Malignant hyperthermia. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Creatine kinase confirms muscle injury after the fact but takes hours to result. Treatment cannot wait for a confirmatory laboratory value in a decompensating patient. <div class="ec-teach"><div class="th">What the findings point to</div> Rising end-tidal carbon dioxide out of proportion to minute ventilation, masseter and generalized muscle rigidity, tachycardia, and climbing temperature after exposure to a volatile anesthetic or succinylcholine define malignant hyperthermia, a pharmacogenetic disorder of the skeletal muscle ryanodine receptor that causes uncontrolled calcium release and hypermetabolism. Every triggering agent must be stopped immediately, and dantrolene, which blocks calcium release at the ryanodine receptor, is the only drug that reverses the process; delaying it while pursuing other measures allows rhabdomyolysis, hyperkalemic arrest, and DIC to develop. <div class="ec-src"><b>Source:</b> Larach MG, Gronert GA, Allen GC, Brandom BW, Lehman EB. Clinical presentation, treatment, and complications of malignant hyperthermia in North America from 1987 to 2006: a report from the North American Malignant Hyperthermia Registry of MHAUS. Anesth Analg 2010;110(2):498-507.</div></div></div> [[Try this question again->Malignant hyperthermia - Rx]] [[Next case →->Hub]] [[Start another case->Hub]] [[Restart this case->Malignant hyperthermia - Rx]]

<span class="ec-case-marker" hidden data-entry="Malignant hyperthermia. Rx"></span><div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Cooling and correcting the potassium address downstream consequences but do not stop the underlying uncontrolled calcium release, which only dantrolene reverses. <div class="ec-teach"><div class="th">What the findings point to</div> Rising end-tidal carbon dioxide out of proportion to minute ventilation, masseter and generalized muscle rigidity, tachycardia, and climbing temperature after exposure to a volatile anesthetic or succinylcholine define malignant hyperthermia, a pharmacogenetic disorder of the skeletal muscle ryanodine receptor that causes uncontrolled calcium release and hypermetabolism. Every triggering agent must be stopped immediately, and dantrolene, which blocks calcium release at the ryanodine receptor, is the only drug that reverses the process; delaying it while pursuing other measures allows rhabdomyolysis, hyperkalemic arrest, and DIC to develop. <div class="ec-src"><b>Source:</b> Larach MG, Gronert GA, Allen GC, Brandom BW, Lehman EB. Clinical presentation, treatment, and complications of malignant hyperthermia in North America from 1987 to 2006: a report from the North American Malignant Hyperthermia Registry of MHAUS. Anesth Analg 2010;110(2):498-507.</div></div></div> [[Try this question again->Malignant hyperthermia - Rx]] [[Next case →->Hub]] [[Start another case->Hub]] [[Restart this case->Malignant hyperthermia - Rx]]