,{type:'mcq',profession:'pa',
  stem:'A PA in urgent care sees a 45yo with productive cough, fever 38.6, and unilateral crackles. CXR shows RLL consolidation. O2 sat 97%. She asks about antibiotic choice. The PA is solo and cannot reach the supervising physician. Which is the MOST appropriate PA action?',
  options:['Wait until the attending is available before treating','Prescribe azithromycin per standard CAP protocol and document the clinical reasoning','Transfer to the ED because this exceeds PA scope','Order labs and send home without antibiotics until review'],
  answer:1,
  explanation:'PA scope includes managing CAP per evidence-based protocols. Azithromycin for outpatient CAP in a low-risk patient (CURB-65 = 1) is within PA scope. Withholding treatment causes harm; waiting for attending is not required for routine decisions within protocol.'},
{type:'mcq',profession:'pa',
  stem:'A PA manages a 68yo with T2DM, HTN, and CKD (CrCl 38) on metformin 1000mg BID. The patient is admitted for a contrast CT. Which action is MOST appropriate regarding metformin?',
  options:['Continue metformin — it is safe with contrast','Hold metformin 48h before and 48h after contrast, restart only if renal function stable','Switch to insulin permanently','Hold metformin only if CrCl drops below 20'],
  answer:1,
  explanation:'Metformin is held around iodinated contrast due to risk of contrast-induced nephropathy leading to metformin-associated lactic acidosis (MALA). Per ADA guidelines, hold 48h before and after, resume only after confirming stable renal function. CrCl 38 puts this patient at higher baseline risk.'},
{type:'mcq',profession:'dentistry',
  stem:'A 55yo male presents with a 1cm white patch on the lateral tongue that cannot be wiped off. He has smoked 1 ppd for 30 years. The lesion has been present for 3 weeks. Vital staining shows irregular uptake in one area. What is the MOST appropriate next step?',
  options:['Reassure the patient and recheck in 6 months','Prescribe antifungal and recheck in 2 weeks','Refer for incisional biopsy within 1-2 weeks','Counsel on smoking cessation only'],
  answer:2,
  explanation:'A non-wipeable white patch (leukoplakia) in a heavy smoker with 3-week duration and irregular vital stain uptake has significant malignant potential. Incisional biopsy is indicated — the lateral tongue is a high-risk site for squamous cell carcinoma. Watchful waiting for more than 2 weeks is inappropriate.'},
{type:'mcq',profession:'dentistry',
  stem:'A 72yo woman on warfarin (INR 2.6) for atrial fibrillation requires extraction of tooth #14. Her cardiologist recommends holding warfarin 5 days before the procedure. Which statement BEST reflects current dental evidence?',
  options:['Always follow the cardiologist recommendation — they own the anticoagulation','Most dental extractions can be safely performed at therapeutic INR with local hemostatic measures','Warfarin must be bridged with heparin for all dental extractions','Hold warfarin only if INR exceeds 3.5'],
  answer:1,
  explanation:'Current evidence (ACCP guidelines, multiple RCTs) supports performing routine dental extractions in anticoagulated patients at therapeutic INR using local hemostatic measures (oxidized cellulose, sutures, tranexamic acid mouthwash). Holding anticoagulation for dental procedures carries greater thromboembolic risk than the procedural bleeding risk.'},
{type:'mcq',profession:'nursing',
  stem:'You are the RN caring for a postpartum patient 20 hours after vaginal delivery. She calls you for a headache. Her BP is 158/106 (was 112/70 in labor). She has new RUQ discomfort and her urine output was 45mL over the last 2 hours. What is the PRIORITY nursing action?',
  options:['Administer acetaminophen per PRN order and reassess in 1 hour','Notify the physician immediately and prepare for possible magnesium sulfate administration','Document the finding and continue routine assessments','Encourage oral hydration to improve urine output'],
  answer:1,
  explanation:'This presentation — new hypertension, severe headache, RUQ pain (hepatic capsule distension), and oliguria in the postpartum period — meets criteria for severe postpartum preeclampsia. This is a medical emergency requiring immediate physician notification. Magnesium sulfate for seizure prophylaxis and antihypertensives may be needed urgently. Delaying by giving acetaminophen first could be catastrophic.'},
{type:'mcq',profession:'nursing',
  stem:'A 79yo patient with dementia is agitated at 0300, trying to climb out of bed, and has pulled out his IV. The Morse Fall Risk Score is 70. A one-to-one sitter is unavailable. Which intervention has the STRONGEST evidence for preventing falls in this situation?',
  options:['Apply wrist restraints to prevent IV removal','Move the patient to a room closer to the nurses station and activate bed/chair alarm','Administer haloperidol 0.5mg IM for behavioral management','Apply a vest restraint for postural support'],
  answer:1,
  explanation:'Physical restraints paradoxically increase fall risk in delirious elderly patients (increased agitation, muscle deconditioning). The HELP protocol and hospital fall prevention evidence support environmental modifications: proximity to nursing station, bed in lowest position, alarm systems, and frequent rounding. Pharmacological sedation carries aspiration and delirium-prolongation risks. Restraints are a last resort and require a physician order.'},
{type:'mcq',profession:'ot',
  stem:'A 7yo boy with autism spectrum disorder (ASD) covers his ears constantly, avoids the cafeteria, and has meltdowns during transitions. Based on Dunn\'s Sensory Processing Model, which quadrant BEST describes his profile?',
  options:['Low Registration — he misses sensory input others notice','Sensation Seeking — he craves intense sensory experiences','Sensory Sensitivity — he notices and is bothered by stimuli others ignore','Sensation Avoiding — he actively limits or controls sensory input'],
  answer:3,
  explanation:'Sensation Avoiding (low threshold + active self-regulation): this child has a low neurological threshold and actively controls input to stay below it — covering ears, avoiding the cafeteria, and using routines/rituals. Sensory Sensitivity (low threshold + passive response) would show distress without behavioral control strategies. The distinction changes intervention: Sensation Avoiding needs predictability and control; Sensory Sensitivity needs graded desensitization.'},
{type:'mcq',profession:'ot',
  stem:'A 68yo woman with HFrEF (EF 32%) reports becoming severely short of breath when showering and cooking. She lives alone. Which energy conservation principle is MOST directly applicable to her showering limitation?',
  options:['Prioritize — eliminate the shower from her daily routine entirely','Pace — use a shower chair and take rest breaks during activity','Position — stand throughout to maintain respiratory mechanics','Plan — shower only when family is present'],
  answer:1,
  explanation:'Pacing (one of the 4Ps: Prioritize, Plan, Pace, Position) directly addresses exertional dyspnea. A shower chair reduces energy expenditure by 30-40% by eliminating the postural work of standing. This allows her to maintain the valued occupation of independent self-care within her cardiac reserve. Elimination of the task is not appropriate — OT seeks adaptation, not avoidance.'},

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<script>
var PUZZLES = [
  {type:'Lab Shift',scenario:'52-year-old male with substernal chest pressure for 2 hours. Your differential: ACS, PE, aortic dissection, pericarditis.',prompt:'Troponin comes back 0.04 ng/mL (normal <0.04). D-dimer is 2,400. What changes in your differential and why?',teaching:'Borderline troponin + markedly elevated D-dimer shifts the probability toward PE over ACS. ACS typically has higher troponin at 2 hours. D-dimer >2000 has high specificity for PE. Aortic dissection can also elevate D-dimer — consider CT angiography.'},
  {type:'Physical Exam Finding',scenario:'68-year-old female with progressive dyspnea over 3 weeks. On exam: JVD, bilateral crackles to mid-lung, S3 gallop, 2+ pitting edema.',prompt:'You find a new harsh systolic murmur loudest at the apex radiating to the axilla. Does this change your working diagnosis of CHF exacerbation? Why or why not?',teaching:'New mitral regurgitation in the setting of CHF changes management significantly. Acute MR can be the CAUSE of the decompensation (papillary muscle rupture, endocarditis, chordal rupture) rather than a consequence. This patient needs an urgent echo to evaluate valve function. The CHF treatment is the same, but the underlying cause matters for definitive management.'},
  {type:'Missing Evidence',scenario:'24-year-old female with sudden-onset pleuritic chest pain, tachycardia, and SpO2 91%. Colleague says: "This is definitely a PE."',prompt:'What single finding, if present, would make you disagree?',teaching:'Fever. PE rarely causes fever >38.5°C. If this patient is febrile, pneumonia or empyema becomes much more likely than PE. Other disconfirming findings: productive purulent sputum (pneumonia), unilateral leg swelling absent (reduces PE probability), pleuritic pain that worsens with inspiration AND position (more consistent with pleurisy/pericarditis).'},
  {type:'Time Pressure',scenario:'You are the overnight resident. 78-year-old male found unresponsive. Nurse reports sudden onset 10 minutes ago. GCS 7 (E1V2M4). Right pupil 6mm fixed, left 3mm reactive.',prompt:'You have 60 seconds before the attending arrives. What do you do RIGHT NOW and why?',teaching:'This is a neurosurgical emergency — herniation syndrome (blown pupil = uncal herniation). Immediate actions: (1) Protect airway — RSI with etomidate/succinylcholine, avoid ketamine. (2) Head of bed 30°. (3) Mannitol 1g/kg or hypertonic saline 23.4% 30mL IV push. (4) Call neurosurgery STAT for emergent decompression. (5) STAT CT head — but do NOT delay treatment for imaging. Every minute of herniation causes irreversible damage.'},
  {type:'Distinguishing Case',scenario:'Two patients in your ED both present with "worst headache of my life." Patient A: sudden onset while lifting weights, neck stiffness, vomiting. Patient B: gradual onset over 6 hours, photophobia, history of migraines.',prompt:'Same chief complaint, very different cases. What is the key distinguishing feature and what diagnosis do you pursue for each?',teaching:'Thunderclap onset (peak in seconds) is the critical distinguishing feature. Patient A: SAH until proven otherwise — CT head → LP if CT negative. The Valsalva trigger (weightlifting) and meningismus support this. Patient B: while "worst headache" is concerning, gradual onset + migraine history makes a severe migraine more likely. Still screen for red flags (new neurological deficits, fever, papilledema) but the pre-test probability for SAH is much lower.'},
  {type:'Source Check',scenario:'35-year-old male with 3 days of right lower quadrant pain, low-grade fever, anorexia. WBC 14,000. You think appendicitis.',prompt:'You are about to call surgery. You have evidence from history and labs. What is your third source, and what specific finding would confirm or refute your diagnosis?',teaching:'Physical exam is your third source — specifically: McBurney point tenderness, rebound tenderness, Rovsing sign, psoas sign, obturator sign. If the exam shows diffuse tenderness without localization, or if the pain is actually in the RUQ (cholecystitis) or suprapubic (UTI), your diagnosis changes. Never commit to a surgical consult on history + labs alone. The three-source rule: history tells you the story, labs quantify it, exam localizes it.'},
  {type:'Risk Priority',scenario:'Your differential for a 45-year-old with acute chest pain includes: GERD (prob: 40%), PE (prob: 15%), ACS (prob: 20%), musculoskeletal (prob: 20%), aortic dissection (prob: 5%).',prompt:'Rank these by which you should work up FIRST, not by probability. Explain your reasoning.',teaching:'The FMEA framework: Probability × Severity × Detectability. Aortic dissection (5% probability) should be worked up before GERD (40% probability) because: (1) Severity if missed = death within hours. (2) Detectability = hard to catch later (no biomarker, requires CT-A). Similarly, ACS and PE rank above GERD despite lower probability because missing them is catastrophic. The clinical rule: "rule out the worst, then work down." Never let a common diagnosis blind you to a lethal one.'},
  {type:'Anchoring Check',scenario:'72-year-old with known COPD presents with dyspnea. You started bronchodilators. Nurse mentions BNP is 1,200.',prompt:'You are anchored on COPD exacerbation. The BNP result just arrived. Walk through your reasoning: should you change your management?',teaching:'BNP >400 strongly suggests heart failure as a contributor. But here is the nuance: COPD and CHF frequently coexist, and COPD exacerbation can mildly elevate BNP (usually <500). BNP >1000 in the context of dyspnea has >90% PPV for heart failure. You should add diuresis to bronchodilators, get an echo, and reassess. The anchoring trap: you saw "COPD + dyspnea" and stopped thinking. The BNP is the evidence that breaks the anchor.'},
  // ── RENAL ──
  {type:'Lab Shift',scenario:'58-year-old male with type 2 diabetes, hypertension, and recent NSAID use presents with fatigue and decreased urine output for 3 days. Creatinine 3.8 (baseline 1.1). Urine shows muddy brown casts.',prompt:'Muddy brown casts on urinalysis. How does this single finding narrow your differential from the broad category of acute kidney injury?',teaching:'Muddy brown casts = acute tubular necrosis (ATN). They represent sloughed tubular epithelial cells — the classic finding of ischemic or nephrotoxic injury to the tubules. This rules out prerenal (hyaline casts or none) and obstructive AKI. NSAIDs cause both direct nephrotoxicity and reduced renal perfusion. Management: stop NSAIDs, IV fluids, nephrology consult — not diuretics yet.'},
  {type:'Distinguishing Case',scenario:'Patient A: creatinine 4.2, FENa 0.3%, urine osmolality 620, specific gravity 1.028. Patient B: creatinine 3.9, FENa 2.8%, urine osmolality 290, specific gravity 1.010.',prompt:'What is the pathophysiology behind each patient's AKI, and how does it change your immediate management?',teaching:'Patient A: FENa <1%, concentrated urine = prerenal AKI. The kidney is intact and trying to conserve sodium — give IV fluids, treat the underlying cause. Patient B: FENa >2%, isotonic urine = intrinsic renal AKI (ATN). The tubules cannot concentrate — IV fluids won't fix this. FENa interpretation caveat: unreliable if the patient is on diuretics — use FeUrea instead (<35% = prerenal).'},
  // ── HEMATOLOGY ──
  {type:'Missing Evidence',scenario:'32-year-old female with 3 days of fatigue, jaundice, and dark urine. Hgb 7.2, reticulocyte count 8%, LDH elevated, haptoglobin undetectable, peripheral smear shows spherocytes. Coombs test positive.',prompt:'The hematologist asks you one question before starting steroids: what critical piece of history must you obtain first?',teaching:'Drug history. Drug-induced immune hemolytic anemia (DIIHA) accounts for 15-20% of positive DAT cases and is treated by removing the offending agent — not steroids. Common culprits: cephalosporins, NSAIDs, penicillins, methyldopa, quinine. If you start prednisone without stopping the drug, the patient continues to hemolyze.'},
  {type:'Risk Priority',scenario:'Your patient has a platelet count of 18,000. The team is debating urgent intervention. Diagnosis is immune thrombocytopenia (ITP).',prompt:'At what platelet threshold and clinical scenario do you treat versus observe? Rank urgency: elective surgery tomorrow, mild gum bleeding, no bleeding, ICH risk.',teaching:'ITP treatment thresholds: (1) ICH/life-threatening bleeding → immediate IVIG + steroids + platelets. (2) Wet bleeding → treat if <30,000. (3) Dry purpura/no bleeding → treat if <20,000-30,000. (4) Elective surgery → target >50,000 (>80,000 neuro/ophth) — postpone if below. Treat based on bleeding risk, not number alone.'},
  // ── NEUROLOGY ──
  {type:'Physical Exam Finding',scenario:'45-year-old male with progressive proximal weakness over 3 weeks, areflexia, mild stocking-glove sensory loss, and prior GI illness 2 weeks ago.',prompt:'This is classic ascending weakness. What single exam finding would make you call neurosurgery instead of neurology?',teaching:'Bowel or bladder dysfunction. Ascending weakness + areflexia = Guillain-Barré (GBS) — neurology emergency. But urinary retention, rectal tone loss, or a sensory level on the trunk = spinal cord compression — neurosurgery emergency. GBS gets IVIG or plasmapheresis; cord compression gets emergent MRI ± surgical decompression. Never skip the sphincter exam in ascending weakness.'},
  {type:'Anchoring Check',scenario:'19-year-old with headache, fever, stiff neck. LP: WBC 840 (98% neutrophils), protein 180, glucose 28 (serum 92). You started empiric ceftriaxone.',prompt:'Your intern says "wait for cultures before adding anything else." What two additional agents must you consider adding immediately and why?',teaching:'(1) Vancomycin — empiric coverage for ceftriaxone-resistant S. pneumoniae (up to 30% resistance in some regions). Do NOT wait for sensitivities. (2) Dexamethasone 0.15mg/kg q6h × 4 days — before or with first antibiotic dose. Reduces mortality and hearing loss in pneumococcal meningitis (NNT ~8). Bacterial meningitis has 20-30% mortality even with correct antibiotics.'},
  // ── RHEUMATOLOGY ──
  {type:'Lab Shift',scenario:'38-year-old female with 6 weeks of symmetric small joint arthritis (MCPs, PIPs), morning stiffness >1 hour, fatigue, and low-grade fever. RF positive, anti-CCP strongly positive, ESR 88.',prompt:'Anti-CCP just came back strongly positive. How does this change your management urgency compared to if it were negative?',teaching:'Anti-CCP is highly specific (>95%) for RA and predicts aggressive, erosive disease. Strongly positive = (1) High risk of rapid joint destruction without treatment. (2) DMARD therapy imperative ideally within 12 weeks of symptom onset. (3) Rheumatology referral within 2 weeks. The window: early methotrexate ± hydroxychloroquine significantly improves long-term joint outcomes.'},
  {type:'Missing Evidence',scenario:'52-year-old male with proximal muscle weakness, difficulty rising from a chair, dysphagia, and heliotrope rash. CK 4,200. You are diagnosing dermatomyositis.',prompt:'Before starting immunosuppression, what workup is non-negotiable — and why would delaying treatment to complete it be wrong?',teaching:'Malignancy screening: dermatomyositis is paraneoplastic in 20-25% of adults (ovarian, lung, colorectal, pancreatic, nasopharyngeal). CT chest/abdomen/pelvis + age-appropriate cancer screening required. But do NOT delay steroids — dysphagia + ILD can be fatal. Run the workup simultaneously. Finding malignancy changes management: treating the cancer may resolve the myositis.'},
  // ── GASTROENTEROLOGY ──
  {type:'Time Pressure',scenario:'62-year-old cirrhotic male with acute hematemesis. BP 88/52, HR 124. Two large-bore IVs placed. The nurse asks what to transfuse first.',prompt:'You have 90 seconds. Blood products, pressors, scopes — what is your exact sequence and why does order matter?',teaching:'(1) pRBCs — target Hgb 7-8 (NOT 10 — over-transfusion raises portal pressure, worsens variceal bleeding). (2) Octreotide 50mcg bolus + 50mcg/hr — reduces splanchnic blood flow. (3) Ceftriaxone 1g IV — SBP prophylaxis reduces mortality 30% (NNT 5). (4) Avoid FFP/platelets unless INR >2.5 or platelets <50k — cirrhotic coagulopathy is complex and FFP increases portal pressure. (5) GI consult for emergent EGD within 12h.'},
  {type:'Distinguishing Case',scenario:'Patient A: 34F, bloody diarrhea 8x/day, tenesmus, colonoscopy shows continuous mucosal inflammation rectum to splenic flexure. Patient B: 28M, RLQ pain, non-bloody diarrhea, 15 lb loss, colonoscopy shows skip lesions, cobblestoning, rectal sparing.',prompt:'Both have IBD. Name one extraintestinal manifestation and one complication more likely in each.',teaching:'Patient A (UC): PSC (occurs in ~5% UC, rare in Crohn's). Complication: toxic megacolon (colon >6cm = surgical emergency). Patient B (Crohn's): perianal fistulae/abscess (pathognomonic for Crohn's). Complication: strictures + obstruction from transmural fibrosis. Key: UC is cured by colectomy; Crohn's is not.'},
  // ── INFECTIOUS DISEASE ──
  {type:'Source Check',scenario:'29-year-old male, 5 days of fever, new murmur, history of IV drug use. Blood cultures pending.',prompt:'Before cultures result, what physical exam findings confirm infective endocarditis — and which finding is the strongest predictor of embolic complications?',teaching:'IE stigmata: Osler nodes (painful finger pads — immune complex), Janeway lesions (painless palms/soles — septic emboli), Roth spots, splinter hemorrhages. Strongest predictor of embolic complications: vegetation >10mm on echo, especially anterior mitral leaflet. Most specific exam finding: Osler nodes (PPV >90%). Do not wait for cultures to get the echo.'},
  {type:'Lab Shift',scenario:'HIV-positive patient, CD4 count 48, not on ART. 2 weeks of headache, fever, mild neck stiffness. LP: opening pressure 28 cmH2O, India ink positive.',prompt:'India ink confirms Cryptococcus. Opening pressure is 28. Your intern says "start fluconazole." What critical intervention is your intern missing?',teaching:'Therapeutic LP for elevated ICP. Remove CSF until opening pressure <20 cmH2O (typically 20-30mL). Elevated ICP is the leading cause of early mortality in crypto meningitis — not fungal burden. Fluconazole is NOT first-line: amphotericin B + flucytosine × 2 weeks, then fluconazole consolidation. Daily LPs until pressure normalizes. Missing ICP management = herniation despite antifungal therapy.'},
  // ── ENDOCRINOLOGY ──
  {type:'Physical Exam Finding',scenario:'24-year-old female, 3 months of palpitations, heat intolerance, 12 lb weight loss, diarrhea. HR 118, tremor, lid lag, smooth diffusely enlarged thyroid. TSH <0.01, free T4 4.8.',prompt:'You hear a bruit over the thyroid. What does this tell you about the etiology, and how does it change your workup?',teaching:'Thyroid bruit = increased blood flow = Graves' disease. Not toxic nodular goiter (focal flow) or thyroiditis (tender, not hypervascular). Workup change: TSI/TRAb antibodies (>90% sensitive for Graves'). This changes treatment choice: RAI preferred in Graves'; surgery preferred for large compressive goiters or coexisting malignancy. Bruit is pathognomonic for Graves' in the right clinical context.'},
  // ── PEDIATRICS ──
  {type:'Time Pressure',scenario:'3-year-old, 3 days of fever 39.8°C, refusal to bear weight on right leg. WBC 18,000, ESR 68, CRP 4.2. Hip held in flexion/external rotation, painful with any motion.',prompt:'What is your decision tree — and what single test result pushes you to the OR tonight vs. morning?',teaching:'4/4 Kocher criteria (fever, non-weight-bearing, ESR >40, WBC >12,000) = >99% predicted probability of septic arthritis. Immediate action: hip ultrasound for effusion → arthrocentesis. Synovial WBC >50,000 = OR tonight for joint washout. Delay = avascular necrosis of the femoral head. Transient synovitis is a diagnosis of exclusion — never assume it with 4/4 Kocher.'},
  // ── PSYCHIATRY ──
  {type:'Missing Evidence',scenario:'28-year-old male, no psychiatric history: 4 days no sleep, pressured speech, believes he was chosen to solve a global crisis, spent $40,000 on a business in 72 hours.',prompt:'Before diagnosing bipolar I mania, what three medical causes must you rule out — and which lab is most commonly missed?',teaching:'Rule out organic mania: (1) Thyroid storm / hyperthyroidism — TSH is the most missed lab; always check free T4 too. (2) Stimulant intoxication — urine drug screen (cocaine, meth, bath salts can be indistinguishable from mania). (3) CNS pathology — new-onset mania after 40 or with focal deficits needs MRI (encephalitis, frontal lobe lesion, HIV encephalopathy). Also: steroid-induced mania, anti-NMDA receptor encephalitis. First-break mania always requires organic workup.'},
  // ── DERMATOLOGY ──
  {type:'Distinguishing Case',scenario:'Patient A: 72F, large tense bullae on urticarial base, flexor surfaces, no mucosal involvement, Nikolsky negative. Patient B: 45M, flaccid easily ruptured bullae, Nikolsky positive, painful oral erosions.',prompt:'Both have autoimmune blistering disorders. What is the pathophysiology of each — and which is immediately life-threatening?',teaching:'Patient A: Bullous Pemphigoid — IgG vs BP180/BP230 (hemidesmosomes). Tense bullae, no mucosa, Nikolsky negative. Managed with steroids. Patient B: Pemphigus Vulgaris — IgG vs desmoglein-3 (desmosome, intraepidermal). Flaccid bullae, mucosal involvement (often first sign), Nikolsky positive. Life-threatening: Pemphigus Vulgaris — severe fluid loss, sepsis, >90% mortality untreated. Nikolsky sign: positive = intraepidermal split (pemphigus); negative = subepidermal split (pemphigoid).'},
  // ── CARDIOLOGY (ADVANCED) ──
  {type:'Anchoring Check',scenario:'66-year-old admitted for "COPD exacerbation," day 2, responding poorly to bronchodilators. New: JVP elevated to jaw angle, distant heart sounds, pulsus paradoxus 18mmHg.',prompt:'You've treated COPD for 36 hours. This constellation has a name. What is it — and what do you do in the next 60 seconds?',teaching:'Beck's triad: hypotension + elevated JVP + muffled sounds = cardiac tamponade. Pulsus paradoxus >10mmHg supports this. Next 60 seconds: (1) Bedside echo STAT — effusion + RA/RV diastolic collapse. (2) Cardiology for emergent pericardiocentesis. (3) 500mL NS bolus — tamponade is preload-dependent. (4) Hold diuretics, beta-blockers, vasodilators — all will kill this patient. The anchor trap: COPD + JVD = cor pulmonale, until pulsus paradoxus breaks it.'},
  {type:'Lab Shift',scenario:'55-year-old male post-CABG day 3. New fever 38.8°C, pleuritic chest pain, friction rub. ECG: diffuse saddle-shaped ST elevation, PR depression in lead II.',prompt:'Your intern calls the cath lab for STEMI. What do you tell them — and what is the single distinguishing ECG feature?',teaching:'This is post-cardiac injury syndrome (Dressler) / pericarditis — NOT STEMI. Distinguishing ECG: pericarditis has diffuse ST elevation (not focal territory), saddle-shape, PR depression (pathognomonic, 80%), no reciprocal changes. STEMI: focal territory, reciprocal depression, hyperacute T-waves, no PR depression. Management: NSAIDs + colchicine × 3 months. PR depression is the single most specific ECG finding for pericarditis.'},
  // ── TOXICOLOGY ──
  {type:'Time Pressure',scenario:'22-year-old unresponsive at a party. HR 42, BP 88/54, RR 8, temp 35.1°C, pupils pinpoint, GCS 6.',prompt:'30 seconds: name the toxidrome, the antidote, and what you check before giving it.',teaching:'Opioid toxidrome: bradycardia, hypotension, respiratory depression, hypothermia, miosis. Antidote: Naloxone 0.4-2mg IV/IM/IN. Before giving: in chronic opioid users, high-dose naloxone precipitates dangerous withdrawal (vomiting + aspiration, catecholamine surge, pulmonary edema). Start with 0.04-0.1mg, titrate to RR >12 — NOT full reversal. Naloxone lasts 1-2h; most opioids last longer — watch for re-sedation.'},
  // ── PULMONARY ──
  {type:'Source Check',scenario:'44-year-old nurse, 6 weeks of productive cough, night sweats, 18 lb weight loss, hemoptysis. CXR: right upper lobe cavitary lesion with surrounding infiltrate.',prompt:'History strongly suggests TB. What are your two required diagnostic sources before starting treatment — and what must happen in the next 5 minutes regardless of results?',teaching:'(1) AFB smear (sputum × 3 early morning samples) — sensitivity 50-80%. (2) Chest CT — characterizes cavity, lymphadenopathy, miliary pattern. The 5-minute action: AIRBORNE ISOLATION. Negative-pressure room immediately — before any test. A healthcare worker with cavitary lesion + hemoptysis is presumed smear-positive TB. Delay in isolation has caused institutional outbreaks. Treatment (RIPE: rifampin, isoniazid, pyrazinamide, ethambutol) starts after 3 AFB smears even if culture pending.'},
  {type:'Anchoring Check',scenario:'45-year-old female with known COPD, 3 days worsening dyspnea on steroids + azithromycin. Day 2: no improvement, HR 108, O2 sat 88%.',prompt:'The team is anchored on COPD exacerbation. What three alternative diagnoses must you actively rule out, and what single test best distinguishes them?',teaching:'Failure to improve on COPD exacerbation treatment is a red flag for missed diagnosis. Rule out: PE (CT-PA using Wells score), pneumonia (CXR + sputum culture), and cardiac decompensation (BNP + echo). CT-PA is most efficient when Wells score is intermediate-high. Anchoring bias kills in COPD — always reassess when the patient is not improving on expected trajectory.'},
  {type:'Risk Priority',scenario:'ED waiting room: A) 72M syncope now asymptomatic. B) 28F worst headache of life, 30 min ago. C) 55M pleuritic chest pain HR 108 recent flight. D) 45F acute monoarthritis fever 38.8. E) 62M crushing chest pain radiating to back.',prompt:'Rank these five patients by priority. For the top two, name the life threat you cannot miss.',teaching:'Priority: E (aortic dissection — tearing pain + back radiation, immediate surgical risk), B (subarachnoid hemorrhage — thunderclap headache, 10% SAH rate, 50% mortality if missed), C (PE — tachycardia + pleuritic pain + recent flight), A (cardiac syncope — ECG risk stratification), D (septic arthritis — urgent but not immediately life-threatening). E and B are simultaneous priorities.'},
  {type:'Source Check',scenario:'Your senior recommends moxifloxacin monotherapy for a hospitalized 58-year-old with community-acquired pneumonia. You recall beta-lactam + macrolide is often preferred.',prompt:'How do you evaluate which approach is more evidence-based without UpToDate? Name two open-access resources and what you are looking for.',teaching:'IDSA/ATS CAP guidelines are freely available at idsociety.org and thoracic.org. Both support beta-lactam + macrolide as preferred for hospitalized non-severe CAP, with fluoroquinolone as alternative when beta-lactam is contraindicated. PubMed search for the guideline is also reliable. The key skill: knowing which professional society owns the guideline for a given disease area.'},
  {type:'Distinguishing Case',scenario:'Two patients with acute knee monoarthritis. Patient A: 55M, obese, large meal with red wine last night, exquisitely tender and hot. Patient B: 62F, chronic RA, started a new biologic 3 weeks ago, swollen and warm.',prompt:'What single test distinguishes gout from septic arthritis, and what findings would you expect in each?',teaching:'Synovial fluid analysis is definitive. Gout: negatively birefringent needle-shaped MSU crystals on polarizing microscopy; WBC 20,000-100,000. Septic arthritis: WBC >50,000 (usually >100,000), PMN predominance, positive Gram stain or culture. Critical: both can coexist. Patient B on a biologic must have septic arthritis ruled out regardless of crystal findings.'},
  {type:'Lab Shift',scenario:'34M IV drug user, 2 weeks of fever, night sweats, new diastolic murmur. Two of three blood cultures return positive for viridans streptococcus. He wants to leave AMA.',prompt:'What is the minimum you must tell him before he leaves, and why is this not safely managed with oral antibiotics?',teaching:'This meets Duke criteria for infective endocarditis. AMA counseling must cover: stroke risk from septic emboli (up to 30%), valve destruction leading to heart failure, and >50% mortality without 4-6 week IV antibiotics. Oral antibiotics are NOT equivalent for native valve IE. Document the conversation in detail. Ensure he has naloxone and harm reduction resources before leaving.'},
  {type:'Time Pressure',scenario:'2 AM: 78-year-old with dementia is acutely confused — significantly different from baseline. Temp 38.6, HR 112, O2 sat 94%. Senior is 10 minutes away.',prompt:'What do you do first, second, and third in the next 10 minutes? What is the most dangerous thing this could be?',teaching:'First: check glucose (hypoglycemia is immediately reversible — 30 seconds). Second: assess vital sign trends and O2 sat trend (94% suggests respiratory cause). Third: collect urine sample and examine for signs of systemic infection. Most dangerous: sepsis — urosepsis in elderly demented patients often presents without localizing symptoms. Also consider: intracranial event (focal deficit?), medication effect, missed dose. Delirium in elderly = medical emergency until proven otherwise.'},
  {type:'Missing Evidence',scenario:'66-year-old female, hypertension, type 2 diabetes, 40 pack-year smoking. Spirometry: FEV1/FVC 0.64, FEV1 62% predicted. No dyspnea complaints. Pulmonologist wants to start a long-acting bronchodilator.',prompt:'What critical piece of evidence is missing before confirming the COPD diagnosis?',teaching:'Post-bronchodilator spirometry. Without it, you cannot distinguish COPD from asthma (which reverses with bronchodilator). A patient with reversible obstruction needs asthma management, not COPD therapy. Post-bronchodilator FEV1/FVC <0.70 is the GOLD standard for COPD diagnosis. This single missing test changes the diagnosis and entire management plan.'},
  {type:'Physical Exam Finding',scenario:'28F, palpitations, 15-pound weight loss over 3 months. HR 118, BP 144/68. Exam: bilateral lid retraction, lid lag, mild proptosis.',prompt:'What exam findings distinguish Graves disease from other causes of hyperthyroidism, and what single lab test confirms autoimmune etiology?',teaching:'Proptosis (exophthalmos) and pretibial myxedema are pathognomonic for Graves — no other cause of hyperthyroidism produces these. Thyroid exam: diffuse smooth non-tender goiter (vs toxic adenoma = single firm nodule). TSH-receptor antibodies (TRAb/TSI) confirm Graves in >95% of cases. Radioactive iodine uptake shows diffuse uptake in Graves vs hot nodule in adenoma.'},
  {type:'Anchoring Check',scenario:'Medical student labels a 44F with known panic disorder as having anxiety-related chest pain. The patient has 4mm ST depression in V4-V6 on ECG.',prompt:'What cognitive bias is being demonstrated, and what are the three steps to correct it before potentially sending this patient home?',teaching:'Premature closure + framing bias. Anxiety cannot explain ST depression — ECG abnormalities are never attributable to psychiatric diagnoses. Correction: (1) Rule out life threats first — ST depression demands serial troponins and cardiology notification regardless of psychiatric history; (2) Always treat the most dangerous diagnosis first; (3) Women are disproportionately harmed by anchoring bias in ACS — this is a documented disparity in outcomes.'},
  {type:'Risk Priority',scenario:'35-year-old G2P1 at 36 weeks, headache, visual changes, BP 162/108, urine protein 3+, brisk bilateral reflexes.',prompt:'What is the diagnosis, the immediate pharmacologic priority, and the definitive treatment?',teaching:'Severe preeclampsia with CNS involvement. Immediate priority: magnesium sulfate 4-6g IV loading dose for seizure prophylaxis — before anything else. Then labetalol or hydralazine for BP control (target <160/105 to prevent stroke). Definitive treatment: delivery. At 36 weeks, delivery is indicated regardless of fetal status. Do not give nimodipine (for SAH, not eclampsia). Phenytoin is inferior to magnesium.'},
  {type:'Lab Shift',scenario:'72-year-old with pneumonia, day 3 of ceftriaxone. Temperature normalized, WBC 9,200. Now develops 8 episodes of watery diarrhea in 12 hours. C. diff PCR returns positive.',prompt:'What is the severity classification and how does it change your treatment choice?',teaching:'Severity (IDSA 2021): Non-severe = WBC <15,000 + Cr <1.5x baseline → vancomycin 125mg QID or fidaxomicin 200mg BID x 10 days. Severe = WBC >15,000 OR Cr >1.5x baseline → vancomycin 125mg QID. Fulminant = hypotension/shock or ileus → vancomycin 500mg QID + IV metronidazole + surgery consult. Fidaxomicin preferred when available — lower recurrence rate (MODIFY trial). Metronidazole is no longer preferred first-line.'},
  {type:'Distinguishing Case',scenario:'Two 65M with LBBB and chest pain. Patient A: LBBB on prior ECG 2 years ago, troponin at upper limit. Patient B: no LBBB on prior ECG, troponin 2.4 (elevated).',prompt:'For Patient B, what scoring system determines if this LBBB is a STEMI equivalent, and what triggers cath lab activation?',teaching:'Patient B has new LBBB with elevated troponin — STEMI equivalent requiring emergent PCI. Sgarbossa criteria: concordant ST elevation ≥1mm (5 points), concordant ST depression ≥1mm in V1-V3 (3 points), discordant ST elevation ≥5mm (2 points). Score ≥3 = high specificity for MI. Modified Sgarbossa (Smith): STE/QRS ratio >0.25 improves sensitivity. New LBBB + chest pain + elevated troponin = activate cath lab without waiting for Sgarbossa score.'},
  {type:'Missing Evidence',scenario:'Synovial fluid WBC 62,000 (PMN 90%), Gram stain negative, culture pending. Patient started on IV cefazolin for presumptive septic arthritis.',prompt:'What critical piece of management is missing that no antibiotic alone can provide?',teaching:'Surgical or arthroscopic joint washout. Antibiotics penetrate synovial fluid but cannot remove the protease-laden purulent material that destroys articular cartilage. Standard of care: antibiotics plus joint drainage. Arthroscopic washout is preferred over serial arthrocentesis for knee septic arthritis. Without drainage, even appropriate antibiotics lead to progressive irreversible joint destruction. Orthopedic surgery must be called immediately.'},
  {type:'Time Pressure',scenario:'19-year-old unrestrained driver, high-speed MVC, GCS 7. Bilateral breath sounds, BP 88/54, HR 142, FAST positive in Morrison\'s pouch and splenorenal space.',prompt:'What are your next three actions in the correct sequence, and what resuscitation strategy does the evidence support?',teaching:'Sequence: (1) Activate massive transfusion protocol — 1:1:1 pRBC:FFP:platelets; (2) Two large-bore IVs or IO access; (3) Emergency trauma surgery consultation for OR. Evidence: crystalloid is harmful in hemorrhagic shock (PROPPR trial). Permissive hypotension (SBP 80-90) is acceptable until hemorrhage controlled. TXA within 3 hours reduces mortality (CRASH-2). Damage control resuscitation = blood products + TXA + early OR.'},
  {type:'Physical Exam Finding',scenario:'55M with cirrhosis: asterixis, mild confusion, jaundice, tense abdomen with shifting dullness. Diagnostic paracentesis performed.',prompt:'What four values from peritoneal fluid diagnose SBP, and what is the treatment if confirmed?',teaching:'SBP diagnosis: PMN count >250 cells/mm³ (most important — treat without waiting for culture), total protein <1 g/dL, SAAG ≥1.1 g/dL (confirms portal hypertension), positive culture (optional — 40% are culture-negative). Treatment: cefotaxime 2g IV q8h x 5 days or ceftriaxone 1g q24h. Albumin 1.5g/kg day 1 + 1g/kg day 3 reduces hepatorenal syndrome and mortality (Sort trial). Norfloxacin for secondary prophylaxis.'},
  {type:'Anchoring Check',scenario:'78F from nursing home, \'not acting right\' for 2 days. Temp 36.8, HR 96, BP 104/62, RR 20. Confused but moving all extremities. Team diagnoses \'altered mental status — likely UTI\' based on positive UA.',prompt:'What is the central error in this reasoning, and what workup must occur before attributing the presentation to a urinary source?',teaching:'Asymptomatic bacteriuria is present in up to 50% of nursing home residents — a positive UA does not diagnose UTI as the cause of delirium. Correct approach: full metabolic panel, blood cultures x2, CXR, CBC to exclude other causes; medication review; only attribute to UTI when other causes are excluded AND the patient has urinary symptoms. Treating asymptomatic bacteriuria does not improve outcomes and increases resistance.'},
  {type:'Source Check',scenario:'Your attending recommends high-dose aspirin (650mg TID) for an acute gout flare, citing its anti-inflammatory effect. You are uncertain this is evidence-based.',prompt:'What is the correct first-line treatment for acute gout, and what specific concern makes high-dose aspirin problematic in this setting?',teaching:'First-line for acute gout: NSAIDs (indomethacin 50mg TID or naproxen 500mg BID x 5-7 days), colchicine (1.2mg then 0.6mg 1h later), or prednisone if NSAIDs/colchicine contraindicated. High-dose aspirin paradoxically worsens gout — at high doses aspirin competes with urate for renal tubular secretion, transiently raising serum uric acid. Neither high nor low-dose aspirin is appropriate. ACR 2020 Gout Guidelines are freely available at rheumatology.org.'},
  {type:'Risk Priority',scenario:'Potassium 7.1 mEq/L. ECG: peaked T waves, PR interval 0.24 seconds. Patient awake, alert, with generalized weakness.',prompt:'What is your treatment sequence? Which intervention stabilizes the membrane, which shifts potassium, and which removes it?',teaching:'Sequence: (1) STABILIZE — calcium gluconate 1-2g IV over 10 min (membrane stabilization, onset 1-3 min; does NOT lower K+); (2) SHIFT — insulin 10 units IV + D50 (onset 15-30 min, lowers K+ ~0.5-1.5 mEq/L) + albuterol 10-20mg nebulized (additive); sodium bicarbonate if pH <7.2; (3) REMOVE — furosemide if making urine, patiromer or sodium polystyrene sulfonate, dialysis if renal failure or refractory. Never give calcium in bicarbonate solution — precipitates.'},
  {type:'Lab Shift',scenario:'32F with SLE: proteinuria 4.2g/24h, hematuria, creatinine rising from 0.9 to 2.8. C3 and C4 very low. Anti-dsDNA highly elevated.',prompt:'What is the likely class of lupus nephritis, why does the class matter, and what treatment does it guide?',teaching:'High proteinuria + hematuria + rapidly rising creatinine + low complement + elevated anti-dsDNA = Class III or IV (proliferative) lupus nephritis — most severe and most treatment-responsive. Class is confirmed by kidney biopsy — treatment decisions depend entirely on it. Class III/IV induction: mycophenolate mofetil 2-3g/day or IV cyclophosphamide (Euro-Lupus protocol) plus high-dose steroids. Hydroxychloroquine for all patients with LN.'},
  {type:'Distinguishing Case',scenario:'Two patients with ascending leg weakness over 5 days. Patient A: 45M, Campylobacter 3 weeks ago, areflexia, facial weakness, albumino-cytologic dissociation on LP. Patient B: 67F, HIV-positive CD4 48, leg weakness + back pain + bladder dysfunction + hyperreflexia.',prompt:'Why do hyperreflexia and bladder symptoms completely change the diagnosis in Patient B?',teaching:'Patient A: Guillain-Barré (ascending weakness, areflexia, post-infectious, albumino-cytologic dissociation). Patient B: hyperreflexia = upper motor neuron = spinal cord, not peripheral nerve. GBS causes areflexia, never hyperreflexia. In HIV with CD4 48: epidural abscess, HIV myelopathy, CMV radiculomyelitis, or lymphomatous cord compression. Emergency MRI spine is the next step — NOT LP until cord compression is excluded.'},
  {type:'Time Pressure',scenario:'3 AM: 82F, post-op day 1 after right hemicolectomy. Nurse calls: increasingly confused, RR 28, O2 sat 88% on 2L. Abdomen soft but distended. BP 108/64.',prompt:'What is your immediate diagnostic priority, and name the four post-operative pulmonary complications to distinguish in the next 10 minutes.',teaching:'Immediate: 100% O2 face mask + ABG + portable CXR while examining. Four post-op pulmonary complications: (1) Atelectasis — most common, fever day 1-2, linear opacity CXR; (2) PE — tachycardia + hypoxia, CXR often normal, needs CT-PA; (3) Aspiration pneumonitis/pneumonia — right lower lobe after general anesthesia; (4) Pulmonary edema — bilateral crackles, post-op fluid overload, elevated BNP. Post-op day 1 + confusion + hypoxia = PE until proven otherwise.'},
  {type:'Missing Evidence',scenario:'24F, no cardiac history, 6 months of exertional dyspnea and palpitations. ECG: short PR (0.10 sec), delta wave on QRS upstroke. She wants to return to competitive swimming.',prompt:'What critical risk stratification is missing before you can counsel her about competitive sports?',teaching:'Electrophysiology study (EPS) for WPW. The danger: if the accessory pathway has a short anterograde refractory period, atrial fibrillation can conduct at >300 bpm causing VF and sudden death. EPS determines: (1) Shortest pre-excited R-R interval during induced AF (SPERRI); (2) Accessory pathway refractory period. SPERRI <250ms = high risk — ablation recommended before any competitive sports. Without EPS, you cannot clear this patient. ACC/AHA sports cardiology guidelines require EPS for all high-risk WPW athletes.'},
  {type:'Anchoring Check',scenario:'62M brought in for confusion. PMH: known alcoholic. Smells of alcohol. Glucose 128. Intern documents \'intoxication\' and plans observation.',prompt:'What three features would confirm this is alcohol intoxication, and what single finding would immediately change your management?',teaching:'To attribute confusion to alcohol: (1) blood alcohol level consistent with degree of confusion; (2) no focal neurological deficits; (3) gradual improvement over time. The one finding that changes everything: any focal neurological deficit — mild unilateral weakness, pronator drift, facial asymmetry, or eye deviation. Subdural hematoma is extremely common in alcoholics due to falls, cortical atrophy, and thrombocytopenia. Alcohol + confusion = CT head, not automatic observation.'},
  {type:'Physical Exam Finding',scenario:'70M, 2 weeks of progressive neck pain and bilateral leg weakness (3/5). Bilateral hyperreflexia at knees and ankles, positive Babinski bilaterally, positive Lhermitte sign.',prompt:'What does this combination of findings tell you about lesion localization, and what is the emergency investigation?',teaching:'Cervical spinal cord lesion — upper motor neuron pattern below the lesion. Lhermitte sign (electric shock sensation down the spine with neck flexion) localizes specifically to the cervical cord, indicating dorsal column compression or demyelination. Bilateral UMN signs with neck pain = cervical cord compression until proven otherwise. Emergency: MRI cervical and thoracic spine with and without contrast. Most common cause in elderly: cervical spondylotic myelopathy. This is a neurological emergency.'},
  {type:'Risk Priority',scenario:'Four simultaneous overnight calls: (1) 58M, 2h post-PCI, BP 78/44, HR 128. (2) 74F, nursing home transfer, temp 39.2. (3) 32M sickle cell pain crisis requesting IV morphine. (4) 28F post-appendectomy day 1 asking for anti-nausea medication.',prompt:'Rank these calls. For Call 1, name the two most dangerous immediate causes of post-PCI hypotension.',teaching:'Priority: Call 1 = IMMEDIATE (you are running). Call 2 = Urgent (febrile elderly = sepsis until proven otherwise). Call 3 = Soon (pain crisis is real; undertreated pain worsens sickling but patient is communicating). Call 4 = Routine. Post-PCI hypotension: (1) Stent thrombosis or coronary re-occlusion — return to cath lab emergently; (2) Cardiac tamponade from coronary perforation — bedside echo immediately. Also consider: retroperitoneal hematoma, vasovagal, contrast reaction.'},
  {type:'Lab Shift',scenario:'56M with acute decompensated heart failure. After 2 days of IV furosemide: creatinine rose from 1.1 to 2.4 (120% increase). Weight down 6kg. Patient feels significantly better.',prompt:'Should you stop the diuresis? Walk through the clinical reasoning.',teaching:'This is diuresis-associated AKI in cardiorenal syndrome — expected with volume removal. Decision framework: (1) Is the patient hemodynamically stable? If yes, often safe to continue; (2) Is output satisfactory? 6kg in 2 days is good progress; (3) Is creatinine plateauing or still rising? If plateauing, may continue with monitoring; (4) Oliguria or hemodynamic decline? Stop. The DOSE trial supports that allowing a modest creatinine rise to achieve decongestion often improves long-term renal outcomes. Treat the fluid status, not the creatinine number in isolation.'},
  {type:'Source Check',scenario:'A student proposes morphine for acute MI, citing that pain and anxiety reduction decreases myocardial oxygen demand. You recall morphine may be harmful in STEMI.',prompt:'What does current evidence say about morphine in ACS, and what analgesic is preferred?',teaching:'The CRUSADE analysis and CIRCUS trial showed morphine delays and reduces absorption of oral P2Y12 inhibitors (clopidogrel, ticagrelor) — dangerous when DAPT is the cornerstone of STEMI treatment. ACC/AHA 2025 ACS guidelines downgraded morphine to Class IIb with a warning about P2Y12 inhibitor interference. Preferred: IV nitrates for ischemic pain if BP permits; fentanyl if opioid is required (less P2Y12 interaction). The pharmacokinetic interaction evidence is compelling even if the oxygen demand rationale is physiologically plausible.'},
  {type:'Distinguishing Case',scenario:'Three patients with severe headache rated 10/10. A: 38M during sexual activity, worst headache of life, neck stiffness, photophobia. B: 52F tension headache history, resolves with ibuprofen in 1 hour. C: 45M occipital headache during Valsalva straining, no neurological deficits.',prompt:'Which patients need CT head, which needs LP even after negative CT, and which can be managed without neuroimaging?',teaching:'Patient A: CT head immediately (thunderclap headache = SAH until proven otherwise). If CT negative within 6 hours of onset, LP may not be required per Ottawa SAH Rule — but if >6h from onset, LP is mandatory (xanthochromia takes hours to develop). Patient C: CT head (Valsalva-triggered thunderclap = high-risk feature regardless). Patient B: does NOT require imaging if this matches her prior pattern, resolves rapidly, and no red flags (first/worst, exertional, fever, focal deficit, age >50, thunderclap onset). Ottawa SAH Rule sensitivity 99%.'},
  {type:'Missing Evidence',scenario:'A 48-year-old male with new monoarthritis of the right knee: synovial WBC 62,000 (PMN 90%), Gram stain negative. Started on IV cefazolin. An EM resident says culture-negative synovitis can be treated with steroids if no organism is identified in 48 hours.',prompt:'What is wrong with this reasoning, and what evidence-based guideline governs the decision to escalate vs de-escalate treatment?',teaching:'Gram stain is negative in up to 50% of bacterial septic arthritis cases — a negative Gram stain never rules out septic arthritis. De-escalation to steroids before cultures finalize (48-72h) is dangerous and not supported by any guideline. Standard of care: continue IV antibiotics + surgical/arthroscopic washout while awaiting cultures; antibiotics should cover S. aureus empirically (ceftriaxone covers gonococcal arthritis in young adults — consider age and sexual history). Steroids are contraindicated in septic arthritis.'},
  {type:'Time Pressure',scenario:'You are called to a code blue. A 67M on the oncology floor is pulseless. CPR in progress. Rhythm on monitor: coarse ventricular fibrillation.',prompt:'Walk through your first 4 minutes of ACLS management including timing, doses, and the single most impactful non-pharmacological intervention.',teaching:'ACLS for VF: (1) Immediate defibrillation — 200J biphasic (most impactful single intervention in VF); resume CPR immediately after shock without rhythm check; (2) Establish IV/IO access during CPR; (3) After 2 minutes (second rhythm check): if VF persists, shock again; give epinephrine 1mg IV every 3-5 min; (4) Third shock if VF persists: amiodarone 300mg IV push (or lidocaine 1-1.5mg/kg). Continuous high-quality CPR (rate 100-120, depth 5-6cm, full recoil, minimize interruptions) is the most impactful modifiable factor. Treat reversible causes (5H and 5T) simultaneously.'},

  // ── PHARMACY ──
  {type:'Mechanism First',profession:'pharmacy',scenario:'A 68-year-old male with heart failure (EF 30%), atrial fibrillation, and CKD stage 3 (GFR 38) is on warfarin, digoxin, lisinopril, furosemide, and amiodarone. He was just started on fluconazole for oral candidiasis.',prompt:'Without looking up a drug interaction table — reason through the mechanism of the two most dangerous interactions in this medication list.',teaching:'(1) Amiodarone + warfarin: amiodarone inhibits CYP2C9 (warfarin metabolism) AND CYP3A4, dramatically increasing warfarin exposure. INR can double or triple over 2-4 weeks. Mechanism: reduced warfarin clearance. Monitor INR closely; reduce warfarin dose 30-50%. (2) Fluconazole + warfarin: fluconazole is a potent CYP2C9 inhibitor — same mechanism as amiodarone, additive effect. Triple interaction (amiodarone + fluconazole + warfarin) is extremely high-risk. Also: digoxin toxicity risk in CKD — renal clearance reduced, narrow therapeutic index.'},
  {type:'Patient Factor',profession:'pharmacy',scenario:'A 52-year-old female with T2DM is on metformin 1000mg BID. New labs: creatinine 1.8 (GFR 32 mL/min/1.73m²). The physician asks if metformin should continue.',prompt:'Use patient-specific factors to reason through this — not just a cutoff. What do you recommend and why?',teaching:'FDA 2016 labeling: metformin is contraindicated when GFR <30; dose reduction recommended GFR 30-45. At GFR 32, the patient is in the warning zone. Risk: lactic acidosis (rare but potentially fatal — mechanism: metformin inhibits hepatic gluconeogenesis and impairs lactate clearance in renal failure). Patient-specific factors that tilt toward stopping: acute illness, iodinated contrast planned, worsening trend, age >65, hepatic disease. Recommendation: reduce to 500mg BID, recheck GFR in 4-6 weeks, hold if contrast or acute illness. Do not stop abruptly without a replacement plan.'},
  {type:'Mechanism First',profession:'pharmacy',scenario:'A transplant patient on tacrolimus has a new prescription for fluconazole for 14 days. Tacrolimus has a narrow therapeutic index.',prompt:'What is the mechanism of this interaction, how significant is it, and what monitoring is required?',teaching:'Fluconazole is a potent CYP3A4 inhibitor. Tacrolimus is primarily metabolized by CYP3A4 (and P-gp). Inhibition dramatically increases tacrolimus exposure — levels can increase 2-4 fold within days. Clinical consequence: nephrotoxicity, neurotoxicity, opportunistic infection (over-immunosuppression). Management: reduce tacrolimus dose empirically 50% at fluconazole initiation; check tacrolimus trough 2-3 days after starting and after stopping fluconazole; therapeutic drug monitoring is non-negotiable. Alternative: nystatin swish-and-swallow if systemic therapy not required.'},
  {type:'Polypharmacy Check',profession:'pharmacy',scenario:'76-year-old female on 14 medications post-hospitalization for hip fracture. Medications include: oxycodone, zolpidem, lorazepam, amitriptyline, oxybutynin, promethazine, and diphenhydramine.',prompt:'Identify the Beers Criteria concerns and prioritize the one change with highest fall/sedation risk.',teaching:'Beers Criteria red flags in this list: oxybutynin (strong anticholinergic, cognitive impairment, falls), amitriptyline (anticholinergic + sedating TCA in elderly), promethazine (anticholinergic + sedating), diphenhydramine (anticholinergic + sedating), zolpidem (Z-drug — falls risk), lorazepam (benzodiazepine — highest fall/fracture risk). Triple/quadruple anticholinergic burden is the most dangerous combination in post-hip-fracture patients. Priority: stop lorazepam (highest evidence for hip fracture) and diphenhydramine (no indication apparent). Anticholinergic burden scale: oxybutynin (3) + amitriptyline (3) + promethazine (2) + diphenhydramine (3) = catastrophic total.'},
  {type:'Missing Evidence',profession:'pharmacy',scenario:'A 28-year-old female with bipolar disorder, currently stable on lithium 900mg/day, lithium level 0.9 mEq/L, presents to pharmacy for a refill. She mentions she just started taking ibuprofen 600mg TID for knee pain and is also starting a new low-sodium diet.',prompt:'What two pharmacokinetic factors are about to significantly change her lithium level, and what is your patient counseling message?',teaching:'(1) NSAIDs reduce renal prostaglandin synthesis → decrease GFR → reduce lithium clearance → lithium toxicity risk. Mechanism: lithium is entirely renally cleared; anything reducing GFR (NSAIDs, ACEi, dehydration) raises levels. (2) Low-sodium diet: lithium is reabsorbed by the same proximal tubule mechanism as sodium. Reduced dietary sodium → kidney retains more lithium. Two simultaneous lithium-elevating factors = high toxicity risk. Counseling: switch to acetaminophen; avoid low-sodium diet while on lithium; signs of toxicity (tremor, ataxia, confusion, GI symptoms); check lithium level in 5-7 days.'},

  // ── PHYSICAL THERAPY ──
  {type:'Red Flag Screen',profession:'pt',scenario:'44-year-old male presents to outpatient PT for low back pain, rated 6/10, 6 weeks duration. He works in construction, no trauma. Pain is constant, worse at night, does not improve with position change. He has lost 12 lbs over 2 months without trying.',prompt:'Before initiating any PT treatment, walk through your red flag screen. What is your disposition?',teaching:'Red flags present: constant pain without mechanical behavior, night pain worse with recumbency (tumor, infection), unexplained weight loss >10 lbs (malignancy screen). Mechanical LBP improves with position and movement — constant non-mechanical pain that disrupts sleep is a cardinal red flag. Action: do NOT initiate PT. Refer immediately to physician/PCP for imaging (MRI lumbar spine) and malignancy workup. Spinal metastasis, primary bone tumor, or spinal infection must be excluded. PT treating this patient delays diagnosis.'},
  {type:'Distinguishing Case',profession:'pt',scenario:'Two patients with lumbar radiculopathy to the right lower extremity. Patient A: 45M, pain radiating from back to great toe, positive straight leg raise at 40°, sensation diminished L4 dermatomal distribution, diminished patellar reflex. Patient B: 58F, bilateral leg pain worse with walking, relieved by sitting or leaning forward, no straight leg raise deficit, normal reflexes.',prompt:'Identify the likely source of each presentation and how it changes your PT approach.',teaching:'Patient A: Disc herniation — L4 nerve root compression (patellar reflex, medial calf/great toe distribution). Positive SLR at 40° is highly specific for nerve root compression. PT: McKenzie extension exercises, neural mobilization, traction may help, but monitor for worsening neurological deficit. Patient B: Spinal stenosis — bilateral symptoms, neurogenic claudication (worse walking, better leaning forward = flexion widens canal), normal SLR. PT: lumbar flexion exercises, aerobic conditioning, aquatic therapy. Key: extension makes stenosis worse; flexion makes disc worse. Getting this backwards worsens both patients.'},
  {type:'Mechanism First',profession:'pt',scenario:'A 32-year-old female runner presents with anterior knee pain worse with descending stairs, prolonged sitting, and squatting. Patellar grind test positive. Quadriceps strength 4-/5, VMO atrophy visible.',prompt:'Explain the biomechanical mechanism driving this presentation and how it directly guides your treatment selection.',teaching:'Patellofemoral pain syndrome: VMO weakness (medial quadriceps) allows lateral patellar tracking — contact area on lateral patellar facet increases, joint stress rises, pain occurs with activities loading the patellofemoral joint. The mechanism directly determines treatment: VMO strengthening (terminal knee extension, step-ups, wall slides at limited range), hip abductor strengthening (controls femoral internal rotation that worsens lateral tracking), taping or bracing to correct lateral tracking acutely, activity modification to limit high-load patellofemoral positions. Patellar mobilization addresses lateral retinacular tightness. Mechanism-first PT avoids treating the symptom instead of the driver.'},
  {type:'Screening Decision',profession:'pt',scenario:'65-year-old female referred to PT for "left shoulder pain." History: 8 weeks of left shoulder aching, no trauma, no overuse history. She also mentions fatigue and left-sided chest heaviness with exertion.',prompt:'What is your decision, and what is the mechanism behind referred pain to the left shoulder?',teaching:'Refer immediately — do not initiate PT. Left shoulder pain + chest heaviness with exertion in a 65-year-old female = cardiac ischemia until proven otherwise. Referred pain mechanism: convergence of afferent pain fibers from the cardiac diaphragmatic/pericardial surface onto C4 and C5 dermatomes (shoulder, neck, jaw referral). Women have higher rates of atypical ACS presentation (fatigue, shoulder pain, exertional dyspnea without classic chest pressure). PT treating this patient as shoulder pathology delays STEMI/unstable angina diagnosis. Call 911 or send directly to ED.'},

  // ── OPTOMETRY ──
  {type:'Ocular-Systemic',profession:'optometry',scenario:'58-year-old male presents with painless, sudden monocular vision loss in the right eye. VA: 20/200 right, 20/20 left. On fundoscopy: cherry-red spot at macula, diffuse retinal whitening, attenuated arterioles. He has hypertension and a 40 pack-year smoking history.',prompt:'Identify the ocular diagnosis, explain the mechanism of the cherry-red spot, and name the three systemic investigations required in the next 24 hours.',teaching:'Central retinal artery occlusion (CRAO). Cherry-red spot mechanism: the fovea receives blood directly from the choroid (not retinal artery); surrounding retina becomes opaque from ischemic edema, while the fovea remains transparent — revealing the red choroidal reflex underneath. The retinal whitening represents ischemic cytotoxic edema. Systemic investigations: (1) ESR/CRP (giant cell arteritis — must exclude to prevent fellow-eye involvement); (2) Carotid Doppler (embolus source); (3) Echocardiogram (cardiac embolus). CRAO is a stroke equivalent — patient needs emergent vascular risk factor evaluation and neurology/ED referral.'},
  {type:'Bidirectional Reasoning',profession:'optometry',scenario:'A 45-year-old female presents for routine exam. Best-corrected VA: 20/20 OU. On slit-lamp exam: bilateral anterior uveitis with 2+ cells and flare, no keratic precipitates. She mentions recurring "achy joints" in her hands and back stiffness in the morning for 30 minutes.',prompt:'The uveitis appears primary ocular. Why should you look systemically, and what is your most important referral?',teaching:'Anterior uveitis (non-granulomatous) is the most common extraocular manifestation of HLA-B27-associated spondyloarthropathies. Morning stiffness >30 minutes + axial pain + bilateral anterior uveitis = ankylosing spondylitis until proven otherwise. HLA-B27 is positive in 90% of AS patients with uveitis. Referral: rheumatology. Additional workup: HLA-B27 typing, sacroiliac joint imaging. Treating the eye without diagnosing the systemic disease leads to recurrent uveitis flares and progressive joint destruction. Bilateral uveitis is more likely systemic than unilateral.'},
  {type:'Missing Evidence',profession:'optometry',scenario:'52-year-old female, new patient, VA 20/20 OU, IOP 28 mmHg OD and 26 mmHg OS, C/D ratio 0.7 OU, normal visual fields, normal OCT nerve fiber layer.',prompt:'Before diagnosing ocular hypertension (OHT) and starting medication, what single measurement is most critical — and how does it change the diagnosis and treatment threshold?',teaching:'Central corneal thickness (CCT). Goldmann applanation tonometry assumes CCT of 520-545 microns — thicker corneas give falsely elevated readings, thinner corneas give falsely low readings. A patient with CCT of 600 microns and IOP of 28 may have a true IOP closer to 22-23 (below treatment threshold). A patient with CCT of 480 and IOP of 22 may have true IOP of 24-25 (higher risk). The Ocular Hypertension Treatment Study (OHTS) found CCT is the strongest predictor of glaucoma conversion in OHT. Never start glaucoma medication without CCT.'},
  {type:'Ocular-Systemic',profession:'optometry',scenario:'32-year-old female with 3 days of right eye pain with eye movement, central scotoma on Amsler grid, and RAPD right eye. VA: 20/200 OD, 20/20 OS. Fundus: normal. MRI brain/orbits pending.',prompt:'What is the most likely diagnosis, what is the key diagnostic finding that localizes it, and why is the fundus normal?',teaching:'Optic neuritis — most commonly associated with multiple sclerosis (50% of ON patients develop MS within 15 years). The RAPD (relative afferent pupillary defect) localizes to the afferent limb — specifically the optic nerve, not the retina or cornea. Fundus is normal in retrobulbar neuritis (posterior to the optic disc — "the patient sees nothing, the doctor sees nothing"). If swollen disc, it is papillitis. Hallmark: pain with eye movement (stretching inflamed optic nerve). Key counseling: >90% recover to 20/40 or better. IV steroids speed recovery but don't change 6-month VA outcome. Refer to neurology for MS workup.'},
  {type:'Distinguishing Case',profession:'optometry',scenario:'Three patients with acute red eye. Patient A: 26F, mild itch, bilateral, watery discharge, no pain. Patient B: 35M, severe unilateral pain, photophobia, circumlimbal injection, 2+ cells on slit lamp, no discharge. Patient C: 68M, unilateral red eye, mid-dilated non-reactive pupil, decreased VA, headache, nausea.',prompt:'Identify each diagnosis and the one that is immediately sight-threatening and life-threatening.',teaching:'Patient A: Allergic conjunctivitis — bilateral, itchy, watery (not purulent). Manage with antihistamines, cold compresses, topical antihistamine/mast cell stabilizer. Patient B: Anterior uveitis — circumlimbal (ciliary) injection, cells/flare on slit lamp, no discharge, photophobia. Needs steroids + cycloplegia; workup for systemic cause. Patient C: ACUTE ANGLE CLOSURE GLAUCOMA — mid-dilated fixed pupil (iris ischemia) + dramatically elevated IOP + GI symptoms (vagal) + decreased VA. Sight AND life threatening (IOP can exceed 60 mmHg, causing optic nerve ischemia within hours). Emergency: topical timolol + pilocarpine, IV acetazolamide, mannitol if needed, emergent laser peripheral iridotomy. Call ophthalmology NOW — this cannot wait.'},

  // ── OCCUPATIONAL THERAPY ──
  {type:'Occupational Profile',profession:'ot',scenario:'78-year-old male, 2 weeks post-right hemisphere stroke with left hemiplegia (3/5), left neglect, and mild dysphagia. Lives alone. Previously independent in all ADLs and IADLs, drove, and volunteered at a food bank 3 days/week.',prompt:'Before selecting any intervention, build his occupational profile. What are the most important occupational performance deficits to prioritize?',teaching:'The occupational profile reveals what this person values and what is lost. Key deficits: (1) Driving — critical for independence and community participation (volunteering); not a realistic short-term goal but essential for discharge planning; (2) Self-care (dressing, bathing) — functional goal addressable in acute/subacute; (3) Left neglect — a safety emergency that affects all ADLs and is the single highest-priority impairment; (4) Meal preparation and dysphagia management — affects nutrition and independence. The volunteering and community role is his occupational identity — discharge planning must include pathways back to meaningful occupation, not just basic ADLs.'},
  {type:'Cognitive Screen',profession:'ot',scenario:'82-year-old female, hospitalized for hip replacement. Post-op day 2: nursing calls OT because she is confused at night, pulled out her IV once, and is calling for family members who are deceased.',prompt:'Distinguish between delirium, dementia, and the common overlap. What assessment confirms your clinical impression, and what is your intervention?',teaching:'Delirium presentation: acute onset (post-op) + fluctuating course (worse at night = sundowning) + inattention + disorganized thinking. Dementia alone doesn't cause acute behavioral change. Delirium superimposed on dementia is the most common scenario in post-op elderly. Assessment: CAM (Confusion Assessment Method) — sensitivity 94%, specificity 89%. CAM positive requires: acute onset + fluctuating course + inattention + EITHER disorganized thinking OR altered consciousness. OT intervention: reorientation (clock, calendar, familiar objects), normalizing day/night cycle (lights/activity during day), early mobilization, remove restraints, involve family, recommend medication review (anticholinergics, opioids, benzodiazepines are primary culprits).'},

  // ── NURSING ──
  {type:'Surveillance',profession:'nursing',scenario:'72-year-old post-op day 1 colectomy. VS at 7am: T 37.2, HR 88, BP 124/78, RR 14, SpO2 97%. At 10am: T 38.3, HR 106, BP 108/72, RR 20, SpO2 94% on 2L. Patient reports increased abdominal pain.',prompt:'What does the trend tell you, and what is your SBAR to the physician?',teaching:'Trend analysis: temp rising, HR rising, BP dropping, RR rising, O2 dropping, pain worsening over 3 hours — this is a clinical deterioration pattern, not stable post-op course. Differential: anastomotic leak, aspiration pneumonia, PE, wound infection with early sepsis. NEWS2 score at 10am: approximately 7-8 = high risk, urgent escalation required. SBAR: Situation — "Mr. Jones, post-op day 1, showing concerning vital sign trend." Background — "Colectomy yesterday, baseline vitals normal at 7am." Assessment — "Appears to be deteriorating: tachycardia, dropping BP and O2, fever, and worsening pain suggesting possible surgical complication." Recommendation — "I need you to come assess now and consider CBC, lactate, CXR, and surgical review."'},
  {type:'Medication Safety',profession:'nursing',scenario:'You are preparing to administer vancomycin 1250mg IV to a 68-year-old with MRSA bacteremia. The pharmacy label says "infuse over 60 minutes." The patient weighs 55kg and has a creatinine of 2.2.',prompt:'What three assessments must you make before hanging this infusion, and what adverse effect is specifically related to infusion rate?',teaching:'(1) Renal function review: creatinine 2.2 = reduced vancomycin clearance. AUC-based monitoring now preferred over trough. Verify with pharmacy that dose and interval are adjusted for CKD. (2) Infusion rate: vancomycin over <60 minutes causes "Red Man Syndrome" — non-immune-mediated histamine release causing flushing, erythema, and hypotension (not an allergy). Slow to 90-120 min if ≥1g. (3) IV site patency: vancomycin is a vesicant — infiltration causes tissue necrosis. Check for pain/swelling at site. Also: establish baseline auditory function (ototoxicity risk), check prior vancomycin levels if available.'},

  // ── MBS / PRE-HEALTH ──
  {type:'Mechanism Bridge',profession:'mbs',scenario:'A first-year MBS student knows that beta-1 adrenergic receptors couple to Gs proteins, activating adenylyl cyclase and increasing cAMP. She is asked why metoprolol (a beta-1 blocker) is used in heart failure.',prompt:'Bridge from the molecular mechanism to the clinical effect — why does blocking a receptor that normally increases heart rate and contractility actually help a failing heart?',teaching:'The mechanism bridge: (1) Molecular: beta-1 blockade → decreased cAMP → decreased PKA activation → reduced calcium influx and release → decreased contractility and heart rate; (2) Pathophysiology: chronic heart failure causes sustained catecholamine excess → beta-1 downregulation, receptor desensitization, and myocyte apoptosis. The failing heart is already maximally stimulated and burning out; (3) Clinical effect: beta-blockade breaks the catecholamine toxicity cycle → upregulation of beta-1 receptors → improved cardiac efficiency, reduced remodeling, reduced sudden death. MERIT-HF trial: metoprolol succinate reduced mortality 34%. The mechanism bridges molecular pharmacology to clinical outcome.'},
  {type:'Mechanism Bridge',profession:'mbs',scenario:'Pre-med student: "I know ACE inhibitors block the conversion of angiotensin I to angiotensin II. Why does this lower blood pressure AND protect the kidneys in diabetes?"',prompt:'Explain both effects through mechanism — why the same drug does two things through the same pathway.',teaching:'The RAAS mechanism bridge: (1) BP reduction: angiotensin II is a potent vasoconstrictor (acts on AT1 receptors on vascular smooth muscle). ACEi → less Ang II → vasodilation → reduced SVR → lower BP. Also: less aldosterone secretion → less sodium retention → reduced volume. (2) Renal protection: angiotensin II preferentially constricts the efferent arteriole of the glomerulus (to maintain filtration pressure). In diabetic nephropathy, this raises intraglomerular pressure, causing hyperfiltration and progressive damage. ACEi → less efferent constriction → reduced intraglomerular pressure → less mechanical stress → slower progression. One drug, one mechanism, two benefits — the pharmacology exam and the clinical exam are the same question.'},
  {type:'Mechanism Bridge',profession:'mbs',scenario:'MCAT-style: A patient with Addison's disease (primary adrenal insufficiency) presents with hyponatremia, hyperkalemia, and hypotension. Without looking at a formula — explain from first principles why all three abnormalities occur.',prompt:'Walk from the gland failure to each electrolyte abnormality using mechanism.',teaching:'First principles: Addison's = destruction of adrenal cortex → loss of both cortisol and aldosterone. (1) Aldosterone normally acts on principal cells of collecting duct: binds mineralocorticoid receptor → increases luminal ENaC (Na+ reabsorption) and ROMK (K+ secretion). Loss of aldosterone → Na+ not reabsorbed → hyponatremia + volume depletion → hypotension. (2) K+ not secreted → hyperkalemia. (3) Hypotension: both hypovolemia (Na+ wasting) and lack of cortisol (which supports vascular tone and catecholamine sensitivity). The MCAT asks you to reason forward from the defect — not memorize "Addison's causes hyponatremia."'}

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,{type:'mcq',
  stem:'A 34yo woman presents with 3 weeks of fatigue and dyspnea. Her hemoglobin is 7.2. The intern anchors on iron-deficiency anemia and orders ferritin. Which cognitive bias does this BEST represent — and what critical information was anchored away from?',
  options:['Availability bias — iron deficiency is common so it comes to mind first','Anchoring bias — the first hypothesis (IDA) prevented considering other causes of anemia in a 34yo woman','Premature closure — a diagnosis was made without completing the history','Framing effect — the word "fatigue" framed the differential toward non-urgent causes'],
  answer:1,
  explanation:'Anchoring: the intern fixed on the most common cause without asking about other critical features. In a 34yo woman with fatigue and Hgb 7.2, the differential includes autoimmune hemolytic anemia, B12/folate deficiency, early leukemia, and hypothyroidism — all of which require different workup. The reticulocyte count and peripheral smear should precede ferritin.'},
{type:'mcq',
  stem:'A physician diagnoses a patient with community-acquired pneumonia and starts azithromycin. Three days later the patient is worse — now requiring O2. A chest CT shows bilateral ground-glass opacities and pleural effusions. Which error in clinical reasoning BEST explains this outcome?',
  options:['Availability bias — pneumonia was the most recently seen diagnosis','Premature closure — diagnosis was accepted before alternative causes were considered','Visceral bias — the physician liked the patient and wanted a benign diagnosis','Framing effect — the word "community-acquired" anchored to outpatient pathogens'],
  answer:1,
  explanation:'Premature closure is the most common diagnostic error in emergency and inpatient medicine. Once pneumonia was diagnosed, the cognitive search stopped. Bilateral GGOs with pleural effusions in a patient who is worsening on appropriate antibiotics should trigger reconsideration: atypical infection, pulmonary edema, vasculitis, or drug reaction. Stopping at "pneumonia" foreclosed the differential.'},
{type:'mcq',profession:'dentistry',
  stem:'A 44yo male presents with trismus (15mm opening), bilateral submandibular swelling, elevated floor of mouth, and difficulty swallowing. Temperature is 39.2°C. Which is the MOST critical immediate action?',
  options:['Prescribe oral amoxicillin-clavulanate and see in 24 hours','Drain the submandibular space in clinic under local anesthesia','Call 911 and prepare for airway emergency — this patient needs immediate hospital transfer','Order a panoramic radiograph to identify the source tooth'],
  answer:2,
  explanation:'Ludwig\'s angina is a life-threatening bilateral submandibular space infection that can cause airway obstruction within hours. The classic triad: bilateral submandibular swelling, elevated/displaced tongue, and trismus. This patient needs emergent transfer — NOT outpatient management. Airway may become impossible to manage if not secured early. IV antibiotics, surgical drainage, and often intubation in an OR setting are required.'},


,{type:'mcq',profession:'medicine',
  stem:'A 58yo diabetic woman presents with 3 hours of dyspnea, nausea, and diaphoresis. She denies chest pain. ECG shows new LBBB. Troponin is pending. Which cognitive error is MOST likely if a physician concludes this is not ACS because of absent chest pain?',
  options:['Availability bias','Premature closure','Representativeness bias — pattern matching to the classic presentation and missing the atypical one','Anchoring bias'],
  answer:2,
  explanation:'Representativeness bias: the physician matches the case to the prototype (crushing chest pain, diaphoresis, middle-aged male) and rejects ACS when the presentation is atypical. Diabetic neuropathy, female sex, and age over 55 are all independent risk factors for silent or atypical MI. New LBBB is a STEMI equivalent. Chest pain is absent in up to 33% of MIs in diabetic women.'},
{type:'mcq',profession:'medicine',
  stem:'A third-year resident has seen 4 cases of pulmonary embolism this month. She now evaluates a 28yo with pleuritic chest pain and mild dyspnea — Wells score 2 (low). She orders a CT-PA immediately without checking a D-dimer. Which bias is MOST operative?',
  options:['Anchoring bias — she fixed on PE from the start','Availability heuristic — recent PE cases make PE feel more likely than base rate warrants','Premature closure — she stopped considering other diagnoses','Commission bias — she prefers action over watchful waiting'],
  answer:1,
  explanation:'Availability heuristic: a diagnosis that comes readily to mind (due to recent experience) is judged as more probable than base rates support. In a low-probability patient, PERC rule or D-dimer should precede CT-PA. Over-ordering CTs exposes low-risk patients to radiation, contrast risk, and incidental findings. The correct debiasing strategy: explicitly invoke pre-test probability and Wells scoring before imaging.'},
{type:'mcq',profession:'medicine',
  stem:'A hospitalist diagnoses a 72yo with confusion, fever, and pyuria as having a UTI and starts nitrofurantoin. He is discharged. She returns 2 days later obtunded with BP 88/56. Blood cultures grow Gram-negative rods. Which error MOST directly caused harm?',
  options:['Premature closure — UTI was accepted as the diagnosis without considering why a 72yo was confused enough to come to the hospital','Anchoring — the urinalysis findings anchored the workup','Availability — UTI is common in elderly women','Framing effect — the ED triage note said "UTI"'],
  answer:0,
  explanation:'Premature closure: the positive UA closed the diagnostic search. But UTI rarely causes acute confusion in isolation — altered mental status in an elderly patient with UTI should trigger evaluation for urosepsis. The confusion was the presenting symptom of bacteremia, not merely a UTI side effect. Nitrofurantoin is also inappropriate for urosepsis — it does not achieve systemic bactericidal levels.'},

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