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`); win.document.close(); setTimeout(() => win.print(), 500); } function dlAllPDF() { if (!PREM.sessions.length) { alert('No sessions to download yet!'); return; } PREM.sessions.forEach((_,i) => setTimeout(() => dlSessionPDF(i), i * 700)); }// ── FORECAST CHART ──────────────────────── let trajChartInst = null; function initForecastChart() { const scores = PREM.scores; if (!scores.length) return; const el = document.getElementById('trajChart'); if (!el) return; const forecast = []; if (scores.length >= 2) { const trend = scores[scores.length-1] - scores[scores.length-2]; for (let w = 1; w <= 4; w++) forecast.push(Math.round(scores[scores.length-1] + trend * w * 0.7)); } const labels = scores.map((_,i) => `NBME ${i+1}`); const fLabels = forecast.map((_,i) => `Week ${i+1}`); if (trajChartInst) trajChartInst.destroy(); trajChartInst = new Chart(el.getContext('2d'), { type: 'line', data: { labels: [...labels, ...fLabels], datasets: [ { label:'Your Scores', data:[...scores,...Array(forecast.length).fill(null)], borderColor:'#0d9488', backgroundColor:'rgba(13,148,136,.08)', borderWidth:2.5, tension:.4, fill:true, pointRadius:5, pointBackgroundColor:'#fff', pointBorderColor:'#0d9488', pointBorderWidth:2 }, { label:'AI Forecast', data:[...Array(scores.length).fill(null), scores[scores.length-1], ...forecast], borderColor:'#7c3aed', backgroundColor:'rgba(124,58,237,.04)', borderWidth:2, tension:.4, fill:false, borderDash:[6,3], pointRadius:4, pointBackgroundColor:'#7c3aed' } ] }, options: { responsive:true, maintainAspectRatio:false, plugins:{ legend:{ labels:{ font:{ family:"'Plus Jakarta Sans'" } } } }, scales:{ y:{ min:185, max:270, grid:{ color:'rgba(0,0,0,.04)' }, ticks:{ color:'#64748b' } }, x:{ grid:{ display:false }, ticks:{ color:'#64748b' } } } } }); if (forecast.length) { const tf = document.getElementById('trajForecast'); if(tf) tf.textContent = forecast[forecast.length-1]; } if (scores.length >= 2) { const diff = scores[scores.length-1] - scores[0]; const tc = document.getElementById('trajChange'); if (tc) { tc.textContent = (diff>=0?'↑ ':'↓ ') + Math.abs(diff) + ' pts from baseline'; tc.style.color = diff >= 0 ? 'var(--green)' : 'var(--red)'; } } }// ── WEEK GRID ───────────────────────────── function renderWeekGrid() { const days = ['Mon','Tue','Wed','Thu','Fri','Sat','Sun']; const today = new Date().getDay(); const checkedDays = JSON.parse(localStorage.getItem('nbme_week_days') || '[]'); const grid = document.getElementById('weekGrid'); if (!grid) return; grid.innerHTML = days.map((d,i) => { const realDay = i === 6 ? 0 : i+1; const isToday = realDay === today; const isDone = checkedDays.includes(new Date().toDateString() + '-' + i); return `

${isDone?'✅':d}

`; }).join(''); }// ── TASK TOGGLE ─────────────────────────── let tasksDone = 0; function toggleTask(el) { el.classList.toggle('done'); const check = el.querySelector('.task-check'); if (el.classList.contains('done')) { check.textContent = '✓'; check.style.background = 'var(--green)'; check.style.borderColor = 'var(--green)'; check.style.color = '#fff'; tasksDone++; } else { check.textContent = ''; check.style.background = ''; check.style.borderColor = 'var(--border)'; check.style.color = ''; tasksDone = Math.max(0, tasksDone-1); } const td = document.getElementById('tasksDone'); if(td) td.textContent = tasksDone + ' / 5'; }// ── LOG DAY ─────────────────────────────── function logDay() { PREM.streak++; try { localStorage.setItem('nbme_streak', PREM.streak); } catch(e){} const sn = document.getElementById('streakNum'); if(sn) sn.textContent = PREM.streak; const hs = document.getElementById('heroPremStreak'); if(hs) hs.textContent = PREM.streak + '🔥'; const btn = document.getElementById('logBtn'); btn.innerHTML = '✅ Day Logged! +1 Streak'; btn.style.background = 'var(--green)'; btn.disabled = true; setTimeout(() => { btn.innerHTML = ' Mark Day Complete'; btn.style.background = 'var(--teal)'; btn.disabled = false; }, 3000); }// ── FALLBACK QUESTIONS — Subject-Specific ─ function getFallbackQs(subject) { const ALL = { 'Pathology': [ {id:1,question:`A 55-year-old smoker presents with hemoptysis, weight loss, and a central lung mass on CXR. Biopsy shows large cells with intercellular bridges and keratin pearls. What is the most likely diagnosis?`,options:['A) Adenocarcinoma','B) Squamous cell carcinoma','C) Small cell carcinoma','D) Large cell carcinoma','E) Carcinoid tumor'],correct:1,explanation:`Squamous cell carcinoma arises centrally from bronchial epithelium. Intercellular bridges (desmosomes) and keratin pearls are hallmarks. Strongly associated with smoking.`,keyPoint:`Squamous cell = central, keratin pearls, intercellular bridges, hypercalcemia (PTHrP)`,difficulty:'Medium'}, {id:2,question:`A 45-year-old presents with fatigue, MCV 110 fL, hypersegmented neutrophils, and normal serum iron. Which process is most likely impaired?`,options:['A) Heme synthesis','B) DNA synthesis','C) Globin chain production','D) Iron absorption','E) Erythropoietin signaling'],correct:1,explanation:`Megaloblastic anemia results from impaired DNA synthesis due to B12 or folate deficiency. This causes large, immature RBCs and hypersegmented neutrophils.`,keyPoint:`Megaloblastic = impaired DNA synthesis; macro-ovalocytes + hypersegmented neutrophils`,difficulty:'Medium'}, {id:3,question:`A 30-year-old man has nephrolithiasis, elevated serum calcium, elevated PTH, and one enlarged parathyroid gland on neck exploration. What is the pathology?`,options:['A) Parathyroid hyperplasia','B) Parathyroid adenoma','C) Parathyroid carcinoma','D) Ectopic PTHrP production','E) Vitamin D toxicity'],correct:1,explanation:`Parathyroid adenoma causes 85% of primary hyperparathyroidism. A single hyperfunctioning gland suppresses the remaining glands.`,keyPoint:`Primary hyperPTH: adenoma (85%) > hyperplasia (15%) > carcinoma (<1%)`,difficulty:'Easy'}, {id:4,question:`A 60-year-old smoker with SCLC develops hyponatremia (Na 118). Labs show low serum osmolality and urine osmolality > serum osmolality. What is the mechanism?`,options:['A) Adrenal insufficiency','B) Ectopic ADH secretion (SIADH)','C) Cerebral salt wasting','D) Hypothyroidism','E) Thiazide diuretic use'],correct:1,explanation:`Small cell carcinoma is neuroendocrine and secretes ectopic ADH, causing SIADH with euvolemic hyponatremia and inappropriately concentrated urine.`,keyPoint:`SCLC ectopic: ADH (SIADH), ACTH (Cushing), anti-Hu antibodies (limbic encephalitis)`,difficulty:'Medium'}, {id:5,question:`A 50-year-old woman has a breast mass biopsy showing cells with E-cadherin loss and cells arranged in a single-file pattern. What is the most likely diagnosis?`,options:['A) Invasive ductal carcinoma','B) Invasive lobular carcinoma','C) Ductal carcinoma in situ','D) Phyllodes tumor','E) Fibroadenoma'],correct:1,explanation:`Invasive lobular carcinoma classically loses E-cadherin expression and shows single-file (Indian file) infiltrating pattern. It is often bilateral and multifocal.`,keyPoint:`Lobular carcinoma = E-cadherin loss, single-file pattern, bilateral tendency`,difficulty:'Hard'} ], 'Pharmacology': [ {id:1,question:`A patient on isoniazid for TB prophylaxis develops peripheral neuropathy. What is the mechanism of this adverse effect?`,options:['A) Direct axonal toxicity','B) Functional pyridoxine (B6) deficiency','C) Folate depletion','D) Mitochondrial dysfunction','E) Demyelination via immune complex'],correct:1,explanation:`Isoniazid inhibits pyridoxal phosphokinase, causing functional B6 deficiency. B6 is essential for myelin synthesis. Supplement B6 to prevent neuropathy.`,keyPoint:`INH: peripheral neuropathy (B6 def), hepatotoxicity, SLE-like; always supplement B6`,difficulty:'Medium'}, {id:2,question:`A 70-year-old man with atrial fibrillation on warfarin starts rifampin for TB. His INR drops from 2.5 to 1.1. Why?`,options:['A) Rifampin inhibits CYP450','B) Rifampin induces CYP450, increasing warfarin metabolism','C) Rifampin binds vitamin K receptors','D) Rifampin inhibits warfarin absorption','E) Rifampin activates clotting factors'],correct:1,explanation:`Rifampin is a potent CYP450 inducer. It accelerates warfarin metabolism, reducing its plasma level and anticoagulant effect. Dose adjustment required.`,keyPoint:`Rifampin = classic CYP inducer (remember: Rifampin, Phenytoin, Carbamazepine, St. John's Wort)`,difficulty:'Medium'}, {id:3,question:`A patient taking sildenafil for erectile dysfunction is brought to the ED with severe hypotension after taking a tablet prescribed for chest pain. What was the second drug?`,options:['A) Aspirin','B) Metoprolol','C) Nitroglycerin','D) Amlodipine','E) Lisinopril'],correct:2,explanation:`Both nitrates and PDE5 inhibitors (sildenafil) increase cGMP and cause vasodilation. Combined use causes dangerous synergistic hypotension. This combination is absolutely contraindicated.`,keyPoint:`Sildenafil + nitrates = life-threatening hypotension; absolute contraindication`,difficulty:'Easy'}, {id:4,question:`A 35-year-old woman with myasthenia gravis is treated with pyridostigmine. Which best describes its mechanism?`,options:['A) Stimulates nicotinic receptors directly','B) Inhibits acetylcholinesterase reversibly','C) Blocks muscarinic receptors','D) Inhibits choline reuptake','E) Releases acetylcholine from nerve terminals'],correct:1,explanation:`Pyridostigmine is a reversible AChE inhibitor. By preventing ACh breakdown at the NMJ, it increases available ACh to compete with autoantibodies blocking nicotinic receptors.`,keyPoint:`Myasthenia = autoAb vs nicotinic receptors; treat with AChE inhibitors (pyridostigmine)`,difficulty:'Medium'}, {id:5,question:`A patient with bipolar disorder on lithium develops tremor, polyuria, and confusion after starting ibuprofen. What is the mechanism?`,options:['A) Ibuprofen inhibits lithium metabolism','B) NSAIDs reduce renal prostaglandins, decreasing lithium excretion','C) Ibuprofen displaces lithium from protein binding','D) NSAIDs enhance lithium CNS penetration','E) Ibuprofen inhibits lithium absorption'],correct:1,explanation:`NSAIDs inhibit prostaglandin synthesis, reducing renal blood flow and GFR. Lithium clearance decreases, leading to toxic accumulation. Use acetaminophen instead.`,keyPoint:`Lithium toxicity: NSAIDs, thiazides, and dehydration all raise lithium levels`,difficulty:'Hard'} ], 'Physiology': [ {id:1,question:`A patient with severe vomiting has pH 7.52, pCO2 48 mmHg, HCO3 38 mEq/L. What is the primary acid-base disorder?`,options:['A) Respiratory alkalosis','B) Metabolic acidosis','C) Metabolic alkalosis with respiratory compensation','D) Respiratory acidosis','E) Mixed metabolic and respiratory alkalosis'],correct:2,explanation:`High pH, high HCO3 = metabolic alkalosis. Elevated pCO2 represents appropriate respiratory compensation (hypoventilation retains CO2). Vomiting causes HCl loss.`,keyPoint:`Metabolic alkalosis: vomiting, antacids, hyperaldosteronism; compensation = hypoventilation`,difficulty:'Medium'}, {id:2,question:`A 25-year-old man is at high altitude (4500m). His pO2 is 55 mmHg. Which response is the FIRST to occur?`,options:['A) Increased erythropoietin production','B) Increased 2,3-DPG in RBCs','C) Hyperventilation via peripheral chemoreceptors','D) Renal HCO3 retention','E) Increased Hb synthesis'],correct:2,explanation:`Peripheral chemoreceptors (carotid and aortic bodies) respond to low pO2 immediately, triggering hyperventilation within minutes. Other adaptations take hours to days.`,keyPoint:`Altitude: immediate = hyperventilation (peripheral chemoreceptors); days = EPO, 2,3-DPG`,difficulty:'Medium'}, {id:3,question:`A patient has a right heart catheterization showing: RA=8, RV=45/8, PA=45/20, PCWP=5 mmHg, CO=4. What is the diagnosis?`,options:['A) Left heart failure','B) Cardiac tamponade','C) Primary pulmonary hypertension','D) Mitral stenosis','E) Tricuspid regurgitation'],correct:2,explanation:`Elevated PA pressure with normal PCWP (wedge pressure) indicates pre-capillary pulmonary hypertension, not left-sided disease. Normal PCWP rules out left heart failure and mitral stenosis.`,keyPoint:`PCWP normal = pre-capillary (pulmonary arterial); PCWP high = post-capillary (left heart)`,difficulty:'Hard'}, {id:4,question:`A 40-year-old has a standing-to-supine blood pressure change of +15 mmHg systolic. What physiologic mechanism explains this?`,options:['A) Decreased venous return in supine position','B) Increased preload (venous return) in supine position increases stroke volume','C) Baroreceptor-mediated vasoconstriction','D) Increased heart rate in supine position','E) Aortic valve closure occurs later supine'],correct:1,explanation:`Lying down increases venous return (preload) by redistributing blood from the lower extremities to the thorax, increasing end-diastolic volume and stroke volume via Frank-Starling.`,keyPoint:`Supine = increased preload → increased SV → increased BP; orthostatic hypotension = opposite`,difficulty:'Easy'}, {id:5,question:`In the loop of Henle, what is the primary mechanism by which the thick ascending limb generates the medullary concentration gradient?`,options:['A) Aquaporin-mediated water reabsorption','B) Na-K-2Cl cotransporter (NKCC2) reabsorbing solute without water','C) Urea recycling from collecting duct','D) Na-H exchanger in proximal tubule','E) Vasopressin-stimulated water channels'],correct:1,explanation:`The thick ascending limb is impermeable to water but actively reabsorbs NaCl via NKCC2, diluting the tubular fluid and concentrating the medullary interstitium.`,keyPoint:`Thick ascending limb: NKCC2 (furosemide target); impermeable to water; diluting segment`,difficulty:'Hard'} ], 'Microbiology': [ {id:1,question:`A 22-year-old college student develops fever, headache, stiff neck, and a petechial rash. CSF shows neutrophils, low glucose, high protein. What is the most likely organism?`,options:['A) Streptococcus pneumoniae','B) Neisseria meningitidis','C) Listeria monocytogenes','D) Haemophilus influenzae','E) Cryptococcus neoformans'],correct:1,explanation:`N. meningitidis causes meningococcemia with classic petechial/purpuric rash. Common in college students in dorms. Treat with penicillin G; prophylax contacts with rifampin.`,keyPoint:`N. meningitidis = petechial rash + meningitis; college students; vaccine preventable`,difficulty:'Medium'}, {id:2,question:`A patient with AIDS (CD4=50) develops ring-enhancing brain lesions. Toxoplasma gondii is suspected. How did this patient most likely acquire this infection?`,options:['A) Direct person-to-person transmission','B) Reactivation of latent cysts acquired from cat feces or undercooked meat','C) Inhalation of spores from soil','D) Mosquito bite','E) Transfusion of infected blood'],correct:1,explanation:`Toxoplasma is acquired via cat feces or undercooked meat. In immunocompromised patients, latent cysts reactivate. In AIDS with CD4<100, prophylax with TMP-SMX.`,keyPoint:`Toxo = ring-enhancing lesions in AIDS; reactivation of latent cysts; treat with pyrimethamine+sulfadiazine`,difficulty:'Medium'}, {id:3,question:`A 5-year-old unvaccinated child presents with "barking cough," inspiratory stridor, and a steeple sign on CXR. What is the causative organism?`,options:['A) Bordetella pertussis','B) Haemophilus influenzae type b','C) Parainfluenza virus','D) RSV','E) Staphylococcus aureus'],correct:2,explanation:`Croup (laryngotracheobronchitis) is caused by parainfluenza virus. The "steeple sign" on AP CXR shows subglottic narrowing. Treat with racemic epinephrine and dexamethasone.`,keyPoint:`Croup = parainfluenza; steeple sign; barking cough; treat with dexamethasone + racemic epi`,difficulty:'Easy'}, {id:4,question:`A traveler returns from Southeast Asia with fever, rigors, and splenomegaly. Thick blood smear shows trophozoites with Schüffner dots and enlarged RBCs. Which Plasmodium species?`,options:['A) P. falciparum','B) P. malariae','C) P. vivax','D) P. ovale','E) P. knowlesi'],correct:2,explanation:`P. vivax (and ovale) cause Schüffner dots and enlarged RBCs. P. vivax is most common cause of malaria globally. Forms hypnozoites in liver requiring primaquine to eliminate.`,keyPoint:`Schuffner dots + enlarged RBCs = vivax/ovale; hypnozoites = primaquine needed`,difficulty:'Medium'}, {id:5,question:`A 65-year-old diabetic develops a rapidly spreading, painful, necrotic wound infection with crepitus after a minor foot injury. X-ray shows gas in soft tissues. What is the most likely cause?`,options:['A) Staphylococcus aureus','B) Group A Streptococcus','C) Clostridium perfringens','D) Bacteroides fragilis','E) Pseudomonas aeruginosa'],correct:2,explanation:`Gas gangrene (clostridial myonecrosis) is caused by C. perfringens. Alpha toxin (lecithinase) destroys cell membranes. Crepitus from CO2/H2 gas production. Treat: surgical debridement + penicillin G.`,keyPoint:`Gas gangrene = C. perfringens alpha toxin; gas in tissue; emergency surgical debridement`,difficulty:'Hard'} ], 'Biochemistry': [ {id:1,question:`A newborn has jaundice, hemolytic anemia, and cataracts after breastfeeding. Urine shows reducing substance but negative glucose oxidase test. What enzyme is deficient?`,options:['A) Glucose-6-phosphatase','B) Galactose-1-phosphate uridyltransferase','C) Galactokinase','D) Fructose-1,6-bisphosphatase','E) Aldolase B'],correct:1,explanation:`Classic galactosemia from galactose-1-phosphate uridyltransferase deficiency. Galactose-1-P accumulates, causing liver damage, cataracts, E. coli sepsis, and intellectual disability.`,keyPoint:`Classic galactosemia: GALT deficiency; jaundice + cataracts + E. coli sepsis in newborn`,difficulty:'Medium'}, {id:2,question:`A 6-year-old boy has recurrent severe hypoglycemia after fasting, hepatomegaly, and elevated lactate. Glucagon injection fails to raise blood glucose. What is the deficiency?`,options:['A) Glycogen phosphorylase','B) Glucose-6-phosphatase (Von Gierke disease)','C) Amylo-1,6-glucosidase','D) Liver phosphorylase kinase','E) Debranching enzyme'],correct:1,explanation:`Von Gierke disease (GSD type I) lacks glucose-6-phosphatase. Glucose cannot be released from liver, causing severe fasting hypoglycemia and lactate/triglyceride accumulation.`,keyPoint:`Von Gierke (GSD I) = no G6Pase; severe fasting hypoglycemia; hepatomegaly; elevated lactate`,difficulty:'Hard'}, {id:3,question:`A patient with PKU (phenylketonuria) must avoid phenylalanine. Which enzyme is deficient in classical PKU?`,options:['A) Tyrosine hydroxylase','B) Phenylalanine hydroxylase','C) Homogentisate oxidase','D) Fumarylacetoacetase','E) Dihydropteridine reductase'],correct:1,explanation:`Classical PKU lacks phenylalanine hydroxylase, which converts phenylalanine to tyrosine. Phenylalanine accumulates and is shunted to phenylketones. Musty body odor, intellectual disability, hypopigmentation.`,keyPoint:`PKU = phenylalanine hydroxylase deficiency; musty odor; avoid Phe; supplement Tyr`,difficulty:'Easy'}, {id:4,question:`A patient's cells cannot synthesize cholesterol despite adequate acetyl-CoA. Which enzyme is the rate-limiting step that is most likely inhibited?`,options:['A) Squalene synthase','B) HMG-CoA synthase','C) HMG-CoA reductase','D) Mevalonate kinase','E) Lanosterol synthase'],correct:2,explanation:`HMG-CoA reductase is the rate-limiting enzyme of cholesterol synthesis (mevalonate pathway). Statins inhibit this enzyme competitively, reducing cholesterol synthesis.`,keyPoint:`HMG-CoA reductase = rate-limiting step; statins inhibit here; occurs in cytoplasm`,difficulty:'Easy'}, {id:5,question:`During intense exercise, muscle cells produce pyruvate faster than the TCA cycle can process it. What happens to the excess pyruvate and why?`,options:['A) Excreted in urine as lactic acid','B) Converted to lactate to regenerate NAD+ for continued glycolysis','C) Stored as glycogen immediately','D) Exported to liver for gluconeogenesis without modification','E) Converted to acetyl-CoA by pyruvate dehydrogenase'],correct:1,explanation:`During anaerobic conditions, lactate dehydrogenase converts pyruvate to lactate, regenerating NAD+ to sustain glycolysis. Lactate is exported to the liver (Cori cycle) for gluconeogenesis.`,keyPoint:`Lactate regenerates NAD+; Cori cycle: lactate to liver → glucose back to muscle`,difficulty:'Medium'} ], 'Anatomy': [ {id:1,question:`A patient has a posterior hip dislocation and cannot abduct the leg or feel the lateral thigh. Which nerve is most likely injured?`,options:['A) Femoral nerve','B) Obturator nerve','C) Superior gluteal nerve','D) Sciatic nerve','E) Inferior gluteal nerve'],correct:2,explanation:`Superior gluteal nerve (L4-S1) innervates gluteus medius and minimus (abductors) and tensor fasciae latae. Posterior hip dislocation commonly injures this nerve, causing Trendelenburg gait.`,keyPoint:`Superior gluteal nerve: gluteus medius/minimus + TFL; injury = Trendelenburg gait (hip drops contralateral)`,difficulty:'Hard'}, {id:2,question:`A 45-year-old man has a stab wound at the midaxillary line at the 6th intercostal space. Which structure is MOST likely injured based on anatomy?`,options:['A) Lung only','B) Liver','C) Spleen','D) Stomach','E) Kidney'],correct:2,explanation:`At the midaxillary line, the 6th intercostal space is below the inferior border of the lung on expiration. On the left side, the spleen lies here. On the right, the liver. This question specifies left side anatomy.`,keyPoint:`Left 6th ICS midaxillary = spleen; right 6th ICS midaxillary = liver; know surface anatomy`,difficulty:'Medium'}, {id:3,question:`A patient has wrist drop after a midshaft humeral fracture. Which nerve is damaged and where?`,options:['A) Ulnar nerve at the medial epicondyle','B) Radial nerve in the spiral groove','C) Median nerve at the carpal tunnel','D) Musculocutaneous nerve in the arm','E) Anterior interosseous nerve'],correct:1,explanation:`The radial nerve winds around the spiral (radial) groove of the humerus. Midshaft fractures commonly injure it here, causing wrist drop (loss of wrist/finger extension) and sensory loss over anatomical snuffbox.`,keyPoint:`Radial nerve in spiral groove: wrist drop; midshaft humerus fracture; loss of finger extension`,difficulty:'Easy'}, {id:4,question:`A 55-year-old has a right lower lobe aspiration pneumonia. In which lung segment would you expect to find the aspirated material if the patient was supine?`,options:['A) Right middle lobe','B) Right upper lobe posterior segment','C) Superior segment of right lower lobe','D) Right lower lobe anterior basal segment','E) Right upper lobe apical segment'],correct:2,explanation:`In the supine position, the most dependent segment of the right lung is the superior segment of the right lower lobe. In the upright position, aspiration goes to the right lower lobe basal segments.`,keyPoint:`Supine aspiration = superior segment RLL; upright = basal segments RLL; right lung preferred`,difficulty:'Medium'}, {id:5,question:`During a femoral hernia repair, the surgeon must identify the femoral canal boundaries. Which structure forms the medial border of the femoral canal?`,options:['A) Femoral vein','B) Femoral artery','C) Lacunar (Gimbernat) ligament','D) Inguinal ligament','E) Pectineal ligament'],correct:2,explanation:`The femoral canal boundaries: anterior = inguinal ligament, posterior = pectineal ligament, lateral = femoral vein, medial = lacunar (Gimbernat) ligament. This is where femoral hernias occur.`,keyPoint:`Femoral canal: NAVEL (from lateral) = Nerve, Artery, Vein, Empty space, Lymphatics`,difficulty:'Hard'} ], 'Immunology': [ {id:1,question:`A 6-month-old boy has recurrent bacterial and fungal infections, low lymphocyte count, absent thymic shadow on CXR, and no response to vaccinations. What is the diagnosis?`,options:['A) X-linked agammaglobulinemia','B) DiGeorge syndrome','C) Severe combined immunodeficiency (SCID)','D) Wiskott-Aldrich syndrome','E) Chronic granulomatous disease'],correct:2,explanation:`SCID involves both T and B cell deficiency. The combination of bacterial, viral, and fungal infections plus absent thymic shadow and lymphopenia all point to SCID. Treat with bone marrow transplant.`,keyPoint:`SCID = absent T and B cells; absent thymus; give irradiated, CMV-negative blood; avoid live vaccines`,difficulty:'Medium'}, {id:2,question:`A 16-year-old with recurrent Neisseria infections (gonorrhea x3, meningitis x1) has normal immunoglobulin levels and normal T cells. What is the deficiency?`,options:['A) IgA deficiency','B) C3 deficiency','C) Terminal complement deficiency (C5-C9)','D) MHC class II deficiency','E) NADPH oxidase deficiency'],correct:2,explanation:`Terminal complement (MAC, C5-C9) forms the membrane attack complex against Neisseria. Deficiency specifically predisposes to recurrent encapsulated infections, especially Neisseria species.`,keyPoint:`Terminal complement (C5-C9) deficiency = recurrent Neisseria; MAC cannot be formed`,difficulty:'Hard'}, {id:3,question:`A patient develops urticaria, hypotension, and bronchospasm within minutes of penicillin injection. What mediates this immediate reaction?`,options:['A) IgG antibodies to penicillin','B) T cell cytotoxicity','C) IgE-mediated mast cell degranulation','D) Immune complex deposition','E) Complement activation'],correct:2,explanation:`Type I (immediate) hypersensitivity: IgE antibodies on mast cells bind penicillin antigen → crosslinking → degranulation → histamine, leukotrienes → anaphylaxis.`,keyPoint:`Type I = IgE + mast cells + basophils; anaphylaxis; urticaria; treat with epinephrine`,difficulty:'Easy'}, {id:4,question:`A patient on long-term penicillin develops hemolytic anemia 10 days after starting the drug. Direct Coombs test is positive. What is the mechanism?`,options:['A) IgE mast cell degranulation','B) Drug-antibody complex deposition on RBCs (Type II)','C) Immune complex deposition in vessel walls','D) T cell delayed hypersensitivity','E) Complement alternative pathway'],correct:1,explanation:`Drug-induced hemolytic anemia is Type II hypersensitivity. Drug (penicillin) binds RBC surface → IgG/IgM antibodies → complement activation → hemolysis. Positive Coombs detects antibody-coated RBCs.`,keyPoint:`Type II = IgG/IgM + complement; targets cells; Coombs positive; hemolytic anemia`,difficulty:'Medium'}, {id:5,question:`A patient with a kidney transplant is started on tacrolimus. What is the primary mechanism by which it prevents rejection?`,options:['A) Blocks mTOR pathway inhibiting T cell proliferation','B) Inhibits calcineurin, preventing IL-2 transcription in T cells','C) Depletes T cells via complement','D) Blocks co-stimulation (CD28-B7 interaction)','E) Inhibits purine synthesis in lymphocytes'],correct:1,explanation:`Tacrolimus (FK506) binds FKBP → inhibits calcineurin → prevents NFAT dephosphorylation → no IL-2 gene transcription → T cell activation blocked. Cyclosporine has same mechanism but different binding protein.`,keyPoint:`Tacrolimus = FKBP → calcineurin inhibition → no IL-2; nephrotoxic; same as cyclosporine target`,difficulty:'Hard'} ], 'Behavioral Science': [ {id:1,question:`A physician tells a terminally ill patient the diagnosis of pancreatic cancer. The patient says "I feel fine, there must be a mistake with the test results." Which defense mechanism is this?`,options:['A) Repression','B) Rationalization','C) Denial','D) Projection','E) Reaction formation'],correct:2,explanation:`Denial is the unconscious refusal to acknowledge a painful reality. The patient is not suppressing the information (repression) but actively disbelieving it. Very common initial response to terminal diagnosis.`,keyPoint:`Denial = refusing to believe reality; first stage of Kubler-Ross grief (DABDA)`,difficulty:'Easy'}, {id:2,question:`In a study, smokers were 5x more likely to develop lung cancer than non-smokers (RR=5). Among 10,000 smokers, 200 developed lung cancer vs. 20 of 5,000 non-smokers. What is the attributable risk?`,options:['A) 0.4%','B) 1.6%','C) 2.0%','D) 0.2%','E) 10x'],correct:1,explanation:`Attributable risk = incidence in exposed - incidence in unexposed = (200/10,000) - (20/5,000) = 2% - 0.4% = 1.6%. This represents the excess risk due to smoking.`,keyPoint:`Attributable risk = incidence exposed - incidence unexposed; measures excess risk due to exposure`,difficulty:'Hard'}, {id:3,question:`A 4-year-old boy uses "baby talk" when his new sibling is born. Previously, he was speaking in full sentences. What defense mechanism is this?`,options:['A) Reaction formation','B) Regression','C) Displacement','D) Undoing','E) Sublimation'],correct:1,explanation:`Regression is returning to an earlier stage of development under stress. The child regresses to infant-like behaviors to cope with the stress of a new sibling competing for attention.`,keyPoint:`Regression = return to earlier behavior under stress; mature defense = sublimation`,difficulty:'Easy'}, {id:4,question:`A researcher finds that a new HIV test has 95% sensitivity and 90% specificity. In a population with 1% HIV prevalence, what is the positive predictive value?`,options:['A) 95%','B) 90%','C) ~8.7%','D) 50%','E) ~99%'],correct:2,explanation:`PPV = TP/(TP+FP). In 10,000 people: 100 HIV+ (TP≈95, FN≈5), 9900 HIV- (FP≈990, TN≈8910). PPV = 95/(95+990) = 95/1085 ≈ 8.7%. Low prevalence greatly reduces PPV even with good test.`,keyPoint:`Low prevalence = low PPV even with high sensitivity; PPV and NPV depend on prevalence`,difficulty:'Hard'}, {id:5,question:`A physician notices a patient is attractive and begins spending extra time with them, bringing gifts, and giving preferential treatment. What ethical principle is most directly violated?`,options:['A) Autonomy','B) Beneficence','C) Non-maleficence','D) Justice','E) Fidelity'],correct:3,explanation:`Justice requires fair and equal treatment of all patients. Providing preferential treatment based on personal attraction violates justice. This behavior also risks boundary violations and may harm the patient.`,keyPoint:`Justice = equal/fair treatment; preferential treatment = justice violation; also boundary issue`,difficulty:'Medium'} ] }; // Return subject-specific questions, fallback to Pathology if unknown subject return ALL[subject] || ALL['Pathology']; }// ── PAGE INIT (log session view) ────────── window.addEventListener('DOMContentLoaded', function() { });

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