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  // ===================== SECTION 1: POISONING =====================
  heading1('SECTION 1: POISONING'),

  heading2('A. Organophosphate Poisoning'),

  q('What is the mechanism of organophosphate (OP) poisoning?'),
  a('Organophosphates irreversibly inhibit acetylcholinesterase (AChE), causing accumulation of acetylcholine (ACh) at both muscarinic and nicotinic receptors, leading to cholinergic toxidrome.'),

  q('What are the muscarinic features of OP poisoning? (Mnemonic: SLUDGE / DUMBELS)'),
  a('SLUDGE: Salivation, Lacrimation, Urination, Defecation, GI distress, Emesis. Also: miosis, bradycardia, bronchospasm, bronchorrhoea, diaphoresis. DUMBELS: Defecation/Diarrhea, Urination, Miosis, Bradycardia/Bronchospasm/Bronchorrhoea, Emesis, Lacrimation, Salivation.'),

  q('What are the nicotinic features of OP poisoning?'),
  a('Muscle fasciculations, weakness, paralysis (including respiratory muscles), tachycardia, hypertension, mydriasis. Remember: "MTWHF" – Mydriasis, Tachycardia, Weakness, Hypertension, Fasciculations.'),

  q('What is the CNS effect of OP poisoning?'),
  a('Anxiety, restlessness, seizures, coma, respiratory depression.'),

  q('What is the "intermediate syndrome" in OP poisoning?'),
  a('Occurs 24-96 hours after the acute cholinergic phase (after atropinization). Features: proximal limb muscle weakness, neck flexor weakness, cranial nerve palsies, respiratory muscle weakness. Does NOT respond to atropine or pralidoxime. Lasts 2-3 weeks.'),

  q('What is the delayed neuropathy in OP poisoning?'),
  a('Organophosphate-induced delayed polyneuropathy (OPIDN). Occurs 2-5 weeks after poisoning. Distal symmetrical sensorimotor polyneuropathy (predominantly motor). Due to TOCP (triorthocresyl phosphate). "Dying back" neuropathy from terminal ends of largest myelinated motor fibres.'),

  q('What is the antidote for organophosphate poisoning?'),
  a('1. ATROPINE: Blocks muscarinic effects. Give 2-4 mg IV, repeat every 5-10 minutes until atropinization (dry secretions, HR >80, dry mouth). NO role in nicotinic/CNS effects.\n2. PRALIDOXIME (2-PAM): Reactivates AChE if given within 24-48 hours (before "ageing"). Dose: 1-2 g IV over 15-30 min, then infusion. Effective for both muscarinic AND nicotinic effects.'),

  q('What is "ageing" in OP poisoning?'),
  a('Once AChE-OP complex undergoes dealkylation (ageing), it becomes permanently inhibited and pralidoxime cannot reactivate it. Ageing time varies by compound - some OP compounds age within minutes (e.g., soman), others take hours to days.'),

  q('What investigations are done in OP poisoning?'),
  a('1. Plasma cholinesterase (pseudocholinesterase) - first to fall, faster to recover\n2. RBC cholinesterase (true AChE) - better correlates with severity, slower to recover\n3. ABG, ECG (QTc prolongation), CXR (aspiration/pulmonary oedema)'),

  q('What is the ECG finding in severe OP poisoning?'),
  a('Prolonged QTc interval (due to cholinergic excess affecting cardiac conduction). Also: bradycardia, heart block, ventricular arrhythmias.'),

  divider(),

  heading2('B. Other Important Poisonings'),

  q('What are the features and antidote of organochlorine (OC) poisoning?'),
  a('Features: CNS excitation, seizures (no cholinergic features - key differentiator from OP). Antidote: No specific antidote. Supportive care, benzodiazepines for seizures. Avoid milk/fats (increase absorption).'),

  q('What are the features of CO (carbon monoxide) poisoning?'),
  a('CO binds Hb with 250x affinity vs O2, forming carboxyhemoglobin (COHb). Features: Headache, dizziness, cherry-red skin, coma, death. SpO2 is falsely normal. Treatment: 100% O2, hyperbaric O2 if severe (COHb >25%, cardiac involvement, neurological features).'),

  q('What are the features and treatment of paracetamol poisoning?'),
  a('Toxic metabolite NAPQI depletes glutathione and causes hepatic necrosis. Stages: 1) 0-24h: N/V, 2) 24-72h: RUQ pain, elevated LFTs, 3) 72-96h: fulminant hepatic failure. Treatment: N-acetylcysteine (NAC) - replenishes glutathione. Effective up to 24h; use Rumack-Matthew nomogram.'),

  q('What are features of opioid poisoning?'),
  a('Classic triad: Miosis (pinpoint pupils), CNS depression, Respiratory depression. Antidote: Naloxone (opioid receptor antagonist) 0.4-2 mg IV/IM, repeat every 2-3 min.'),

  q('What are features of tricyclic antidepressant (TCA) poisoning?'),
  a('3 Cs: Cardiotoxicity (wide QRS, QTc prolongation, ventricular arrhythmias), Convulsions, Coma. Also anticholinergic features (dry, hot, dilated). Treatment: Sodium bicarbonate (narrows QRS, prevents arrhythmias).'),

  q('What are features and treatment of methanol poisoning?'),
  a('Toxin: formic acid (from methanol metabolism by ADH) damages optic nerve and causes high AG metabolic acidosis. Features: visual disturbances, blindness, severe metabolic acidosis. Treatment: Fomepizole (ADH inhibitor) or ethanol (competitive ADH substrate), folate, dialysis.'),

  q('What are features and treatment of benzodiazepine poisoning?'),
  a('CNS and respiratory depression (milder than opioids). Antidote: Flumazenil (competitive GABA-A antagonist). Caution: do NOT use in chronic BZD users or TCA co-ingestion (precipitates seizures).'),

  q('What are the features of cyanide poisoning?'),
  a('Inhibits cytochrome c oxidase (Complex IV) - blocks cellular respiration. Features: bitter almond breath, rapid coma, "venous blood appears arterial" (high venous pO2). Treatment: Hydroxocobalamin (preferred), sodium nitrite + sodium thiosulfate.'),

  q('What is the approach to an unconscious poisoned patient?'),
  a('A-B-C first. DONT: Dextrose 50ml IV, O2, Naloxone 0.4mg IV, Thiamine 100mg IV. Then: identify poison, decontaminate (activated charcoal if <1h, alert, no contraindications), specific antidote, supportive care.'),

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  // ===================== SECTION 2: CARDIOMEGALY =====================
  heading1('SECTION 2: CARDIOMEGALY'),

  q('How is cardiomegaly defined on a chest X-ray?'),
  a('Cardiothoracic ratio (CTR) > 0.5 on a PA CXR. (Heart diameter / widest thoracic diameter). On an AP view, CTR > 0.55 is used (AP views slightly magnify the heart).'),

  q('What are the causes of cardiomegaly?'),
  a('Mnemonic: "PAID HEART"\nP - Pericardial effusion (most common cause of globular/flask-shaped enlargement)\nA - Anaemia (chronic)\nI - Ischaemic cardiomyopathy\nD - Dilated cardiomyopathy\nH - Hypertensive heart disease / High output states (thyrotoxicosis, AV fistula, beriberi)\nE - Endocrine (acromegaly, hypothyroidism)\nA - Amyloidosis / Athletes heart (physiological)\nR - Rheumatic heart disease / Regurgitant valvular lesions (AR, MR)\nT - Toxins (alcohol, doxorubicin)'),

  q('How do you differentiate pericardial effusion from cardiomegaly on CXR?'),
  a('Pericardial effusion: "Flask-shaped" or "water bottle" heart, clear lung fields (no pulmonary oedema), rapidly changing cardiac silhouette over days. True cardiomegaly: irregular or specific chamber enlargement, pulmonary plethora/oedema may be present. Echocardiography is gold standard to differentiate.'),

  q('What are the CXR features of left ventricular enlargement?'),
  a('Boot-shaped heart (coeur en sabot). Lateral CXR: LV extends posteriorly. Causes: hypertension, aortic stenosis, aortic regurgitation, hypertrophic cardiomyopathy, DCMP.'),

  q('What are the CXR features of right ventricular enlargement?'),
  a('On PA CXR: RV enlargement is not prominent in PA view. On lateral CXR: RV fills the retrosternal space (loss of retrosternal air space). Causes: pulmonary hypertension, pulmonary stenosis, ASD, Cor pulmonale.'),

  q('What are the CXR features of left atrial enlargement?'),
  a('Double opacity at right cardiac border, elevation of left main bronchus (angle >70 degrees), splaying of carina, prominent left atrial appendage (loss of left heart border concavity). Causes: mitral stenosis (classic).'),

  q('What is the echocardiographic approach to cardiomegaly?'),
  a('Assess: 1) LV size and function (EF, wall motion), 2) RV size and function, 3) Pericardial effusion, 4) Wall thickness (hypertrophy vs dilation), 5) Valvular lesions, 6) Regional wall motion abnormalities.'),

  q('What blood tests are done in cardiomegaly workup?'),
  a('CBC (anaemia), TFT (hypothyroidism, thyrotoxicosis), LFT, RFT, FBS, Lipid profile, ECG, BNP/NT-proBNP, Cardiac biomarkers (troponin), Chest X-ray, Echo.'),

  divider(),

  // ===================== SECTION 3: MYOCARDITIS =====================
  heading1('SECTION 3: MYOCARDITIS'),

  q('What is myocarditis? What are its causes?'),
  a('Inflammation of the myocardium. Causes:\n1. VIRAL (most common - 50%): Coxsackievirus B (most common), adenovirus, parvovirus B19, HIV, CMV, influenza, COVID-19\n2. BACTERIAL: Diphtheria (myocarditis is leading cause of death), typhoid, leptospirosis, Chagas disease (T. cruzi)\n3. PARASITIC: Trypanosoma cruzi (Chagas - chronic dilated cardiomyopathy), Toxoplasma\n4. DRUGS/TOXINS: Anthracyclines, clozapine, cocaine, alcohol\n5. AUTOIMMUNE: SLE, sarcoidosis, giant cell myocarditis\n6. IDIOPATHIC: ~50% of cases'),

  q('What is the most common viral cause of myocarditis?'),
  a('Coxsackievirus B (Group B Coxsackievirus) - an enterovirus. Epidemics occur in summer and early autumn. More common in males and children.'),

  q('What are the clinical features of myocarditis?'),
  a('1. Prodrome: 1-2 weeks prior viral illness (fever, URI, GI symptoms)\n2. Chest pain (can mimic MI - precordial, continuous, pleuritic component)\n3. Dyspnea, fatigue, palpitations\n4. Signs of heart failure: tachycardia, S3 gallop, pulmonary oedema\n5. Arrhythmias and conduction blocks\n6. In severe cases: cardiogenic shock, sudden death'),

  q('What are the ECG findings in myocarditis?'),
  a('Non-specific ST-T changes, sinus tachycardia, PR prolongation, bundle branch blocks, ventricular arrhythmias. ST elevation can mimic MI (diffuse ST elevation without reciprocal changes - similar to pericarditis). AV blocks are common with Lyme disease and diphtheria.'),

  q('What are the investigations in myocarditis?'),
  a('1. ECG: ST-T changes, arrhythmias\n2. Troponin I/T: elevated (myocyte necrosis) - marker of severity\n3. BNP/NT-proBNP: elevated in heart failure\n4. Echo: LV dysfunction, wall motion abnormalities, pericardial effusion\n5. Cardiac MRI: gold standard for non-invasive diagnosis - shows myocardial oedema (T2), late gadolinium enhancement (LGE) in a non-ischaemic pattern (mid-wall or epicardial)\n6. Endomyocardial biopsy: definitive/gold standard, used in severe/refractory cases. Shows: lymphocytic infiltration + myocyte necrosis (Dallas criteria)'),

  q('What are the Dallas criteria for myocarditis on endomyocardial biopsy?'),
  a('Active myocarditis: inflammatory infiltrate (predominantly lymphocytes) + myocyte necrosis/damage.\nBorderline myocarditis: inflammatory infiltrate without myocyte necrosis (repeat biopsy recommended).'),

  q('What is the treatment of myocarditis?'),
  a('1. SUPPORTIVE: Rest (restrict activity for 6 months in athletes), treat HF (ACEi, beta-blockers, diuretics, spironolactone), antiarrhythmics\n2. NO NSAIDs (worsen myocardial damage in early phase)\n3. SPECIFIC:\n  - Viral: Antiviral if specific (e.g., HIV - ART; CMV - ganciclovir)\n  - Diphtheria: Antitoxin + penicillin (prevent cardiac death)\n  - Lyme: Doxycycline or ceftriaxone\n  - Autoimmune/Giant cell: Immunosuppression (steroids + azathioprine)\n  - Chagas: Benznidazole or nifurtimox (in acute phase)\n4. IVIG: Used in pediatric myocarditis and fulminant myocarditis\n5. Mechanical support: IABP, VAD in cardiogenic shock\n6. Heart transplant: end-stage'),

  q('What is fulminant myocarditis?'),
  a('Acute onset severe cardiac dysfunction with haemodynamic compromise (cardiogenic shock). Despite severity, prognosis is better than non-fulminant myocarditis with aggressive support. "Recovery or death" pattern - survivors have near-normal cardiac function. More often caused by viral infections. Requires mechanical circulatory support.'),

  q('What are the complications of myocarditis?'),
  a('1. Dilated cardiomyopathy (most important long-term complication) - 10-20% progress\n2. Arrhythmias and sudden cardiac death\n3. Complete heart block\n4. Cardiac tamponade (if associated pericarditis)\n5. Cardiogenic shock'),

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  // ===================== SECTION 4: PERICARDIAL EFFUSION =====================
  heading1('SECTION 4: PERICARDIAL EFFUSION'),

  q('What is a pericardial effusion?'),
  a('Abnormal accumulation of fluid in the pericardial space. Normal pericardial fluid: 15-50 mL. Effusions are classified by size: Small <100 mL, Moderate 100-500 mL, Large >500 mL. Also classified by type: transudative, exudative, haemorrhagic, chylous.'),

  q('What are the causes of pericardial effusion?'),
  a('Mnemonic: "CARDIAC MITES"\nC - Cancer (metastatic - lung, breast most common; lymphoma)\nA - Autoimmune (SLE - most common autoimmune, RA, scleroderma)\nR - Renal (uraemia - uraemic pericarditis)\nD - Drugs (hydralazine, procainamide, isoniazid, doxorubicin, cyclosporine)\nI - Infectious (viral >bacterial; TB - common in endemic areas, HIV)\nA - After MI (Dressler syndrome - autoimmune, 2-10 weeks post-MI)\nC - Cardiac (post-cardiac surgery, post-pericardiotomy syndrome)\n\nM - Myxoedema (hypothyroidism - classic cause of large effusion)\nI - Idiopathic (most common cause in developed countries)\nT - Trauma\nE - post-radiation pericarditis\nS - Sarcoidosis'),

  q('What is Beck\'s triad?'),
  a('Classic triad of cardiac tamponade:\n1. Hypotension (decreased cardiac output)\n2. Raised JVP (JVD - distended neck veins)\n3. Muffled/distant heart sounds\nRemember: "HMJ" - Hypotension, Muffled sounds, JVD'),

  q('What is pulsus paradoxus?'),
  a('Exaggerated decrease in systolic BP >10 mmHg during inspiration (normal is ≤10 mmHg). Mechanism: Inspiration → increased RV filling → septum shifts left → reduced LV filling → reduced SV → reduced BP. Seen in: cardiac tamponade, severe asthma/COPD, constrictive pericarditis.'),

  q('When does pulsus paradoxus NOT occur despite tamponade?'),
  a('1. Severe aortic regurgitation\n2. Atrial septal defect\n3. Pre-existing elevated LV diastolic pressure (LV failure)\n4. Regional (loculated) tamponade\n5. Severe pulmonary hypertension'),

  q('What is Ewart\'s sign in pericardial effusion?'),
  a('In large pericardial effusion: dullness to percussion, bronchial breathing, and aegophony below the angle of the left scapula (due to compression of left lower lobe). Also called "Pins sign."'),

  q('What are the ECG findings in pericardial effusion?'),
  a('1. Low voltage complexes (QRS amplitude <5 mm in limb leads, <10 mm in chest leads)\n2. Electrical alternans (beat-to-beat variation in QRS amplitude/axis) - PATHOGNOMONIC of cardiac tamponade - heart swinging in pericardial fluid\n3. Sinus tachycardia'),

  q('What are the CXR findings in pericardial effusion?'),
  a('1. Cardiomegaly - "Water bottle" or "flask-shaped" heart\n2. Obliteration of normal cardiac contours\n3. Clear lung fields (distinguishes from cardiac failure)\n4. "Fat pad sign" - separation between pericardial fat lines (rarely seen)'),

  q('What is the echocardiographic finding in cardiac tamponade?'),
  a('1. Diastolic collapse of the right atrium (first sign - most sensitive)\n2. Diastolic collapse of the right ventricle (more specific for tamponade)\n3. IVC plethora (dilated IVC >2.1 cm without inspiratory collapse)\n4. Respiratory variation in mitral/tricuspid inflow velocities >25%\n5. Swinging motion of the heart'),

  q('What is the treatment of pericardial effusion?'),
  a('Depends on cause and haemodynamic significance:\n1. TREAT UNDERLYING CAUSE: antibiotics, antitubercular therapy, steroids for autoimmune\n2. NSAIDs + Colchicine: for inflammatory pericardial effusion\n3. PERICARDIOCENTESIS: Indicated in cardiac tamponade (emergency), large effusion, diagnostic tap for unknown cause. Approach: subxiphoid (most common), apical, parasternal. Echo-guided preferred.\n4. PERICARDIOSTOMY/WINDOW: for recurrent effusions\n5. PERICARDIECTOMY: for constrictive pericarditis'),

  q('What is the Dressler\'s syndrome?'),
  a('Post-MI pericarditis (also called post-cardiac injury syndrome). Onset: 2-10 weeks after MI or cardiac surgery. Mechanism: autoimmune (anti-heart antibodies). Features: fever, pleuritic chest pain, pericardial effusion, elevated ESR, CRP. Treatment: NSAIDs (aspirin preferred post-MI), colchicine, steroids.'),

  q('What is the difference between cardiac tamponade and constrictive pericarditis?'),
  a('Feature | Tamponade | Constriction\nJVP: Elevated, absent y descent | Elevated, prominent x AND y descent (Friedreich\'s sign)\nPulsus paradoxus: Present | Usually absent (may be present)\nKussmaul\'s sign: Absent | Present (JVP rises on inspiration)\nECG: Electrical alternans | Low voltage, no alternans\nEcho: RA/RV collapse, IVC plethora | Septal bounce (septal "knock")\nPericardium: Effusion | Thickened, calcified'),

  q('What is Kussmaul\'s sign?'),
  a('Paradoxical rise (or failure to fall) of JVP on inspiration. Normally JVP falls on inspiration. Seen in: Constrictive pericarditis (most classic), RV failure, RV infarction, restrictive cardiomyopathy, cardiac tamponade (rarely).'),

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  divider(),
  spacer(),
  new Paragraph({
    children: [new TextRun({ text: 'HOW TO USE THIS FILE', bold: true, size: 24, color: '1F3864' })],
    spacing: { after: 60 },
  }),
  bullet('Each case is followed by structured questions with marks weightage (10 or 5 marks)'),
  bullet('Answer each question before looking at the model answer'),
  bullet('10-mark answers: Write 8-10 points with headings (Classification / Pathophysiology / Clinical / Ix / Management)'),
  bullet('5-mark answers: Write 4-6 focused points'),
  bullet('Examiner tip boxes are included to highlight what examiners look for'),
  spacer(),
  divider(),
);

// ═══════════════════════════════════════════════════════════════
// SECTION 1: POISONING CASES
// ═══════════════════════════════════════════════════════════════
children.push(sectionTitle('SECTION 1: POISONING'), spacer());

// ── CASE 1 (10-mark) ─────────────────────────────────────────
children.push(
  h2('CASE 1'),
  caseBox([
    'A 32-year-old farmer is brought to the emergency department by his family.',
    'He was found unconscious in his field 2 hours ago. His clothes smell of a chemical.',
    'On examination: GCS 8/15, pupils bilaterally pinpoint (miosis), HR 46/min,',
    'BP 90/60 mmHg, RR 28/min, SpO2 88% on room air.',
    'Excessive secretions from mouth and nose are noted. Diffuse wheeze on auscultation.',
    'Muscle fasciculations are seen over both thighs. Bladder is palpable.',
  ]),
  spacer(),
  markBadge('10 MARKS'),
  questionPara(1, 'What is the most likely diagnosis? Discuss the pathophysiology, clinical features, investigations, and management of this condition. (10 marks)'),
  spacer(),

  answerHeading('Organophosphate (OP) Poisoning'),
  spacer(),

  h2('1. Diagnosis'),
  bullet('Organophosphate poisoning (pesticide/insecticide exposure in a farmer)'),
  bullet('Classic triad: miosis + bradycardia + secretions (cholinergic toxidrome)'),
  bullet('Chemical smell on clothes, fasciculations, bladder retention, bronchospasm'),
  spacer(),

  h2('2. Pathophysiology (2 marks)'),
  bullet('OPs irreversibly inhibit acetylcholinesterase (AChE)'),
  bullet('→ Accumulation of acetylcholine (ACh) at synapses'),
  bullet('→ Excessive stimulation of:'),
  subBullet('Muscarinic receptors (smooth muscle, glands, heart)'),
  subBullet('Nicotinic receptors (NMJ, autonomic ganglia)'),
  subBullet('Central nervous system receptors'),
  bullet('"Ageing": irreversible phosphorylation of AChE over time (hours to days) → pralidoxime ineffective after ageing'),
  spacer(),

  h2('3. Clinical Features (2 marks)'),
  bullet('MUSCARINIC ("SLUDGE / DUMBELS"):'),
  subBullet('Salivation, Lacrimation, Urination, Defecation, GI cramps, Emesis'),
  subBullet('Miosis, Bradycardia, Bronchospasm + Bronchorrhoea, Diaphoresis'),
  bullet('NICOTINIC:'),
  subBullet('Muscle fasciculations → weakness → flaccid paralysis (including respiratory)'),
  subBullet('Tachycardia, Hypertension, Mydriasis (can oppose muscarinic miosis)'),
  bullet('CNS: anxiety, seizures, coma, respiratory depression'),
  spacer(),

  h2('4. Investigations (2 marks)'),
  bullet('RBC cholinesterase (true AChE): best correlates with severity, slow to recover'),
  bullet('Plasma (pseudo)cholinesterase: first to fall, faster to recover'),
  bullet('ABG: hypoxia, metabolic acidosis'),
  bullet('ECG: prolonged QTc, bradycardia, heart block'),
  bullet('Blood glucose, electrolytes, RFT, LFT'),
  bullet('Urine: organophosphate metabolites (alkyl phosphates)'),
  spacer(),

  h2('5. Management (4 marks)'),
  bullet('IMMEDIATE: ABC stabilization, remove contaminated clothing (decontamination)'),
  bullet('High-flow O2, IV access, cardiac monitor'),
  bullet('ATROPINE (Muscarinic blocker):'),
  subBullet('2-4 mg IV bolus, repeat every 5-10 minutes'),
  subBullet('End point: ATROPINIZATION - dry secretions, HR >80/min, clear chest, dry skin (NOT pupil dilation)'),
  subBullet('May need 20-100 mg in severe cases'),
  subBullet('No role against nicotinic or CNS effects'),
  bullet('PRALIDOXIME (2-PAM, Oxime):'),
  subBullet('1-2 g IV over 15-30 min, then 500 mg/hr infusion'),
  subBullet('Reactivates AChE BEFORE ageing'),
  subBullet('Give within 24-48 hours of exposure'),
  subBullet('Effective against nicotinic AND muscarinic effects'),
  bullet('BENZODIAZEPINES: for seizures (diazepam 5-10 mg IV)'),
  bullet('Avoid succinylcholine (cholinesterase substrate - prolonged paralysis)'),
  bullet('ICU monitoring, ventilator support if respiratory failure'),
  spacer(),

  keypoint('The end point of atropinization is DRY secretions and clear chest - NOT dilated pupils. Pupils are an unreliable end point.'),
  keypoint('Intermediate syndrome (24-96h): proximal weakness, respiratory failure - does NOT respond to atropine or pralidoxime.'),
  divider(),
);

// ── CASE 2 (5-mark) ──────────────────────────────────────────
children.push(
  h2('CASE 2'),
  caseBox([
    'A 28-year-old medical student is brought to casualty after being found unresponsive',
    'in his hostel room. Empty blister packs of a tablet are found nearby.',
    'Examination: GCS 9/15, bilaterally pinpoint pupils, RR 8/min, SpO2 84%,',
    'HR 58/min. No other significant findings.',
  ]),
  spacer(),
  markBadge('5 MARKS'),
  questionPara(2, 'What is the most likely diagnosis? What is the antidote and its mechanism? What are the precautions when using the antidote? (5 marks)'),
  spacer(),

  answerHeading('Opioid Poisoning (Overdose)'),
  spacer(),

  h2('Diagnosis (1 mark)'),
  bullet('Classic triad: Miosis (pinpoint pupils) + CNS depression + Respiratory depression'),
  bullet('Opioid overdose (likely oral opioid tablets from blister packs)'),
  spacer(),

  h2('Antidote and Mechanism (2 marks)'),
  bullet('NALOXONE (Narcan) - competitive opioid receptor antagonist'),
  bullet('Mechanism: competes with opioids at mu (µ), kappa (κ), delta (δ) receptors - blocks and reverses all opioid effects'),
  bullet('Dose: 0.4-2 mg IV/IM/intranasal, repeat every 2-3 minutes (max 10 mg)'),
  bullet('Onset: IV 1-2 min, IM 5 min. Duration: 30-90 min (shorter than most opioids)'),
  bullet('Watch for re-narcotization: naloxone wears off before opioid → repeat doses or infusion may be needed'),
  spacer(),

  h2('Precautions (2 marks)'),
  bullet('Precipitates acute opioid withdrawal in dependent users (agitation, seizures, pulmonary oedema)'),
  bullet('Short half-life → re-sedation common; observe for minimum 4-6 hours after last dose'),
  bullet('In opioid-dependent patients: start with low dose (0.1-0.4 mg) to avoid abrupt withdrawal'),
  bullet('Naloxone infusion if long-acting opioids (methadone, fentanyl patch): 2/3 of initial effective dose/hour'),
  bullet('Not effective for non-opioid respiratory depression (benzodiazepines need flumazenil)'),
  spacer(),

  keypoint('Pinpoint pupils + respiratory depression + response to naloxone = opioid toxidrome. Miosis + CNS depression WITHOUT respiratory depression suggests other causes.'),
  divider(),
);

// ── CASE 3 (5-mark) ──────────────────────────────────────────
children.push(
  h2('CASE 3'),
  caseBox([
    'A 45-year-old woman is brought to casualty with altered consciousness.',
    'Husband reports she took 30 tablets of paracetamol (500 mg each) 18 hours ago.',
    'She has nausea and vomiting, RUQ abdominal pain.',
    'Labs: AST 2400 IU/L, ALT 1980 IU/L, PT 28 seconds, Creatinine 2.1 mg/dL.',
  ]),
  spacer(),
  markBadge('5 MARKS'),
  questionPara(3, 'Discuss the pathophysiology of liver injury in paracetamol poisoning and its management. (5 marks)'),
  spacer(),

  answerHeading('Paracetamol (Acetaminophen) Poisoning'),
  spacer(),

  h2('Pathophysiology of Liver Injury (2 marks)'),
  bullet('Normal metabolism: 90% via glucuronidation/sulfation → non-toxic conjugates'),
  bullet('Toxic dose: CYP2E1 pathway overwhelmed → forms NAPQI (N-acetyl-p-benzoquinone imine)'),
  bullet('NAPQI normally detoxified by glutathione (GSH)'),
  bullet('Toxic dose depletes GSH → NAPQI accumulates → covalent binding to hepatocytes → Zone 3 (centrilobular) necrosis'),
  bullet('Stages: Stage 1 (0-24h): N/V | Stage 2 (24-72h): LFT rise, RUQ pain | Stage 3 (72-96h): fulminant hepatic failure | Stage 4 (4d-2wk): recovery or death'),
  spacer(),

  h2('Management (3 marks)'),
  bullet('N-ACETYLCYSTEINE (NAC) - cornerstone of treatment:'),
  subBullet('Replenishes glutathione stores'),
  subBullet('IV protocol: 150 mg/kg in 200 mL D5W over 1h, then 50 mg/kg over 4h, then 100 mg/kg over 16h'),
  subBullet('Effective up to 24h; continue even beyond 24h in severe cases'),
  bullet('Use RUMACK-MATTHEW nomogram: plot serum paracetamol level vs time post-ingestion to guide NAC use'),
  bullet('Activated charcoal: if within 1-2 hours of ingestion (alert patient, no contraindications)'),
  bullet('Monitor: LFT, PT/INR, RFT, blood glucose (hypoglycaemia common)'),
  bullet('Liver transplant criteria (King\'s College Criteria): pH <7.3, OR all three: PT >100s + creatinine >3.4 mg/dL + Grade III/IV encephalopathy'),
  spacer(),

  keypoint('NAC is most effective if given within 8 hours of ingestion. Do NOT wait for LFT results before starting NAC in a patient with known paracetamol overdose.'),
  divider(),
);

// ═══════════════════════════════════════════════════════════════
// SECTION 2: CARDIOMEGALY CASES
// ═══════════════════════════════════════════════════════════════
children.push(sectionTitle('SECTION 2: CARDIOMEGALY'), spacer());

// ── CASE 4 (10-mark) ─────────────────────────────────────────
children.push(
  h2('CASE 4'),
  caseBox([
    'A 52-year-old man presents with progressive exertional dyspnoea for 6 months,',
    'orthopnea, and bilateral pedal oedema. He is a chronic alcoholic.',
    'On examination: BP 110/70 mmHg, HR 112/min (irregular), JVP raised 5 cm,',
    'apex beat displaced to 6th intercostal space, anterior axillary line.',
    'S3 gallop heard. Bibasal crepitations. 2+ pitting oedema up to knees.',
    'CXR: Cardiothoracic ratio 0.62, upper lobe diversion, Kerley B lines.',
  ]),
  spacer(),
  markBadge('10 MARKS'),
  questionPara(4, 'Discuss cardiomegaly - its causes, radiological assessment, and the approach to this patient including investigations and management. (10 marks)'),
  spacer(),

  answerHeading('Cardiomegaly - Dilated Cardiomyopathy (Alcoholic)'),
  spacer(),

  h2('1. Definition and Radiological Criteria (1 mark)'),
  bullet('Cardiothoracic ratio (CTR) > 0.5 on PA CXR'),
  bullet('This patient: CTR 0.62 (significantly enlarged)'),
  spacer(),

  h2('2. Causes of Cardiomegaly - Mnemonic PAID HEART (2 marks)'),
  bullet('P - Pericardial effusion (water-bottle heart, clear lungs)'),
  bullet('A - Anaemia (chronic, high-output failure)'),
  bullet('I - Ischaemic cardiomyopathy (post-MI, coronary artery disease)'),
  bullet('D - Dilated cardiomyopathy (familial, viral, alcohol, peripartum)'),
  bullet('H - Hypertensive heart disease / High-output (thyrotoxicosis, AV fistula, beriberi)'),
  bullet('E - Endocrine (hypothyroidism, acromegaly)'),
  bullet('A - Amyloidosis / Athletes heart'),
  bullet('R - Rheumatic heart disease / Regurgitant lesions (AR, MR)'),
  bullet('T - Toxins (ALCOHOL - this patient, doxorubicin, cocaine)'),
  spacer(),

  h2('3. Radiological Features in this Patient (1 mark)'),
  bullet('CTR > 0.5: cardiomegaly'),
  bullet('Upper lobe diversion (pulmonary venous hypertension - PCWP >12 mmHg)'),
  bullet('Kerley B lines (interstitial oedema - PCWP >18 mmHg)'),
  bullet('Displaced apex (left ventricular enlargement)'),
  spacer(),

  h2('4. Diagnosis: Dilated Cardiomyopathy (DCM) (1 mark)'),
  bullet('Alcoholic DCM: chronic alcohol toxic to myocytes (acetaldehyde + oxidative stress)'),
  bullet('Criteria: LV EF <45% with LV dilation, no ischaemia/valvular cause'),
  spacer(),

  h2('5. Investigations (2 marks)'),
  bullet('ECG: AF (irregular - noted here), LBBB, LVH, non-specific ST-T changes'),
  bullet('Echocardiography (MOST IMPORTANT): LV dilation, reduced EF (<40%), global hypokinesia, functional MR/TR'),
  bullet('BNP/NT-proBNP: elevated (mirrors severity)'),
  bullet('CBC (anaemia), LFT (alcohol related), RFT, TFT, Serum ferritin (haemochromatosis)'),
  bullet('Coronary angiography: to exclude ischaemic cause'),
  bullet('Cardiac MRI: assess fibrosis, etiology'),
  spacer(),

  h2('6. Management (3 marks)'),
  bullet('LIFESTYLE: STRICT ALCOHOL ABSTINENCE (can reverse alcoholic DCM if early)'),
  bullet('HEART FAILURE PHARMACOTHERAPY:'),
  subBullet('ACE inhibitor (enalapril/ramipril) - reduces preload + afterload, improves survival'),
  subBullet('Beta-blocker (carvedilol/metoprolol succinate) - start after stabilisation'),
  subBullet('Spironolactone/Eplerenone - aldosterone antagonist, reduces mortality'),
  subBullet('Loop diuretic (furosemide) - symptom relief, reduce oedema'),
  subBullet('SGLT2 inhibitor (dapagliflozin/empagliflozin) - now standard in HFrEF'),
  bullet('AF management: rate control (digoxin/beta-blocker), anticoagulation (CHA2DS2-VASc ≥2)'),
  bullet('DEVICE THERAPY: CRT (if LBBB + EF <35% + NYHA II-IV), ICD (EF <35% despite 3 months optimal therapy)'),
  bullet('Heart transplant: refractory end-stage HF'),
  spacer(),

  keypoint('Alcoholic DCM can REVERSE with abstinence. Even 50% improvement in EF possible within 6-18 months. This is unique among cardiomyopathies.'),
  divider(),
);

// ── CASE 5 (5-mark) ──────────────────────────────────────────
children.push(
  h2('CASE 5'),
  caseBox([
    'A 38-year-old woman, known case of hypothyroidism (non-compliant with thyroxine),',
    'presents with progressive dyspnoea and facial puffiness.',
    'Examination: HR 58/min, BP 100/70 mmHg, dry coarse skin, puffy face, slow relaxing reflexes.',
    'CXR shows massive cardiomegaly with clear lung fields.',
    'Echo: Large circumferential pericardial effusion. LVEF 55%.',
  ]),
  spacer(),
  markBadge('5 MARKS'),
  questionPara(5, 'Explain how hypothyroidism causes cardiomegaly and discuss the management. (5 marks)'),
  spacer(),

  answerHeading('Hypothyroidism causing Pericardial Effusion + Cardiomegaly'),
  spacer(),

  h2('Mechanism of Cardiomegaly in Hypothyroidism (2 marks)'),
  bullet('Hypothyroidism → ↑ capillary permeability + ↓ lymphatic drainage → protein-rich (cholesterol-rich) pericardial effusion'),
  bullet('This is a TRANSUDATIVE effusion (low protein) - actually the fluid is a "myxoedematous" effusion'),
  bullet('Accumulates slowly → can become MASSIVE without tamponade (slow accumulation allows pericardium to stretch)'),
  bullet('Direct myocardial effect: thyroid hormone deficiency → ↓ cardiac contractility, ↓ HR, diastolic dysfunction'),
  bullet('CXR shows massive cardiomegaly with CLEAR lung fields (no pulmonary oedema) → classic for pericardial effusion'),
  spacer(),

  h2('Management (3 marks)'),
  bullet('PRIMARY TREATMENT: Thyroid hormone replacement (L-thyroxine)'),
  subBullet('Start low and go slow (elderly/cardiac disease: 12.5-25 mcg/day)'),
  subBullet('Effusion resolves with treatment in most cases - no drainage needed'),
  bullet('PERICARDIOCENTESIS only if: haemodynamic compromise (tamponade) or effusion fails to resolve with T4 therapy'),
  bullet('Monitor TFT: target TSH in normal range'),
  bullet('ECG changes in hypothyroidism: sinus bradycardia, low voltage, prolonged QTc, flattened/inverted T waves'),
  bullet('Avoid over-rapid correction - can precipitate angina/cardiac ischaemia'),
  spacer(),

  keypoint('Hypothyroid pericardial effusion = clear lungs + massive cardiomegaly + normal LVEF + bradycardia + clinical myxoedema features. Treatment is T4 replacement, NOT pericardiocentesis.'),
  divider(),
);

// ═══════════════════════════════════════════════════════════════
// SECTION 3: MYOCARDITIS CASES
// ═══════════════════════════════════════════════════════════════
children.push(sectionTitle('SECTION 3: MYOCARDITIS'), spacer());

// ── CASE 6 (10-mark) ─────────────────────────────────────────
children.push(
  h2('CASE 6'),
  caseBox([
    'A 19-year-old male college student presents with chest pain, dyspnoea and',
    'palpitations for 4 days. He had a "flu-like illness" 10 days ago with fever,',
    'sore throat and myalgia which resolved spontaneously.',
    'Examination: HR 118/min, BP 98/64 mmHg, RR 26/min, Temperature 38.2°C.',
    'S3 gallop present. JVP raised. No murmur. SpO2 94% on room air.',
    'ECG: Diffuse ST elevation with PR depression. No reciprocal changes.',
    'Troponin I: 4.8 ng/mL (elevated). Echo: EF 32%, global LV hypokinesia,',
    'small pericardial effusion. BNP: 1200 pg/mL.',
  ]),
  spacer(),
  markBadge('10 MARKS'),
  questionPara(6, 'Discuss the diagnosis, pathophysiology, investigations, and management of this condition. How would you differentiate it from acute MI? (10 marks)'),
  spacer(),

  answerHeading('Acute Myocarditis (Viral / Post-Infectious)'),
  spacer(),

  h2('1. Diagnosis (1 mark)'),
  bullet('Acute myocarditis - post-viral (likely Coxsackievirus B)'),
  bullet('Evidence: young patient, preceding viral illness, chest pain + HF symptoms, elevated troponin, reduced EF, small pericardial effusion (myopericarditis)'),
  spacer(),

  h2('2. Pathophysiology (2 marks)'),
  bullet('Phase 1 (Viral entry, day 0-3): Direct viral invasion of myocytes via receptors (CAR receptor for Coxsackievirus B). Viral replication → myocyte lysis'),
  bullet('Phase 2 (Immune activation, day 4-14): NK cells, macrophages → release cytokines (TNF-α, IL-1, IL-6). Autoantibodies formed against myosin, troponin, β-adrenergic receptors'),
  bullet('Phase 3 (Chronic, weeks-months): Persistent inflammation → myocyte apoptosis + fibrosis → dilated cardiomyopathy (10-20%)'),
  bullet('Autoimmune mechanism: molecular mimicry - viral peptides resemble cardiac proteins → cross-reactive immune response'),
  spacer(),

  h2('3. Differentiation from Acute MI (2 marks)'),
  bullet('Age: Myocarditis - young; MI - older, risk factors'),
  bullet('ECG: Myocarditis - diffuse ST elevation, PR depression, NO reciprocal changes; MI - territorial ST elevation WITH reciprocal changes, Q waves'),
  bullet('Troponin pattern: Myocarditis - slow rise and fall (days); MI - rapid rise and fall (hours)'),
  bullet('Echo: Myocarditis - global hypokinesia, no culprit vessel territory; MI - regional wall motion abnormality (coronary territory)'),
  bullet('Cardiac MRI (gold standard non-invasive): Myocarditis - non-ischaemic LGE pattern (mid-wall/epicardial); MI - subendocardial/transmural LGE in coronary territory'),
  bullet('Coronary angiography: Myocarditis - normal coronaries; MI - culprit stenosis/occlusion'),
  spacer(),

  h2('4. Investigations (2 marks)'),
  bullet('Troponin I/T: elevated, correlates with severity'),
  bullet('BNP/NT-proBNP: elevated (HF severity marker)'),
  bullet('ECG: diffuse ST elevation + PR depression (pericardial involvement)'),
  bullet('Echocardiography: global LV dysfunction, ± pericardial effusion, wall motion'),
  bullet('Cardiac MRI (gold standard non-invasive):'),
  subBullet('T2-weighted: myocardial oedema (increased signal)'),
  subBullet('T1 with gadolinium: early gadolinium enhancement (hyperaemia)'),
  subBullet('Late gadolinium enhancement (LGE): non-ischaemic mid-wall/epicardial pattern'),
  bullet('Endomyocardial biopsy (definitive): lymphocytic infiltrate + myocyte necrosis (Dallas criteria). Reserved for severe/fulminant cases.'),
  bullet('Viral serology: acute and convalescent titres (Coxsackievirus, adenovirus, parvovirus B19)'),
  spacer(),

  h2('5. Management (3 marks)'),
  bullet('ACTIVITY RESTRICTION: complete rest, avoid strenuous activity for 3-6 months (risk of SCD)'),
  bullet('HEART FAILURE TREATMENT:'),
  subBullet('ACE inhibitor/ARB + Beta-blocker (start when stabilised) + MRA + Loop diuretic'),
  subBullet('SGLT2i (dapagliflozin) - now included in HFrEF protocols'),
  bullet('NO NSAIDs in acute phase (worsen myocardial inflammation)'),
  bullet('ANTIARRHYTHMICS: amiodarone for ventricular arrhythmias'),
  bullet('ANTICOAGULATION: if LV thrombus or AF present'),
  bullet('IMMUNOSUPPRESSION:'),
  subBullet('Giant cell myocarditis: steroids + azathioprine (often refractory)'),
  subBullet('Autoimmune/sarcoid myocarditis: corticosteroids'),
  subBullet('Viral myocarditis: NOT recommended routinely'),
  bullet('IVIG: in paediatric and fulminant myocarditis (evidence limited)'),
  bullet('MECHANICAL SUPPORT: IABP/VA-ECMO/LVAD for cardiogenic shock'),
  spacer(),

  keypoint('Fulminant myocarditis = abrupt onset cardiogenic shock. Paradoxically has BETTER long-term prognosis than acute non-fulminant - survivors recover near-normal EF. Aggressive support is life-saving.'),
  keypoint('Myocarditis in a young person + Coxsackievirus B = classic exam scenario. Remember: diffuse ST elevation (no reciprocal changes) + normal coronaries distinguishes from MI.'),
  divider(),
);

// ── CASE 7 (5-mark) ──────────────────────────────────────────
children.push(
  h2('CASE 7'),
  caseBox([
    'A 9-year-old child is brought with high fever (39.5°C), sore throat for 5 days.',
    'On day 4, the child developed a bull-neck appearance.',
    'Examination: HR 38/min, BP 80/50 mmHg, grey-white membrane over tonsils.',
    'ECG shows complete heart block (P waves dissociated from QRS).',
    'Throat swab: Gram-positive bacilli with metachromatic granules.',
  ]),
  spacer(),
  markBadge('5 MARKS'),
  questionPara(7, 'What is the diagnosis? How does this organism cause myocarditis and heart block? Outline the treatment. (5 marks)'),
  spacer(),

  answerHeading('Diphtheria with Myocarditis and Complete Heart Block'),
  spacer(),

  h2('Diagnosis (1 mark)'),
  bullet('Diphtheria: Corynebacterium diphtheriae (Gram-positive, clubbed bacilli, Babes-Ernst/metachromatic granules)'),
  bullet('Bull-neck (bull-neck lymphadenopathy + pseudomembrane), complete heart block, myocarditis'),
  spacer(),

  h2('Mechanism of Myocarditis (2 marks)'),
  bullet('C. diphtheriae produces a powerful EXOTOXIN (encoded by bacteriophage gene tox+)'),
  bullet('Toxin mechanism: inhibits protein synthesis by ADP-ribosylation of EF-2 (Elongation Factor-2)'),
  bullet('Cardiac involvement:'),
  subBullet('Toxin targets cardiac myocytes and conduction tissue preferentially'),
  subBullet('→ Myocarditis (fatty degeneration + necrosis of myocytes)'),
  subBullet('→ Involvement of AV node → heart block (most common cause of death in diphtheria)'),
  bullet('Onset: 1-2 weeks after pharyngeal infection'),
  bullet('Leading cause of death in diphtheria (arrhythmias > heart block > cardiac failure)'),
  spacer(),

  h2('Treatment (2 marks)'),
  bullet('DIPHTHERIA ANTITOXIN (DAT): MOST IMPORTANT - neutralizes circulating toxin (does NOT reverse already-bound toxin). Give IM/IV without waiting for lab confirmation.'),
  bullet('ANTIBIOTICS: Penicillin G or Erythromycin (eliminate organism, reduce toxin production)'),
  bullet('COMPLETE HEART BLOCK: Temporary pacemaker (transcutaneous/transvenous) - until block resolves'),
  bullet('STRICT BED REST: avoid exertion (risk of sudden death from arrhythmia)'),
  bullet('Isolation, ICU monitoring, close ECG monitoring'),
  bullet('VACCINATION (DPT/DT) after recovery: infection does not confer immunity'),
  spacer(),

  keypoint('Diphtheria antitoxin must be given on CLINICAL diagnosis without waiting for culture. Delay increases mortality dramatically. Antitoxin is effective only against FREE toxin, not cell-bound toxin.'),
  divider(),
);

// ═══════════════════════════════════════════════════════════════
// SECTION 4: PERICARDIAL EFFUSION CASES
// ═══════════════════════════════════════════════════════════════
children.push(sectionTitle('SECTION 4: PERICARDIAL EFFUSION'), spacer());

// ── CASE 8 (10-mark) ─────────────────────────────────────────
children.push(
  h2('CASE 8'),
  caseBox([
    'A 55-year-old woman with known lung cancer (adenocarcinoma) presents with',
    'worsening dyspnoea, dizziness, and near-syncope over the past 3 days.',
    'She appears anxious and distressed. BP 80/60 mmHg, HR 138/min (sinus tachycardia).',
    'JVP raised to angle of jaw. Heart sounds are soft and distant.',
    'During BP measurement, systolic BP drops by 18 mmHg during inspiration.',
    'ECG: Sinus tachycardia, low voltage QRS, electrical alternans.',
    'CXR: Massive cardiomegaly ("water-bottle heart"), clear lung fields.',
  ]),
  spacer(),
  markBadge('10 MARKS'),
  questionPara(8, 'What is the diagnosis? Discuss the pathophysiology, clinical features, investigations, and emergency management of this condition. (10 marks)'),
  spacer(),

  answerHeading('Cardiac Tamponade (Malignant Pericardial Effusion)'),
  spacer(),

  h2('1. Diagnosis (1 mark)'),
  bullet('Cardiac tamponade complicating malignant pericardial effusion (lung cancer)'),
  bullet('Evidence: Beck\'s triad + pulsus paradoxus (18 mmHg) + electrical alternans'),
  spacer(),

  h2('2. Pathophysiology (2 marks)'),
  bullet('Pericardial sac is inextensible → fluid accumulation raises intrapericardial pressure'),
  bullet('Rapidly: even 150-200 mL can cause tamponade (fast accumulation)'),
  bullet('Slowly: up to 2 litres can accumulate without tamponade (chronic, allows pericardial stretch)'),
  bullet('Mechanism of haemodynamic compromise:'),
  subBullet('↑ Intrapericardial pressure → compresses all cardiac chambers'),
  subBullet('→ ↓ Diastolic filling (especially RV first, then LV)'),
  subBullet('→ ↓ Stroke volume → ↓ CO → cardiogenic shock'),
  bullet('Inspiration: ↑ RV filling → IVS shifts left → ↓ LV filling → ↓ BP (pulsus paradoxus)'),
  bullet('Compensatory: tachycardia + peripheral vasoconstriction (maintains BP temporarily)'),
  spacer(),

  h2('3. Clinical Features - Beck\'s Triad (1 mark)'),
  bullet('HYPOTENSION (↓ BP 80/60 mmHg): ↓ cardiac output'),
  bullet('RAISED JVP (raised to angle of jaw): obstructed venous return'),
  bullet('MUFFLED/DISTANT HEART SOUNDS: fluid surrounding heart'),
  bullet('ADDITIONAL: Pulsus paradoxus >10 mmHg, tachycardia, Kussmaul\'s sign (absent in tamponade - present in constrictive pericarditis)'),
  spacer(),

  h2('4. Pulsus Paradoxus (1 mark)'),
  bullet('Definition: ↓ systolic BP >10 mmHg during normal inspiration'),
  bullet('Normal: slight ↓ (≤10 mmHg) during inspiration is physiological'),
  bullet('Mechanism in tamponade: inspiration → ↑ RV volume → septum bows left → ↓ LV filling → ↓ SV → ↓ BP'),
  bullet('Absent in: severe AR, ASD, LV failure, regional tamponade'),
  spacer(),

  h2('5. Investigations (2 marks)'),
  bullet('ECG: sinus tachycardia + low voltage QRS + ELECTRICAL ALTERNANS (beat-to-beat variation in QRS axis = heart swinging in fluid = PATHOGNOMONIC of tamponade)'),
  bullet('CXR: water-bottle/flask-shaped cardiomegaly + clear lungs'),
  bullet('ECHOCARDIOGRAPHY (investigation of choice):'),
  subBullet('Circumferential pericardial effusion'),
  subBullet('RA diastolic collapse (earliest and most sensitive sign)'),
  subBullet('RV diastolic collapse (more specific for tamponade)'),
  subBullet('IVC plethora (dilated >2.1 cm, no inspiratory collapse)'),
  subBullet('Respiratory variation in mitral inflow >25% (by Doppler)'),
  spacer(),

  h2('6. Emergency Management (3 marks)'),
  bullet('IMMEDIATE: IV fluid challenge (250-500 mL NS) - temporary measure to maintain preload'),
  bullet('AVOID: diuretics, vasodilators, beta-blockers (reduce preload/HR → catastrophic)'),
  bullet('PERICARDIOCENTESIS (definitive emergency treatment):'),
  subBullet('Subxiphoid approach (most common - safest, away from coronary arteries)'),
  subBullet('Echo-guided (preferred - safer, real-time guidance)'),
  subBullet('Needle inserted at 45° angle toward left shoulder'),
  subBullet('Remove fluid → immediate BP improvement'),
  subBullet('"Haemorrhagic aspirate" test: blood from heart clots, pericardial blood does NOT clot'),
  bullet('PERICARDIAL DRAIN: leave in situ for 24-48h to prevent reaccumulation'),
  bullet('TREAT UNDERLYING CAUSE:'),
  subBullet('Malignant effusion: intrapericardial chemotherapy, systemic treatment'),
  subBullet('Pericardial window/pericardiectomy for recurrent malignant effusions'),
  bullet('FLUID ANALYSIS: cytology, cultures, LDH/protein (exudate vs transudate)'),
  spacer(),

  keypoint('ELECTRICAL ALTERNANS = pathognomonic of cardiac tamponade. This is a HIGH-YIELD ECG finding for exams. Beat-to-beat alternation in QRS amplitude = heart swinging in a large pericardial effusion.'),
  keypoint('Never give diuretics in cardiac tamponade - the patient is preload-dependent. Pericardiocentesis is the only treatment.'),
  divider(),
);

// ── CASE 9 (5-mark) ──────────────────────────────────────────
children.push(
  h2('CASE 9'),
  caseBox([
    'A 48-year-old man presents with sharp left-sided chest pain that worsens',
    'on lying down and improves on leaning forward. He had a myocardial infarction',
    '6 weeks ago and was treated with thrombolysis.',
    'Examination: Temperature 38.4°C, friction rub heard at left lower sternal border.',
    'ECG: Diffuse ST elevation with PR depression in multiple leads.',
    'Echo: Small pericardial effusion, LVEF 48%. ESR 86 mm/hr, CRP 42 mg/L.',
  ]),
  spacer(),
  markBadge('5 MARKS'),
  questionPara(9, 'What is the diagnosis? Discuss its pathogenesis and management. (5 marks)'),
  spacer(),

  answerHeading("Dressler's Syndrome (Post-Cardiac Injury Syndrome)"),
  spacer(),

  h2('Diagnosis (1 mark)'),
  bullet("Dressler's syndrome (post-MI pericarditis / post-cardiac injury syndrome)"),
  bullet('Classic history: pericarditis developing 2-10 weeks after myocardial infarction'),
  bullet('Features: fever + pleuritic chest pain + friction rub + ECG changes + elevated inflammatory markers'),
  spacer(),

  h2('Pathogenesis (2 marks)'),
  bullet("Autoimmune mechanism: myocardial necrosis after MI → release of cardiac antigens"),
  bullet('→ Formation of anti-myocardial antibodies (anti-sarcolemmal, anti-myosin antibodies)'),
  bullet('→ Type III hypersensitivity (immune complex deposition) in pericardium → pericarditis'),
  bullet('Can also occur after cardiac surgery (post-pericardiotomy syndrome), cardiac catheterisation, pacemaker insertion'),
  bullet("Distinction from early post-MI pericarditis (fibrinous pericarditis days 1-4 after MI = direct extension of infarct, NOT Dressler's)"),
  spacer(),

  h2('Management (2 marks)'),
  bullet('ASPIRIN (preferred post-MI): 650 mg every 6-8 hours for 2-4 weeks (then taper). First choice as NSAIDs other than aspirin may impair infarct healing and increase LV remodelling.'),
  bullet('COLCHICINE: 0.5 mg twice daily for 3 months - reduces recurrence by ~50%. Should be added to aspirin.'),
  bullet('NSAIDS (ibuprofen): alternative if aspirin not tolerated, but use with caution post-MI'),
  bullet('CORTICOSTEROIDS (prednisolone): only if aspirin/NSAIDs/colchicine fail or contraindicated. Associated with ↑ recurrence risk if used early.'),
  bullet('Avoid anticoagulation (↑ risk of haemopericardium if using warfarin/heparin)'),
  bullet('Activity restriction until resolution of symptoms'),
  spacer(),

  keypoint("Dressler's = 2-10 weeks post-MI. Early post-MI pericarditis = 1-4 DAYS post-MI. Both are important exam distinctions. In Dressler's, aspirin + colchicine is the treatment, NOT steroids as first line."),
  divider(),
);

// ── CASE 10 (5-mark) ─────────────────────────────────────────
children.push(
  h2('CASE 10'),
  caseBox([
    'A 35-year-old HIV-positive man (not on ART, CD4 count 180 cells/μL)',
    'presents with evening fever, weight loss, night sweats for 3 months.',
    'He has now developed progressive breathlessness.',
    'Examination: raised JVP with prominent x AND y descent, BP 110/70 mmHg,',
    'Kussmaul\'s sign positive. No pulsus paradoxus. Pericardial knock heard.',
    'CXR: Calcification of pericardium, no significant cardiac enlargement.',
    'Echo: Thickened pericardium, normal LV and RV size, septal bounce.',
  ]),
  spacer(),
  markBadge('5 MARKS'),
  questionPara(10, 'What is the diagnosis? How do you differentiate this from cardiac tamponade? Outline management. (5 marks)'),
  spacer(),

  answerHeading('Constrictive Pericarditis (Tuberculous)'),
  spacer(),

  h2('Diagnosis (1 mark)'),
  bullet('Tuberculous constrictive pericarditis in an HIV-positive patient'),
  bullet('TB is the most common cause of constrictive pericarditis in developing countries/HIV patients'),
  spacer(),

  h2('Tamponade vs Constrictive Pericarditis (2 marks)'),

  new Table({
    width: { size: 100, type: WidthType.PERCENTAGE },
    rows: [
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        children: [
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          new TableCell({ children: [new Paragraph({ children: [new TextRun({ text: 'Cardiac Tamponade', bold: true, size: 20, color: 'FFFFFF' })] })], shading: { type: ShadingType.SOLID, color: '1F3864' }, margins: { top: 60, bottom: 60, left: 120, right: 120 } }),
          new TableCell({ children: [new Paragraph({ children: [new TextRun({ text: 'Constrictive Pericarditis', bold: true, size: 20, color: 'FFFFFF' })] })], shading: { type: ShadingType.SOLID, color: '1F3864' }, margins: { top: 60, bottom: 60, left: 120, right: 120 } }),
        ],
      }),
      ...([
        ['JVP waveform', 'Absent y descent (x descent preserved)', 'Prominent x AND y descent (Friedreich sign)'],
        ['Pulsus paradoxus', 'Present (>10 mmHg)', 'Usually absent'],
        ["Kussmaul's sign", 'Absent', 'Present (JVP rises on inspiration)'],
        ['Heart sounds', 'Muffled/distant', 'Pericardial knock (early S3-like)'],
        ['ECG', 'Electrical alternans, low voltage', 'Low voltage, no alternans'],
        ['Echo', 'RA/RV diastolic collapse, IVC plethora', 'Septal bounce, thickened pericardium'],
        ['CXR', 'Flask-shaped cardiomegaly', 'Pericardial calcification (30%)'],
        ['Treatment', 'Pericardiocentesis (emergency)', 'Pericardiectomy (surgical)'],
      ].map((row, i) =>
        new TableRow({
          children: row.map(cell =>
            new TableCell({
              children: [new Paragraph({ children: [new TextRun({ text: cell, size: 20 })], spacing: { before: 40, after: 40 } })],
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              margins: { top: 60, bottom: 60, left: 120, right: 120 },
            })
          ),
        })
      )),
    ],
  }),

  spacer(),

  h2('Management (2 marks)'),
  bullet('ANTITUBERCULAR THERAPY (ATT): standard 6-9 month regimen (HRZE x 2 months, then HR x 4-7 months)'),
  bullet('CORTICOSTEROIDS: prednisolone 1 mg/kg/day tapering over 6-8 weeks - reduces progression to constriction, improves outcomes (evidence for TB pericarditis)'),
  bullet('ART for HIV: improves immune function, reduces TB activity'),
  bullet('PERICARDIECTOMY (surgical decortication): definitive treatment for established constrictive pericarditis. Indicated when symptoms persist despite medical therapy.'),
  bullet('Monitor for IRIS (immune reconstitution inflammatory syndrome) when starting ART + ATT simultaneously'),
  spacer(),

  keypoint("Kussmaul's sign (JVP rises on inspiration) + Friedreich's sign (prominent y descent) + pericardial knock + septal bounce on echo = constrictive pericarditis. Calcification on CXR is pathognomonic."),
  divider(),
);

// ── SUMMARY TABLE ────────────────────────────────────────────
children.push(
  sectionTitle('QUICK SUMMARY: HIGH-YIELD EXAM POINTS'),
  spacer(),
  new Paragraph({
    children: [new TextRun({ text: 'POISONING KEY FACTS', bold: true, size: 24, color: 'C00000' })],
    spacing: { after: 60 },
  }),
  bullet('OP Poisoning antidote: ATROPINE (muscarinic) + PRALIDOXIME (reactivates AChE before ageing)'),
  bullet('Intermediate syndrome: 24-96h, proximal weakness, does NOT respond to atropine'),
  bullet('Opioid antidote: Naloxone | Paracetamol antidote: N-acetylcysteine | CO: 100% O2'),
  bullet('TCA poisoning: wide QRS → Sodium bicarbonate | Methanol: Fomepizole'),
  spacer(),
  new Paragraph({
    children: [new TextRun({ text: 'CARDIOMEGALY KEY FACTS', bold: true, size: 24, color: 'C00000' })],
    spacing: { after: 60 },
  }),
  bullet('CTR >0.5 on PA CXR = cardiomegaly'),
  bullet('Flask-shaped heart + clear lungs = pericardial effusion (NOT cardiomegaly from HF)'),
  bullet('Hypothyroid large effusion = treat with T4, not pericardiocentesis'),
  bullet('Alcoholic DCM can reverse with abstinence (unique)'),
  spacer(),
  new Paragraph({
    children: [new TextRun({ text: 'MYOCARDITIS KEY FACTS', bold: true, size: 24, color: 'C00000' })],
    spacing: { after: 60 },
  }),
  bullet('Most common viral cause: Coxsackievirus B'),
  bullet('Diphtheria myocarditis: #1 cause of death; treat with antitoxin FIRST'),
  bullet('Cardiac MRI = best non-invasive; Endomyocardial biopsy = gold standard (Dallas criteria)'),
  bullet('Fulminant myocarditis: worse acutely, BETTER long-term prognosis'),
  bullet('NO NSAIDs in myocarditis'),
  spacer(),
  new Paragraph({
    children: [new TextRun({ text: 'PERICARDIAL EFFUSION KEY FACTS', bold: true, size: 24, color: 'C00000' })],
    spacing: { after: 60 },
  }),
  bullet("Beck's triad: Hypotension + Raised JVP + Muffled heart sounds = Tamponade"),
  bullet('Electrical alternans = PATHOGNOMONIC of cardiac tamponade'),
  bullet('Pulsus paradoxus >10 mmHg = tamponade'),
  bullet("Dressler's (2-10 weeks post-MI): Aspirin + Colchicine"),
  bullet("Constrictive pericarditis: Kussmaul's sign + Friedreich's sign + pericardial knock + calcification"),
  bullet('Tamponade: absent y descent | Constriction: prominent x AND y descent'),
  spacer(),
);

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