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HKMLE CARDIOVASCULAR PHARMACOLOGY - ANKI FLASHCARD DECK
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Generated from: Cardio 💊.pdf (High-Yield HKMLE Notes)
Card count: 120+
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SECTION 1: ACE INHIBITORS (-PRILS)
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[CARD 1 - Type 3: Mnemonic]
Q: What is the mnemonic for ACEi side effects?
A: CAPTOPRIL = Cough, Angioedema, Potassium ↑, Teratogenic, low bP, Renal failure, Increased renin, Liver problems

[CARD 2 - Type 1: Basic Q&A]
Q: What is the mechanism of ACE inhibitors?
A: Block ACE → ↓ angiotensin II → vasodilation + ↓ aldosterone; also prevent bradykinin breakdown → dry cough.

[CARD 3 - Type 2: Cloze]
[c] ACE inhibitors [/c] cause dry cough because they prevent bradykinin breakdown (bradykinin accumulates → irritates airways).

[CARD 4 - Type 1: Basic Q&A]
Q: Name 5 key indications for ACE inhibitors.
A: Hypertension, HFrEF, Post-MI, Diabetic nephropathy, Proteinuria.

[CARD 5 - Type 1: Basic Q&A]
Q: Name 4 contraindications to ACE inhibitors.
A: Pregnancy (teratogen), Bilateral renal artery stenosis, Hyperkalaemia, Prior angioedema.

[CARD 6 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: A patient on ACEi develops cough. What is the next step?
A: Switch to an ARB (-sartan) — ARBs have the same hemodynamic benefit without causing cough.
[Trap: Do NOT rechallenge with a different ACEi — the cough is a class effect via bradykinin.]

[CARD 7 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: A patient on ACEi develops bilateral leg oedema of the face and tongue. What is the diagnosis and management?
A: Angioedema (ACEi-induced) — stop the ACEi immediately; do NOT switch to another ACEi or ARB (ARBs very rarely cause it but can).
[Trap: Angioedema is an ACEi class effect — ARBs can theoretically cause it but far less commonly; in practice the correct answer is to avoid ACEi.]

[CARD 8 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: An ACEi is started in a patient with bilateral renal artery stenosis. What happens?
A: Acute kidney injury — the ACEi removes angiotensin II-driven efferent arteriole constriction, dropping GFR precipitously.

[CARD 9 - Type 1: Basic Q&A]
Q: Which ACEi is used in hypertensive crisis (IV route)?
A: Captopril (also enalaprilat IV).

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SECTION 2: ANGIOTENSIN RECEPTOR BLOCKERS (ARBs, -SARTANS)
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[CARD 10 - Type 3: Mnemonic]
Q: What is the mnemonic for ARBs?
A: "SARTANS SPARE THE COUGH" — ARBs block AT1 receptor but do NOT affect bradykinin, so no cough.

[CARD 11 - Type 1: Basic Q&A]
Q: What is the mechanism of ARBs?
A: Block AT1 receptor → same hemodynamic effect as ACEi, but NO bradykinin effect (no cough, no angioedema).

[CARD 12 - Type 2: Cloze]
[c] ARBs [/c] do NOT cause cough because they block the AT1 receptor without affecting bradykinin metabolism.

[CARD 13 - Type 1: Basic Q&A]
Q: Name 4 ARB drugs (HKMLE key drugs).
A: Losartan, Valsartan, Candesartan, Irbesartan.

[CARD 14 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Can you combine an ACEi and an ARB in heart failure?
A: No — combination increases renal failure risk with no additional mortality benefit; avoid ACEi + ARB dual blockade.
[Trap: Some older guidelines mentioned dual blockade for proteinuria — HKMLE expects you to know this combination is now contraindicated.]

[CARD 15 - Type 1: Basic Q&A]
Q: Name the contraindications shared by both ACEi and ARBs.
A: Pregnancy, bilateral renal artery stenosis, hyperkalaemia.

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SECTION 3: BETA-BLOCKERS (-OLOLS)
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[CARD 16 - Type 3: Mnemonic]
Q: What is the mnemonic for beta-blocker side effects?
A: BASH = Bradycardia, Asthma (contraindicated), Sexual dysfunction, HF (use cautiously — only start when stable).

[CARD 17 - Type 3: Mnemonic]
Q: What is the mnemonic for beta-blocker contraindications?
A: ABCDE = Asthma, Bradycardia, Cardiogenic shock, Diabetes (relative — masks hypoglycaemia), Elevated K is the effect not a CI.

[CARD 18 - Type 1: Basic Q&A]
Q: What is the mechanism of beta-blockers?
A: β1-blockade → ↓ HR, ↓ contractility, ↓ renin; non-selective β2-blockade also causes bronchoconstriction.

[CARD 19 - Type 1: Basic Q&A]
Q: Name 5 key indications for beta-blockers.
A: HFrEF (mortality benefit), Post-MI, Angina, AF rate control, SVT, Hyperthyroidism/thyroid storm.

[CARD 20 - Type 1: Basic Q&A]
Q: Which beta-blockers are cardioselective (β1-selective)?
A: Metoprolol, Atenolol, Bisoprolol — safer in COPD patients.
[Trap: "Cardioselective" does not mean completely safe in severe asthma — they are still relatively contraindicated.]

[CARD 21 - Type 2: Cloze]
[c] Propranolol [/c] is a non-selective beta-blocker used for portal hypertension, migraine prophylaxis, and essential tremor (in addition to cardiac indications).

[CARD 22 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which beta-blockers have proven mortality benefit in HFrEF?
A: Bisoprolol, Carvedilol, and Metoprolol succinate — only these three are evidence-based for HFrEF.
[Trap: Not all beta-blockers reduce mortality in HF — only these three are approved/tested.]

[CARD 23 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: When should you NOT start a beta-blocker in heart failure?
A: Do NOT initiate in decompensated (acutely worsening) HF — only start when the patient is stable.

[CARD 24 - Type 1: Basic Q&A]
Q: Which beta-blocker is given IV for acute SVT in the emergency setting?
A: Esmolol (short-acting IV beta-blocker).

[CARD 25 - Type 2: Cloze]
[c] Non-selective beta-blockers [/c] can mask hypoglycaemia symptoms in diabetics because they block the adrenergic response (tachycardia, tremor) to low blood glucose.

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SECTION 4: CALCIUM CHANNEL BLOCKERS (CCBs)
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[CARD 26 - Type 3: Mnemonic]
Q: What is the mnemonic to distinguish DHP vs Non-DHP CCBs?
A: DHP = "Dilate Peripheral vessels" (vascular selectivity); Non-DHP = "Node-slowing" (AV node effects).

[CARD 27 - Type 1: Basic Q&A]
Q: Name the dihydropyridine (DHP) CCBs and their key use.
A: Amlodipine, Nifedipine, Felodipine — used for hypertension and angina (peripheral vasodilation).

[CARD 28 - Type 1: Basic Q&A]
Q: Name the non-DHP CCBs and their key use.
A: Verapamil and Diltiazem — used for AF rate control, SVT, and angina (slow AV node).

[CARD 29 - Type 1: Basic Q&A]
Q: What are the side effects of DHP CCBs (e.g. amlodipine)?
A: Peripheral oedema, flushing, reflex tachycardia.

[CARD 30 - Type 1: Basic Q&A]
Q: What are the side effects of non-DHP CCBs (verapamil/diltiazem)?
A: Bradycardia, heart block, constipation (especially verapamil).

[CARD 31 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What happens if you combine verapamil with a beta-blocker?
A: Complete heart block — this combination is contraindicated.
[Trap: Diltiazem + beta-blocker also risks heart block, but the verapamil combination is the classic HKMLE trap.]

[CARD 32 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which CCB is safe to use for hypertension in a patient with HFrEF?
A: Amlodipine — it is the only CCB considered safe in HFrEF (for hypertension control); non-DHPs are contraindicated in HFrEF.

[CARD 33 - Type 1: Basic Q&A]
Q: What is the contraindication of short-acting nifedipine?
A: Unstable angina — short-acting nifedipine causes reflex tachycardia which can worsen ischaemia.

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SECTION 5: DIURETICS
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--- LOOP DIURETICS ---

[CARD 34 - Type 3: Mnemonic]
Q: What is the mnemonic for loop diuretic electrolyte effects?
A: "FUROSEMIDE FLUSHES EVERYTHING" — loses K, Na, Mg, Ca (hypokalaemia, hyponatraemia, hypomagnesaemia, hypocalcaemia).

[CARD 35 - Type 1: Basic Q&A]
Q: What is the mechanism of loop diuretics?
A: Block Na-K-2Cl cotransporter in the thick ascending limb of the Loop of Henle.

[CARD 36 - Type 1: Basic Q&A]
Q: Name 4 key indications for furosemide.
A: Acute pulmonary oedema, decompensated HF, oedema (cirrhosis/nephrotic), hypercalcaemia.

[CARD 37 - Type 1: Basic Q&A]
Q: Name 4 side effects of loop diuretics.
A: Hypokalaemia, hyponatraemia, metabolic alkalosis, ototoxicity (high doses), hyperuricaemia (gout).

[CARD 38 - Type 2: Cloze]
[c] Furosemide [/c] causes metabolic alkalosis because it increases H+ excretion in the collecting duct via a compensatory mechanism for sodium loss.

--- THIAZIDE DIURETICS ---

[CARD 39 - Type 3: Mnemonic]
Q: What is the mnemonic for thiazide electrolyte effects?
A: "THIAZIDES TAKE AWAY K, Mg, Na - but KEEP calcium" — causes hypokalaemia, hypomagnesaemia, hyponatraemia, but hypercalcaemia.

[CARD 40 - Type 1: Basic Q&A]
Q: What is the mechanism of thiazide diuretics?
A: Block Na-Cl cotransporter in the distal convoluted tubule.

[CARD 41 - Type 1: Basic Q&A]
Q: Name 4 indications for thiazide diuretics.
A: Hypertension (first-line), mild HF, calcium kidney stones (reduces urinary Ca), nephrogenic DI.

[CARD 42 - Type 1: Basic Q&A]
Q: What are the metabolic side effects of thiazides?
A: Hypokalaemia, hyperuricaemia (gout), hyperglycaemia, hyperlipidaemia, hypercalcaemia.

[CARD 43 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: How does the calcium effect of loop vs thiazide diuretics differ?
A: Loop diuretics cause hypocalcaemia (used in hypercalcaemia); thiazides cause hypercalcaemia (used in calcium kidney stones).
[Trap: Both are diuretics but they have OPPOSITE effects on calcium — a classic HKMLE distinction.]

--- POTASSIUM-SPARING DIURETICS ---

[CARD 44 - Type 1: Basic Q&A]
Q: What is the mechanism of spironolactone?
A: Aldosterone antagonist → blocks Na retention and K excretion in the collecting duct.

[CARD 45 - Type 1: Basic Q&A]
Q: What is the key HKMLE indication for spironolactone?
A: HFrEF (mortality benefit - RALES trial), secondary hyperaldosteronism, ascites.

[CARD 46 - Type 2: Cloze]
[c] Spironolactone [/c] causes gynaecomastia because it blocks androgen receptors (in addition to aldosterone receptors).

[CARD 47 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: A male patient on spironolactone develops gynaecomastia. What should you switch to?
A: Eplerenone — selective aldosterone antagonist with fewer androgen side effects (no gynaecomastia).

[CARD 48 - Type 1: Basic Q&A]
Q: What is the most important side effect of all potassium-sparing diuretics?
A: Hyperkalaemia — avoid combination with ACEi/ARB unless carefully monitored.

[CARD 49 - Type 1: Basic Q&A]
Q: What is the mechanism of amiloride?
A: Blocks ENaC (epithelial Na channel) in the collecting duct → K sparing without aldosterone antagonism.

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SECTION 6: NITRATES
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[CARD 50 - Type 3: Mnemonic]
Q: What is the mnemonic for nitrate mechanism?
A: "NITRATES = NO → cGMP → relax smooth muscle" — venodilation (↓ preload) at low doses; arterial dilation (↓ afterload) at high doses.

[CARD 51 - Type 1: Basic Q&A]
Q: Name 3 key indications for nitrates.
A: Acute angina (sublingual GTN), angina prophylaxis, acute HF (↓ preload), hypertensive emergency with pulmonary oedema.

[CARD 52 - Type 1: Basic Q&A]
Q: What are the side effects of nitrates?
A: Headache (most common), hypotension, reflex tachycardia, tolerance with continuous use.

[CARD 53 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: A patient takes GTN (glyceryl trinitrate) and sildenafil together. What happens?
A: Potentially fatal hypotension — GTN + any PDE-5 inhibitor (sildenafil, tadalafil, vardenafil) is absolutely contraindicated.
[Trap: The question may use trade names (Viagra, Cialis) — always recognise PDE-5 inhibitors and flag the GTN interaction.]

[CARD 54 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: How do you prevent nitrate tolerance?
A: Allow an 8-12 hour nitrate-free period each day (typically overnight).

[CARD 55 - Type 1: Basic Q&A]
Q: Name 4 contraindications to nitrates.
A: Concurrent PDE-5 inhibitors, HOCM (hypertrophic obstructive cardiomyopathy), severe aortic stenosis, right ventricular infarction.

[CARD 56 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why are nitrates contraindicated in RV infarction?
A: RV infarction requires adequate preload to maintain cardiac output — nitrate-induced venodilation drops preload and causes severe hypotension.

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SECTION 7: ANTIARRHYTHMIC DRUGS (VAUGHAN-WILLIAMS)
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[CARD 57 - Type 3: Mnemonic]
Q: What is the mnemonic for the Vaughan-Williams classification?
A: "1 Na, 2 Beta, 3 K (prolong), 4 Ca" — Class I: Na channel blockers; II: Beta-blockers; III: K channel blockers (prolong QT); IV: Ca channel blockers.

--- CLASS I ---

[CARD 58 - Type 1: Basic Q&A]
Q: What is the mechanism of Class IA antiarrhythmics (quinidine, procainamide, disopyramide)?
A: Block Na+ channels (slow phase 0) AND prolong repolarisation → risk of QT prolongation and Torsades de Pointes.

[CARD 59 - Type 2: Cloze]
[c] Procainamide [/c] causes drug-induced lupus (SLE-like syndrome) with long-term use — an important HKMLE side effect.

[CARD 60 - Type 2: Cloze]
[c] Quinidine [/c] causes cinchonism (tinnitus, headache, visual disturbance) as a characteristic side effect.

[CARD 61 - Type 1: Basic Q&A]
Q: What is the mechanism of Class IB antiarrhythmics (lidocaine, mexiletine)?
A: Block Na+ channels selectively in ischaemic tissue (shorten phase 3) — used for ventricular arrhythmias post-MI.

[CARD 62 - Type 1: Basic Q&A]
Q: What are the CNS side effects of lidocaine toxicity?
A: Nystagmus, seizures, confusion (CNS toxicity is dose-dependent).

[CARD 63 - Type 1: Basic Q&A]
Q: What is the mechanism of Class IC antiarrhythmics (flecainide, propafenone)?
A: Markedly slow phase 0 (strongest Na+ channel block) → most potent sodium channel blockers.

[CARD 64 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: When is flecainide contraindicated?
A: Structural heart disease (post-MI, LV dysfunction) — Class IC drugs are proarrhythmic in structural disease (CAST trial).
[Trap: Flecainide is safe for AF in structurally normal hearts ("pill in pocket") — do NOT give in post-MI patients.]

--- CLASS II ---
[Cards covered in Beta-Blockers section above]

--- CLASS III: AMIODARONE ---

[CARD 65 - Type 3: Mnemonic]
Q: What is the mnemonic for amiodarone toxicity?
A: THYROID LUNGS LIVER EYES SKIN = TFT (thyroid), PFTs/CXR (lungs), LFTs (liver), corneal microdeposits (eyes), photodermatitis/slate-grey skin.

[CARD 66 - Type 1: Basic Q&A]
Q: What is amiodarone's primary mechanism?
A: Primarily Class III (K+ channel block → prolongs phase 3 → ↑ refractory period); also has Class I, II, and IV properties — "multi-class."

[CARD 67 - Type 1: Basic Q&A]
Q: Name 3 key indications for amiodarone.
A: AF (rhythm control), refractory VT/VF, WPW syndrome with AF.

[CARD 68 - Type 1: Basic Q&A]
Q: What monitoring is required for patients on amiodarone?
A: TFTs, LFTs, CXR, and PFTs every 6-12 months.

[CARD 69 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: A patient on amiodarone and warfarin has a rising INR. Why?
A: Amiodarone inhibits CYP2C9 → slows warfarin metabolism → potentiates warfarin effect → higher INR.
[Trap: Always halve the warfarin dose and increase INR monitoring when starting amiodarone.]

[CARD 70 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: A patient on amiodarone and digoxin develops bradycardia and signs of digoxin toxicity. Why?
A: Amiodarone raises digoxin levels by inhibiting P-glycoprotein and reducing renal clearance — reduce digoxin dose by 50%.

[CARD 71 - Type 2: Cloze]
[c] Amiodarone [/c] causes both hypothyroidism AND hyperthyroidism because it contains iodine (37% by weight) and blocks peripheral T4→T3 conversion.

--- ADENOSINE ---

[CARD 72 - Type 1: Basic Q&A]
Q: What is the mechanism of adenosine?
A: Activates A1 receptors → hyperpolarises AV node → transiently blocks AV conduction.

[CARD 73 - Type 1: Basic Q&A]
Q: Name 2 key indications for adenosine.
A: First-line treatment for acute SVT termination; diagnostic tool to unmask atrial flutter (exposes flutter waves).

[CARD 74 - Type 1: Basic Q&A]
Q: Name 2 contraindications to adenosine.
A: Asthma (use verapamil instead); WPW + AF (risk of triggering VF by blocking AV node and forcing conduction down accessory pathway).
[Trap: In WPW + AF, adenosine is dangerous — it blocks the AV node and forces ALL conduction down the fast accessory pathway → VF.]

[CARD 75 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What drugs block adenosine's effect?
A: Caffeine and theophylline — they block adenosine A1 receptors; higher doses of adenosine are needed in patients on these drugs.

[CARD 76 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: How should adenosine be administered?
A: Rapid IV bolus into a large vein (antecubital or central) — its half-life is ~10 seconds, so slow administration fails.

--- DIGOXIN ---

[CARD 77 - Type 1: Basic Q&A]
Q: What is the mechanism of digoxin?
A: Inhibits Na+/K+ ATPase → ↑ intracellular Ca2+ (positive inotropy); also ↑ vagal tone → slows AV node (rate control).

[CARD 78 - Type 1: Basic Q&A]
Q: Name 2 key indications for digoxin.
A: AF rate control (especially in HF + AF); symptomatic HFrEF added to ACEi + beta-blocker.

[CARD 79 - Type 2: Cloze]
[c] Digoxin toxicity [/c] can cause ANY arrhythmia — bradycardia, heart block, VT, or VF — making arrhythmia in a digoxin patient the classic HKMLE toxicity scenario.

[CARD 80 - Type 3: Mnemonic]
Q: What is the mnemonic for digoxin toxicity precipitants?
A: DIAL = Diuretics (hypokalaemia), Impaired renal function, Amiodarone, Low Mg (hypomagnesaemia).

[CARD 81 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why does hypokalaemia precipitate digoxin toxicity?
A: K+ and digoxin compete for the same binding site on Na+/K+ ATPase — low K+ means more digoxin binds → toxicity at normal serum digoxin levels.
[Trap: A patient on furosemide + digoxin is at HIGH risk — the diuretic causes hypokalaemia → digoxin toxicity.]

[CARD 82 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: How do you treat severe digoxin toxicity?
A: Correct electrolytes (K+, Mg2+) + digoxin-specific antibody fragments (Digifab/DigiBind).

[CARD 83 - Type 1: Basic Q&A]
Q: Name 3 contraindications to digoxin.
A: HOCM (obstructs outflow tract), WPW + AF (same reason as adenosine — dangerous), AV block.

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SECTION 8: STATINS
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[CARD 84 - Type 1: Basic Q&A]
Q: What is the mechanism of statins?
A: Block HMG-CoA reductase → ↓ hepatic cholesterol synthesis → upregulate LDL receptors → ↓ serum LDL.

[CARD 85 - Type 1: Basic Q&A]
Q: What are the major HKMLE side effects of statins?
A: Myopathy/myalgia (check CK), rhabdomyolysis (rare but serious), hepatotoxicity (raised ALT).

[CARD 86 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which combination is most likely to cause statin-induced rhabdomyolysis?
A: Simvastatin + gemfibrozil — gemfibrozil inhibits CYP3A4 → raises statin levels → rhabdomyolysis.
[Trap: Gemfibrozil and statins should NOT be combined; fenofibrate is the safer fibrate if needed with a statin.]

[CARD 87 - Type 1: Basic Q&A]
Q: When is a statin indicated post-MI, regardless of baseline LDL?
A: Always — statins reduce cardiovascular events post-MI through plaque-stabilising (anti-inflammatory) effects, not just LDL lowering.

[CARD 88 - Type 1: Basic Q&A]
Q: Name the two highest-potency statins.
A: Rosuvastatin and Atorvastatin.

[CARD 89 - Type 1: Basic Q&A]
Q: Name 2 contraindications to statins.
A: Pregnancy, active liver disease.

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SECTION 9: ANTIPLATELET DRUGS
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[CARD 90 - Type 1: Basic Q&A]
Q: What is the mechanism of aspirin as an antiplatelet?
A: Irreversibly blocks COX-1 → ↓ TXA2 → ↓ platelet aggregation (effect lasts for platelet lifespan, ~7-10 days).

[CARD 91 - Type 1: Basic Q&A]
Q: What is the mechanism of clopidogrel?
A: Irreversibly blocks P2Y12 ADP receptor → inhibits platelet aggregation.

[CARD 92 - Type 1: Basic Q&A]
Q: What is the mechanism of ticagrelor vs clopidogrel?
A: Ticagrelor reversibly blocks P2Y12 (unlike clopidogrel which is irreversible).

[CARD 93 - Type 2: Cloze]
[c] Ticagrelor [/c] causes dyspnoea as a unique side effect — it is not bronchospasm and does not indicate lung disease; the mechanism is unclear.
[Trap: Do NOT stop ticagrelor for dyspnoea unless severe — this is NOT an asthma attack.]

[CARD 94 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is DAPT and how long is it continued post-ACS/PCI?
A: Dual antiplatelet therapy = aspirin + P2Y12 inhibitor (clopidogrel, ticagrelor, or prasugrel) for 12 months post-ACS or PCI.

[CARD 95 - Type 1: Basic Q&A]
Q: When should prasugrel be avoided?
A: Prior stroke/TIA, age >75 years, weight <60 kg — higher bleeding risk in these groups.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 10: ANTICOAGULANTS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 96 - Type 1: Basic Q&A]
Q: What is the mechanism of warfarin?
A: Vitamin K antagonist — inhibits clotting factors II, VII, IX, X and proteins C and S.

[CARD 97 - Type 1: Basic Q&A]
Q: How is warfarin reversed urgently vs non-urgently?
A: Urgently: FFP (fresh frozen plasma) or PCC (prothrombin complex concentrate); Non-urgently: Vitamin K (slow onset, 6-12h).

[CARD 98 - Type 2: Cloze]
[c] Warfarin [/c] is the ONLY anticoagulant appropriate for patients with mechanical heart valves — DOACs are contraindicated in this setting.

[CARD 99 - Type 1: Basic Q&A]
Q: Name 3 drugs that potentiate warfarin (increase INR).
A: Amiodarone, metronidazole, fluconazole (all inhibit CYP2C9).

[CARD 100 - Type 1: Basic Q&A]
Q: Name 2 drugs that reduce warfarin effect (decrease INR).
A: Rifampicin, carbamazepine (CYP enzyme inducers — increase warfarin metabolism).

[CARD 101 - Type 1: Basic Q&A]
Q: What is the mechanism of unfractionated heparin (UFH)?
A: Activates antithrombin III → inactivates thrombin (IIa) and Factor Xa.

[CARD 102 - Type 1: Basic Q&A]
Q: How is UFH reversed?
A: Protamine sulfate.

[CARD 103 - Type 1: Basic Q&A]
Q: What is the mechanism of LMWH (enoxaparin)?
A: Activates antithrombin III → mainly inhibits Factor Xa (less thrombin effect vs UFH).

[CARD 104 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: A patient on heparin develops a drop in platelets and new thrombosis. What is the diagnosis and management?
A: Heparin-induced thrombocytopaenia (HIT) — STOP all heparin immediately, switch to argatroban or fondaparinux. Do NOT give platelets (paradoxically thrombogenic).
[Trap: Never transfuse platelets in HIT — it worsens thrombosis. This is a classic HKMLE trap.]

[CARD 105 - Type 1: Basic Q&A]
Q: Name the 2 DOAC types and their mechanisms.
A: Anti-Xa: rivaroxaban, apixaban; Anti-IIa (thrombin): dabigatran.

[CARD 106 - Type 1: Basic Q&A]
Q: What are the reversal agents for DOACs?
A: Dabigatran: idarucizumab; Xa inhibitors (rivaroxaban/apixaban): andexanet alfa.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 11: ACS MANAGEMENT
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 107 - Type 3: Mnemonic]
Q: What is the mnemonic for acute ACS management?
A: MONA = Morphine (pain), Oxygen (only if SpO2 <94%), Nitrates (GTN sublingual), Aspirin 300mg loading dose.

[CARD 108 - Type 3: Mnemonic]
Q: What is the mnemonic for post-MI secondary prevention?
A: ABCDE = Aspirin + P2Y12 (DAPT), Beta-blocker, Cholesterol (statin), DAPT continued + ACEi/ARB, Exercise/Eplerenone (if HF post-MI).

[CARD 109 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: When should oxygen NOT be given in ACS?
A: Do not give oxygen if SpO2 ≥94% — routine oxygen in normoxic ACS patients may increase infarct size.

[CARD 110 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why is morphine used cautiously in NSTEMI?
A: Morphine may increase mortality in NSTEMI — it delays absorption of oral antiplatelets (e.g. ticagrelor) via slowing gastric motility.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 12: HEART FAILURE - DRUG MANAGEMENT
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 111 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which drugs have proven MORTALITY BENEFIT in HFrEF?
A: ACEi/ARB, Beta-blocker (bisoprolol/carvedilol/metoprolol), Spironolactone/Eplerenone, Sacubitril/Valsartan (ARNI), SGLT2 inhibitors (dapagliflozin).
[Trap: Furosemide and digoxin provide SYMPTOM RELIEF only — no mortality benefit.]

[CARD 112 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is the "fantastic four" in modern HFrEF treatment?
A: ACEi (or ARNI) + Beta-blocker + Aldosterone antagonist + SGLT2 inhibitor — all four have mortality benefit.

[CARD 113 - Type 2: Cloze]
[c] Sacubitril/valsartan (ARNI) [/c] replaces ACEi in HFrEF when a patient remains symptomatic on ACEi + beta-blocker + aldosterone antagonist.

[CARD 114 - Type 1: Basic Q&A]
Q: What is the mechanism of ivabradine?
A: Blocks the "funny current" (If) in the SA node → slows HR only (no effect on contractility or blood pressure).

[CARD 115 - Type 1: Basic Q&A]
Q: What are the indications for ivabradine in HF?
A: HFrEF with HR >70 bpm, in sinus rhythm, on maximum tolerated beta-blocker dose.

[CARD 116 - Type 1: Basic Q&A]
Q: What is the unique visual side effect of ivabradine?
A: Phosphenes — transient visual bright spots/flashes.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 13: VASODILATORS / OTHERS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 117 - Type 1: Basic Q&A]
Q: What is the mechanism and key use of hydralazine?
A: Direct arteriolar vasodilator → used for hypertensive crisis in pregnancy (eclampsia) and HF in pregnancy (safe).

[CARD 118 - Type 2: Cloze]
[c] Hydralazine [/c] causes drug-induced lupus with long-term use (same as procainamide and isoniazid).

[CARD 119 - Type 3: Mnemonic]
Q: What is the mnemonic for drugs causing drug-induced lupus?
A: SHIPS = Sulfonamides, Hydralazine, Isoniazid, Procainamide, Statins (rare).

[CARD 120 - Type 1: Basic Q&A]
Q: What is the mechanism of sodium nitroprusside?
A: Releases NO → ↓ both preload and afterload (venous + arterial dilation).

[CARD 121 - Type 1: Basic Q&A]
Q: What is the serious toxicity of prolonged sodium nitroprusside infusion?
A: Cyanide (thiocyanate) toxicity — risk with prolonged high-dose IV infusion.

[CARD 122 - Type 1: Basic Q&A]
Q: Name 2 key indications for sodium nitroprusside.
A: Hypertensive emergency (IV only); aortic dissection (reduces aortic wall stress rapidly).

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
BONUS: DRUG INTERACTION CARDS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 123 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Name 3 drugs that increase warfarin effect (raise INR).
A: Amiodarone, metronidazole, fluconazole — all inhibit CYP2C9 (warfarin metabolism).

[CARD 124 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Name 2 drugs that decrease warfarin effect (lower INR).
A: Rifampicin and carbamazepine — enzyme inducers that accelerate warfarin metabolism.

[CARD 125 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What drug interaction causes simvastatin rhabdomyolysis?
A: Gemfibrozil + simvastatin — gemfibrozil inhibits CYP3A4 → statin accumulates → rhabdomyolysis.

[CARD 126 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: A patient on amiodarone has a rising digoxin level despite unchanged dose. Why?
A: Amiodarone inhibits P-glycoprotein and reduces renal digoxin clearance — reduce digoxin dose by ~50%.

[CARD 127 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why is the combination of verapamil + beta-blocker dangerous?
A: Both slow AV conduction — the combination can cause complete heart block.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
BONUS: CARDIAC DRUGS IN PREGNANCY
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 128 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Name 4 cardiac drugs that are UNSAFE in pregnancy.
A: ACEi and ARBs (teratogenic — renal agenesis/oligohydramnios), warfarin (teratogenic in 1st trimester), statins (teratogenic).

[CARD 129 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which cardiac drugs are SAFE in pregnancy?
A: Methyldopa (first-line hypertension), hydralazine, labetalol, heparin/LMWH (anticoagulation — do not cross placenta).

[CARD 130 - Type 1: Basic Q&A]
Q: Which anticoagulant is safe throughout pregnancy?
A: Heparin (UFH or LMWH) — does not cross the placenta; warfarin and DOACs are avoided.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
BONUS: HIGH-YIELD TRAP SUMMARY
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 131]
Q: HKMLE Trap: Patient on furosemide + digoxin develops toxicity. Why?
A: Furosemide causes hypokalaemia → K+ and digoxin compete for Na+/K+ ATPase → digoxin toxicity at normal levels.

[CARD 132]
Q: HKMLE Trap: Patient with WPW + AF is given adenosine. What happens?
A: Adenosine blocks the AV node → all conduction goes down the fast accessory pathway → extremely rapid ventricular rate → VF.

[CARD 133]
Q: HKMLE Trap: Flecainide is prescribed for a post-MI patient with AF. What is the danger?
A: Flecainide is proarrhythmic in structural heart disease — contraindicated post-MI (CAST trial showed increased mortality).

[CARD 134]
Q: HKMLE Trap: Platelets are given for a patient with HIT and low platelet count. What is wrong?
A: NEVER give platelets in HIT — it is paradoxically thrombogenic and can trigger life-threatening clots.

[CARD 135]
Q: HKMLE Trap: Patient with bilateral renal artery stenosis is started on an ARB. What happens?
A: Acute kidney injury — same mechanism as ACEi. Both are contraindicated in bilateral RAS.

[CARD 136]
Q: HKMLE Trap: A patient needs anticoagulation with a mechanical heart valve. Is a DOAC acceptable?
A: NO — DOACs are contraindicated in mechanical heart valves. Warfarin is the only approved anticoagulant.

[CARD 137]
Q: HKMLE Trap: Patient with HF is given verapamil for rate control. What is the concern?
A: Non-DHP CCBs (verapamil, diltiazem) are contraindicated in HFrEF — they depress myocardial contractility further. Use amlodipine if a CCB is needed.

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END OF DECK — 137 CARDS TOTAL
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HKMLE ANTIBIOTICS & ANTIFUNGALS - ANKI FLASHCARD DECK
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Generated from: Antibiotics and anti fungal 💊.pdf
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MASTER MECHANISM OVERVIEW
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 1 - Type 3: Mnemonic]
Q: What is the mnemonic for antibiotic mechanisms by target?
A: CATCH ME = Cell wall (β-lactams, glycopeptides), Aminoglycosides (30S), Tetracyclines (30S), Cell membrane (polymyxins, daptomycin), Macrolides/Linezolid (50S), Metronidazole (DNA damage), quinolonEs (DNA gyrase/topo IV)

[CARD 2 - Type 3: Mnemonic]
Q: What is the mnemonic for 30S ribosome inhibitors?
A: "30 AT" = Aminoglycosides, Tetracyclines

[CARD 3 - Type 3: Mnemonic]
Q: What is the mnemonic for 50S ribosome inhibitors?
A: "50 MCCL" = Macrolides, Clindamycin, Chloramphenicol, Linezolid

[CARD 4 - Type 3: Mnemonic]
Q: What is the mnemonic for cell wall synthesis drugs?
A: PGC = Penicillins, cephalosporins, Glycopeptides (vancomycin), Carbapenems

[CARD 5 - Type 3: Mnemonic]
Q: What is the mnemonic for DNA mechanism drugs?
A: "FluoroMet" = Fluoroquinolones (DNA gyrase), Metronidazole (DNA damage)

[CARD 6 - Type 1: Basic Q&A]
Q: Which antibiotic class inhibits folate synthesis (step 1)?
A: Sulfonamides (inhibit dihydropteroate synthase).

[CARD 7 - Type 1: Basic Q&A]
Q: Which antibiotic class inhibits folate reduction (step 2)?
A: Trimethoprim (inhibits dihydrofolate reductase).

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 1: PENICILLINS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 8 - Type 3: Mnemonic]
Q: What is the mnemonic for penicillins?
A: "Penicillins Prevent Peptidoglycan Production - Prone to Penicillinase"

[CARD 9 - Type 1: Basic Q&A]
Q: What is the mechanism of penicillins?
A: Bind penicillin-binding proteins (PBPs) → inhibit transpeptidation → ↓ cell wall cross-linking → bactericidal (time-dependent killing).

[CARD 10 - Type 1: Basic Q&A]
Q: What are the two mechanisms of penicillin resistance?
A: β-lactamase (penicillinase) production; altered PBPs (MRSA mechanism).

[CARD 11 - Type 1: Basic Q&A]
Q: What is the drug of choice for MSSA infections?
A: Flucloxacillin (anti-staphylococcal penicillin).
[Trap: Flucloxacillin covers MSSA ONLY — it does NOT cover MRSA.]

[CARD 12 - Type 2: Cloze]
[c] Flucloxacillin [/c] must be taken 30 minutes before food because food significantly reduces its oral absorption.

[CARD 13 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: A young patient with EBV (mononucleosis) is given ampicillin and develops a widespread rash. Is this a true penicillin allergy?
A: No — ampicillin rash in EBV is a non-allergic maculopapular rash; it is NOT a true penicillin allergy and the patient can receive penicillins in the future.
[Trap: This is a classic HKMLE trap — do not label the patient as penicillin-allergic.]

[CARD 14 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is the cross-reactivity rate between penicillin and cephalosporins?
A: ~1-2% (NOT 10% as historically cited); major penicillin allergy (anaphylaxis) = avoid all β-lactams; minor rash = cephalosporins usually safe.
[Trap: The old "10% cross-reactivity" figure is outdated — HKMLE uses the current ~1-2% figure.]

[CARD 15 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: An elderly male on prolonged co-amoxiclav develops jaundice. What is the diagnosis?
A: Co-amoxiclav (amoxicillin-clavulanate) cholestatic hepatotoxicity — especially in elderly males on prolonged courses.

[CARD 16 - Type 1: Basic Q&A]
Q: Which penicillin covers Listeria (important in neonatal meningitis)?
A: Ampicillin or amoxicillin.

[CARD 17 - Type 1: Basic Q&A]
Q: Which penicillin combination covers Pseudomonas?
A: Piperacillin-tazobactam (Tazocin) — must be combined with a β-lactamase inhibitor.

[CARD 18 - Type 1: Basic Q&A]
Q: What is the role of clavulanate in co-amoxiclav?
A: Clavulanate is a β-lactamase inhibitor — it protects amoxicillin from β-lactamase degradation, broadening coverage to include MSSA, anaerobes, and some gram-negatives.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 2: CEPHALOSPORINS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 19 - Type 3: Mnemonic]
Q: What is the mnemonic for cephalosporin generations?
A: "GAPS get Bigger with generation — 1st = MSSA/Strep; 5th = MRSA"

[CARD 20 - Type 1: Basic Q&A]
Q: What is the gold standard surgical prophylaxis cephalosporin?
A: 1st generation — cefazolin (IV) or cefalexin (oral).

[CARD 21 - Type 1: Basic Q&A]
Q: Which 3rd generation cephalosporin is drug of choice for bacterial meningitis?
A: Ceftriaxone (+ ampicillin to cover Listeria empirically).

[CARD 22 - Type 1: Basic Q&A]
Q: Which 3rd generation cephalosporin covers Pseudomonas?
A: Ceftazidime — the only 3rd gen cephalosporin with anti-pseudomonal activity.
[Trap: Ceftriaxone and cefotaxime do NOT cover Pseudomonas — only ceftazidime among 3rd gen.]

[CARD 23 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which cephalosporin covers MRSA?
A: Only ceftaroline (5th generation) — no other cephalosporin covers MRSA.
[Trap: A common wrong answer is ceftriaxone for MRSA — it has no MRSA activity.]

[CARD 24 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Do cephalosporins cover Enterococcus?
A: No — no cephalosporin reliably covers Enterococcus; use penicillin or vancomycin.

[CARD 25 - Type 1: Basic Q&A]
Q: What is the unique side effect of ceftriaxone in children?
A: Biliary sludge/pseudolithiasis (ceftriaxone precipitates in bile).

[CARD 26 - Type 1: Basic Q&A]
Q: Which cephalosporin is used for single-dose IM treatment of gonorrhoea?
A: Ceftriaxone (3rd gen, IM single dose).

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 3: CARBAPENEMS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 27 - Type 3: Mnemonic]
Q: What is the mnemonic for carbapenems?
A: "Carbapenems = Carpet-bomb everything (widest β-lactam spectrum) — but NOT MRSA"

[CARD 28 - Type 1: Basic Q&A]
Q: What is the coverage of carbapenems?
A: Extremely broad — gram+, gram-, anaerobes, Pseudomonas (imipenem/meropenem); NOT MRSA, NOT Stenotrophomonas.

[CARD 29 - Type 2: Cloze]
[c] Imipenem [/c] causes seizures more than other carbapenems because it is a GABA receptor antagonist; meropenem is preferred for CNS infections.

[CARD 30 - Type 1: Basic Q&A]
Q: Why is imipenem always combined with cilastatin?
A: Cilastatin inhibits renal dehydropeptidase-I, preventing renal metabolism of imipenem (and reducing nephrotoxicity).

[CARD 31 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which carbapenem does NOT cover Pseudomonas?
A: Ertapenem — no Pseudomonas or Acinetobacter coverage; used for ESBL gram-negatives without Pseudomonas risk.

[CARD 32 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Carbapenem-resistant Enterobacteriaceae (CRE/KPC) — what do you treat with?
A: Colistin/polymyxin B or newer agents (ceftazidime-avibactam) — classic HKMLE MDR scenario.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 4: AZTREONAM (MONOBACTAM)
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 33 - Type 1: Basic Q&A]
Q: What is the coverage of aztreonam?
A: Gram-negative aerobic organisms only (including Pseudomonas) — NO gram-positive, NO anaerobes.

[CARD 34 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: When is aztreonam the preferred choice?
A: Gram-negative infections in patients with severe penicillin/β-lactam allergy — aztreonam has minimal cross-reactivity with other β-lactams.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 5: GLYCOPEPTIDES — VANCOMYCIN & TEICOPLANIN
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 35 - Type 3: Mnemonic]
Q: What is the mnemonic for vancomycin?
A: "VanCOMycin = VAN for MRSA, COM-plications: Red man, neCROsis (nephro/oto)"

[CARD 36 - Type 3: Mnemonic]
Q: What is the mnemonic for vancomycin toxicities?
A: "RED MAN" = Renal (nephrotoxicity), Ear (ototoxicity), Drip-rate reaction (red man syndrome)

[CARD 37 - Type 1: Basic Q&A]
Q: What is the mechanism of vancomycin?
A: Binds D-Ala-D-Ala terminus of peptidoglycan precursors → inhibits cell wall synthesis (different site from β-lactams — NOT cross-resistant).

[CARD 38 - Type 1: Basic Q&A]
Q: What is the coverage of vancomycin?
A: Gram-positive only — MRSA, MSSA, Enterococcus, Streptococcus; oral only for C. difficile (not absorbed systemically).

[CARD 39 - Type 2: Cloze]
[c] Red man syndrome [/c] is caused by rapid vancomycin infusion triggering histamine release → flushing, rash, hypotension — it is NOT a true allergy; slow the infusion rate and premedicate with antihistamine.
[Trap: Red man syndrome is NOT an allergy — do not label the patient allergic to vancomycin; slow the infusion instead.]

[CARD 40 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: A patient on oral vancomycin for C. difficile — will it treat MRSA bacteraemia?
A: No — oral vancomycin stays in the gut (not absorbed); IV vancomycin is required for systemic MRSA infections.
[Trap: Oral vs IV vancomycin have completely different indications — a classic HKMLE distinction.]

[CARD 41 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What dangerous combination significantly increases nephrotoxicity with vancomycin?
A: Vancomycin + aminoglycosides — synergistic nephrotoxicity; avoid this combination.

[CARD 42 - Type 1: Basic Q&A]
Q: What vancomycin monitoring levels are targeted for MRSA bacteraemia/endocarditis?
A: Trough levels 15-20 µg/mL (or AUC/MIC ≥400 preferred in modern practice).

[CARD 43 - Type 1: Basic Q&A]
Q: What is used instead of vancomycin for VRE infections?
A: Linezolid or daptomycin.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 6: AMINOGLYCOSIDES
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 44 - Type 3: Mnemonic]
Q: What is the mnemonic for aminoglycosides?
A: "AMINO = Always Monitor (nephro/oto toxic), Never Once without Oxygen (aerobes only), Inject IV"

[CARD 45 - Type 3: Mnemonic]
Q: What is the memory aid for aminoglycoside use?
A: "GET SMART" = Gentamicin, tobramycin — Synergy, Monitoring, Aerobic only, Renal/ear Toxicity

[CARD 46 - Type 1: Basic Q&A]
Q: What is the mechanism of aminoglycosides?
A: Bind 30S ribosomal subunit → misreading of mRNA → abnormal protein synthesis → bactericidal; concentration-dependent killing.

[CARD 47 - Type 1: Basic Q&A]
Q: Why do aminoglycosides NOT work against anaerobes?
A: Aminoglycosides require oxygen for active uptake into bacteria — anaerobic environments prevent drug entry.

[CARD 48 - Type 2: Cloze]
[c] Aminoglycosides [/c] cause irreversible ototoxicity affecting both cochlear (hearing loss) and vestibular (balance) function.
[Trap: Ototoxicity from aminoglycosides is IRREVERSIBLE — this distinguishes it from vancomycin ototoxicity which is often reversible if caught early.]

[CARD 49 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What two drug combinations significantly increase aminoglycoside toxicity?
A: Aminoglycosides + loop diuretics (furosemide) = ↑ ototoxicity; aminoglycosides + vancomycin = ↑ nephrotoxicity.

[CARD 50 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why are aminoglycosides contraindicated in myasthenia gravis?
A: They cause neuromuscular blockade — exacerbates myasthenic weakness and can trigger respiratory failure.

[CARD 51 - Type 1: Basic Q&A]
Q: Which aminoglycoside is used for TB and plague?
A: Streptomycin.

[CARD 52 - Type 1: Basic Q&A]
Q: Which aminoglycoside is given inhaled for cystic fibrosis?
A: Tobramycin (inhaled for Pseudomonas in CF).

[CARD 53 - Type 1: Basic Q&A]
Q: What is the role of gentamicin in endocarditis?
A: Synergy with β-lactams or vancomycin for Enterococcus and Streptococcus endocarditis (low-dose synergistic dosing).

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 7: MACROLIDES
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 54 - Type 3: Mnemonic]
Q: What is the mnemonic for macrolides?
A: "MAcrolides = Motility promoters (GI prokinetic), Atypical cover, CYP inhibitors (drug interactions)"

[CARD 55 - Type 1: Basic Q&A]
Q: What is the mechanism of macrolides?
A: Bind 50S ribosomal subunit (23S rRNA) → inhibit translocation → bacteriostatic (bactericidal at high doses).

[CARD 56 - Type 1: Basic Q&A]
Q: Name 3 atypical organisms covered by macrolides.
A: Mycoplasma, Chlamydia, Legionella (also Bordetella pertussis, H. pylori with clarithromycin).

[CARD 57 - Type 1: Basic Q&A]
Q: Which macrolide is used as a single 1g dose for Chlamydia?
A: Azithromycin (single dose 1g oral — longest half-life due to tissue accumulation).

[CARD 58 - Type 2: Cloze]
[c] Clarithromycin [/c] is the strongest CYP3A4 inhibitor among macrolides — raising warfarin (↑ INR) and statin (rhabdomyolysis risk) levels.

[CARD 59 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which macrolide is teratogenic and must be avoided in pregnancy?
A: Clarithromycin — animal studies show teratogenicity; use erythromycin base or azithromycin instead.
[Trap: Not all macrolides are the same in pregnancy — erythromycin BASE is safe; clarithromycin is NOT.]

[CARD 60 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which macrolide causes cholestatic jaundice and is avoided in pregnancy?
A: Erythromycin estolate (the estolate salt form) — use erythromycin base instead in pregnancy.

[CARD 61 - Type 2: Cloze]
[c] All macrolides [/c] prolong the QT interval — azithromycin has the highest QT-prolonging risk among the class.

[CARD 62 - Type 1: Basic Q&A]
Q: Which macrolide has a GI prokinetic effect and is used for gastroparesis?
A: Erythromycin (motilin receptor agonist → stimulates gastric motility).

[CARD 63 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Clarithromycin + simvastatin — what is the risk?
A: Rhabdomyolysis — clarithromycin inhibits CYP3A4 → raises statin levels → myotoxicity.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 8: FLUOROQUINOLONES
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 64 - Type 3: Mnemonic]
Q: What is the mnemonic for fluoroquinolone side effects?
A: FLOX = Football (tendon rupture), Liver (hepatotoxicity), QT prolongation, X-ray (avoid in children — cartilage damage)

[CARD 65 - Type 1: Basic Q&A]
Q: What is the mechanism of fluoroquinolones?
A: Inhibit DNA gyrase (gram-negative) and Topoisomerase IV (gram-positive) → prevent DNA replication → bactericidal (concentration-dependent).

[CARD 66 - Type 1: Basic Q&A]
Q: Name 4 key side effects of fluoroquinolones.
A: Tendinopathy/tendon rupture (Achilles), QT prolongation, CNS effects (seizures, insomnia), C. difficile colitis, photosensitivity.

[CARD 67 - Type 2: Cloze]
[c] Fluoroquinolones [/c] cause Achilles tendon rupture — risk is highest in elderly patients on concurrent corticosteroids or with renal failure.
[Trap: The classic HKMLE scenario is elderly patient + steroids + fluoroquinolone → tendon rupture.]

[CARD 68 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Ciprofloxacin + theophylline — what is the danger?
A: Ciprofloxacin inhibits CYP1A2 → raises theophylline levels → toxicity (arrhythmia, seizures).
[Trap: This is a classic HKMLE drug interaction — always check theophylline levels when starting ciprofloxacin.]

[CARD 69 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why is moxifloxacin NOT used for UTI?
A: Moxifloxacin is hepatically eliminated with low urinary excretion — it does not achieve therapeutic levels in urine.
[Trap: Common wrong answer is moxifloxacin for UTI — use ciprofloxacin or levofloxacin instead.]

[CARD 70 - Type 1: Basic Q&A]
Q: Which fluoroquinolone has the best anti-pseudomonal activity?
A: Ciprofloxacin (highest anti-pseudomonal activity among fluoroquinolones).

[CARD 71 - Type 1: Basic Q&A]
Q: Which fluoroquinolones are "respiratory quinolones" (better gram-positive/atypical coverage)?
A: Levofloxacin and moxifloxacin — used for CAP when atypical cover is needed.

[CARD 72 - Type 3: Mnemonic]
Q: What is the mnemonic for organisms causing C. difficile (common culprit antibiotics)?
A: "C's and A's" = Cephalosporins, Clindamycin, Co-amoxiclav, Aminopenicillins, And fluoroquinolones

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 9: TETRACYCLINES
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 73 - Type 3: Mnemonic]
Q: What is the mnemonic for tetracycline features?
A: TETRACYCLE = Teeth stain, Embryo harm, Treats atypicals, Rickettsiae, Acne, C. pylori (historical), Young children avoid, Cross BBB, Light sensitivity, Esophageal irritation

[CARD 74 - Type 1: Basic Q&A]
Q: What is the mechanism of tetracyclines?
A: Bind 30S ribosome → block aminoacyl-tRNA binding → inhibit protein synthesis → bacteriostatic.

[CARD 75 - Type 1: Basic Q&A]
Q: Name 4 organisms where tetracyclines (doxycycline) are the drug of choice.
A: Rickettsia (RMSF — DOC!), Chlamydia, Lyme disease (Borrelia), Brucellosis.

[CARD 76 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is the drug of choice for Rocky Mountain Spotted Fever (RMSF), even in children?
A: Doxycycline — the risk of untreated RMSF (life-threatening) outweighs the dental risk; the <8 years rule is relaxed here.
[Trap: Do NOT withhold doxycycline in RMSF because of patient age — this is an exam-tested exception.]

[CARD 77 - Type 2: Cloze]
[c] Tetracyclines [/c] are contraindicated in children under 8 years because they bind calcium in developing teeth and bones → permanent discolouration and enamel hypoplasia.

[CARD 78 - Type 2: Cloze]
[c] Tetracyclines [/c] are chelated by divalent cations (Ca2+, Mg2+, Al3+, Fe2+) in antacids, milk, and iron supplements → dramatically reduced oral absorption; take separately by 2-3 hours.

[CARD 79 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which tetracycline is safe in renal failure?
A: Doxycycline — hepatically eliminated, not renally; does not accumulate in CKD. All other tetracyclines are avoided in renal failure.

[CARD 80 - Type 1: Basic Q&A]
Q: What is a unique rare CNS side effect of tetracyclines?
A: Pseudotumour cerebri (benign intracranial hypertension — ↑ ICP, headache, papilloedema).

[CARD 81 - Type 1: Basic Q&A]
Q: Which tetracycline has the broadest coverage including MDR gram-negatives and anaerobes?
A: Tigecycline (IV only) — broadest tetracycline but NOT Pseudomonas.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 10: METRONIDAZOLE
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 82 - Type 3: Mnemonic]
Q: What is the mnemonic for metronidazole?
A: "METRO = Must avoid alcohol, Then DNA damaged (anaerobes), Reduces warfarin clearance (inhibits CYP), Obese bugs and protozoa killed (anaerobes + protozoa)"

[CARD 83 - Type 1: Basic Q&A]
Q: What is the mechanism of metronidazole?
A: Prodrug activated by bacterial/protozoal nitroreductases → forms reactive intermediates → DNA strand breaks → bactericidal.

[CARD 84 - Type 1: Basic Q&A]
Q: What organisms does metronidazole cover?
A: Obligate anaerobes (Bacteroides fragilis, Clostridium) and protozoa (Giardia, Entamoeba, Trichomonas) — NO aerobic bacteria.

[CARD 85 - Type 2: Cloze]
[c] Metronidazole [/c] causes a disulfiram-like reaction with alcohol (flushing, nausea, vomiting, hypotension) due to acetaldehyde accumulation — also triggered by alcohol-containing mouthwashes.

[CARD 86 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Metronidazole + warfarin — what happens?
A: ↑ INR — metronidazole inhibits CYP2C9 → ↓ warfarin metabolism → potentiated anticoagulant effect.
[Trap: Classic HKMLE drug interaction — always check INR when starting metronidazole in a patient on warfarin.]

[CARD 87 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: C. difficile treatment — mild/moderate vs severe?
A: Mild/moderate = oral metronidazole (or oral vancomycin); Severe = oral vancomycin or fidaxomicin.

[CARD 88 - Type 1: Basic Q&A]
Q: Why must metronidazole always be combined with another antibiotic in mixed infections?
A: Metronidazole does NOT cover aerobic bacteria — it must be paired with a broad-spectrum agent for mixed aerobic/anaerobic coverage.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 11: LINEZOLID (OXAZOLIDINONE)
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 89 - Type 3: Mnemonic]
Q: What is the mnemonic for linezolid?
A: "LINEZOLID = Last resort, Inhibits 50S, No MAO (MAOI activity), Expensive, Zaps MRSA/VRE, Orange-ish (serotonin risk), Lowers platelet count, Inhibits bone marrow"

[CARD 90 - Type 1: Basic Q&A]
Q: What is the mechanism of linezolid?
A: Binds 50S ribosomal subunit (unique site: 23S rRNA-peptidyl transferase centre) → prevents formation of 70S initiation complex → bacteriostatic (bactericidal vs Streptococcus).

[CARD 91 - Type 1: Basic Q&A]
Q: What is the coverage of linezolid?
A: Gram-positive only — MRSA, VRE, drug-resistant Streptococcus, MSSA (backup).

[CARD 92 - Type 2: Cloze]
[c] Linezolid [/c] is a reversible MAO inhibitor — combining it with SSRIs, SNRIs, or tramadol causes serotonin syndrome.
[Trap: Do NOT combine linezolid with any serotonergic drug — this is a classic HKMLE drug interaction.]

[CARD 93 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why is linezolid preferred over daptomycin for MRSA pneumonia?
A: Daptomycin is inactivated by pulmonary surfactant → cannot be used for lung infections; linezolid achieves excellent lung penetration.
[Trap: Common wrong answer is daptomycin for MRSA pneumonia — always use linezolid for MRSA lung infections.]

[CARD 94 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is the unique pharmacokinetic advantage of linezolid?
A: 100% oral bioavailability — oral linezolid is as effective as IV; allows seamless step-down from hospital to home.

[CARD 95 - Type 1: Basic Q&A]
Q: What haematological side effect requires weekly FBC monitoring with linezolid?
A: Myelosuppression — thrombocytopaenia is most common (monitor FBC weekly for courses >2 weeks).

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 12: CLINDAMYCIN
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 96 - Type 1: Basic Q&A]
Q: What is the mechanism of clindamycin?
A: Binds 50S ribosome → blocks translocation → bacteriostatic.

[CARD 97 - Type 1: Basic Q&A]
Q: What is the key anaerobic coverage difference between clindamycin and metronidazole?
A: Clindamycin covers anaerobes ABOVE the diaphragm (e.g. aspiration pneumonia, dental/oral); metronidazole is preferred for below-diaphragm anaerobes.

[CARD 98 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which antibiotic carries the HIGHEST risk of C. difficile colitis?
A: Clindamycin — always warn patients to report diarrhoea immediately when prescribing.
[Trap: While many antibiotics cause C. diff, clindamycin is the classic highest-risk answer on HKMLE.]

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 13: CO-TRIMOXAZOLE (TMP-SMX)
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 99 - Type 1: Basic Q&A]
Q: What is the mechanism of co-trimoxazole (TMP-SMX)?
A: Sequential double block of folate synthesis — sulfamethoxazole inhibits dihydropteroate synthase; trimethoprim inhibits dihydrofolate reductase → synergistic bactericidal effect.

[CARD 100 - Type 1: Basic Q&A]
Q: What is the primary indication for co-trimoxazole in immunocompromised patients?
A: PCP (Pneumocystis jirovecii pneumonia) — first-line for prophylaxis AND treatment in HIV/immunocompromised.

[CARD 101 - Type 2: Cloze]
[c] Co-trimoxazole [/c] causes Stevens-Johnson syndrome (SJS/TEN) — a severe blistering skin reaction from the sulfonamide component.

[CARD 102 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: A patient on TMP-SMX and ACEi develops hyperkalaemia. Why?
A: Trimethoprim blocks potassium excretion in the collecting duct (amiloride-like ENaC block) — combined with ACEi, hyperkalaemia can be severe.
[Trap: TMP-SMX hyperkalaemia is a classic HKMLE trap — especially dangerous in patients already on ACEi/ARBs/spironolactone.]

[CARD 103 - Type 1: Basic Q&A]
Q: Name 3 contraindications to co-trimoxazole.
A: Severe renal impairment, pregnancy (folate antagonism → neural tube defects — give folic acid), G6PD deficiency (haemolysis from sulfa component).

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 14: ANTIFUNGALS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 104 - Type 3: Mnemonic]
Q: What is the mnemonic for antifungal targets?
A: "EEE" = Ergosterol binding (polyenes/amphotericin B), Ergosterol synthesis (azoles), Exoskeleton/cell wall glucan (echinocandins)

--- AMPHOTERICIN B ---

[CARD 105 - Type 3: Mnemonic]
Q: What is the mnemonic for amphotericin B?
A: "Ampho-TERRIBLE = Terrible side effects but Terrific spectrum"

[CARD 106 - Type 1: Basic Q&A]
Q: What is the mechanism of amphotericin B?
A: Binds ergosterol in fungal cell membrane → forms pores → K+ leakage → cell death (fungicidal).

[CARD 107 - Type 1: Basic Q&A]
Q: What is the coverage of amphotericin B?
A: Broadest antifungal — Candida, Aspergillus, Cryptococcus, Mucor, Histoplasma, Coccidioides, Blastomyces; also Leishmaniasis.

[CARD 108 - Type 1: Basic Q&A]
Q: Name 3 major side effects of amphotericin B.
A: "Shake and bake" (rigors + fever during infusion), nephrotoxicity (hypokalaemia, hypomagnesaemia, renal tubular acidosis — dose-limiting), anaemia (↓ EPO).

[CARD 109 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: How do you reduce amphotericin B nephrotoxicity?
A: Use liposomal amphotericin B (AmBisome) — same antifungal efficacy, much less nephrotoxicity; preferred in renal impairment.

[CARD 110 - Type 1: Basic Q&A]
Q: How do you premedicate before amphotericin B infusion to reduce infusion reactions?
A: Paracetamol + antihistamine + hydrocortisone before infusion; monitor and correct K+ and Mg2+ throughout treatment.

--- AZOLE ANTIFUNGALS ---

[CARD 111 - Type 3: Mnemonic]
Q: What is the mnemonic for azole antifungals?
A: "AZOLES = All inhibit CYP (P450), Zero gram+/gram- activity, Only fungi, Liver monitoring, Ergosterol synthesis blocked"

[CARD 112 - Type 1: Basic Q&A]
Q: What is the mechanism of azole antifungals?
A: Inhibit fungal CYP51 (lanosterol 14α-demethylase) → ↓ ergosterol synthesis → altered membrane function → fungistatic.

[CARD 113 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Does fluconazole cover Aspergillus?
A: NO — fluconazole does NOT cover Aspergillus; use voriconazole for invasive aspergillosis.
[Trap: This is the most tested azole coverage gap — fluconazole only covers Candida and Cryptococcus.]

[CARD 114 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is the first-line treatment for invasive aspergillosis?
A: Voriconazole (IV/oral) — first-line for invasive aspergillosis.

[CARD 115 - Type 1: Basic Q&A]
Q: What unique visual side effect does voriconazole cause?
A: Visual disturbances — hallucinations, photopsia (seeing lights/flashes); this is a characteristic side effect unique to voriconazole.

[CARD 116 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which azole is contraindicated in heart failure?
A: Itraconazole — it has a negative inotropic effect (↓ cardiac contractility); contraindicated in HF.
[Trap: Other azoles do not have this cardiac effect — itraconazole HF contraindication is a unique HKMLE point.]

[CARD 117 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which antifungals cover Mucormycosis (Mucor/Rhizopus)?
A: Liposomal amphotericin B (first-line), then posaconazole or isavuconazole (step-down); fluconazole and voriconazole do NOT cover Mucor.
[Trap: Voriconazole has NO activity against Mucor — a classic coverage gap tested on HKMLE.]

[CARD 118 - Type 1: Basic Q&A]
Q: Which azole is used for maintenance therapy of Cryptococcal meningitis after induction?
A: Fluconazole (fluconazole consolidation/maintenance after amphotericin B + flucytosine induction).

[CARD 119 - Type 2: Cloze]
[c] All azoles [/c] inhibit CYP3A4 → raise warfarin (↑ INR), statin (rhabdomyolysis), and tacrolimus/cyclosporin (nephrotoxicity) levels — monitor closely.

[CARD 120 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why must posaconazole be taken with food?
A: Posaconazole requires food (fatty meal) for adequate absorption — TDM (therapeutic drug monitoring) is also required.

--- ECHINOCANDINS ---

[CARD 121 - Type 3: Mnemonic]
Q: What is the mnemonic for echinocandins?
A: "Echinocandins = Echo = They WALL off fungi (inhibit cell wall β-1,3-glucan synthesis)"

[CARD 122 - Type 1: Basic Q&A]
Q: What is the mechanism of echinocandins?
A: Inhibit β-1,3-glucan synthase → ↓ fungal cell wall synthesis (unique fungal target → excellent safety profile).

[CARD 123 - Type 1: Basic Q&A]
Q: What is the coverage of echinocandins?
A: Candida (including azole-resistant species), Aspergillus (not first-line); NOT Cryptococcus, NOT Mucor.

[CARD 124 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is the first-line antifungal for invasive candidiasis in ICU/haemodynamically unstable patients?
A: Echinocandin (caspofungin or micafungin) — first-line in ICU or azole-exposed patients.

[CARD 125 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Are echinocandins available as oral formulations?
A: No — echinocandins are IV only (no oral formulation available); plan accordingly for step-down therapy.

--- FLUCYTOSINE ---

[CARD 126 - Type 1: Basic Q&A]
Q: What is the mechanism of flucytosine?
A: Converted to 5-fluorouracil (5-FU) inside fungal cells → inhibits DNA/RNA synthesis.

[CARD 127 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: When is flucytosine used and why is it never used alone?
A: Flucytosine is used in combination for Cryptococcal meningitis (+ amphotericin B for 2-week induction) — monotherapy causes rapid resistance.

[CARD 128 - Type 1: Basic Q&A]
Q: What toxicities require monitoring during flucytosine therapy?
A: Myelosuppression (leucopenia, thrombocytopaenia) and hepatotoxicity — monitor FBC and LFTs.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 15: KEY DRUG INTERACTIONS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 129 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Metronidazole + warfarin — effect and mechanism?
A: ↑ INR — metronidazole inhibits CYP2C9 → ↓ warfarin breakdown → increased bleeding risk.

[CARD 130 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Metronidazole + alcohol — what happens?
A: Disulfiram-like reaction (flushing, vomiting, hypotension) — metronidazole blocks aldehyde dehydrogenase → acetaldehyde accumulates. Also triggered by alcohol-containing mouthwashes.

[CARD 131 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Ciprofloxacin + theophylline — effect and mechanism?
A: ↑ Theophylline toxicity (arrhythmia, seizures) — ciprofloxacin inhibits CYP1A2 → ↓ theophylline metabolism.

[CARD 132 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Rifampicin + warfarin/OCP/ART/tacrolimus — what happens?
A: ↓ Efficacy of all co-administered drugs — rifampicin is a potent CYP450 inducer → accelerates drug metabolism.
[Trap: Rifampicin reduces the effectiveness of the OCP — a classic missed contraception trap.]

[CARD 133 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Fluconazole + warfarin — effect and mechanism?
A: Significantly ↑ INR — fluconazole inhibits CYP2C9 → ↓ warfarin metabolism → bleeding risk.

[CARD 134 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Linezolid + SSRIs — what is the risk?
A: Serotonin syndrome — linezolid is a reversible MAO inhibitor; combining with any serotonergic drug is dangerous.

[CARD 135 - Type 1: Basic Q&A]
Q: Clarithromycin + simvastatin — what is the risk and mechanism?
A: Rhabdomyolysis — clarithromycin inhibits CYP3A4 → statin accumulates → myotoxicity.

[CARD 136 - Type 1: Basic Q&A]
Q: Aminoglycosides + furosemide — what is the risk?
A: Additive ototoxicity — both are independently ototoxic; combination greatly ↑ cochlear/vestibular damage risk.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 16: ANTIBIOTICS IN PREGNANCY
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 137 - Type 3: Mnemonic]
Q: What is the mnemonic for antibiotics safe in pregnancy?
A: "SAFE MOM" = Safest: Penicillins, Azithromycin, FEw cephalosporins, Erythromycin base, Metronidazole (avoid T1)

[CARD 138 - Type 3: Mnemonic]
Q: What is the mnemonic for antibiotics to avoid in pregnancy?
A: "FCAT" = Fluoroquinolones, Cotrimoxazole (T1), Aminoglycosides (streptomycin — fetal ototoxicity), Tetracyclines

[CARD 139 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which antibiotics are SAFE throughout pregnancy?
A: Penicillins (all), cephalosporins, erythromycin BASE, azithromycin, clindamycin.

[CARD 140 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why is trimethoprim avoided in the 1st trimester of pregnancy?
A: Trimethoprim is a folate antagonist → risk of neural tube defects in T1; if must be used, give folic acid supplementation.

[CARD 141 - Type 2: Cloze]
[c] Chloramphenicol [/c] causes Grey Baby Syndrome near term — neonatal cardiovascular collapse due to inability to metabolise the drug.

[CARD 142 - Type 1: Basic Q&A]
Q: Why is nitrofurantoin avoided near term (3rd trimester)?
A: Risk of haemolytic anaemia in the neonate due to immature erythrocyte glutathione pathways (G6PD-like vulnerability at term).

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 17: ORGANISM-TO-DRUG COVERAGE CHEAT CARDS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 143 - Type 1: Basic Q&A]
Q: First-line IV treatment for MRSA bacteraemia/serious systemic infection?
A: Vancomycin IV (trough 15-20 µg/mL for bacteraemia/endocarditis).

[CARD 144 - Type 1: Basic Q&A]
Q: First-line treatment for community-acquired MRSA skin/soft tissue infection?
A: Doxycycline or TMP-SMX (co-trimoxazole).

[CARD 145 - Type 1: Basic Q&A]
Q: First-line antibiotic coverage for Pseudomonas aeruginosa?
A: Piperacillin-tazobactam, ceftazidime, cefepime, meropenem, or ciprofloxacin (contextually dependent).

[CARD 146 - Type 1: Basic Q&A]
Q: Treatment for ESBL gram-negative infection?
A: Meropenem (or ertapenem if Pseudomonas not a concern).

[CARD 147 - Type 1: Basic Q&A]
Q: Treatment for severe C. difficile?
A: Oral vancomycin or fidaxomicin (fidaxomicin preferred if available — lower recurrence).

[CARD 148 - Type 1: Basic Q&A]
Q: Three-phase treatment of Cryptococcal meningitis?
A: Induction: amphotericin B + flucytosine (2 weeks) → Consolidation: fluconazole (8 weeks) → Maintenance: fluconazole.

[CARD 149 - Type 1: Basic Q&A]
Q: First-line treatment for atypical pneumonia (Mycoplasma, Chlamydia)?
A: Macrolide (azithromycin) or doxycycline or levofloxacin.

[CARD 150 - Type 1: Basic Q&A]
Q: Drug of choice for Legionella pneumonia?
A: Levofloxacin or azithromycin.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
BONUS: HIGH-YIELD TRAP SUMMARY CARDS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 151]
Q: HKMLE Trap: Patient with EBV gets ampicillin and develops a rash — is this a penicillin allergy?
A: NO — ampicillin + EBV rash is a non-allergic drug-virus interaction; do NOT label as penicillin-allergic.

[CARD 152]
Q: HKMLE Trap: Patient needs antifungal for invasive aspergillosis. Is fluconazole appropriate?
A: NO — fluconazole has NO activity against Aspergillus; use voriconazole (first-line).

[CARD 153]
Q: HKMLE Trap: Patient with MRSA pneumonia is given daptomycin. What is the problem?
A: Daptomycin is inactivated by pulmonary surfactant — it CANNOT treat lung infections; use linezolid or vancomycin for MRSA pneumonia.

[CARD 154]
Q: HKMLE Trap: Oral vancomycin is prescribed for MRSA bloodstream infection. Will it work?
A: NO — oral vancomycin is NOT absorbed systemically; it only treats C. difficile in the gut. Use IV vancomycin for MRSA bacteraemia.

[CARD 155]
Q: HKMLE Trap: Patient with HF is started on itraconazole for onychomycosis. What is the concern?
A: Itraconazole has negative inotropic effects — contraindicated in heart failure.

[CARD 156]
Q: HKMLE Trap: Moxifloxacin is prescribed for a complicated UTI. What is wrong?
A: Moxifloxacin has negligible urinary excretion — it does NOT achieve therapeutic levels in urine; use ciprofloxacin or levofloxacin.

[CARD 157]
Q: HKMLE Trap: Patient starts ciprofloxacin while on theophylline — what must you do?
A: Check theophylline levels — ciprofloxacin inhibits CYP1A2 and can cause life-threatening theophylline toxicity (arrhythmia, seizures).

[CARD 158]
Q: HKMLE Trap: Flucytosine is given alone for Cryptococcal meningitis. What is the problem?
A: Flucytosine monotherapy rapidly develops resistance — it is ONLY used in combination with amphotericin B.

[CARD 159]
Q: HKMLE Trap: Doxycycline is withheld from a child with Rocky Mountain Spotted Fever because of age. What is the risk?
A: RMSF is life-threatening — doxycycline is the DOC even in children <8 years; the dental risk is outweighed by the mortality risk.

[CARD 160]
Q: HKMLE Trap: A patient on linezolid is prescribed sertraline (SSRI) for depression. What happens?
A: Serotonin syndrome — linezolid's MAO-inhibiting activity + SSRI = potentially fatal combination.

================================================================
END OF DECK — 160 CARDS TOTAL
================================================================

================================================================
HKMLE EMERGENCY & TOXICOLOGY — ANKI FLASHCARD DECK
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Generated from: Emergency and toxicology 💊.pdf
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SECTION 1: APPROACH TO POISONING & TOXIDROMES
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 1 - Type 3: Mnemonic]
Q: What is the mnemonic for the approach to poisoning?
A: DRIED = Decontaminate, Resuscitate, Identify toxidrome, Enhance elimination, Deliver antidote

[CARD 2 - Type 3: Mnemonic]
Q: What is the mnemonic for the toxidrome categories?
A: SODA-C = Sympathomimetic, Opioid, Downer (cholinergic/sedative), Anticholinergic, CNS syndromes

[CARD 3 - Type 1: Basic Q&A]
Q: What are the classic features of the sympathomimetic toxidrome?
A: ↑HR, ↑BP, dilated pupils (mydriasis), ↑temp, ↑sweating, agitation, seizures, hyperthermia.
Causes: cocaine, amphetamines, MDMA.

[CARD 4 - Type 1: Basic Q&A]
Q: What is the classic opioid triad?
A: Coma + Miosis (pinpoint pupils) + Respiratory depression.

[CARD 5 - Type 3: Mnemonic]
Q: What is the mnemonic for anticholinergic toxidrome features?
A: "Hot as hell, Mad as a hatter, Dry as a bone, Blind as a bat, Red as a beet" = Hyperthermia, Delirium, Dry skin, Mydriasis, Flushing + urinary retention.

[CARD 6 - Type 1: Basic Q&A]
Q: Name 4 causes of anticholinergic toxidrome.
A: TCAs, antihistamines, atropine, scopolamine.

[CARD 7 - Type 3: Mnemonic]
Q: What is the mnemonic for cholinergic toxidrome symptoms?
A: SLUDGE = Salivation, Lacrimation, Urination, Defecation, GI cramps, Emesis
(Also DUMBELS = Diarrhoea, Urination, Miosis, Bradycardia/bronchospasm, Emesis, Lacrimation, Salivation)

[CARD 8 - Type 1: Basic Q&A]
Q: What are the pupils in cholinergic vs anticholinergic toxidrome?
A: Cholinergic = pinpoint (miosis); Anticholinergic = dilated (mydriasis).
[Trap: Both opioid AND cholinergic toxidromes cause miosis — distinguish by other features: cholinergic has SLUDGE, opioid has respiratory depression.]

[CARD 9 - Type 1: Basic Q&A]
Q: What distinguishes sedative/hypnotic overdose pupils from opioid overdose pupils?
A: Sedative/hypnotic = normal or mildly small pupils; Opioid = pinpoint (miosis).
[Trap: Normal pupils in sedated patient suggest BZD/barbiturate, not opioids — do NOT give naloxone first.]

[CARD 10 - Type 1: Basic Q&A]
Q: What is the clinical triad of serotonin syndrome?
A: Altered mental status + neuromuscular abnormalities (clonus, hyperreflexia) + autonomic instability (↑HR, ↑BP, ↑temp, diaphoresis).

[CARD 11 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What distinguishes serotonin syndrome from NMS clinically?
A: Serotonin syndrome = fast onset (hours), clonus/hyperreflexia, caused by serotonergic drugs; NMS = slow onset (days), lead-pipe rigidity, markedly ↑CK, caused by antipsychotics (dopamine blockade).
[Trap: Both have hyperthermia and rigidity — key distinctions are onset speed, cause, and type of rigidity.]

[CARD 12 - Type 3: Mnemonic]
Q: What is the mnemonic for NMS features?
A: "FEVER" = Fever, Encephalopathy, Vital signs unstable, Elevated CK, Rigidity (lead-pipe)

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 2: ACTIVATED CHARCOAL
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 13 - Type 1: Basic Q&A]
Q: What is the mechanism of activated charcoal?
A: Porous carbon adsorbs drugs/toxins in the GI lumen → prevents systemic absorption; does NOT enter bloodstream.

[CARD 14 - Type 1: Basic Q&A]
Q: Within what time window is activated charcoal most effective?
A: Within 1 hour of ingestion.

[CARD 15 - Type 3: Mnemonic]
Q: What is the mnemonic for substances activated charcoal does NOT work for?
A: LIAP = Lithium, Iron, Alcohols (methanol, ethanol, ethylene glycol), Potassium (also: lead, heavy metals, cyanide)
[Trap: Activated charcoal is often listed as a generic antidote — HKMLE always tests its specific failures, especially Lithium and Iron.]

[CARD 16 - Type 1: Basic Q&A]
Q: Name 5 drugs that benefit from multi-dose activated charcoal.
A: Theophylline, digoxin, phenobarbital, carbamazepine, quinine — all undergo enterohepatic recirculation.

[CARD 17 - Type 1: Basic Q&A]
Q: Name 3 contraindications to activated charcoal.
A: Reduced GCS/unprotected airway (aspiration risk), caustic ingestion (acid/alkali), intestinal obstruction or absent bowel sounds.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 3: ANTIDOTES — MASTER TABLE
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 18 - Type 1: Basic Q&A]
Q: What is the antidote for paracetamol overdose?
A: N-Acetylcysteine (NAC) — replenishes glutathione and detoxifies NAPQI.

[CARD 19 - Type 1: Basic Q&A]
Q: What is the antidote for opioid overdose?
A: Naloxone — competitive μ-opioid receptor antagonist.

[CARD 20 - Type 1: Basic Q&A]
Q: What is the antidote for benzodiazepine overdose?
A: Flumazenil — competitive GABA-A receptor antagonist at the BZD binding site.

[CARD 21 - Type 1: Basic Q&A]
Q: What are the two antidotes for organophosphate poisoning?
A: Atropine (blocks muscarinic receptors) + Pralidoxime (reactivates acetylcholinesterase before ageing).

[CARD 22 - Type 1: Basic Q&A]
Q: What is the antidote for TCA and salicylate overdose?
A: Sodium bicarbonate — alkalinises blood (reduces TCA Na-channel binding) and urine (traps salicylate for excretion).

[CARD 23 - Type 1: Basic Q&A]
Q: What is the antidote for warfarin overdose?
A: Vitamin K (non-urgent, slow onset) + PCC/FFP (urgent, immediate factor replacement).

[CARD 24 - Type 1: Basic Q&A]
Q: What is the antidote for heparin overdose?
A: Protamine sulfate (binds heparin ionically → neutralises anticoagulant effect).

[CARD 25 - Type 1: Basic Q&A]
Q: What is the antidote for dabigatran overdose?
A: Idarucizumab (anti-dabigatran monoclonal antibody Fab fragment).

[CARD 26 - Type 1: Basic Q&A]
Q: What is the antidote for rivaroxaban/apixaban (Xa inhibitor) overdose?
A: Andexanet alfa (recombinant Xa decoy protein).

[CARD 27 - Type 1: Basic Q&A]
Q: What is the antidote for digoxin toxicity?
A: Digoxin-specific Fab antibody fragments (DigiFab) — bind free digoxin → renal excretion.

[CARD 28 - Type 1: Basic Q&A]
Q: What is the preferred antidote for cyanide poisoning?
A: Hydroxocobalamin 5g IV — binds cyanide directly → forms cyanocobalamin (B12) → renally excreted.

[CARD 29 - Type 1: Basic Q&A]
Q: What is the antidote for carbon monoxide poisoning?
A: 100% high-flow O2 (displaces CO from Hb); hyperbaric O2 if COHb >25%, pregnancy, loss of consciousness, or cardiac/neurological features.

[CARD 30 - Type 1: Basic Q&A]
Q: What is the preferred antidote for methanol and ethylene glycol poisoning?
A: Fomepizole (inhibits alcohol dehydrogenase → blocks formation of toxic metabolites).

[CARD 31 - Type 1: Basic Q&A]
Q: What is the antidote for iron overdose?
A: Deferoxamine (chelates free iron → excreted in urine).

[CARD 32 - Type 1: Basic Q&A]
Q: What is the antidote for lead poisoning?
A: DMSA (succimer) or EDTA (chelate lead).

[CARD 33 - Type 1: Basic Q&A]
Q: What is the antidote for methotrexate toxicity?
A: Leucovorin (folinic acid) — bypasses DHFR blockade to provide active folate.

[CARD 34 - Type 1: Basic Q&A]
Q: What drug is used for serotonin syndrome?
A: Cyproheptadine (5-HT2A antagonist) + supportive care (cooling, BZDs for agitation).

[CARD 35 - Type 1: Basic Q&A]
Q: What drugs are used for malignant hyperthermia and NMS?
A: Dantrolene (blocks ryanodine receptor → ↓ Ca2+ release → ↓ muscle rigidity) ± bromocriptine (D2 agonist for NMS).

[CARD 36 - Type 1: Basic Q&A]
Q: What is the role of calcium gluconate in hyperkalaemia?
A: Membrane stabilisation (cardiac protection) — does NOT lower serum K+.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 4: NALOXONE
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 37 - Type 1: Basic Q&A]
Q: What is the mechanism of naloxone?
A: Competitive μ-opioid receptor antagonist (also κ and δ) → reverses opioid-induced CNS and respiratory depression.

[CARD 38 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: How much naloxone should you give in opioid OD — enough to wake the patient up fully?
A: No — titrate naloxone to RESTORE BREATHING only; do NOT fully reverse opioid (precipitates acute withdrawal: agitation, vomiting, pulmonary oedema).
[Trap: Common wrong answer is "full reversal of consciousness" — the clinical endpoint is restoration of adequate respiration, not full wakefulness.]

[CARD 39 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why does naloxone require repeated doses or infusion for methadone overdose?
A: Naloxone t½ is ~1 hour — much shorter than methadone (t½ 24-36h); re-narcotisation occurs after each dose → infusion or repeated dosing needed.

[CARD 40 - Type 2: Cloze]
[c] Naloxone [/c] precipitates acute opioid withdrawal if given in excess — features include agitation, vomiting, tachycardia, hypertension, and non-cardiogenic pulmonary oedema.

[CARD 41 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Tramadol overdose — does naloxone reverse the seizures?
A: No — tramadol-induced seizures are NOT reversed by naloxone (they are due to serotonergic/noradrenergic mechanisms); treat seizures with benzodiazepines.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 5: FLUMAZENIL
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 42 - Type 1: Basic Q&A]
Q: What is the mechanism of flumazenil?
A: Competitive GABA-A receptor antagonist at the benzodiazepine binding site → reverses BZD-induced sedation.

[CARD 43 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: NEVER give flumazenil in which scenario?
A: Suspected TCA overdose — removing BZD sedation unmasks TCA-induced seizures → fatal status epilepticus.
[Trap: This is the #1 flumazenil trap on HKMLE — if TCA OD is suspected, BZDs are protective; flumazenil removes that protection.]

[CARD 44 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why is flumazenil dangerous in BZD-dependent patients?
A: Precipitates acute benzodiazepine withdrawal → seizures; use only when BZD dependence is excluded.

[CARD 45 - Type 2: Cloze]
[c] Flumazenil [/c] has a short half-life (~1 hour) — resedation can occur after initial reversal; repeat doses or infusion may be needed.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 6: N-ACETYLCYSTEINE (NAC) — PARACETAMOL OD
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 46 - Type 1: Basic Q&A]
Q: What is the mechanism of NAC in paracetamol overdose?
A: Glutathione precursor → replenishes hepatic glutathione → detoxifies NAPQI (the toxic CYP2E1 metabolite).

[CARD 47 - Type 1: Basic Q&A]
Q: What are the 4 clinical phases of paracetamol overdose?
A: Phase 1 (0-24h): N/V/malaise; Phase 2 (24-72h): RUQ pain, ↑ALT/AST, ↑INR; Phase 3 (72-96h): peak hepatotoxicity, jaundice, coagulopathy, renal failure; Phase 4: recovery or death.

[CARD 48 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Within what window is NAC most effective for paracetamol OD?
A: Most effective within 8-10 hours of ingestion — but still give NAC even if >10h as it reduces hepatic failure risk.
[Trap: Do NOT withhold NAC because the patient presents late — late NAC still reduces mortality.]

[CARD 49 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: When can you NOT use the Rumack-Matthew nomogram?
A: Staggered overdose (multiple ingestions over time) — nomogram only valid for single acute ingestion; treat empirically if >75mg/kg ingested or timing unclear.

[CARD 50 - Type 2: Cloze]
[c] NAC (N-acetylcysteine) [/c] causes anaphylactoid reactions (urticaria, flushing, bronchospasm) — NOT IgE-mediated; treat by slowing infusion + antihistamine; do NOT permanently stop NAC.
[Trap: NAC reactions are anaphylactoid NOT allergic — never permanently stop NAC for this; slow the infusion and premedicate.]

[CARD 51 - Type 1: Basic Q&A]
Q: What are the King's College Criteria for liver transplant assessment in paracetamol OD?
A: pH <7.3 OR (PT >100s + Creatinine >300 µmol/L + Grade III-IV hepatic encephalopathy) — any one criterion = consider transplant.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 7: ORGANOPHOSPHATE POISONING
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 52 - Type 3: Mnemonic]
Q: What is the mnemonic for organophosphate/atropine treatment?
A: "ATROPINE = Anticholinergic Treatment; PRALIDOXIME = reactivates cholinesterase before ageing"

[CARD 53 - Type 1: Basic Q&A]
Q: What is the mechanism of organophosphate toxicity?
A: Irreversibly inhibit acetylcholinesterase → ACh accumulates at all synapses → muscarinic + nicotinic + CNS effects.

[CARD 54 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is the correct endpoint of atropine therapy in organophosphate poisoning?
A: Drying of secretions — NOT pupil size and NOT heart rate.
[Trap: Common wrong answers are HR normalisation or miosis reversal — the only correct endpoint is dry secretions/clear chest.]

[CARD 55 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why must pralidoxime be given early in organophosphate poisoning?
A: Pralidoxime only works BEFORE "ageing" (irreversible covalent bonding of OP to AChE after hours) — delayed pralidoxime is ineffective.

[CARD 56 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Should pralidoxime be given for carbamate poisoning?
A: No — carbamates reversibly inhibit AChE (no ageing); pralidoxime is not needed and may be harmful. Use atropine only.
[Trap: Do NOT give pralidoxime for carbamate insecticides — only for organophosphates.]

[CARD 57 - Type 1: Basic Q&A]
Q: What are the nicotinic effects of organophosphate poisoning?
A: Muscle fasciculations → paralysis (including respiratory muscles), tachycardia (can mask bradycardia).

[CARD 58 - Type 1: Basic Q&A]
Q: What is the starting dose of atropine in severe organophosphate poisoning?
A: 2-4mg IV, doubled every 5-10 minutes — may need 100+ mg in severe poisoning; titrate to dry secretions.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 8: SODIUM BICARBONATE
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 59 - Type 1: Basic Q&A]
Q: What are the two mechanisms of sodium bicarbonate in TCA overdose?
A: Alkalinises blood → raises pH → ion-trapping reduces TCA binding to Na+ channels; also corrects metabolic acidosis.

[CARD 60 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: TCA overdose + QRS >120ms — what is the immediate treatment?
A: Sodium bicarbonate IV (target serum pH 7.45-7.55) — narrows QRS and prevents VT/VF.
[Trap: Do NOT use phenytoin for TCA seizures — it worsens Na-channel blockade; use benzodiazepines instead.]

[CARD 61 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What ECG finding is highly specific for TCA poisoning?
A: R wave in aVR ≥3mm (plus QRS >120ms and prolonged QTc).

[CARD 62 - Type 2: Cloze]
[c] Sodium bicarbonate [/c] is used in salicylate poisoning to alkalinise the urine (target urine pH 7.5-8) → ionised salicylate is trapped in tubular lumen → increased renal excretion.

[CARD 63 - Type 1: Basic Q&A]
Q: In which cardiac arrest scenarios is sodium bicarbonate specifically indicated?
A: Hyperkalaemic arrest, TCA-induced arrest, prolonged arrest (>10-15 min) with severe acidosis.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 9: TCA OVERDOSE
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 64 - Type 3: Mnemonic]
Q: What is the mnemonic for the 3 killers in TCA overdose?
A: "TCA OD = 3 killers: Na-channel blockade (arrhythmia), Anticholinergic (tachycardia/hyperthermia), Alpha-1 blockade (hypotension)"

[CARD 65 - Type 1: Basic Q&A]
Q: What are the 4 mechanisms of TCA toxicity?
A: Na+ channel blockade (QRS widening → arrhythmia), anticholinergic effects, alpha-1 blockade (hypotension), antihistamine (sedation) + GABA-A antagonism (seizures).

[CARD 66 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What two drugs must NEVER be given in TCA overdose?
A: Flumazenil (precipitates fatal seizures by removing BZD protection) and physostigmine (worsens arrhythmias).
[Trap: Both are commonly considered antidotes in sedated/confused patients — both are deadly in TCA OD.]

[CARD 67 - Type 1: Basic Q&A]
Q: What is used to treat seizures in TCA overdose?
A: Benzodiazepines (diazepam/lorazepam) — NOT phenytoin (worsens Na-channel blockade).

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 10: SALICYLATE (ASPIRIN) OVERDOSE
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 68 - Type 3: Mnemonic]
Q: What is the mnemonic for salicylate toxicity features?
A: SALE = Salicylates cause: Acidosis (metabolic), Lungs (non-cardiogenic pulmonary oedema), Ears (tinnitus), Early alkalosis (initial respiratory alkalosis)

[CARD 69 - Type 1: Basic Q&A]
Q: What is the classic ABG pattern in salicylate poisoning?
A: Mixed respiratory alkalosis + metabolic acidosis (initial hyperventilation from direct respiratory centre stimulation, then metabolic acidosis from lactic acid + salicylate).

[CARD 70 - Type 1: Basic Q&A]
Q: What are the indications for haemodialysis in salicylate poisoning?
A: Severe poisoning, renal failure, pulmonary oedema, neurological features, salicylate level >700mg/L.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 11: LITHIUM TOXICITY
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 71 - Type 1: Basic Q&A]
Q: What is the therapeutic window for lithium?
A: 0.4-1.0 mmol/L; >1.5 = mild toxicity; >2.0 = moderate; >2.5 = severe.

[CARD 72 - Type 1: Basic Q&A]
Q: What are the features of lithium toxicity?
A: Coarse tremor (first sign), N/V/D, ataxia, confusion, dysarthria, muscle twitching, seizures, coma, cardiac arrhythmias.

[CARD 73 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Name 4 drugs/situations that raise lithium levels to toxic range.
A: NSAIDs, ACEi/ARBs, thiazide diuretics, dehydration — all increase renal tubular reabsorption of lithium.
[Trap: NSAIDs are the classic exam interaction — a patient on lithium who starts ibuprofen for pain can develop lithium toxicity rapidly.]

[CARD 74 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Does activated charcoal work for lithium overdose?
A: No — lithium is not adsorbed by activated charcoal (it is LIAP — a classic charcoal failure); use IV 0.9% NaCl and haemodialysis.

[CARD 75 - Type 1: Basic Q&A]
Q: What are the indications for haemodialysis in lithium toxicity?
A: Lithium level >2.5-3.0 mmol/L with neurological features.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 12: DIGOXIN TOXICITY
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 76 - Type 1: Basic Q&A]
Q: What is the most common arrhythmia in digoxin toxicity?
A: Bradycardia + AV block; any arrhythmia is possible; bidirectional VT is pathognomonic.

[CARD 77 - Type 1: Basic Q&A]
Q: What is the "digoxin effect" on ECG (not toxicity)?
A: Down-sloping ST depression — "reverse tick" or "hockey stick" pattern (sign of digoxin effect, not toxicity).

[CARD 78 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why is calcium contraindicated in digoxin toxicity?
A: Hypercalcaemia has the same cellular effect as digoxin (↑ intracellular Ca2+) → worsens toxicity → "stone heart" (irreversible contracture); calcium is absolutely contraindicated.
[Trap: Calcium is used for hyperkalaemia — but if the patient is on digoxin, giving calcium can be lethal.]

[CARD 79 - Type 3: Mnemonic]
Q: What is the mnemonic for digoxin toxicity management?
A: "K up, Mg up, Ca down, DigiFab for life-threatening" = correct hypokalaemia + hypomagnesaemia, avoid calcium, give DigiFab for severe arrhythmias.

[CARD 80 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What are the indications for DigiFab (digoxin Fab antibodies)?
A: Life-threatening arrhythmias (VT, VF, complete heart block), severe bradycardia unresponsive to atropine, digoxin level >10 ng/mL, acute ingestion >10mg.

[CARD 81 - Type 3: Mnemonic]
Q: What is the mnemonic for the hyperkalaemia management sequence?
A: C-BIG-K-Drop = Calcium (stabilise heart), Bicarbonate, Insulin + Glucose, Kayexalate (remove K+), Dialysis (definitive)

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 13: THEOPHYLLINE TOXICITY
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 82 - Type 1: Basic Q&A]
Q: What are the key features of theophylline toxicity?
A: Severe N/V, refractory seizures, tachyarrhythmias (SVT, AF, VT), hypokalaemia, hyperglycaemia, metabolic acidosis.

[CARD 83 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: How do you manage theophylline toxicity seizures?
A: Benzodiazepines — NOT phenytoin (ineffective for theophylline seizures); multi-dose activated charcoal for elimination; haemodialysis if severe.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 14: METHANOL & ETHYLENE GLYCOL POISONING
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 84 - Type 1: Basic Q&A]
Q: What is the toxic metabolite of methanol?
A: Formic acid (via formaldehyde) — damages optic nerve → blindness.

[CARD 85 - Type 1: Basic Q&A]
Q: What is the toxic metabolite of ethylene glycol?
A: Oxalic acid (via glycolic acid) — precipitates as calcium oxalate crystals in renal tubules → renal failure.

[CARD 86 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: High anion gap metabolic acidosis + elevated osmolar gap — what is the diagnosis until proven otherwise?
A: Methanol or ethylene glycol poisoning — osmolar gap = measured osmolality - calculated osmolality (normal <10).
[Trap: Do NOT forget the osmolar gap — anion gap alone is non-specific; osmolar gap distinguishes toxic alcohol ingestion from other causes of HAGMA.]

[CARD 87 - Type 1: Basic Q&A]
Q: What is the mechanism of fomepizole?
A: Inhibits alcohol dehydrogenase → prevents conversion of methanol/ethylene glycol to their toxic metabolites.

[CARD 88 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What unique symptom distinguishes methanol from ethylene glycol poisoning?
A: Visual disturbance progressing to blindness (formic acid damages the optic nerve) — specific to methanol; ethylene glycol causes renal failure without visual symptoms.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 15: CARBON MONOXIDE POISONING
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 89 - Type 3: Mnemonic]
Q: What is the mnemonic for carbon monoxide poisoning?
A: "CO = Cherry red lips (rare), Confused, CO-Hb on ABG (NOT on pulse ox!)"

[CARD 90 - Type 1: Basic Q&A]
Q: Why does pulse oximetry give a falsely normal reading in CO poisoning?
A: Pulse oximetry cannot distinguish oxyhaemoglobin from carboxyhaemoglobin → reads COHb as O2Hb → falsely normal SpO2.
[Trap: Normal SpO2 on pulse oximetry does NOT exclude CO poisoning — always order ABG with co-oximetry if CO is suspected.]

[CARD 91 - Type 1: Basic Q&A]
Q: What is the mechanism of CO toxicity?
A: CO binds Hb with 250x affinity vs O2 → carboxyhaemoglobin → ↓ O2-carrying capacity + left-shifts O2-Hb curve + inhibits cytochrome c oxidase (mitochondrial poisoning).

[CARD 92 - Type 1: Basic Q&A]
Q: What are the indications for hyperbaric oxygen in CO poisoning?
A: COHb >25%, any CO exposure in pregnancy (any COHb level), loss of consciousness, cardiac/neurological features.

[CARD 93 - Type 2: Cloze]
[c] 100% high-flow O2 [/c] reduces COHb half-life from 5 hours to ~1 hour; hyperbaric O2 reduces it further to ~20 minutes.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 16: CYANIDE POISONING
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 94 - Type 1: Basic Q&A]
Q: What is the mechanism of cyanide toxicity?
A: Binds cytochrome c oxidase (complex IV) → blocks mitochondrial electron transport → histotoxic hypoxia → lactic acidosis despite adequate O2 delivery.

[CARD 95 - Type 1: Basic Q&A]
Q: What is the classic clinical finding pointing to cyanide poisoning in a fire victim?
A: Severe lactic acidosis + haemodynamic instability despite high O2; "arterialized" venous blood (high PvO2 — cells not extracting O2).

[CARD 96 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why is hydroxocobalamin preferred over sodium nitrite + thiosulfate in smoke inhalation?
A: Smoke inhalation patients often have co-existing CO poisoning — sodium nitrite induces methemoglobinaemia, which further reduces O2-carrying capacity and is dangerous with concurrent CO; hydroxocobalamin avoids this.
[Trap: Classic HKMLE scenario — always use hydroxocobalamin for house fire/smoke inhalation cyanide poisoning.]

[CARD 97 - Type 2: Cloze]
[c] Hydroxocobalamin [/c] causes transient red/pink discolouration of skin and body fluids and interferes with pulse oximetry and colorimetric lab tests — these are harmless and expected.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 17: MALIGNANT HYPERTHERMIA & NMS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 98 - Type 3: Mnemonic]
Q: What is the mnemonic for malignant hyperthermia management?
A: "STOP sux/volatile → DANTROLENE" — stop the triggering agent immediately, give dantrolene 2.5mg/kg IV bolus.

[CARD 99 - Type 1: Basic Q&A]
Q: What triggers malignant hyperthermia (MH)?
A: Volatile anaesthetics (halothane, sevoflurane, desflurane) and suxamethonium.

[CARD 100 - Type 1: Basic Q&A]
Q: What is the mechanism of dantrolene?
A: Blocks ryanodine receptor in sarcoplasmic reticulum → inhibits Ca2+ release → reduces skeletal muscle contraction and rigidity.

[CARD 101 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: How does MH differ from NMS in trigger and onset?
A: MH: triggered by suxamethonium/volatile anaesthetics, onset within minutes in the OR, masseter spasm + extreme hyperthermia. NMS: triggered by antipsychotics (dopamine blockade), onset over hours-days, lead-pipe rigidity + elevated CK.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 18: ANAPHYLAXIS MANAGEMENT
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 102 - Type 3: Mnemonic]
Q: What is the mnemonic for anaphylaxis management?
A: SAFE = Stop trigger, Adrenaline (IM) FIRST, Fluid resuscitation, Extra drugs (antihistamine/steroids as adjuncts)

[CARD 103 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is the FIRST treatment for anaphylaxis?
A: Adrenaline (epinephrine) 0.5mg IM into anterolateral thigh (1:1000 solution) — antihistamines and steroids are adjuncts only, not first-line.
[Trap: Common wrong answer is antihistamine first — this treats urticaria but does NOT treat airway/cardiovascular collapse.]

[CARD 104 - Type 1: Basic Q&A]
Q: What are the 3 receptor effects of adrenaline in anaphylaxis?
A: α1 (vasoconstriction → reverses hypotension and angioedema), β1 (↑HR/contractility → improves cardiac output), β2 (bronchodilation + ↓ mediator release from mast cells).

[CARD 105 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: When is IV adrenaline used in anaphylaxis (vs IM)?
A: IV adrenaline only for refractory anaphylaxis or cardiac arrest — IM is safe and effective for standard anaphylaxis; IV risks severe hypertension and arrhythmias if not carefully titrated.
[Trap: IV adrenaline for standard anaphylaxis is NOT correct — IM is the standard route.]

[CARD 106 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: A patient on beta-blockers has anaphylaxis refractory to adrenaline. What do you add?
A: Glucagon — bypasses β-receptor blockade by stimulating cAMP via a different mechanism.

[CARD 107 - Type 1: Basic Q&A]
Q: Why are corticosteroids given in anaphylaxis?
A: To prevent biphasic reaction (recurrence up to 72h later) — they take hours to act and are adjuncts, not acute treatment.

[CARD 108 - Type 1: Basic Q&A]
Q: What is the purpose of the antihistamine (chlorphenamine) in anaphylaxis?
A: Treats urticaria and itching only — does NOT treat airway compromise or cardiovascular collapse.

[CARD 109 - Type 1: Basic Q&A]
Q: How long should patients be observed after anaphylaxis and why?
A: 4-6 hours minimum — biphasic reaction (second wave of anaphylaxis) can occur up to 72 hours later.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 19: RSI DRUGS — INDUCTION AGENTS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 110 - Type 3: Mnemonic]
Q: What is the mnemonic for RSI induction agent selection?
A: "Haemodynamic instability = Etomidate; Asthma/bronchospasm = Ketamine; ICU/elective = Propofol"

[CARD 111 - Type 1: Basic Q&A]
Q: What is the mechanism and key property of ketamine?
A: NMDA receptor antagonist → dissociative anaesthesia; causes ↑HR and ↑BP (sympathomimetic), bronchodilator — ideal for asthma and haemodynamically unstable patients.

[CARD 112 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why is ketamine avoided in severe hypertension?
A: Ketamine is sympathomimetic — raises HR and BP further; also historically avoided in raised ICP (though newer evidence suggests it is safe in practice).

[CARD 113 - Type 1: Basic Q&A]
Q: What is a unique side effect of ketamine requiring co-prescription of a benzodiazepine?
A: Emergence reactions (hallucinations, dissociation on recovery) — co-prescribe midazolam to reduce this.

[CARD 114 - Type 1: Basic Q&A]
Q: What is the mechanism and key advantage of etomidate?
A: GABA-A potentiation (imidazole); most haemodynamically stable induction agent — minimal BP/HR changes; preferred for IHD and elderly.

[CARD 115 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is the important endocrine side effect of etomidate?
A: Adrenal suppression (↓ cortisol for 24-48h after a single dose) — controversial in sepsis; use with caution in adrenal insufficiency.

[CARD 116 - Type 2: Cloze]
[c] Propofol [/c] causes hypotension (vasodilation + ↓ cardiac output) and is contraindicated in haemodynamic instability; Propofol Infusion Syndrome (lactic acidosis + multi-organ failure) occurs with high-dose prolonged infusions.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 20: RSI DRUGS — NEUROMUSCULAR BLOCKERS (PARALYTICS)
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 117 - Type 3: Mnemonic]
Q: What is the mnemonic for suxamethonium contraindications?
A: BUCKS = Burns (after 24h), Uraemia (hyperkalaemia), Crush injury, K+ high (hyperkalaemia), Spinal cord/denervation injury

[CARD 118 - Type 1: Basic Q&A]
Q: What is the mechanism of suxamethonium (succinylcholine)?
A: Depolarising NMB — mimics ACh at nicotinic receptor → sustained depolarisation → paralysis; causes fasciculations before block.

[CARD 119 - Type 2: Cloze]
[c] Suxamethonium [/c] raises serum K+ by 0.5-1 mmol/L in normal patients — this is fatal in patients with hyperkalaemia, burns (after 24h), crush injury, prolonged immobility, or denervating conditions (spinal cord injury, stroke, Guillain-Barré).
[Trap: Suxamethonium is safe in acute burns within the first 24 hours — the hyperkalaemia risk starts AFTER 24h due to upregulation of extrajunctional ACh receptors.]

[CARD 120 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which drugs trigger malignant hyperthermia?
A: Suxamethonium and volatile anaesthetic agents (halothane, sevoflurane, isoflurane, desflurane) — treat immediately with dantrolene.

[CARD 121 - Type 1: Basic Q&A]
Q: What is the mechanism of rocuronium and how is it reversed?
A: Non-depolarising NMB — competes with ACh at nicotinic receptors; reversed with sugammadex (encapsulates drug → excreted renally).

[CARD 122 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: "Cannot intubate, cannot oxygenate" — what do you do if rocuronium was used?
A: Give sugammadex immediately to reverse rocuronium → patient regains spontaneous breathing; this is the life-saving advantage of rocuronium over suxamethonium in a failed airway.
[Trap: Suxamethonium CANNOT be reversed — if you used sux and can't intubate, you cannot chemically reverse the paralysis.]

[CARD 123 - Type 1: Basic Q&A]
Q: What is the advantage of rocuronium over suxamethonium for RSI?
A: No risk of hyperkalaemia, no malignant hyperthermia trigger, reversible with sugammadex — equivalent onset at 1.2mg/kg dose.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 21: CARDIAC ARREST RESUSCITATION DRUGS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 124 - Type 3: Mnemonic]
Q: What is the mnemonic for cardiac arrest drugs?
A: "AAA + MCS" = Adrenaline x2 (all rhythms), Amiodarone (shockable), Magnesium (TdP), Calcium (hyperkalaemia/CCB/hypocalcaemia), Sodium bicarb (hyperkalaemia/TCA/prolonged arrest)

[CARD 125 - Type 3: Mnemonic]
Q: What is the mnemonic for cardiac arrest drugs dosing?
A: "1mg Adrenaline every 3-5 min; 300mg Amiodarone after 3rd shock; 150mg after 5th shock; Magnesium 2g IV for TdP"

[CARD 126 - Type 1: Basic Q&A]
Q: When is adrenaline given in VF/pVT vs PEA/asystole during cardiac arrest?
A: VF/pVT: after 3rd shock; PEA/asystole: as soon as IV/IO access achieved.

[CARD 127 - Type 1: Basic Q&A]
Q: What is the drug of choice for Torsades de Pointes (TdP)?
A: Magnesium sulfate 2g IV over 15 minutes (faster if TdP in arrest).
[Trap: Amiodarone is NOT the first-line for TdP — magnesium is. Amiodarone can actually prolong QT and worsen TdP.]

[CARD 128 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: In which cardiac arrest scenarios is calcium gluconate specifically indicated?
A: Hyperkalaemic arrest, hypocalcaemic arrest, CCB overdose arrest, hypermagnesaemia — but NEVER in digoxin toxicity.

[CARD 129 - Type 1: Basic Q&A]
Q: What is lidocaine's role in cardiac arrest?
A: Alternative to amiodarone for refractory VF/pVT (100mg IV) — used when amiodarone is unavailable.

[CARD 130 - Type 3: Mnemonic]
Q: What is the mnemonic for reversible causes of cardiac arrest?
A: 4H4T = Hypoxia, Hypovolaemia, Hypo/hyperkalaemia + metabolic, Hypothermia + Thrombosis (PE/MI), Tension pneumothorax, Tamponade (cardiac), Toxins (drug OD/poisoning)

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 22: HAEMODIALYSIS — INDICATIONS FOR ELIMINATION
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 131 - Type 1: Basic Q&A]
Q: Name 5 toxins/drugs that require haemodialysis for enhanced elimination.
A: Lithium, methanol, ethylene glycol, salicylate, theophylline — mnemonic: "LEAST" = Lithium, Ethylene glycol, Aspirin (salicylate), Salicylate, Theophylline.
[Trap: Activated charcoal is NOT an alternative to dialysis for lithium — charcoal does not adsorb lithium at all.]

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
BONUS: HIGH-YIELD TRAP SUMMARY CARDS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 132]
Q: HKMLE Trap: Patient with mixed TCA + BZD overdose is given flumazenil. What happens?
A: Flumazenil removes BZD protection against TCA-induced seizures → fatal status epilepticus.

[CARD 133]
Q: HKMLE Trap: Naloxone is given to fully wake up an unconscious opioid OD patient. What is the risk?
A: Acute opioid withdrawal (agitation, vomiting, hypertension, non-cardiogenic pulmonary oedema) — titrate to restore breathing only.

[CARD 134]
Q: HKMLE Trap: SpO2 is 99% on a patient rescued from a house fire. Is CO poisoning excluded?
A: No — pulse oximetry reads COHb as oxyhaemoglobin → falsely normal SpO2; always order ABG with co-oximetry to measure COHb directly.

[CARD 135]
Q: HKMLE Trap: Activated charcoal given for lithium overdose. Will it help?
A: No — lithium is NOT adsorbed by activated charcoal (LIAP failure); use IV saline and haemodialysis.

[CARD 136]
Q: HKMLE Trap: Calcium gluconate given to a patient with digoxin toxicity and hyperkalaemia. What is the danger?
A: Calcium potentiates digoxin toxicity → worsens arrhythmias → "stone heart"; calcium is absolutely contraindicated in digoxin toxicity regardless of the K+ level.

[CARD 137]
Q: HKMLE Trap: Phenytoin given for seizures in TCA overdose. What is the problem?
A: Phenytoin worsens Na-channel blockade in TCA poisoning → worsens arrhythmias; use benzodiazepines for TCA seizures.

[CARD 138]
Q: HKMLE Trap: Suxamethonium given to a patient with burns from 3 days ago. What is the danger?
A: Burns after 24h cause upregulation of extrajunctional ACh receptors — suxamethonium causes massive K+ efflux → fatal hyperkalaemia/VF.

[CARD 139]
Q: HKMLE Trap: Pralidoxime given for carbamate insecticide poisoning. Is it appropriate?
A: No — carbamates reversibly inhibit AChE without ageing; pralidoxime is not needed and may worsen outcome; use atropine only.

[CARD 140]
Q: HKMLE Trap: Anaphylaxis treated with chlorphenamine (antihistamine) first. What is the error?
A: Antihistamine treats urticaria only — it does NOT treat airway compromise or distributive shock; adrenaline IM FIRST is the correct priority.

[CARD 141]
Q: HKMLE Trap: Rocuronium is given for RSI and intubation fails — "can't intubate, can't oxygenate." What is the rescue?
A: Sugammadex IV immediately — encapsulates rocuronium → rapid reversal → patient regains spontaneous breathing (this is not possible with suxamethonium).

[CARD 142]
Q: HKMLE Trap: Sodium nitrite + thiosulfate given to a house fire victim with suspected cyanide poisoning. What is the danger?
A: Sodium nitrite induces methemoglobinaemia — dangerous if co-existing CO poisoning (further reduces O2-carrying capacity); use hydroxocobalamin instead.

[CARD 143]
Q: HKMLE Trap: NAC infusion is stopped because the patient developed urticaria and flushing. Is this correct?
A: No — NAC anaphylactoid reactions are NOT IgE-mediated; slow the infusion and give antihistamine; do NOT permanently stop NAC as the patient still needs treatment.

================================================================
END OF DECK — 143 CARDS TOTAL
================================================================

================================================================
HKMLE CNS PHARMACOLOGY — ANKI FLASHCARD DECK
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Generated from: CNS 💊.pdf
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SECTION 1: SSRIs
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 1 - Type 3: Mnemonic]
Q: What is the mnemonic for SSRI side effects?
A: SSRI = Sexual dysfunction, Serotonin syndrome risk, SIADH (hyponatraemia), Initial anxiety/activation (early worsening)

[CARD 2 - Type 1: Basic Q&A]
Q: What is the mechanism of SSRIs?
A: Block serotonin (5-HT) reuptake transporter → ↑ synaptic serotonin.

[CARD 3 - Type 1: Basic Q&A]
Q: Name 5 key indications for SSRIs.
A: Depression (first-line), GAD, panic disorder, PTSD, OCD, social phobia, bulimia (fluoxetine).

[CARD 4 - Type 1: Basic Q&A]
Q: What is the most common SSRI side effect?
A: Sexual dysfunction (↓ libido, anorgasmia, delayed ejaculation) — affects the majority of patients.

[CARD 5 - Type 2: Cloze]
[c] SSRIs [/c] cause hyponatraemia (SIADH) by stimulating ADH release — especially dangerous in elderly patients on diuretics.

[CARD 6 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: SSRI + MAOI — what happens?
A: Serotonin syndrome: hyperthermia, clonus, agitation, diarrhoea, autonomic instability — potentially fatal; never combine.
[Trap: The washout period is NOT the same in both directions — MAOI → SSRI needs 2 weeks; fluoxetine → MAOI needs 5 weeks (due to fluoxetine's long t½).]

[CARD 7 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: How long does an antidepressant take to work — and what must you tell patients?
A: 2-4 weeks for antidepressant effect — patients must be warned to continue the drug even if they feel no benefit initially.

[CARD 8 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which SSRI is preferred in pregnancy?
A: Fluoxetine — longest half-life (1-4 days), fewest discontinuation symptoms; most safety data in pregnancy.
[Trap: Paroxetine is the SSRI to avoid in pregnancy — it has the most discontinuation symptoms and highest teratogenicity concern among SSRIs.]

[CARD 9 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which SSRI causes the most discontinuation symptoms on stopping, and why?
A: Paroxetine — shortest half-life among commonly used SSRIs → most abrupt drop in serotonin when stopped.

[CARD 10 - Type 1: Basic Q&A]
Q: Which SSRI is used for OCD (and has the most CYP interactions)?
A: Fluvoxamine (also clarithromycin-level CYP1A2/2C19 inhibitor — most drug interactions of SSRIs).

[CARD 11 - Type 1: Basic Q&A]
Q: What is the black box warning for SSRIs in young adults?
A: Increased risk of suicidal ideation in patients ≤24 years — monitor closely especially in first weeks of treatment.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 2: SNRIs
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 12 - Type 1: Basic Q&A]
Q: What is the mechanism of SNRIs?
A: Block both serotonin AND noradrenaline reuptake.

[CARD 13 - Type 1: Basic Q&A]
Q: Name 3 indications for duloxetine (beyond depression).
A: Neuropathic pain, fibromyalgia, stress urinary incontinence.

[CARD 14 - Type 2: Cloze]
[c] SNRIs [/c] can cause hypertension (due to noradrenaline reuptake inhibition) — check BP before and during treatment.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 3: TCAs (TRICYCLIC ANTIDEPRESSANTS)
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 15 - Type 3: Mnemonic]
Q: What is the mnemonic for TCAs?
A: "TCAs = Toxic in overdose, Cardiotoxic, Anticholinergic"

[CARD 16 - Type 3: Mnemonic]
Q: What is the mnemonic for TCA overdose features?
A: 3 C's = Convulsions, Coma, Cardiac arrhythmia → treat with NaHCO3

[CARD 17 - Type 1: Basic Q&A]
Q: What is the mechanism of TCAs?
A: Block 5-HT + noradrenaline reuptake; also block muscarinic, histamine, and α1 receptors — explaining anticholinergic, sedative, and hypotensive effects.

[CARD 18 - Type 1: Basic Q&A]
Q: Name 4 indications for TCAs (beyond depression).
A: Neuropathic pain (amitriptyline), migraine prophylaxis (amitriptyline), enuresis in children (imipramine), panic disorder.

[CARD 19 - Type 1: Basic Q&A]
Q: Name 4 contraindications to TCAs.
A: Recent MI, arrhythmias, narrow-angle glaucoma, prostatic hypertrophy (all due to anticholinergic/cardiac effects).

[CARD 20 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: TCA overdose ECG sign and treatment?
A: Wide QRS (>120ms) + prolonged QTc → sodium bicarbonate IV (target pH 7.45-7.55); also treat hypotension with IV fluids.
[Trap: Do NOT give physostigmine (worsens arrhythmias) or flumazenil (precipitates seizures) in TCA OD.]

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 4: MAOIs
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 21 - Type 3: Mnemonic]
Q: What is the mnemonic for MAOIs?
A: "MAOIs = Must Avoid Old cheese (tyramine), Must Avoid Other serotonergics"

[CARD 22 - Type 1: Basic Q&A]
Q: What is the mechanism of MAOIs?
A: Inhibit monoamine oxidase → ↑ serotonin, dopamine, and noradrenaline in CNS.

[CARD 23 - Type 2: Cloze]
[c] MAOIs [/c] cause hypertensive crisis when tyramine-rich foods are eaten (cheese, red wine, cured meats) because MAO normally breaks down tyramine in the gut — inhibition allows tyramine to enter circulation → massive noradrenaline release.

[CARD 24 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Washout period when switching from MAOI to SSRI — and from fluoxetine to MAOI?
A: MAOI → SSRI = 2 weeks; fluoxetine → MAOI = 5 weeks (fluoxetine's long t½ means serotonin levels remain elevated long after stopping).
[Trap: The 5-week washout for fluoxetine is unique — other SSRIs only need 2 weeks washout before starting an MAOI.]

[CARD 25 - Type 1: Basic Q&A]
Q: Which MAOI has fewer dietary restrictions and why?
A: Moclobemide — reversible MAO inhibitor (RIMA); tyramine can displace it from MAO, so the interaction is much less dangerous.

[CARD 26 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Pethidine (meperidine) + MAOI — what happens?
A: Serotonin syndrome (pethidine has serotonergic properties) — this combination is absolutely contraindicated; use morphine instead.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 5: OTHER ANTIDEPRESSANTS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 27 - Type 1: Basic Q&A]
Q: What is the mechanism of mirtazapine and its key clinical features?
A: α2 antagonist + 5-HT2/5-HT3 antagonist → ↑ noradrenaline + serotonin; causes weight gain + sedation (antihistaminic), NO sexual dysfunction — good for elderly/underweight patients.

[CARD 28 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Bupropion — what two conditions is it used for, and what is its main risk?
A: Smoking cessation AND depression; lowers seizure threshold — avoid in bulimia, anorexia, and epilepsy.

[CARD 29 - Type 2: Cloze]
[c] Trazodone [/c] causes priapism as a rare but characteristic side effect — a prolonged painful erection requiring urgent urological management.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 6: TYPICAL ANTIPSYCHOTICS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 30 - Type 3: Mnemonic]
Q: What is the mnemonic distinguishing typical vs atypical antipsychotics?
A: "Typical = D2 block (motor side effects); Atypical = D2 + 5-HT2 block (less EPS, more metabolic)"

[CARD 31 - Type 1: Basic Q&A]
Q: What is the mechanism of typical antipsychotics?
A: Block D2 dopamine receptors.

[CARD 32 - Type 3: Mnemonic]
Q: What is the mnemonic for EPS timeline with antipsychotics?
A: "Acutely Agitated Patients Take Drugs" = Acute dystonia (hours-days) → Akathisia (days-weeks) → Parkinsonism (weeks-months) → Tardive dyskinesia (months-years)

[CARD 33 - Type 1: Basic Q&A]
Q: What is acute dystonia and how is it treated?
A: Sudden painful muscle spasm (torticollis, oculogyric crisis) occurring hours to days after starting antipsychotic — treat with IM procyclidine or benztropine.

[CARD 34 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: A patient on haloperidol complains of restlessness and inability to sit still. What is the diagnosis and management?
A: Akathisia — reduce dose, add propranolol or benzodiazepine; often mistaken for anxiety → do NOT increase the antipsychotic dose.
[Trap: Akathisia is commonly misidentified as worsening psychosis or anxiety — increasing the antipsychotic makes it worse.]

[CARD 35 - Type 2: Cloze]
[c] Tardive dyskinesia [/c] is characterised by oro-facial movements (lip smacking, tongue protrusion) appearing months-years after antipsychotic use — it can be irreversible; stop the drug if possible.

[CARD 36 - Type 1: Basic Q&A]
Q: What is the treatment for antipsychotic-induced Parkinsonism?
A: Anticholinergics (procyclidine, benztropine, trihexyphenidyl) — reduce dose or switch to atypical antipsychotic.

[CARD 37 - Type 1: Basic Q&A]
Q: What are the common indications for haloperidol specifically?
A: Schizophrenia (acute), delirium, Tourette's syndrome; high-potency = more EPS, less sedation.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 7: NEUROLEPTIC MALIGNANT SYNDROME (NMS)
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 38 - Type 3: Mnemonic]
Q: What is the mnemonic for NMS features?
A: FALTER = Fever, Altered consciousness, Lead-pipe rigidity, Tachycardia/autonomic instability, Elevated CK, Rhabdomyolysis

[CARD 39 - Type 1: Basic Q&A]
Q: What causes NMS?
A: Any antipsychotic (typical > atypical); also sudden withdrawal of dopaminergic drugs.

[CARD 40 - Type 1: Basic Q&A]
Q: What is the treatment for NMS?
A: Stop antipsychotic immediately; supportive care (cooling, hydration); dantrolene (muscle relaxant); bromocriptine (D2 agonist to restore dopamine tone).

[CARD 41 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Key clinical differences between NMS and serotonin syndrome?
A: NMS = lead-pipe rigidity, slow onset (days), normal/small pupils, high CK, caused by antipsychotics; serotonin syndrome = clonus/hyperreflexia, rapid onset (hours), dilated pupils, diarrhoea, caused by serotonergic drugs.
[Trap: Both have hyperthermia and altered consciousness — the key differentiators are type of muscle tone abnormality and speed of onset.]

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 8: ATYPICAL ANTIPSYCHOTICS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 42 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which antipsychotic is used for treatment-resistant schizophrenia?
A: Clozapine — only option after failure of 2 antipsychotics; requires mandatory weekly FBC monitoring for agranulocytosis.
[Trap: Clozapine is NOT used as first-line — it is reserved for treatment-resistant schizophrenia only.]

[CARD 43 - Type 2: Cloze]
[c] Clozapine [/c] causes agranulocytosis in ~1-2% of patients — FBC must be monitored weekly for 18 weeks, then monthly; neutropenia = stop immediately.

[CARD 44 - Type 1: Basic Q&A]
Q: What other serious side effect of clozapine requires monitoring?
A: Myocarditis (especially in the first 4 weeks) — monitor troponin and ECG at baseline and early treatment.

[CARD 45 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Aripiprazole — what is unique about its mechanism vs other antipsychotics?
A: Aripiprazole is a PARTIAL D2 agonist (not a pure antagonist) — it stabilises dopamine pathways rather than fully blocking them; least metabolic side effects.
[Trap: Common wrong answer is "D2 antagonist" for aripiprazole — it is a partial agonist, which is an exam-tested distinction.]

[CARD 46 - Type 1: Basic Q&A]
Q: Which atypical antipsychotic causes the most metabolic syndrome (weight gain, diabetes, dyslipidaemia)?
A: Olanzapine — highest risk of metabolic syndrome among atypicals.

[CARD 47 - Type 1: Basic Q&A]
Q: Which atypical antipsychotic is most useful for bipolar depression?
A: Quetiapine — most used for bipolar depression; also causes most sedation and postural hypotension.

[CARD 48 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which antipsychotic is used if psychosis develops in Parkinson's disease?
A: Quetiapine or clozapine — least D2 blockade; all other antipsychotics worsen Parkinson's motor symptoms.
[Trap: Never give haloperidol, risperidone, or olanzapine to a Parkinson's patient — these have high D2 block and will worsen motor function catastrophically.]

[CARD 49 - Type 2: Cloze]
[c] Risperidone [/c] causes the most hyperprolactinaemia of all atypical antipsychotics (galactorrhoea, amenorrhoea, sexual dysfunction) and causes EPS at high doses.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 9: BENZODIAZEPINES
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 50 - Type 3: Mnemonic]
Q: What is the mnemonic for benzodiazepines?
A: "BZDs = Bind GABA, Big sedation, Beware dependence"

[CARD 51 - Type 1: Basic Q&A]
Q: What is the mechanism of benzodiazepines?
A: Positive allosteric modulator at GABA-A receptor → ↑ frequency of Cl- channel opening → CNS depression (enhances GABA effect, does NOT replace it).

[CARD 52 - Type 1: Basic Q&A]
Q: Name 5 key indications for benzodiazepines.
A: Acute anxiety/panic, alcohol withdrawal (first-line), acute seizures/status epilepticus, procedural sedation, muscle spasm.

[CARD 53 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: First-line treatment for status epilepticus?
A: IV lorazepam (or rectal/buccal diazepam if IV access unavailable) → if fails, phenytoin/levetiracetam → then phenobarbitone.

[CARD 54 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why is diazepam (not lorazepam) used for alcohol withdrawal?
A: Diazepam has long-acting active metabolites (t½ days) → provides smooth taper effect, prevents withdrawal seizures and delirium tremens.
[Trap: Lorazepam can be used for acute withdrawal seizures, but diazepam is preferred for the overall withdrawal management due to long t½.]

[CARD 55 - Type 1: Basic Q&A]
Q: What are the contraindications to benzodiazepines?
A: Sleep apnoea, severe respiratory depression, pregnancy (cleft palate risk), myasthenia gravis.

[CARD 56 - Type 2: Cloze]
[c] BZD + opioid combination [/c] carries a black box warning for additive respiratory depression — avoid concurrent use unless absolutely necessary and with close monitoring.

[CARD 57 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Flumazenil reverses BZD sedation — what are its limitations?
A: Very short-acting (t½ ~1h) → re-sedation can occur; does NOT reverse respiratory depression from other drugs; precipitates withdrawal seizures in BZD-dependent patients.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 10: Z-DRUGS & BUSPIRONE
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 58 - Type 1: Basic Q&A]
Q: What is the mechanism of Z-drugs (zolpidem, zopiclone, zaleplon)?
A: Same GABA-A site as BZDs but more selective for α1 subunit → more hypnotic, less anxiolytic/anticonvulsant.

[CARD 59 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Are Z-drugs significantly safer than BZDs for dependence?
A: No — Z-drugs have similar dependence potential to BZDs; NICE recommends short-term use only (2-4 weeks max).
[Trap: Z-drugs are often thought to be "safer" than BZDs — this is false for dependence risk.]

[CARD 60 - Type 1: Basic Q&A]
Q: What is the mechanism and key advantage of buspirone for GAD?
A: 5-HT1A partial agonist; no dependence, no sedation, no cognitive impairment — but delayed onset (2-4 weeks); cannot replace BZDs acutely.
[Trap: Buspirone cannot abort an acute anxiety attack — it has no cross-tolerance with BZDs and takes weeks to work.]

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 11: ANTIEPILEPTIC DRUGS (AEDs)
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 61 - Type 3: Mnemonic]
Q: What is the mnemonic for AED mechanisms?
A: "Sodium Blocks Fits, Calcium Crushes Absence, GABA Guards neurons"

[CARD 62 - Type 3: Mnemonic]
Q: What is the mnemonic for AED seizure type matching?
A: Absence = Ethosuximide; Myoclonic = Valproate; Focal = Carbamazepine

--- SODIUM VALPROATE ---

[CARD 63 - Type 3: Mnemonic]
Q: What is the mnemonic for valproate toxicity?
A: HALT = Hepatotoxicity, Alopecia, Liver failure, Teratogen (neural tube defects)

[CARD 64 - Type 1: Basic Q&A]
Q: What is the mechanism of sodium valproate?
A: ↑ GABA, ↓ Na+ channels, ↓ T-type Ca2+ channels → broad spectrum (all seizure types including absence).

[CARD 65 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is the most important contraindication to valproate in women?
A: Women of childbearing age — highest teratogen risk of all AEDs (neural tube defects, spina bifida, neurodevelopmental delay); avoid unless no alternative + document risks + ensure contraception.

[CARD 66 - Type 1: Basic Q&A]
Q: Name 5 side effects of valproate.
A: Hepatotoxicity, weight gain, tremor, alopecia, neural tube defects (teratogen), thrombocytopenia, PCOS, pancreatitis.

--- CARBAMAZEPINE ---

[CARD 67 - Type 1: Basic Q&A]
Q: What is the mechanism of carbamazepine?
A: Blocks voltage-gated Na+ channels.

[CARD 68 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which seizure types should carbamazepine NOT be used for?
A: Absence seizures and myoclonic seizures — carbamazepine can worsen both of these.
[Trap: Carbamazepine is often chosen as a "broad AED" — it is NOT broad spectrum and worsens absence/myoclonic seizures.]

[CARD 69 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Carbamazepine + Asian patients — what must you check first?
A: HLA-B*1502 allele (common in Han Chinese, Vietnamese, Thai) — associated with severe Stevens-Johnson syndrome; screen before prescribing carbamazepine in Asian patients.

[CARD 70 - Type 2: Cloze]
[c] Carbamazepine [/c] is a potent CYP450 inducer — it reduces the efficacy of warfarin, the OCP, and many other drugs by accelerating their metabolism.

[CARD 71 - Type 1: Basic Q&A]
Q: What are the serious haematological side effects of carbamazepine?
A: Aplastic anaemia, agranulocytosis (rare), hyponatraemia (SIADH — most common electrolyte effect).

--- PHENYTOIN ---

[CARD 72 - Type 3: Mnemonic]
Q: What is the mnemonic for phenytoin side effects?
A: GANG = Gingival hyperplasia, Ataxia, Nystagmus (toxicity sign), hirsutism, coarse facies (also megaloblastic anaemia, teratogen)

[CARD 73 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is special about phenytoin's pharmacokinetics?
A: Zero-order (saturation) kinetics — at therapeutic levels, small dose increases cause disproportionately large rises in plasma levels → narrow therapeutic window (10-20 µg/mL); toxic level causes nystagmus → ataxia → seizures.
[Trap: Most drugs follow first-order kinetics — phenytoin's zero-order kinetics means doubling the dose can triple or quadruple the blood level.]

[CARD 74 - Type 1: Basic Q&A]
Q: What are the signs of phenytoin toxicity in order of increasing severity?
A: Nystagmus (earliest) → ataxia/diplopia → dysarthria → sedation/encephalopathy → seizures.

[CARD 75 - Type 1: Basic Q&A]
Q: What is phenytoin used for in the emergency setting?
A: IV phenytoin for status epilepticus (second-line after benzodiazepines); also IV loading for acute seizure prevention.

--- LAMOTRIGINE ---

[CARD 76 - Type 1: Basic Q&A]
Q: What is the mechanism of lamotrigine?
A: Blocks voltage-gated Na+ channels.

[CARD 77 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Lamotrigine + valproate — what is the risk and why?
A: Lamotrigine + valproate greatly increases SJS risk AND valproate doubles lamotrigine levels (inhibits its glucuronidation) → titrate lamotrigine very slowly when adding to valproate.
[Trap: Rapid titration of lamotrigine (especially with valproate) is the most common cause of drug-induced SJS — always titrate slowly.]

[CARD 78 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which AED is considered safest in pregnancy?
A: Lamotrigine (lowest risk among older AEDs); levetiracetam increasingly preferred; levels drop in pregnancy so dose increase needed.

--- LEVETIRACETAM ---

[CARD 79 - Type 1: Basic Q&A]
Q: What is the mechanism of levetiracetam?
A: Binds SV2A synaptic vesicle protein → broad spectrum (focal, generalised, myoclonic).

[CARD 80 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is the key advantage of levetiracetam over older AEDs?
A: Renally cleared, minimal drug interactions, increasing first-line use — but can cause behavioural/psychiatric side effects (irritability, depression).

--- ETHOSUXIMIDE ---

[CARD 81 - Type 1: Basic Q&A]
Q: What is the mechanism of ethosuximide and what is it used for?
A: Blocks T-type Ca2+ channels in thalamus → used ONLY for pure absence (petit mal) seizures — does NOT work for other seizure types.
[Trap: Ethosuximide only treats absence seizures — if the patient also has generalised tonic-clonic seizures, use valproate instead.]

--- PHENOBARBITONE ---

[CARD 82 - Type 1: Basic Q&A]
Q: What is the mechanism of phenobarbitone?
A: ↑ GABA-A Cl- channel duration of opening → CNS depression; used for neonatal seizures (IV) and status epilepticus (third-line).

--- GABAPENTIN / PREGABALIN ---

[CARD 83 - Type 1: Basic Q&A]
Q: What is the mechanism of gabapentin and pregabalin?
A: Bind α2δ subunit of voltage-gated Ca2+ channels → ↓ excitatory neurotransmitter release.

[CARD 84 - Type 1: Basic Q&A]
Q: Name 3 indications for pregabalin beyond epilepsy.
A: Neuropathic pain, fibromyalgia, GAD (pregabalin specifically licensed for anxiety).

[CARD 85 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is the abuse concern with pregabalin?
A: Pregabalin has significant abuse/misuse potential — scheduled as Class C (Schedule 3) in the UK; prescribe cautiously in patients with substance misuse history.

--- TOPIRAMATE ---

[CARD 86 - Type 2: Cloze]
[c] Topiramate [/c] causes weight LOSS (unlike most AEDs which cause weight gain) — used as an add-on therapy and for migraine prophylaxis; causes cognitive dulling ("Dope-amax") and kidney stones (carbonic anhydrase inhibition).

--- AED SEIZURE TYPE SELECTION ---

[CARD 87 - Type 1: Basic Q&A]
Q: What is the first-line AED for focal (partial) seizures?
A: Carbamazepine, lamotrigine, or levetiracetam (avoid valproate in women of childbearing age).

[CARD 88 - Type 1: Basic Q&A]
Q: What is the first-line AED for generalised tonic-clonic seizures?
A: Valproate, lamotrigine, or levetiracetam (carbamazepine may worsen absence/myoclonic components).

[CARD 89 - Type 1: Basic Q&A]
Q: What is the drug of choice for pure absence seizures?
A: Ethosuximide (pure absence) or valproate (if mixed with other generalised seizure types).
[Trap: Carbamazepine and phenytoin can WORSEN absence seizures — never use for pure absence.]

[CARD 90 - Type 1: Basic Q&A]
Q: What is the first-line treatment for myoclonic seizures?
A: Valproate, levetiracetam, or clonazepam.
[Trap: Carbamazepine and phenytoin worsen myoclonic seizures — never use for myoclonic epilepsy (e.g. juvenile myoclonic epilepsy).]

--- AEDs IN PREGNANCY ---

[CARD 91 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What folic acid dose do women on AEDs need pre-conception and early pregnancy?
A: 5mg/day (NOT the standard 400mcg/day — higher dose required for all women on AEDs).
[Trap: The standard 400mcg folic acid is insufficient for women on AEDs — 5mg/day is the correct dose on HKMLE.]

[CARD 92 - Type 1: Basic Q&A]
Q: Which AED causes fetal hydantoin syndrome?
A: Phenytoin — cleft palate, digit defects, developmental delay.

[CARD 93 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Valproate in pregnancy — what is the risk?
A: Highest teratogen risk of all AEDs: neural tube defects (1-2%), spina bifida, facial abnormalities, and long-term neurodevelopmental delay in the child.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 12: PARKINSON'S DISEASE DRUGS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 94 - Type 3: Mnemonic]
Q: What is the mnemonic for Parkinson's drugs?
A: LMAD = Levodopa/carbidopa, MAO-B inhibitors, Agonists (DA), DOPA decarboxylase inhibitor (carbidopa reminder)

[CARD 95 - Type 1: Basic Q&A]
Q: What is the mechanism of levodopa + carbidopa (co-careldopa)?
A: Levodopa → dopamine in CNS; carbidopa blocks peripheral dopa decarboxylase → ↓ peripheral conversion → more L-DOPA crosses BBB + reduced peripheral side effects (nausea, hypotension).
[Trap: Carbidopa does NOT cross the BBB — it only reduces peripheral side effects; it does NOT reduce central dopamine effects.]

[CARD 96 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is the on-off phenomenon in Parkinson's disease?
A: Motor fluctuations with long-term levodopa — "on" (drug works, good mobility) alternates with "off" (drug wears off, immobility); managed by adding COMT inhibitors, MAO-B inhibitors, or dopamine agonists.

[CARD 97 - Type 2: Cloze]
[c] Levodopa [/c] causes dyskinesias (involuntary writhing movements) at high doses after years of therapy — this is a sign of dopamine overstimulation, not disease progression.

[CARD 98 - Type 1: Basic Q&A]
Q: What are dopamine agonists used for in Parkinson's disease?
A: Early PD in younger patients (delays levodopa start), adjunct to levodopa, restless legs syndrome; examples: pramipexole, ropinirole, rotigotine (patch).

[CARD 99 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Dopamine agonists and impulse control disorders — what must you warn patients about?
A: Impulse control disorders (pathological gambling, hypersexuality, binge eating) — a characteristic and frequently tested side effect of dopamine agonists.

[CARD 100 - Type 1: Basic Q&A]
Q: What is the mechanism of MAO-B inhibitors in Parkinson's disease?
A: Block MAO-B → ↓ dopamine breakdown in CNS → ↑ CNS dopamine levels; used as monotherapy in early PD or adjunct.

[CARD 101 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Selegiline (MAO-B inhibitor) + pethidine — what happens?
A: Serotonin syndrome — pethidine has serotonergic properties; this combination is absolutely contraindicated.
[Trap: MAO-B inhibitors are more selective than MAO-A/B inhibitors but still interact dangerously with pethidine and SSRIs.]

[CARD 102 - Type 1: Basic Q&A]
Q: What is the mechanism of COMT inhibitors (entacapone, tolcapone)?
A: Block catechol-O-methyltransferase → ↓ peripheral levodopa breakdown → more L-DOPA enters brain; given with EVERY dose of levodopa.

[CARD 103 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why is tolcapone more dangerous than entacapone?
A: Tolcapone causes hepatotoxicity (requires LFT monitoring) — entacapone is preferred; tolcapone reserved for refractory cases.

[CARD 104 - Type 1: Basic Q&A]
Q: What are anticholinergics used for in Parkinson's disease?
A: Tremor-predominant PD (especially in younger patients), drug-induced parkinsonism, and acute dystonia; AVOID in elderly (confusion, falls, urinary retention).

[CARD 105 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is amantadine's unique indication in Parkinson's disease?
A: Reducing levodopa-induced dyskinesias in late/advanced PD — this is its unique niche indication (also mild early PD).

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 13: DEMENTIA DRUGS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 106 - Type 3: Mnemonic]
Q: What is the mnemonic for dementia drugs?
A: "4 drugs: 3 AChE inhibitors (donepezil, rivastigmine, galantamine) + 1 NMDA antagonist (memantine)"

[CARD 107 - Type 1: Basic Q&A]
Q: What is the mechanism of donepezil, rivastigmine, and galantamine?
A: Reversible acetylcholinesterase (AChE) inhibitors → ↑ ACh in synaptic cleft → symptomatic improvement in cognition.

[CARD 108 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which is the only AChEI approved for severe (not just mild-moderate) Alzheimer's disease?
A: Donepezil — licensed for mild, moderate, AND severe AD; rivastigmine and galantamine are only for mild-moderate.

[CARD 109 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which AChEI is approved for Parkinson's disease dementia?
A: Rivastigmine — also inhibits BuChE (butyrylcholinesterase); the only AChEI with this specific indication; available as transdermal patch (better GI tolerability).

[CARD 110 - Type 2: Cloze]
[c] Donepezil [/c] can cause bradycardia (via cholinergic stimulation of the heart) — monitor closely in patients with sick sinus syndrome or cardiac conduction defects.

[CARD 111 - Type 1: Basic Q&A]
Q: What is the mechanism of memantine?
A: Non-competitive NMDA receptor antagonist → blocks excessive glutamate (excitotoxicity) → used for moderate-severe AD.

[CARD 112 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Antipsychotics in Lewy body dementia — what is the risk?
A: Severely contraindicated — even small doses of typical or atypical antipsychotics (except quetiapine/clozapine) cause severe irreversible Parkinsonism and can be fatal in Lewy body dementia.
[Trap: AChEIs are actually USEFUL in Lewy body dementia — the trap is giving antipsychotics for behavioural symptoms.]

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 14: OPIOID ANALGESICS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 113 - Type 3: Mnemonic]
Q: What is the mnemonic for opioid side effects?
A: OPIOIDS = Oppressive (respiratory depression), Pupils (miosis), Itching (pruritus), Overdose risk, Ileus (constipation), Dependence, Sedation

[CARD 114 - Type 3: Mnemonic]
Q: What is the mnemonic for opioid overdose triad?
A: RMP = Respiratory depression, Miosis (pinpoint pupils), coma (unconscious/Mood-altered)

[CARD 115 - Type 1: Basic Q&A]
Q: What is the mechanism of opioids?
A: Agonists at μ (mu), κ (kappa), δ (delta) opioid receptors → ↓ pain transmission, ↓ cough reflex, ↓ GI motility.

[CARD 116 - Type 1: Basic Q&A]
Q: Which opioid side effect does tolerance NOT develop to?
A: Constipation — always prescribe laxatives with opioids; tolerance develops to sedation and nausea but never to constipation.
[Trap: Many students think tolerance develops to all opioid side effects — constipation is the exception.]

[CARD 117 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why does morphine accumulate in renal failure?
A: Active metabolite morphine-6-glucuronide (M6G) is renally cleared — accumulates in CKD → prolonged opioid effect/toxicity; use fentanyl or oxycodone instead in renal failure.

[CARD 118 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why is codeine dangerous in ultra-rapid CYP2D6 metabolisers?
A: Codeine is a prodrug — CYP2D6 converts it to morphine; ultra-rapid metabolisers convert too much → morphine toxicity; avoid in children post-tonsillectomy (multiple deaths reported).
[Trap: Poor CYP2D6 metabolisers get NO analgesia from codeine (can't convert it); ultra-rapid metabolisers get toxicity — both extremes are problematic.]

[CARD 119 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Tramadol — why is it more dangerous than a simple opioid?
A: Tramadol is a weak μ agonist + SNRI (inhibits serotonin/noradrenaline reuptake) → lowers seizure threshold + serotonin syndrome risk with SSRIs; not reversed by naloxone alone.

[CARD 120 - Type 2: Cloze]
[c] Pethidine (meperidine) [/c] causes seizures via its toxic metabolite norpethidine — avoid in renal failure and in Parkinson's patients on MAO-B inhibitors (serotonin syndrome risk).

[CARD 121 - Type 1: Basic Q&A]
Q: What is buprenorphine used for and why is it safer for dependence treatment?
A: Opioid dependence treatment — partial μ agonist with ceiling effect on respiratory depression; combined with naloxone (Suboxone) to deter IV misuse.

[CARD 122 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why does methadone require extra cardiac monitoring?
A: Methadone prolongs QT interval — risk of Torsades de Pointes, especially with other QT-prolonging drugs; also has unpredictable long t½.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 15: MIGRAINE DRUGS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 123 - Type 1: Basic Q&A]
Q: What is the mechanism of triptans (e.g. sumatriptan)?
A: 5-HT1B/1D agonist → vasoconstriction of meningeal vessels + ↓ neuropeptide (CGRP) release → aborts migraine attack.

[CARD 124 - Type 1: Basic Q&A]
Q: Name 3 contraindications to triptans.
A: Ischaemic heart disease (IHD), uncontrolled hypertension, hemiplegic migraine (risk of stroke).

[CARD 125 - Type 1: Basic Q&A]
Q: What is the first-line prophylaxis for migraine?
A: Propranolol (β-blocker) — contraindicated in asthma; alternatives include amitriptyline, topiramate, valproate.

[CARD 126 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is the newest class of migraine preventives tested on HKMLE?
A: CGRP monoclonal antibodies (erenumab, fremanezumab) — used for refractory migraine prophylaxis; injection site reactions and constipation are side effects.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 16: SUBSTANCE MISUSE / DEPENDENCE
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 127 - Type 1: Basic Q&A]
Q: What is the mechanism of disulfiram and what does it do?
A: Blocks aldehyde dehydrogenase (ALDH) → acetaldehyde accumulates → flushing, nausea, headache, hypotension when alcohol is consumed; deters drinking in motivated patients.

[CARD 128 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What drug causes the same reaction as disulfiram when taken with alcohol?
A: Metronidazole — also inhibits ALDH → acetaldehyde accumulation → disulfiram-like reaction (flushing, vomiting, hypotension).
[Trap: The disulfiram reaction is not unique to disulfiram — metronidazole, tinidazole, and some cephalosporins cause the same reaction.]

[CARD 129 - Type 1: Basic Q&A]
Q: What is acamprosate's mechanism in alcohol dependence?
A: GABA agonist / NMDA antagonist → reduces craving; started after detox; does NOT work if patient is still drinking.

[CARD 130 - Type 1: Basic Q&A]
Q: What is naltrexone used for in addiction medicine?
A: Opioid receptor antagonist — reduces alcohol craving (mechanism unclear) in alcohol dependence AND prevents opioid relapse; oral or monthly injection.

[CARD 131 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is the most effective single agent for smoking cessation?
A: Varenicline (Champix) — partial α4β2 nicotinic ACh receptor agonist; more effective than NRT or bupropion alone; carry a neuropsychiatric warning (depression, suicidal ideation).

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 17: SEROTONIN SYNDROME vs NMS — COMPARISON
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 132 - Type 1: Basic Q&A]
Q: What are the causes of serotonin syndrome vs NMS?
A: Serotonin syndrome = excess serotonin (SSRI + MAOI, SSRI + tramadol, SSRI + linezolid); NMS = dopamine blockade (antipsychotics) or sudden DA drug withdrawal.

[CARD 133 - Type 1: Basic Q&A]
Q: What is the muscle tone in serotonin syndrome vs NMS?
A: Serotonin syndrome = clonus, hyperreflexia, myoclonus; NMS = lead-pipe rigidity.

[CARD 134 - Type 1: Basic Q&A]
Q: What are the pupil findings in serotonin syndrome vs NMS?
A: Serotonin syndrome = dilated (mydriasis); NMS = normal or small pupils.

[CARD 135 - Type 1: Basic Q&A]
Q: What is the CK level in serotonin syndrome vs NMS?
A: Serotonin syndrome = normal or mildly elevated CK; NMS = markedly elevated CK (rhabdomyolysis).

[CARD 136 - Type 1: Basic Q&A]
Q: What is the treatment for serotonin syndrome?
A: Cyproheptadine (5-HT antagonist), supportive care, BZDs for agitation, cooling; stop all serotonergic drugs.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
BONUS: HIGH-YIELD TRAP CARDS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 137]
Q: HKMLE Trap: SSRI is stopped suddenly after 6 months of treatment. The patient develops dizziness, electric shock sensations, and flu-like symptoms. What is this?
A: SSRI discontinuation syndrome — NOT relapse; taper slowly over weeks (especially paroxetine which has the worst discontinuation syndrome due to short t½).

[CARD 138]
Q: HKMLE Trap: Ethosuximide is prescribed for a patient with absence + tonic-clonic seizures. What is wrong?
A: Ethosuximide only treats pure absence seizures — it has no effect on tonic-clonic seizures; use valproate for mixed generalised epilepsy.

[CARD 139]
Q: HKMLE Trap: Carbamazepine prescribed for a patient with juvenile myoclonic epilepsy. What is the problem?
A: Carbamazepine worsens myoclonic and absence seizures — use valproate or levetiracetam for myoclonic epilepsy.

[CARD 140]
Q: HKMLE Trap: Phenytoin dose is increased from 250mg to 300mg daily. The patient develops nystagmus and ataxia. Why?
A: Phenytoin has zero-order kinetics — a small dose increase causes a disproportionately large rise in plasma levels → toxicity; check serum level immediately.

[CARD 141]
Q: HKMLE Trap: Haloperidol prescribed for a Parkinson's patient with psychosis. What is the danger?
A: Haloperidol is a high-potency D2 blocker — severely worsens motor symptoms in Parkinson's; use quetiapine or clozapine only for psychosis in PD.

[CARD 142]
Q: HKMLE Trap: Typical antipsychotic is continued in a patient developing high fever, lead-pipe rigidity, and elevated CK. What must you do?
A: Stop the antipsychotic immediately — this is NMS; continuing it can be fatal.

[CARD 143]
Q: HKMLE Trap: A woman aged 25 with epilepsy is started on valproate. What must be done first?
A: Discuss teratogenicity risks, document the discussion, ensure effective contraception (valproate PREVENT programme), and consider an alternative AED — all women of childbearing age must be counselled before starting valproate.

[CARD 144]
Q: HKMLE Trap: Antipsychotics given for behavioural symptoms in Lewy body dementia. What is the risk?
A: Severely contraindicated — even small doses cause irreversible severe Parkinsonism and death in Lewy body dementia; use non-pharmacological approaches and AChEIs instead.

[CARD 145]
Q: HKMLE Trap: Z-drugs prescribed as a "safer" long-term alternative to BZDs for chronic insomnia. What is wrong?
A: Z-drugs have similar dependence and tolerance potential to BZDs — they are NOT safer for long-term use; maximum 2-4 weeks only.

[CARD 146]
Q: HKMLE Trap: Standard folic acid 400mcg prescribed to a woman on carbamazepine planning pregnancy. What is the correct dose?
A: 5mg/day folic acid is required for all women on AEDs — the standard 400mcg dose is insufficient to protect against AED-associated neural tube defects.

================================================================
END OF DECK — 146 CARDS TOTAL
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HKMLE ENDOCRINE PHARMACOLOGY — ANKI FLASHCARD DECK
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Generated from: Endocrine 💊.pdf
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SECTION 1: INSULIN
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 1 - Type 3: Mnemonic]
Q: What is the mnemonic for insulin types?
A: "RAP = Rapid-acting, Aspart/Lispro, Prandial" | "NGL = NPH Goes Long" | "Glargine = Gliding basal (no peak)"

[CARD 2 - Type 1: Basic Q&A]
Q: Which insulin types can be given IV?
A: Only Regular (short-acting/soluble) insulin and rapid-acting analogues (lispro, aspart) — NPH and long-acting insulins are NEVER given IV.
[Trap: NPH (intermediate-acting) is IV-capable is a classic wrong answer — it is ALWAYS subcutaneous only.]

[CARD 3 - Type 1: Basic Q&A]
Q: What is the onset, peak, and duration of rapid-acting insulin (lispro, aspart)?
A: Onset 15-30 min, peak 30-90 min, duration 3-5h — give 15 minutes before a meal.

[CARD 4 - Type 1: Basic Q&A]
Q: What is the onset, peak, and duration of Regular (short-acting) insulin?
A: Onset 30 min, peak 1-3h, duration 6-8h — give 30 minutes before a meal; used for IV infusions (DKA).

[CARD 5 - Type 1: Basic Q&A]
Q: What is the key clinical feature of long-acting insulin (glargine)?
A: No peak (flat profile) → least risk of nocturnal hypoglycaemia; given once daily as basal insulin.

[CARD 6 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which insulin is used for IV infusion in DKA?
A: Short-acting Regular (soluble) insulin only — rapid-acting analogues can also be used IV; NPH and long-acting insulins must never be given IV.

[CARD 7 - Type 1: Basic Q&A]
Q: What electrolyte disturbance does insulin cause and why is this critical in DKA?
A: Insulin drives K+ into cells → hypokalaemia; in DKA, K+ must be replaced before/with insulin to prevent fatal hypokalaemia.
[Trap: DKA patients appear to have normal or high K+ initially (due to acidosis), but total body K+ is low — hypokalaemia develops rapidly once insulin is started.]

[CARD 8 - Type 1: Basic Q&A]
Q: What is lipodystrophy and how is it prevented?
A: Lipoatrophy or lipohypertrophy at insulin injection sites — prevented by rotating injection sites with each dose.

[CARD 9 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: All insulins cause weight gain — which diabetes drug is weight-neutral or causes weight loss?
A: Metformin (weight-neutral/slight loss), GLP-1 agonists (significant weight loss), SGLT2 inhibitors (modest weight loss) — these are preferred in obese T2DM patients.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 2: METFORMIN
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 10 - Type 3: Mnemonic]
Q: What is the mnemonic for metformin?
A: "Metformin = Must exclude renal failure, Metabo-protective, Minimal hypoglycaemia"

[CARD 11 - Type 3: Mnemonic]
Q: What is the mnemonic for metformin contraindications?
A: CRASH = CKD (eGFR <30), Radiological contrast (hold 48h), Alcoholism, Serious illness/surgery, Hepatic failure

[CARD 12 - Type 1: Basic Q&A]
Q: What is the mechanism of metformin?
A: Activates AMPK → ↓ hepatic gluconeogenesis (primary action), ↑ peripheral insulin sensitivity, ↓ GI glucose absorption.

[CARD 13 - Type 1: Basic Q&A]
Q: What is the first-line drug for T2DM (all guidelines)?
A: Metformin — also used for PCOS and prediabetes prevention.

[CARD 14 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Does metformin cause hypoglycaemia as monotherapy?
A: No — metformin does not stimulate insulin release; hypoglycaemia only occurs if combined with insulin or sulfonylurea.
[Trap: Common wrong answer is that metformin causes hypoglycaemia — it does NOT as monotherapy.]

[CARD 15 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why must metformin be held before IV contrast?
A: Iodinated contrast can cause acute kidney injury → reduces metformin clearance → lactic acidosis; hold 48h before and until renal function confirmed stable after contrast.

[CARD 16 - Type 2: Cloze]
[c] Metformin [/c] causes lactic acidosis in patients with renal failure (eGFR <30) because reduced renal clearance leads to metformin accumulation → impaired mitochondrial function → lactic acid buildup.

[CARD 17 - Type 1: Basic Q&A]
Q: What long-term deficiency does metformin cause with chronic use?
A: Vitamin B12 deficiency — monitor B12 annually in long-term users; can cause peripheral neuropathy if untreated.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 3: SULFONYLUREAS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 18 - Type 3: Mnemonic]
Q: What is the mnemonic for sulfonylureas?
A: "SULFONYLureas = SULK if no glucose = Stimulate insulin regardless of sugar level" (glucose-independent mechanism)

[CARD 19 - Type 1: Basic Q&A]
Q: What is the mechanism of sulfonylureas?
A: Close ATP-sensitive K+ channels on pancreatic β-cells → membrane depolarisation → Ca2+ influx → insulin secretion (glucose-independent).

[CARD 20 - Type 2: Cloze]
[c] Sulfonylureas [/c] cause hypoglycaemia because they stimulate insulin release independently of blood glucose — insulin is secreted even when glucose is normal or low.

[CARD 21 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which sulfonylurea is safest in renal impairment, and which is most dangerous?
A: Gliclazide is safest (hepatically metabolised, shorter-acting); glibenclamide is most dangerous (active metabolites accumulate in CKD → prolonged severe hypoglycaemia).
[Trap: Common wrong answer is to continue glibenclamide in elderly or CKD patients — it causes the most severe and prolonged hypoglycaemia of all sulfonylureas.]

[CARD 22 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Can sulfonylureas be used in T1DM?
A: No — sulfonylureas require functioning β-cells to work; T1DM has destroyed β-cells; insulin is the only treatment for T1DM.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 4: SGLT2 INHIBITORS (GLIFLOZINS)
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 23 - Type 3: Mnemonic]
Q: What is the mnemonic for SGLT2 inhibitor side effects?
A: FUNGUS = Female genital mycosis, UTI, Nocturia/diuresis, Glycosuria, Urinary frequency, Skin (Fournier's gangrene)

[CARD 24 - Type 1: Basic Q&A]
Q: What is the mechanism of SGLT2 inhibitors?
A: Inhibit SGLT2 in the proximal tubule → block renal glucose reabsorption → glycosuria → lower BGL; also causes natriuresis and osmotic diuresis.

[CARD 25 - Type 1: Basic Q&A]
Q: Name 3 cardiovascular/renal indications for SGLT2 inhibitors (beyond glucose control).
A: T2DM + HFrEF (↓ hospitalisation), T2DM + established CVD (↓ CV mortality — EMPA-REG), T2DM + CKD (↓ progression); also HFrEF and CKD without diabetes.

[CARD 26 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Euglycaemic DKA — what is it and which drug causes it?
A: SGLT2 inhibitors cause ketoacidosis with near-normal blood glucose — easy to miss because glucose is not markedly elevated; test ketones in any unwell patient on SGLT2i.
[Trap: DKA is defined by ketosis + acidosis, NOT by hyperglycaemia — SGLT2i-induced DKA can have glucose in the normal range.]

[CARD 27 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What must you do with SGLT2 inhibitors before surgery?
A: Hold SGLT2 inhibitors 3 days before planned surgery — risk of perioperative euglycaemic DKA.

[CARD 28 - Type 2: Cloze]
[c] SGLT2 inhibitors [/c] cause Fournier's gangrene (necrotising fasciitis of the perineum) — a rare but life-threatening complication requiring immediate surgical debridement.

[CARD 29 - Type 1: Basic Q&A]
Q: Which SGLT2 inhibitor has the most evidence for heart failure (with and without diabetes)?
A: Dapagliflozin (DAPA-HF trial — HFrEF with or without T2DM); empagliflozin also approved for HFrEF.

[CARD 30 - Type 1: Basic Q&A]
Q: Do SGLT2 inhibitors cause hypoglycaemia as monotherapy?
A: No — glycosuria only increases when blood glucose is elevated; mechanism is glucose-independent only at the renal level, not via insulin stimulation.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 5: GLP-1 RECEPTOR AGONISTS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 31 - Type 3: Mnemonic]
Q: What is the mnemonic for GLP-1 receptor agonists?
A: "GLP-1 = Gut slows (↓ gastric emptying), Less appetite (hypothalamus), Pumps insulin when glucose HIGH (glucose-dependent), 1 injection weekly/daily"

[CARD 32 - Type 1: Basic Q&A]
Q: What is the mechanism of GLP-1 receptor agonists?
A: Mimic incretin hormone GLP-1 → glucose-dependent insulin secretion, ↓ glucagon, ↓ gastric emptying (→ satiety), ↓ appetite via hypothalamus.

[CARD 33 - Type 1: Basic Q&A]
Q: What is the most important contraindication to GLP-1 receptor agonists?
A: Personal or family history of medullary thyroid carcinoma (MTC) or MEN type 2 — black box warning (C-cell tumours in rodent studies).
[Trap: Common wrong answer is to avoid in pancreatitis only — the MTC/MEN2 contraindication is the more critical HKMLE-tested contraindication.]

[CARD 34 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Do GLP-1 agonists cause hypoglycaemia as monotherapy?
A: No — insulin secretion is glucose-dependent; GLP-1 agonists only stimulate insulin when blood glucose is elevated.

[CARD 35 - Type 1: Basic Q&A]
Q: Which GLP-1 agonist has the most potent weight loss effect?
A: Semaglutide (up to 15% body weight loss with 2.4mg/week = Wegovy for obesity); also available orally.

[CARD 36 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which GLP-1 agonist and SGLT2 inhibitor are best for T2DM + established CVD?
A: GLP-1 agonists: liraglutide (LEADER trial) or semaglutide; SGLT2 inhibitors: empagliflozin (EMPA-REG) or canagliflozin.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 6: DPP-4 INHIBITORS (GLIPTINS)
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 37 - Type 3: Mnemonic]
Q: What is the mnemonic for DPP-4 inhibitors (gliptins)?
A: "Gliptins = Gentle (no hypo, no weight), nasty joints (arthralgia)"

[CARD 38 - Type 1: Basic Q&A]
Q: What is the mechanism of DPP-4 inhibitors?
A: Inhibit DPP-4 enzyme → prevent GLP-1 and GIP degradation → ↑ endogenous incretin levels → glucose-dependent insulin secretion, ↓ glucagon.

[CARD 39 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which gliptin does NOT require renal dose adjustment?
A: Linagliptin — hepatically eliminated; all other gliptins require dose reduction in renal impairment.
[Trap: Common wrong answer is sitagliptin (most widely used) — sitagliptin DOES need renal dose adjustment; linagliptin is the exception.]

[CARD 40 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which gliptin specifically increases heart failure risk?
A: Saxagliptin (SAVOR-TIMI trial) — avoid in HF; other gliptins are generally HF-neutral.

[CARD 41 - Type 1: Basic Q&A]
Q: What is the black box warning for DPP-4 inhibitors?
A: Severe joint pain (arthralgia) — can be disabling; reversible on stopping the drug.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 7: THIAZOLIDINEDIONES (TZDs / GLITAZONES)
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 42 - Type 3: Mnemonic]
Q: What is the mnemonic for TZD side effects?
A: "TZDs = Thick fluid (oedema), Zero bone (fractures), Dangerous heart (HF)"

[CARD 43 - Type 1: Basic Q&A]
Q: What is the mechanism of TZDs (pioglitazone)?
A: Activate PPAR-γ nuclear receptor → ↑ insulin sensitivity in muscle, liver, and adipose tissue (insulin sensitiser — do NOT stimulate insulin release).

[CARD 44 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why are TZDs absolutely contraindicated in heart failure?
A: TZDs cause fluid retention and peripheral oedema → directly worsen HF in all classes; hard contraindication.
[Trap: Common wrong answer is that TZDs are safe in compensated HF — they are contraindicated in ALL classes of HF.]

[CARD 45 - Type 2: Cloze]
[c] Pioglitazone [/c] is associated with bladder cancer with long-term use — screen for haematuria and avoid in patients with a history of bladder cancer.

[CARD 46 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why was rosiglitazone withdrawn from the market?
A: Increased myocardial infarction risk — rosiglitazone was withdrawn due to CV safety; pioglitazone is the only TZD still available.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 8: DIABETES DRUG QUICK-SELECT
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 47 - Type 1: Basic Q&A]
Q: First-line drug for T2DM?
A: Metformin (all guidelines, unless contraindicated).

[CARD 48 - Type 1: Basic Q&A]
Q: Preferred add-on drug for T2DM + HFrEF?
A: SGLT2 inhibitor (dapagliflozin or empagliflozin) — mortality benefit in HFrEF with or without diabetes.

[CARD 49 - Type 1: Basic Q&A]
Q: Preferred drug for T2DM + obesity (weight loss is priority)?
A: GLP-1 receptor agonist (semaglutide or liraglutide).

[CARD 50 - Type 1: Basic Q&A]
Q: Preferred antidiabetic drugs in the elderly (to minimise hypoglycaemia)?
A: DPP-4 inhibitor (gliptin) or gliclazide (shortest-acting sulfonylurea) — avoid glibenclamide.

[CARD 51 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which antidiabetic is preferred in T2DM + CKD (eGFR 25-45)?
A: Dapagliflozin (also renoprotective); avoid metformin if eGFR <30; dose-adjust other drugs accordingly.

[CARD 52 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is the only treatment for T1DM?
A: Insulin — no oral antidiabetic drug works without functioning β-cells; T1DM requires insulin replacement.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 9: THYROID DRUGS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 53 - Type 3: Mnemonic]
Q: What is the mnemonic for thyroid drug choice in pregnancy?
A: "PTU = 1st trimester; Carbimazole = after 1st trimester" (PTU safer in T1; switch at T2 because PTU is hepatotoxic long-term)

[CARD 54 - Type 1: Basic Q&A]
Q: What is the mechanism of carbimazole and PTU (shared)?
A: Block thyroid peroxidase → ↓ iodination of tyrosine residues → ↓ T3/T4 synthesis.

[CARD 55 - Type 1: Basic Q&A]
Q: What additional mechanism does PTU have that carbimazole lacks?
A: PTU also blocks peripheral T4 → T3 conversion (deiodinase inhibition) — important in thyroid storm.

[CARD 56 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which antithyroid drug is used in the 1st trimester of pregnancy and why?
A: PTU — carbimazole is associated with aplasia cutis and choanal atresia in the fetus during 1st trimester organogenesis.
[Trap: Common wrong answer is carbimazole throughout pregnancy — PTU is required in T1, then switch to carbimazole in T2/T3 (PTU is more hepatotoxic long-term).]

[CARD 57 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: A patient on carbimazole develops a sore throat and fever. What must you do?
A: Stop carbimazole immediately and check FBC — this may be agranulocytosis (0.5% incidence); a life-threatening complication.
[Trap: Never reassure and continue the drug — ANY sore throat/fever in a patient on antithyroids = stop and check FBC immediately.]

[CARD 58 - Type 2: Cloze]
[c] Antithyroid drugs [/c] take 6-8 weeks to achieve a euthyroid state because they block NEW hormone synthesis but do not remove pre-formed thyroid hormone already stored in the gland.

[CARD 59 - Type 3: Mnemonic]
Q: What is the mnemonic for thyroid storm management?
A: BIIP = Block synthesis (PTU), Iodine (Lugol's — given AFTER PTU, NOT before), Iodide uptake block (β-blocker/propranolol), Prednisolone (hydrocortisone)

[CARD 60 - Type 1: Basic Q&A]
Q: What are the 4 drug classes used in thyroid storm management?
A: PTU (high dose), Lugol's iodine (given AFTER PTU), propranolol IV (rate control + ↓ T4→T3 conversion), hydrocortisone IV (↓ T4→T3 conversion + adrenal support).

[CARD 61 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why must Lugol's iodine be given AFTER PTU in thyroid storm?
A: If iodine is given before PTU, the iodine load is used to synthesise MORE thyroid hormone (Jod-Basedow effect) — PTU must first block synthesis, then iodine is given to inhibit hormone release.
[Trap: Giving iodine first is a dangerous error — always give PTU first, then iodine at least 1 hour later.]

[CARD 62 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why is aspirin avoided in thyroid storm hyperpyrexia?
A: Aspirin displaces thyroid hormone from binding proteins → raises free T4/T3 levels → worsens the storm; use paracetamol for fever instead.

--- LEVOTHYROXINE ---

[CARD 63 - Type 3: Mnemonic]
Q: What is the mnemonic for levothyroxine?
A: "Levothyroxine = Long half-life (7 days), one morning dose (empty stomach), Less interaction with food"

[CARD 64 - Type 1: Basic Q&A]
Q: What is the mechanism of levothyroxine?
A: Synthetic T4 → converted to active T3 in peripheral tissues by deiodinase.

[CARD 65 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why must levothyroxine be started LOW and titrated slowly in elderly patients with IHD?
A: Levothyroxine increases myocardial O2 demand → can precipitate angina or MI in those with underlying IHD; start at 25-50 mcg and increase slowly.

[CARD 66 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why must steroids be given BEFORE levothyroxine in combined pituitary failure?
A: In combined hypothyroidism + adrenal insufficiency, starting levothyroxine first increases cortisol metabolism → precipitates adrenal crisis; always start hydrocortisone first.
[Trap: Starting levothyroxine first in panhypopituitarism is a classic HKMLE management trap that can be fatal.]

[CARD 67 - Type 1: Basic Q&A]
Q: When should TSH be rechecked after changing levothyroxine dose?
A: 6 weeks — levothyroxine has a long t½ (7 days); TSH takes ~6 weeks to reach new steady state after dose adjustment.

[CARD 68 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Levothyroxine dose in pregnancy — does it need adjustment?
A: Yes — increase dose by ~25-50% in the 1st trimester (↑ TBG demand, ↑ placental T4 transfer); check TSH early and often.

[CARD 69 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Management of myxoedema coma?
A: IV T3 (liothyronine) or IV T4 + IV hydrocortisone + rewarming + ICU admission; hydrocortisone given empirically to prevent adrenal crisis.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 10: CORTICOSTEROIDS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 70 - Type 3: Mnemonic]
Q: What is the mnemonic for corticosteroid side effects?
A: STEROIDS = Sugar↑ (hyperglycaemia), Thin skin/bones (osteoporosis), Edema, Raised BP, Obesity (cushingoid), Infections↑ (TB reactivation), Delayed healing, Suppression of HPA axis

[CARD 71 - Type 1: Basic Q&A]
Q: What is the relative glucocorticoid potency order?
A: Dexamethasone (25-30x) > methylprednisolone (5x) > prednisolone (4x) > hydrocortisone (1x reference).

[CARD 72 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which steroid has no mineralocorticoid activity?
A: Dexamethasone (mineralocorticoid potency = 0) — used when fluid retention must be avoided (e.g. cerebral oedema, fetal lung maturation, suppression test).

[CARD 73 - Type 1: Basic Q&A]
Q: What are the 3 key indications for dexamethasone?
A: Cerebral oedema, fetal lung maturation (antenatal), dexamethasone suppression test (Cushing's diagnosis), croup, anti-emetic (chemotherapy), severe COVID-19.

[CARD 74 - Type 1: Basic Q&A]
Q: What is fludrocortisone used for?
A: Mineralocorticoid replacement in primary adrenal insufficiency (Addison's disease) — high mineralocorticoid potency (250x hydrocortisone), negligible glucocorticoid effect.

[CARD 75 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why must steroids never be stopped abruptly after >3 weeks of use?
A: HPA axis suppression → adrenal cortex cannot produce cortisol after exogenous steroid withdrawal → adrenal crisis (hypotension, hypoglycaemia, collapse); taper gradually.
[Trap: Any patient on ≥5mg prednisolone/day for >3 weeks needs a taper — do NOT stop abruptly.]

[CARD 76 - Type 2: Cloze]
[c] Corticosteroids [/c] increase risk of tuberculosis reactivation — always screen with IGRA (interferon-gamma release assay) before starting long-term steroids and consider TB prophylaxis if positive.

[CARD 77 - Type 1: Basic Q&A]
Q: What bone complication of steroids requires urgent orthopaedic assessment?
A: Avascular necrosis of the femoral head — hip pain + restricted movement in a patient on steroids = urgent MRI.

[CARD 78 - Type 1: Basic Q&A]
Q: Which steroid is used for IV pulse therapy (MS relapse, lupus nephritis, transplant rejection)?
A: Methylprednisolone (IV high-dose pulse).

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 11: ADRENAL INSUFFICIENCY MANAGEMENT
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 79 - Type 3: Mnemonic]
Q: What is the mnemonic for adrenal crisis treatment?
A: HISS = Hydrocortisone IV (100mg bolus), IV saline (0.9% large volume), Sugar (IV dextrose if hypoglycaemic), Support vitals

[CARD 80 - Type 1: Basic Q&A]
Q: What are the clinical features of adrenal crisis?
A: Hypotension, hypoglycaemia, hyponatraemia, hyperkalaemia, fever, vomiting, altered GCS.

[CARD 81 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Should you delay hydrocortisone while waiting for cortisol results in suspected adrenal crisis?
A: No — do NOT delay treatment if adrenal crisis is strongly suspected; give hydrocortisone 100mg IV immediately, take blood for cortisol before injection if possible but do not wait.

[CARD 82 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What are the sick day rules for a patient on long-term hydrocortisone?
A: Double the hydrocortisone dose during fever or infection; if vomiting (cannot absorb oral) → give IM/IV hydrocortisone immediately.
[Trap: Patients on chronic steroids who are vomiting and do not inject IM hydrocortisone can develop life-threatening adrenal crisis — always give parenteral steroids if unable to take oral.]

[CARD 83 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What perioperative steroid cover is needed for a patient on long-term prednisolone?
A: Stress-dose steroids perioperatively — typically IV hydrocortisone 25-100mg at induction and post-operatively; failure to do so → intraoperative adrenal crisis.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 12: BISPHOSPHONATES
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 84 - Type 3: Mnemonic]
Q: What is the mnemonic for bisphosphonate side effects?
A: BONE SNAP = Bisphosphonate ONJ (osteonecrosis jaw), Esophagitis, Snap fractures (atypical femur), Nephrological (avoid in CKD)

[CARD 85 - Type 3: Mnemonic]
Q: What is the mnemonic for bisphosphonate counselling (oral)?
A: STOP EAT = Stay upright (30-60 min), Take on empty stomach, Only water with tablet, Pre-dental check (ONJ risk)

[CARD 86 - Type 1: Basic Q&A]
Q: What is the mechanism of bisphosphonates?
A: Bind hydroxyapatite → inhibit osteoclast activity → ↓ bone resorption → ↑ bone mineral density.

[CARD 87 - Type 1: Basic Q&A]
Q: Name 5 indications for bisphosphonates.
A: Postmenopausal osteoporosis, glucocorticoid-induced osteoporosis, Paget's disease (zoledronic acid), hypercalcaemia of malignancy, bone metastases (pain/fracture prevention).

[CARD 88 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is osteonecrosis of the jaw (ONJ) and when does it occur?
A: Exposed necrotic bone in the jaw — most common after IV bisphosphonates (higher dose) combined with dental procedures/extractions; advise dental review before starting bisphosphonate.
[Trap: ONJ risk is not exclusive to IV bisphosphonates — oral bisphosphonates also carry a risk, but IV (zoledronic acid) is higher.]

[CARD 89 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Oral bisphosphonate administration rules — what happens if the patient lies down after taking it?
A: Oesophagitis and oesophageal ulceration — patients must remain upright for 30 minutes (alendronate) or 60 minutes (risedronate) after taking the tablet.

[CARD 90 - Type 2: Cloze]
[c] IV bisphosphonates [/c] cause an acute phase reaction (fever, myalgia, flu-like symptoms) after the first dose — caused by activation of γδ T cells; usually resolves within 3 days; premedicate with paracetamol.

[CARD 91 - Type 1: Basic Q&A]
Q: Which bisphosphonate is given once yearly IV and is first-line for Paget's disease?
A: Zoledronic acid (highest potency among bisphosphonates).

[CARD 92 - Type 1: Basic Q&A]
Q: What is the contraindication to bisphosphonates in renal failure?
A: eGFR <30-35 — bisphosphonates are renally cleared; accumulation causes severe nephrotoxicity; avoid oral and IV forms.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 13: DENOSUMAB
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 93 - Type 3: Mnemonic]
Q: What is the mnemonic for denosumab?
A: "Denosumab DENies osteoclasts (RANK-L)" — monoclonal antibody blocks RANK-L → prevents osteoclast formation.

[CARD 94 - Type 1: Basic Q&A]
Q: What is the mechanism of denosumab?
A: Monoclonal antibody against RANK-L → prevents osteoclast formation and activation → ↓ bone resorption.

[CARD 95 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why is denosumab preferred over bisphosphonates in severe CKD?
A: Denosumab is not renally cleared (it is a monoclonal antibody) — safe in any stage of CKD including dialysis; bisphosphonates are contraindicated below eGFR 30-35.
[Trap: Denosumab still causes hypocalcaemia (higher risk in CKD) — always supplement calcium + vitamin D.]

[CARD 96 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What happens if denosumab is stopped abruptly?
A: Rebound vertebral fractures — sudden loss of RANK-L suppression causes a surge in osteoclast activity → multiple crush fractures; must transition to bisphosphonate when stopping denosumab.
[Trap: Simply stopping denosumab without transitioning to a bisphosphonate is a dangerous error — fracture risk is higher than at baseline.]

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 14: CALCITONIN & TERIPARATIDE
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 97 - Type 1: Basic Q&A]
Q: What is the mechanism and key indication for calcitonin?
A: Inhibits osteoclasts + ↓ renal calcium reabsorption → used for acute hypercalcaemia (rapid-acting, short-term) and acute pain from osteoporotic vertebral fracture (intranasal).

[CARD 98 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: In hypercalcaemia of malignancy — calcitonin vs bisphosphonate, which is better long-term?
A: IV bisphosphonate (zoledronic acid) is superior long-term; calcitonin is used for immediate/rapid effect only (within hours) while bisphosphonate takes 2-4 days to work — use both together in acute hypercalcaemia.

[CARD 99 - Type 2: Cloze]
[c] Calcitonin [/c] causes tachyphylaxis (rapid tolerance) within days of repeated use — it cannot be used for chronic management of hypercalcaemia; bisphosphonates are used for maintenance.

[CARD 100 - Type 1: Basic Q&A]
Q: What is the mechanism of teriparatide and how does it differ from bisphosphonates?
A: Recombinant PTH 1-34 → intermittent pulsed stimulation of osteoblasts → bone formation (anabolic); bisphosphonates are antiresorptive — teriparatide BUILDS new bone.
[Trap: Continuous PTH causes bone resorption; only PULSED/intermittent PTH is anabolic — this pharmacokinetic paradox is exam-tested.]

[CARD 101 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What are the key limitations of teriparatide?
A: Maximum 2 years lifetime use; contraindicated in Paget's disease, prior radiation to skeleton, bone metastases, hyperparathyroidism; causes hypercalcaemia.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 15: DESMOPRESSIN (DDAVP)
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 102 - Type 3: Mnemonic]
Q: What is the mnemonic for desmopressin?
A: "DDAVP = Dry the tap (antidiuretic) without the pressure (no vasoconstriction — V2 only, not V1)"

[CARD 103 - Type 1: Basic Q&A]
Q: What is the mechanism of desmopressin?
A: Synthetic V2-receptor agonist (vasopressin analogue) → ↑ water reabsorption in collecting duct; no V1 pressor effect (unlike vasopressin).

[CARD 104 - Type 1: Basic Q&A]
Q: Name 4 indications for desmopressin.
A: Central diabetes insipidus (treatment of choice), nocturnal enuresis (children), von Willebrand disease type 1 (↑ vWF release), Haemophilia A (↑ Factor VIII release).

[CARD 105 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Central DI vs nephrogenic DI — how do you distinguish them and treat each?
A: Central DI responds to desmopressin (water deprivation test + desmopressin challenge); Nephrogenic DI does NOT respond to desmopressin — treat with thiazide diuretics (paradoxical antidiuresis) and low-sodium diet.
[Trap: Desmopressin is useless in nephrogenic DI — the kidneys cannot respond to ADH regardless of dose; thiazides are the paradoxical treatment.]

[CARD 106 - Type 2: Cloze]
[c] Desmopressin [/c] causes hyponatraemia and water intoxication — the most important side effect, especially in children with enuresis; restrict fluid intake after dosing.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 16: SOMATOSTATIN ANALOGUES & OTHER PITUITARY DRUGS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 107 - Type 3: Mnemonic]
Q: What is the mnemonic for octreotide?
A: "OctREOtide = Octopus grabs all the excess hormones" — inhibits GH, insulin, glucagon, TSH, and gut hormones.

[CARD 108 - Type 1: Basic Q&A]
Q: What is the mechanism of somatostatin analogues (octreotide)?
A: Mimic somatostatin → inhibit GH, insulin, glucagon, TSH, and gut hormone secretion; reduce splanchnic blood flow.

[CARD 109 - Type 1: Basic Q&A]
Q: Name 4 key indications for octreotide.
A: Acromegaly (post-surgical), carcinoid syndrome (symptom control), variceal bleeding (↓ portal pressure), VIPoma/glucagonoma/gastrinoma.

[CARD 110 - Type 2: Cloze]
[c] Somatostatin analogues (octreotide) [/c] cause gallstones because they reduce gallbladder motility → bile stasis → stone formation; monitor with biliary ultrasound.

[CARD 111 - Type 1: Basic Q&A]
Q: What is the mechanism of cabergoline and what is it used for?
A: Dopamine D2 agonist → ↓ prolactin secretion; first-line for prolactinoma; also used in Parkinson's (bromocriptine) and acromegaly (adjunct).

[CARD 112 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: High-dose cabergoline for prolactinoma — what cardiac side effect requires monitoring?
A: Cardiac valve fibrosis (regurgitation) — requires periodic echocardiogram monitoring with long-term high-dose cabergoline.

[CARD 113 - Type 1: Basic Q&A]
Q: What is the mechanism of GnRH agonists (leuprolide, goserelin) and why do they decrease sex hormones with chronic use?
A: Continuous GnRH agonist stimulation downregulates pituitary GnRH receptors → paradoxically ↓ LH/FSH → ↓ testosterone/oestrogen; used for prostate cancer, endometriosis, precocious puberty.

[CARD 114 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which drug is used for acromegaly when somatostatin analogues fail?
A: Pegvisomant — GH receptor antagonist → ↓ IGF-1; requires LFT monitoring.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
BONUS: HIGH-YIELD TRAP CARDS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 115]
Q: HKMLE Trap: Patient on metformin has IV contrast for CT scan without holding the drug. What is the risk?
A: Lactic acidosis — contrast-induced AKI reduces metformin clearance → accumulation → lactic acidosis; hold metformin 48h before contrast and until renal function is confirmed stable.

[CARD 116]
Q: HKMLE Trap: NPH insulin is ordered as an IV infusion for DKA. What is the error?
A: NPH (intermediate-acting) must NEVER be given IV — only Regular (short-acting) or rapid-acting insulin are IV-capable.

[CARD 117]
Q: HKMLE Trap: SGLT2 inhibitor patient presents with nausea, vomiting, and blood glucose of 12 mmol/L. What diagnosis must not be missed?
A: Euglycaemic DKA — glucose is only mildly elevated but the patient is in ketoacidosis; check blood/urine ketones in any unwell patient on SGLT2i.

[CARD 118]
Q: HKMLE Trap: Carbimazole prescribed throughout pregnancy for Graves' disease. What is the risk in T1?
A: Aplasia cutis and choanal atresia — carbimazole is teratogenic in the 1st trimester; use PTU in T1, switch to carbimazole in T2/T3.

[CARD 119]
Q: HKMLE Trap: Lugol's iodine given BEFORE PTU in thyroid storm. What happens?
A: Iodine load stimulates MORE thyroid hormone synthesis (Jod-Basedow effect) — always give PTU first to block synthesis, then give iodine at least 1 hour later.

[CARD 120]
Q: HKMLE Trap: Levothyroxine is started first in a patient with combined hypothyroidism and adrenal insufficiency. What is the danger?
A: Adrenal crisis — levothyroxine increases cortisol metabolism; without adrenal reserve, starting T4 first precipitates crisis; always give hydrocortisone first.

[CARD 121]
Q: HKMLE Trap: Prednisolone is stopped abruptly after 6 weeks of treatment. What can happen?
A: Adrenal crisis — HPA axis is suppressed; abrupt cessation causes acute cortisol deficiency; taper gradually over weeks.

[CARD 122]
Q: HKMLE Trap: Bisphosphonate prescribed for a patient with eGFR 20 ml/min. What is the concern?
A: Contraindicated below eGFR 30-35 — use denosumab instead (not renally cleared); supplement calcium and vitamin D with denosumab.

[CARD 123]
Q: HKMLE Trap: Denosumab stopped without transitioning to bisphosphonate. What is the risk?
A: Rebound vertebral fractures — RANK-L suppression suddenly lifted → osteoclast surge → multiple crush fractures; always transition to bisphosphonate when stopping denosumab.

[CARD 124]
Q: HKMLE Trap: Desmopressin given for nephrogenic DI. Will it work?
A: No — nephrogenic DI is caused by renal V2 receptor resistance; desmopressin has no effect; treat with thiazide diuretics (paradoxical antidiuresis) instead.

[CARD 125]
Q: HKMLE Trap: Patient with T2DM on glibenclamide develops prolonged hypoglycaemia. What should the sulfonylurea be changed to?
A: Gliclazide (hepatically metabolised, shorter-acting) — glibenclamide active metabolites accumulate, causing prolonged dangerous hypoglycaemia especially in elderly/CKD.

================================================================
END OF DECK — 125 CARDS TOTAL
================================================================

================================================================
HKMLE RESPIRATORY PHARMACOLOGY — ANKI FLASHCARD DECK
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Generated from: Resp 💊.pdf
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━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 1: SHORT-ACTING β2 AGONISTS (SABAs)
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 1 - Type 3: Mnemonic]
Q: What is the mnemonic for SABAs?
A: "SABA = Salbutamol = Seconds to work = Save acute attacks"

[CARD 2 - Type 1: Basic Q&A]
Q: What is the mechanism of SABAs (salbutamol)?
A: Stimulate β2 receptors → ↑ cAMP → airway smooth muscle relaxation → bronchodilation.

[CARD 3 - Type 1: Basic Q&A]
Q: What are the 3 key indications for SABAs?
A: Acute asthma (first-line reliever), acute COPD exacerbation, exercise-induced bronchospasm (prophylaxis — take before exercise).

[CARD 4 - Type 2: Cloze]
[c] Salbutamol (SABA) [/c] causes hypokalaemia at high doses because β2 stimulation drives K+ into cells via Na+/K+-ATPase activation — a classic HKMLE exam side effect.

[CARD 5 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: SABA overuse — what does it signal?
A: Overuse of SABA (>3 canisters/month) signals poor asthma control — step up treatment, do NOT simply increase SABA.
[Trap: Increasing SABA frequency to manage worsening asthma is a wrong answer — it signals the need for step-up with ICS or ICS + LABA.]

[CARD 6 - Type 1: Basic Q&A]
Q: What are the main side effects of SABAs?
A: Tremor (most common), tachycardia, palpitations, hypokalaemia (high doses), headache.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 2: LONG-ACTING β2 AGONISTS (LABAs)
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 7 - Type 3: Mnemonic]
Q: What is the mnemonic for LABAs?
A: "LABAs Last Long — but NEVER Alone in asthma"

[CARD 8 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Can a LABA be used as monotherapy for asthma?
A: No — LABA monotherapy in asthma is associated with increased asthma-related death (black box warning); always combine with ICS.
[Trap: LABA alone for asthma is a classic wrong answer — must always be paired with ICS in asthma.]

[CARD 9 - Type 1: Basic Q&A]
Q: What is the standard step-up combination for uncontrolled asthma at Step 3?
A: ICS + LABA (e.g. fluticasone + salmeterol = Seretide/Advair; budesonide + formoterol = Symbicort).

[CARD 10 - Type 1: Basic Q&A]
Q: Name 3 LABAs and their durations.
A: Salmeterol (12h), formoterol (12h), indacaterol (24h — COPD only).

[CARD 11 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which LABA can be used as BOTH preventer and reliever in Symbicort MART?
A: Formoterol — fast-onset LABA; salmeterol CANNOT be used as a reliever due to slow onset.
[Trap: Salmeterol is not fast enough for reliever use — only formoterol-containing inhalers are used in MART regimens.]

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 3: SHORT-ACTING MUSCARINIC ANTAGONISTS (SAMAs)
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 12 - Type 3: Mnemonic]
Q: What is the mnemonic for ipratropium?
A: "IPRAtropium = I PRefer Airways Relaxed — COPD not asthma first-line"

[CARD 13 - Type 1: Basic Q&A]
Q: What is the mechanism of ipratropium?
A: Blocks M3 muscarinic receptors → ↓ bronchoconstriction + ↓ mucus secretion → bronchodilation.

[CARD 14 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is the role of ipratropium in acute severe asthma in the ED?
A: Add ipratropium nebulisation to salbutamol for additive bronchodilation in acute severe asthma — it does not replace SABA; used as an adjunct.
[Trap: Ipratropium replacing SABA in acute asthma is wrong — it is always an adjunct, never first-line alone.]

[CARD 15 - Type 1: Basic Q&A]
Q: What are the key side effects of ipratropium (anticholinergic)?
A: Dry mouth (most common), urinary retention, constipation, blurred vision, paradoxical tachycardia.

[CARD 16 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which condition is ipratropium contraindicated in and why?
A: Narrow-angle glaucoma (especially if nebuliser spray contacts the eyes) — avoid getting the mist near the eyes; also caution in prostatic hypertrophy (urinary retention).

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 4: LONG-ACTING MUSCARINIC ANTAGONISTS (LAMAs)
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 17 - Type 3: Mnemonic]
Q: What is the mnemonic for tiotropium?
A: "TIOtropium = TImes Once daily = COPD controller"

[CARD 18 - Type 1: Basic Q&A]
Q: What is tiotropium's main indication and dosing advantage?
A: First-line COPD maintenance therapy — once daily (superior to ipratropium 4x daily); also reduces exacerbations.

[CARD 19 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Can tiotropium (LAMA) be used in asthma?
A: Yes — tiotropium is licensed as add-on therapy in severe asthma (≥6 years) when ICS + LABA is insufficient (Step 4-5).
[Trap: LAMAs are COPD-first but are also a valid asthma add-on — not exclusive to COPD.]

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 5: INHALED CORTICOSTEROIDS (ICS)
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 20 - Type 3: Mnemonic]
Q: What is the mnemonic for ICS side effects?
A: "ICS = Inflammation Controlled & Suppressed — but watch the MOUTH (candida)"

[CARD 21 - Type 1: Basic Q&A]
Q: What is the mechanism of ICS?
A: Bind glucocorticoid receptors → ↓ inflammatory cytokines, ↓ eosinophils, ↓ airway oedema → ↓ bronchial hyperresponsiveness.

[CARD 22 - Type 1: Basic Q&A]
Q: What is the most common local side effect of ICS?
A: Oropharyngeal candidiasis (thrush) — prevented by rinsing mouth and gargling with water after every dose.

[CARD 23 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: How do you prevent oral candidiasis from ICS?
A: Rinse mouth and gargle with water after EVERY dose — this is standard patient education and is exam-tested counselling.
[Trap: A common wrong answer is to reduce the dose of ICS — the correct answer is rinse mouth after each use; do NOT stop or reduce the ICS.]

[CARD 24 - Type 2: Cloze]
[c] Inhaled corticosteroids [/c] cause dysphonia (hoarse voice) because steroid deposition on the larynx causes local myopathy of the vocal cords — improved by using a spacer or rinsing mouth.

[CARD 25 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which ICS is safest in pregnancy?
A: Budesonide (Category B) — the preferred ICS during pregnancy; do NOT stop asthma ICS in pregnancy (uncontrolled asthma is more harmful to the fetus).
[Trap: Stopping ICS in pregnancy to avoid fetal harm is wrong — uncontrolled asthma is more dangerous; continue budesonide.]

[CARD 26 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Can ICS be used to treat an acute asthma attack?
A: No — ICS takes days to weeks to reduce airway inflammation; it has NO role in acute bronchospasm; use SABA (salbutamol) for acute attacks.
[Trap: Using ICS for acute asthma attack is a wrong answer — ICS is a preventer/controller, not a reliever.]

[CARD 27 - Type 1: Basic Q&A]
Q: What systemic side effects occur with HIGH-dose ICS?
A: Adrenal suppression, growth suppression in children, osteoporosis — at standard therapeutic doses, systemic effects are minimal.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 6: COMBINED INHALERS (ICS + LABA)
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 28 - Type 1: Basic Q&A]
Q: What are the 3 main ICS + LABA combination inhalers?
A: Seretide (fluticasone + salmeterol), Symbicort (budesonide + formoterol), Relvar Ellipta (fluticasone furoate + vilanterol — once daily, COPD).

[CARD 29 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is Symbicort MART and how does it work?
A: Symbicort MART (Maintenance And Reliever Therapy) = patient uses Symbicort as BOTH daily preventer AND as-needed reliever — possible only because formoterol has fast onset; Seretide CANNOT be used this way (salmeterol is too slow).
[Trap: Using Seretide (salmeterol-containing) as reliever is wrong — salmeterol onset is too slow; only formoterol-containing inhalers can be used as MART.]

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 7: THEOPHYLLINE
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 30 - Type 3: Mnemonic]
Q: What is the mnemonic for theophylline toxicity?
A: CANT = Cardiac arrhythmia, Agitation/seizures, Nausea/vomiting, Tremor

[CARD 31 - Type 1: Basic Q&A]
Q: What is the mechanism of theophylline?
A: Non-selective phosphodiesterase (PDE) inhibitor → ↑ cAMP → bronchodilation; also adenosine receptor antagonist.

[CARD 32 - Type 1: Basic Q&A]
Q: What is theophylline's therapeutic range and why does it matter?
A: 10-20 mg/L — narrow therapeutic index; levels above 20 mg/L cause serious toxicity (arrhythmias, seizures); monitor drug levels regularly.

[CARD 33 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why do smokers need higher theophylline doses, and what happens when they quit?
A: Smoking induces CYP1A2 → faster theophylline metabolism → lower levels; when a smoker quits, levels rise → toxicity risk; must reduce dose on smoking cessation.
[Trap: Assuming smokers need lower doses is wrong — they need HIGHER doses due to CYP1A2 induction; levels rise (and toxicity ensues) when they quit.]

[CARD 34 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which drugs increase theophylline levels (toxicity risk)?
A: Erythromycin, ciprofloxacin (CYP inhibitors), cimetidine, allopurinol, fluconazole — inhibit theophylline metabolism → levels rise → toxicity.
[Trap: Adding ciprofloxacin or erythromycin to a patient on theophylline without dose reduction = theophylline toxicity.]

[CARD 35 - Type 1: Basic Q&A]
Q: Which drugs decrease theophylline levels?
A: Rifampicin, phenytoin, carbamazepine, phenobarbitone (all CYP inducers), and smoking — increase theophylline metabolism → sub-therapeutic levels.

[CARD 36 - Type 2: Cloze]
[c] Theophylline [/c] causes seizures and arrhythmias in toxicity because at supratherapeutic levels, excess adenosine antagonism and PDE inhibition cause CNS excitation and cardiac instability — check drug levels immediately in any patient on theophylline who develops these symptoms.

[CARD 37 - Type 1: Basic Q&A]
Q: What is IV aminophylline used for?
A: Acute severe asthma unresponsive to salbutamol, ipratropium, and steroids in hospital — IV aminophylline is a last-resort bronchodilator.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 8: MONTELUKAST (LTRA)
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 38 - Type 1: Basic Q&A]
Q: What is the mechanism of montelukast?
A: Blocks cysteinyl leukotriene CysLT1 receptors → ↓ bronchoconstriction, ↓ mucus production, ↓ eosinophilic inflammation.

[CARD 39 - Type 1: Basic Q&A]
Q: Name 3 key indications for montelukast.
A: Mild persistent asthma (especially children), allergic rhinitis (dual indication), aspirin-exacerbated respiratory disease (AERD/Samter's triad), exercise-induced bronchospasm.

[CARD 40 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Classic scenario for montelukast?
A: Child with asthma + allergic rhinitis → montelukast treats BOTH with a single oral tablet daily; preferred when parents want to avoid ICS due to growth concerns.

[CARD 41 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is the black box warning for montelukast?
A: Neuropsychiatric effects — agitation, depression, sleep disturbances, and suicidal ideation; warn patients/parents and review if behavioural changes occur.

[CARD 42 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Can montelukast be used for an acute asthma attack?
A: No — montelukast has no bronchodilator action; it is a preventer only; use SABA for acute attacks.
[Trap: Using montelukast for acute bronchospasm is wrong — it has no acute effect; SABA is always the acute reliever.]

[CARD 43 - Type 2: Cloze]
[c] Montelukast [/c] is associated with EGPA (eosinophilic granulomatosis with polyangiitis / Churg-Strauss syndrome) — a rare complication triggered when oral steroids are reduced in steroid-dependent asthmatics who are on LTRAs, unmasking underlying vasculitis.

[CARD 44 - Type 1: Basic Q&A]
Q: What drug interaction does zafirlukast (another LTRA) have?
A: Zafirlukast inhibits CYP → increases warfarin levels (↑ INR); monitor closely if both are prescribed.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 9: MAST CELL STABILISERS (CROMOLYN)
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 45 - Type 3: Mnemonic]
Q: What is the mnemonic for cromolyn (sodium cromoglicate)?
A: CROMO = Can't be used acutely, Reduces mast cell degranulation, Only prophylaxis, Must dose 3-4x daily, Old drug (declining use)

[CARD 46 - Type 1: Basic Q&A]
Q: What is the mechanism of cromolyn (sodium cromoglicate)?
A: Inhibits mast cell degranulation → blocks histamine and leukotriene release before allergen/exercise exposure (prophylaxis only).

[CARD 47 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Is cromolyn useful for an acute asthma attack?
A: No — cromolyn has NO bronchodilator action; it is prophylaxis only; must be taken BEFORE allergen or exercise exposure to prevent (not treat) attacks.
[Trap: Using cromolyn to treat acute bronchospasm is wrong — it has no acute effect at all.]

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 10: BIOLOGICS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 48 - Type 3: Mnemonic]
Q: What is the mnemonic for omalizumab?
A: "OMALizumab = OMAkes IgE useless" — anti-IgE monoclonal antibody

[CARD 49 - Type 1: Basic Q&A]
Q: What is the mechanism of omalizumab?
A: Monoclonal antibody against free IgE → prevents IgE binding to mast cells and basophils → ↓ allergic cascade.

[CARD 50 - Type 1: Basic Q&A]
Q: What is the indication for omalizumab?
A: Severe allergic (IgE-mediated) asthma uncontrolled on high-dose ICS + LABA — requires confirmed elevated serum IgE + positive skin prick test or RAST.

[CARD 51 - Type 3: Mnemonic]
Q: What is the mnemonic for mepolizumab?
A: "MEPO = MEans eosino-PHils Out" — anti-IL-5 monoclonal antibody

[CARD 52 - Type 1: Basic Q&A]
Q: What is the mechanism of mepolizumab?
A: Monoclonal antibody against IL-5 → ↓ eosinophil production and survival → ↓ eosinophilic airway inflammation.

[CARD 53 - Type 1: Basic Q&A]
Q: What is the indication for mepolizumab?
A: Severe eosinophilic asthma uncontrolled on high-dose ICS + LABA — requires blood eosinophils ≥300 cells/µL.

[CARD 54 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: How do you choose between omalizumab and mepolizumab?
A: Elevated total IgE + positive allergy test → omalizumab (anti-IgE); elevated blood eosinophils (≥300/µL) → mepolizumab or benralizumab (anti-IL-5).
[Trap: Giving omalizumab to a non-allergic eosinophilic asthmatic is wrong — check the biomarker first: IgE = omalizumab; eosinophils = mepolizumab.]

[CARD 55 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: At which asthma step do biologics get added?
A: Step 5 (refractory asthma) — patient must already be on step 4 (high-dose ICS + LABA + LAMA/LTRA) before biologics are considered.

[CARD 56 - Type 1: Basic Q&A]
Q: What monitoring is required after omalizumab injection?
A: Observe for 30 minutes after each SC injection — risk of anaphylaxis (adrenaline must be available).

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 11: TB DRUGS — "RIPE" REGIMEN
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 57 - Type 3: Mnemonic]
Q: What is the mnemonic for TB drugs?
A: RIPE = Rifampicin (R), Isoniazid (I/H), Pyrazinamide (P/Z), Ethambutol (E)

[CARD 58 - Type 1: Basic Q&A]
Q: What is the standard TB treatment regimen for pulmonary TB?
A: 2 months RIPE (intensive phase) → 4 months RI (continuation phase) = 6 months total; CNS/bone TB requires 9+ months.

[CARD 59 - Type 1: Basic Q&A]
Q: What is the mechanism of rifampicin?
A: Inhibits bacterial RNA polymerase → ↓ bacterial RNA synthesis.

[CARD 60 - Type 2: Cloze]
[c] Rifampicin [/c] causes orange/red discolouration of urine, tears, and sweat — warn patients before starting to prevent alarm; this is harmless but commonly tested in HKMLE patient education questions.

[CARD 61 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is the most important drug interaction of rifampicin?
A: Rifampicin is a potent CYP450 inducer — reduces levels of OCP (use barrier contraception), warfarin, cyclosporin, antiretrovirals, and many other drugs.
[Trap: Continuing OCP without additional contraception while on rifampicin leads to contraceptive failure — always advise barrier contraception.]

[CARD 62 - Type 1: Basic Q&A]
Q: What is the mechanism of isoniazid (INH)?
A: Inhibits mycolic acid synthesis (target: InhA enzyme) → disrupts mycobacterial cell wall.

[CARD 63 - Type 2: Cloze]
[c] Isoniazid [/c] causes peripheral neuropathy because it competes with pyridoxine (Vitamin B6) for enzyme binding — always co-prescribe pyridoxine (B6) with isoniazid to prevent neuropathy.

[CARD 64 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What must always be co-prescribed with isoniazid and why?
A: Pyridoxine (Vitamin B6) — isoniazid depletes B6 → peripheral neuropathy; B6 supplementation prevents this complication.
[Trap: Forgetting pyridoxine with isoniazid is a common HKMLE management error — always co-prescribe.]

[CARD 65 - Type 1: Basic Q&A]
Q: What is the most serious hepatotoxic TB drug?
A: All 4 RIPE drugs are hepatotoxic — check LFTs before starting and monitor during treatment; isoniazid and rifampicin carry the highest hepatotoxicity risk.

[CARD 66 - Type 1: Basic Q&A]
Q: What is the mechanism of pyrazinamide and its key side effect?
A: Disrupts membrane energy metabolism in acidic environments (active against dormant/intracellular bacilli); key side effect = hyperuricaemia → gout.

[CARD 67 - Type 3: Mnemonic]
Q: What is the mnemonic for pyrazinamide's side effect?
A: "PyraZINamide → ZINC → Gout (uric acid)" — hyperuricaemia is the signature side effect.

[CARD 68 - Type 1: Basic Q&A]
Q: What is the mechanism of ethambutol and its key side effect?
A: Inhibits arabinosyl transferase → ↓ cell wall arabinogalactan synthesis; key side effect = optic neuritis (red-green colour blindness, ↓ visual acuity).

[CARD 69 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What monitoring is mandatory for patients on ethambutol?
A: Monthly visual acuity and colour vision testing — optic neuritis can cause irreversible blindness if not detected early; stop ethambutol immediately if visual changes occur.
[Trap: Missing the monthly visual monitoring for ethambutol is a common HKMLE omission error — it is mandatory.]

[CARD 70 - Type 3: Mnemonic]
Q: What is the mnemonic for TB drug side effects?
A: Red urine = Rifampicin | Injury to nerves + B6 = Isoniazid | Pyrazinamide → Gout | Eyes (optic neuritis) = Ethambutol

[CARD 71 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which TB drug is used as monotherapy for latent TB prophylaxis?
A: Isoniazid monotherapy for 9 months — used for latent TB treatment (positive IGRA or Mantoux with no active disease).

[CARD 72 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is MDR-TB and how is it treated?
A: Resistance to at least rifampicin + isoniazid (the two most potent drugs) → requires second-line drugs: fluoroquinolones (moxifloxacin), amikacin, bedaquiline; treat for 18-24 months.

[CARD 73 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which TB drug should be avoided in pregnancy?
A: Streptomycin — ototoxic to the fetus; RIPE drugs are generally safe in pregnancy (pyrazinamide: WHO says safe, but some guidelines avoid in T1 if uncertain).

[CARD 74 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: When should ART be started in a patient with TB and HIV?
A: Start ART 2-8 weeks after TB treatment is initiated — starting too early risks immune reconstitution inflammatory syndrome (IRIS); rifampicin interactions with antiretrovirals must be managed.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 12: PNEUMONIA ANTIBIOTICS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 75 - Type 3: Mnemonic]
Q: What is the mnemonic for CAP severity scoring?
A: CURB-65 = Confusion, Urea >7 mmol/L, Respiratory rate >30, Blood pressure <90/60, age ≥65 — 1 point each; score 0-1 = mild; 2 = moderate; ≥3 = severe.

[CARD 76 - Type 1: Basic Q&A]
Q: What is the antibiotic regimen for mild CAP (CURB-65 0-1) managed outpatient?
A: Amoxicillin 500mg TDS x 5 days OR doxycycline — covers Streptococcus pneumoniae (most common CAP pathogen).

[CARD 77 - Type 1: Basic Q&A]
Q: What is the antibiotic regimen for moderate CAP (CURB-65 2) requiring admission?
A: IV amoxicillin-clavulanate + azithromycin (or clarithromycin) — covers both typical and atypical organisms.

[CARD 78 - Type 1: Basic Q&A]
Q: What is the antibiotic regimen for severe CAP (CURB-65 ≥3) in ICU?
A: Co-amoxiclav or ceftriaxone IV + azithromycin OR respiratory fluoroquinolone (levofloxacin) — broad-spectrum including atypical cover.

[CARD 79 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why do atypical organisms (Mycoplasma, Legionella, Chlamydia) not respond to amoxicillin?
A: Atypical organisms have no cell wall → β-lactam antibiotics (penicillins, cephalosporins) cannot work; use macrolides (azithromycin), tetracyclines (doxycycline), or fluoroquinolones.
[Trap: Prescribing amoxicillin alone for Mycoplasma or Legionella pneumonia is wrong — always add atypical cover with a macrolide or doxycycline.]

[CARD 80 - Type 3: Mnemonic]
Q: What is the mnemonic for atypical pneumonia organisms?
A: My Leg Chills = Mycoplasma, Legionella, Chlamydophila

[CARD 81 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: How is Legionella pneumonia diagnosed and treated?
A: Diagnosed with urinary Legionella antigen test; treated with fluoroquinolone (levofloxacin) or azithromycin — macrolides or fluoroquinolones, NOT β-lactams.

[CARD 82 - Type 1: Basic Q&A]
Q: What antibiotic is used in CAP with penicillin allergy?
A: Respiratory fluoroquinolone (levofloxacin or moxifloxacin) — broad-spectrum coverage including both typical and atypical organisms.

[CARD 83 - Type 1: Basic Q&A]
Q: What are the key organisms in hospital-acquired pneumonia (HAP)/VAP?
A: Gram-negative rods (Pseudomonas aeruginosa, Klebsiella, E. coli, Acinetobacter) and MRSA.

[CARD 84 - Type 1: Basic Q&A]
Q: What is the antibiotic regimen for HAP/VAP?
A: Anti-pseudomonal β-lactam (piperacillin-tazobactam or cefepime) ± aminoglycoside ± vancomycin (for MRSA coverage).

[CARD 85 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: When is HAP defined and why does it matter for antibiotic choice?
A: Pneumonia developing ≥48 hours after hospital admission — implies resistant organisms; empirical narrow-spectrum antibiotics (like amoxicillin) are insufficient.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 13: INHALER DEVICES
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 86 - Type 3: Mnemonic]
Q: What is the mnemonic for inhaler device choice?
A: "MDI needs coordination, DPI needs force, Spacer helps kids"

[CARD 87 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What inhaler device should be used for a child under 8 years?
A: MDI + spacer — children <8 cannot coordinate MDI actuation with inhalation, and cannot generate sufficient inspiratory flow for DPI.
[Trap: Prescribing DPI for a child under 8 is wrong — they lack the inspiratory force required; MDI + spacer is mandatory.]

[CARD 88 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which inhaler device is appropriate for acute severe asthma?
A: Nebuliser (oxygen-driven or air-driven) — patient is too breathless to coordinate MDI or generate flow for DPI; delivers continuous high-dose bronchodilator (salbutamol + ipratropium).
[Trap: Prescribing DPI in acute severe asthma is wrong — the patient cannot generate enough inspiratory flow when severely breathless.]

[CARD 89 - Type 1: Basic Q&A]
Q: What is the advantage of MDI + spacer over MDI alone for ICS delivery?
A: Spacer holds the aerosol cloud, eliminating the need for breath-MDI coordination AND reducing oropharyngeal deposition → less oral candidiasis from ICS.

[CARD 90 - Type 1: Basic Q&A]
Q: Why can't DPI be used in acute severe asthma?
A: DPI requires adequate inspiratory flow to disperse the powder — a severely breathless patient cannot generate sufficient flow.

[CARD 91 - Type 1: Basic Q&A]
Q: What are the 6 steps of correct MDI technique (exam-tested)?
A: 1. Shake inhaler. 2. Breathe out fully. 3. Seal lips around mouthpiece. 4. Press + inhale slowly and deeply simultaneously. 5. Hold breath 10 seconds. 6. Wait 30-60 sec before second puff.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 14: ASTHMA STEP-UP THERAPY
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 92 - Type 1: Basic Q&A]
Q: What is the treatment at Asthma Step 1 (mild intermittent)?
A: SABA as needed (reliever only) — no regular preventer required.

[CARD 93 - Type 1: Basic Q&A]
Q: What is the treatment at Asthma Step 2 (mild persistent)?
A: Low-dose ICS (daily preventer) + SABA PRN.

[CARD 94 - Type 1: Basic Q&A]
Q: What is the treatment at Asthma Step 3 (moderate persistent)?
A: Low-dose ICS + LABA (e.g. Symbicort or Seretide) + SABA PRN — LABA must ALWAYS be combined with ICS.

[CARD 95 - Type 1: Basic Q&A]
Q: What is the treatment at Asthma Step 4 (severe persistent)?
A: Medium/high-dose ICS + LABA + additional controller (LAMA and/or LTRA) + SABA PRN.

[CARD 96 - Type 1: Basic Q&A]
Q: What is the treatment at Asthma Step 5 (refractory)?
A: Add biologic (omalizumab if allergic, mepolizumab if eosinophilic) or low-dose oral prednisolone.

[CARD 97 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is the reliever at EVERY step of asthma management?
A: SABA (salbutamol) PRN remains the reliever at all steps — never remove SABA access regardless of preventer therapy.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 15: COPD DRUG MANAGEMENT
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 98 - Type 1: Basic Q&A]
Q: What is the first-line drug therapy for any COPD patient?
A: SABA (salbutamol) + SAMA (ipratropium) PRN — for symptomatic relief of all COPD patients.

[CARD 99 - Type 1: Basic Q&A]
Q: What is maintenance therapy for COPD with MRC dyspnoea ≥2 or CAT ≥10?
A: LAMA (tiotropium) OR LABA — long-acting bronchodilator as regular maintenance.

[CARD 100 - Type 1: Basic Q&A]
Q: When is ICS added in COPD?
A: Frequent exacerbations + blood eosinophils ≥300/µL — add ICS to LABA + LAMA triple therapy.

[CARD 101 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is the oxygen target in an acute COPD exacerbation and why?
A: Target SpO2 88-92% — high-flow O2 removes the hypoxic drive in CO2 retainers → CO2 retention and hypercapnic respiratory failure; do NOT target 94-98% in COPD.
[Trap: Targeting SpO2 94-98% in a COPD patient on O2 is a very common HKMLE trap — always target 88-92% in COPD exacerbations.]

[CARD 102 - Type 1: Basic Q&A]
Q: What is the antibiotic regimen for COPD exacerbation with purulent sputum?
A: Amoxicillin, doxycycline, or co-amoxiclav (oral) — only give antibiotics if sputum is purulent/there are signs of infection.

[CARD 103 - Type 1: Basic Q&A]
Q: What steroid is used in acute COPD exacerbation and for how long?
A: Oral prednisolone 30mg x 5 days — shortens recovery time and reduces treatment failure.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 16: DRUGS TO AVOID IN ASTHMA
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 104 - Type 3: Mnemonic]
Q: What is the mnemonic for drugs to AVOID in asthma?
A: BANNS = Beta-blockers (non-selective), Aspirin/NSAIDs (in AERD), NSAIDS, Non-selective beta-blockers, Sulfites

[CARD 105 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why are non-selective beta-blockers contraindicated in asthma?
A: β2 blockade causes bronchoconstriction — even topical beta-blockers (e.g. timolol eye drops for glaucoma) can trigger fatal bronchoconstriction in asthmatics.
[Trap: Assuming topical/ophthalmic beta-blockers are safe in asthma is wrong — systemic absorption can cause fatal bronchospasm.]

[CARD 106 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is Samter's triad (AERD) and which drug class triggers it?
A: Asthma + nasal polyps + aspirin/NSAID sensitivity — NSAIDs trigger bronchospasm by diverting arachidonic acid from COX to lipoxygenase pathway → ↑ leukotriene production; treat with montelukast.

[CARD 107 - Type 3: Mnemonic]
Q: What is the mnemonic for drugs safe in asthma in pregnancy?
A: SAFE = Salbutamol, Antihistamines, Fluticasone/budesonide (ICS), Eformoterol (LABA)

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
BONUS: HIGH-YIELD TRAP CARDS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 108]
Q: HKMLE Trap: LABA prescribed alone as the sole therapy for uncontrolled asthma. What is the problem?
A: LABA monotherapy in asthma is associated with increased asthma-related death (FDA black box warning) — must always combine with ICS; LABA alone is never acceptable in asthma.

[CARD 109]
Q: HKMLE Trap: Patient on theophylline starts ciprofloxacin for a UTI. What must be done?
A: Reduce theophylline dose and monitor drug levels — ciprofloxacin inhibits CYP1A2 → theophylline levels rise → toxicity risk (arrhythmia, seizures).

[CARD 110]
Q: HKMLE Trap: COPD patient given high-flow O2 targeting SpO2 >98% — what is the danger?
A: CO2 retention and hypercapnic respiratory failure — COPD patients with chronic hypercapnia lose their CO2 drive and rely on hypoxic drive; high-flow O2 removes this → respiratory arrest.

[CARD 111]
Q: HKMLE Trap: ICS prescribed to treat an acute asthma attack. Correct?
A: No — ICS has no bronchodilator action; it does not work in acute attacks; use SABA (salbutamol) for acute relief.

[CARD 112]
Q: HKMLE Trap: Ethambutol started for TB but no monitoring is arranged. What is the risk?
A: Optic neuritis — can cause irreversible red-green colour blindness and ↓ visual acuity; monthly visual acuity + colour vision testing is mandatory while on ethambutol.

[CARD 113]
Q: HKMLE Trap: Isoniazid prescribed for TB without pyridoxine. What complication may occur?
A: Peripheral neuropathy — isoniazid depletes vitamin B6; always co-prescribe pyridoxine 10-25mg daily with isoniazid.

[CARD 114]
Q: HKMLE Trap: Rifampicin started for TB in a patient on the OCP. What must be advised?
A: Rifampicin is a potent CYP inducer → reduces OCP efficacy → contraceptive failure; advise additional barrier contraception for the duration of rifampicin treatment and for 4 weeks after.

[CARD 115]
Q: HKMLE Trap: DPI prescribed for a 6-year-old child with asthma. What is the correct device?
A: MDI + spacer — children under 8 cannot generate sufficient inspiratory flow for DPI; MDI + spacer is the correct device.

[CARD 116]
Q: HKMLE Trap: Amoxicillin prescribed alone for Legionella pneumonia. Will it work?
A: No — Legionella is an atypical organism with no cell wall; β-lactams are ineffective; treat with fluoroquinolone (levofloxacin) or azithromycin.

[CARD 117]
Q: HKMLE Trap: Montelukast given for an acute asthma exacerbation in the ED. Correct?
A: No — montelukast has no bronchodilator action; it cannot treat acute bronchospasm; SABA (salbutamol) is first-line for acute attacks.

[CARD 118]
Q: HKMLE Trap: Seretide (fluticasone + salmeterol) used as MART regimen. Correct?
A: No — only formoterol-based combinations (e.g. Symbicort) can be used as MART because formoterol has fast onset; salmeterol is slow-onset and cannot be used as a reliever.

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END OF DECK — 118 CARDS TOTAL
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HKMLE GI PHARMACOLOGY — ANKI FLASHCARD DECK
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Generated from: GI 💊.pdf
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SECTION 1: PROTON PUMP INHIBITORS (PPIs)
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 1 - Type 3: Mnemonic]
Q: What is the mnemonic for PPI long-term side effects?
A: PPI CHOB = C. difficile infection, Hypomagnesaemia, Osteoporosis/fractures, B12 deficiency

[CARD 2 - Type 1: Basic Q&A]
Q: What is the mechanism of PPIs?
A: Prodrug → activated in acidic environment → irreversibly binds H+/K+-ATPase (proton pump) on gastric parietal cells → ↓ acid secretion (most potent acid suppressant).

[CARD 3 - Type 1: Basic Q&A]
Q: When should PPIs be taken and why?
A: 30-60 minutes before a meal — proton pumps are activated by food; drug works best when pumps are active and being stimulated.
[Trap: Taking PPIs at any time or after meals is wrong — efficacy is significantly reduced if not taken before food.]

[CARD 4 - Type 1: Basic Q&A]
Q: Name 5 indications for PPIs.
A: Peptic ulcer disease, H. pylori eradication (triple/quadruple therapy), GORD/GERD, stress ulcer prophylaxis (ICU), NSAID-induced ulcer prevention, Zollinger-Ellison syndrome (high dose).

[CARD 5 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which PPI should be used in a patient also taking clopidogrel?
A: Pantoprazole — least CYP2C19 inhibition → least reduction of clopidogrel activation (a prodrug requiring CYP2C19); omeprazole/esomeprazole inhibit CYP2C19 most.
[Trap: Omeprazole + clopidogrel is a dangerous combination — omeprazole reduces clopidogrel antiplatelet effect by inhibiting its activation via CYP2C19; use pantoprazole instead.]

[CARD 6 - Type 2: Cloze]
[c] PPIs (long-term) [/c] cause hypomagnesaemia because chronic acid suppression reduces active Mg2+ absorption in the gut — this can cascade to cause hypocalcaemia and hypokalaemia; monitor Mg2+ with prolonged PPI use.

[CARD 7 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What happens when a long-term PPI is stopped abruptly?
A: Rebound acid hypersecretion — upregulated proton pumps suddenly produce excessive acid; taper gradually after long-term use.
[Trap: Abrupt PPI discontinuation after long-term use causes rebound symptoms — do NOT stop suddenly; taper the dose.]

[CARD 8 - Type 2: Cloze]
[c] Long-term PPIs [/c] increase risk of C. difficile infection because reduced gastric acid allows C. difficile spores to survive transit to the colon — an important long-term risk to counsel patients about.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 2: H2 RECEPTOR ANTAGONISTS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 9 - Type 3: Mnemonic]
Q: What is the mnemonic for H2 blockers?
A: "H2 = Half as good as PPIs but fewer long-term risks"

[CARD 10 - Type 1: Basic Q&A]
Q: What is the mechanism of H2 receptor antagonists?
A: Competitively block histamine H2 receptors on gastric parietal cells → ↓ acid secretion (less potent and reversible compared to PPIs).

[CARD 11 - Type 2: Cloze]
[c] Cimetidine [/c] causes gynaecomastia and impotence in men because it is an anti-androgen — it blocks testosterone synthesis and androgen receptors; use ranitidine or famotidine instead.

[CARD 12 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which H2 blocker has the most drug interactions and why?
A: Cimetidine — potent CYP450 inhibitor; increases levels of warfarin, theophylline, phenytoin; famotidine and ranitidine have fewer interactions.
[Trap: Assuming all H2 blockers share the same drug interactions is wrong — cimetidine is unique in its CYP inhibition and anti-androgen effects.]

[CARD 13 - Type 1: Basic Q&A]
Q: What are the key side effects of H2 receptor antagonists?
A: Generally well tolerated; cimetidine = gynaecomastia/impotence (anti-androgen), CYP inhibitor; ranitidine = headache; tolerance develops with prolonged use.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 3: H. PYLORI ERADICATION
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 14 - Type 3: Mnemonic]
Q: What is the mnemonic for H. pylori triple therapy?
A: PAC = PPI + Amoxicillin + Clarithromycin (x 7-14 days)

[CARD 15 - Type 3: Mnemonic]
Q: What is the mnemonic for H. pylori quadruple therapy?
A: PBMT = PPI + Bismuth + Metronidazole + Tetracycline (x 10-14 days — used if clarithromycin resistance or triple therapy failed)

[CARD 16 - Type 1: Basic Q&A]
Q: When is H. pylori quadruple therapy used?
A: When clarithromycin resistance is suspected, when triple therapy has failed, or as first-line in areas with high clarithromycin resistance.

[CARD 17 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: How do you confirm H. pylori eradication after treatment?
A: Urea breath test (UBT) — NOT serology; antibodies remain positive for months after eradication and cannot confirm cure; UBT performed ≥4 weeks after completing treatment (and ≥2 weeks off PPI).
[Trap: Using serology (IgG) to confirm H. pylori eradication is wrong — antibodies persist; UBT (or stool antigen) confirms eradication.]

[CARD 18 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is the penicillin allergy alternative for H. pylori triple therapy?
A: Replace amoxicillin with metronidazole → PPI + Metronidazole + Clarithromycin; or use quadruple (PBMT) therapy.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 4: ANTACIDS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 19 - Type 1: Basic Q&A]
Q: What is the key side effect of aluminium-containing antacids?
A: Constipation — aluminium salts slow gut motility; also causes aluminium toxicity in renal failure (accumulation).

[CARD 20 - Type 1: Basic Q&A]
Q: What is the key side effect of magnesium-containing antacids?
A: Diarrhoea — magnesium salts are osmotic; also hypermagnesaemia in renal failure (avoid Mg-antacids in renal failure).

[CARD 21 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What drugs do antacids chelate and what is the rule?
A: Antacids chelate tetracyclines, quinolones (fluoroquinolones), and iron → significantly ↓ absorption; do NOT take within 2 hours of these drugs.
[Trap: Taking tetracycline or ciprofloxacin simultaneously with antacids is wrong — chelation reduces drug absorption by up to 90%; separate by at least 2 hours.]

[CARD 22 - Type 1: Basic Q&A]
Q: What is the danger of long-term sodium bicarbonate use as an antacid?
A: Metabolic alkalosis and sodium load — avoid in hypertension and heart failure.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 5: SUCRALFATE
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 23 - Type 1: Basic Q&A]
Q: What is the mechanism of sucralfate?
A: Aluminium salt → polymerises in acidic pH → viscous gel forms → coats ulcer base → physical barrier against acid, pepsin, and bile; also ↑ local prostaglandin synthesis.

[CARD 24 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why must sucralfate NOT be co-administered with antacids or PPIs?
A: Sucralfate requires acidic pH to polymerise and form its protective gel — antacids and PPIs raise the pH, abolishing its mechanism of action.
[Trap: Co-prescribing sucralfate with a PPI for stress ulcer prophylaxis is a common error — the PPI alkalinises the stomach, preventing sucralfate from working.]

[CARD 25 - Type 1: Basic Q&A]
Q: When should sucralfate be taken?
A: On an empty stomach, 1 hour before meals and at bedtime — food interferes with coating the ulcer surface.

[CARD 26 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What drugs does sucralfate reduce absorption of?
A: Quinolones, tetracyclines, phenytoin, and digoxin — give sucralfate at least 2 hours apart from these drugs.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 6: MISOPROSTOL
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 27 - Type 3: Mnemonic]
Q: What is the mnemonic for misoprostol?
A: "MISOPROStol = MISery Prevention (NSAID ulcers) + MISCARRIAGE (uterine contractions = contraindicated in pregnancy unless inducing)"

[CARD 28 - Type 1: Basic Q&A]
Q: What is the mechanism of misoprostol?
A: Synthetic PGE1 prostaglandin analogue → ↑ mucus + bicarbonate secretion (cytoprotection), ↓ acid secretion, ↑ mucosal blood flow; also causes uterine contractions.

[CARD 29 - Type 1: Basic Q&A]
Q: Name 4 indications for misoprostol.
A: NSAID-induced gastric ulcer prevention, medical termination of pregnancy (with mifepristone), cervical ripening, postpartum haemorrhage.

[CARD 30 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: PPI vs misoprostol — which is preferred for NSAID ulcer prevention?
A: PPI (omeprazole/lansoprazole) is preferred — better tolerated, fewer GI side effects; misoprostol is an alternative but diarrhoea and cramping limit its use.

[CARD 31 - Type 2: Cloze]
[c] Misoprostol [/c] is absolutely contraindicated in pregnancy (when not used for termination) because it causes uterine contractions that can lead to miscarriage, premature labour, or fetal distress.
[Trap: Prescribing misoprostol for NSAID ulcer prevention to a pregnant woman is dangerous — it is a potent abortifacient.]

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 7: PROKINETICS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 32 - Type 1: Basic Q&A]
Q: What is the mechanism of metoclopramide?
A: D2 receptor antagonist (and weak 5-HT3 antagonist) → enhances gastric motility + raises lower oesophageal sphincter tone; also antiemetic via central D2 blockade in the CTZ.

[CARD 33 - Type 1: Basic Q&A]
Q: What are the key indications for metoclopramide?
A: Nausea/vomiting (post-op, chemotherapy, migraine), gastroparesis (diabetic), GORD (improve LOS tone), promoting GI motility.

[CARD 34 - Type 2: Cloze]
[c] Metoclopramide [/c] causes extrapyramidal side effects (EPS) — acute dystonia, akathisia, tardive dyskinesia — because it blocks dopamine D2 receptors in the basal ganglia; treat acute dystonia with procyclidine or benztropine.
[Trap: Not recognising tardive dyskinesia as a long-term metoclopramide side effect is a common HKMLE error — it is dose- and duration-dependent; avoid long-term use.]

[CARD 35 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: A patient on long-term metoclopramide develops involuntary facial movements. What is this and how is it treated?
A: Tardive dyskinesia — a potentially irreversible extrapyramidal side effect; stop metoclopramide immediately; acute dystonic reactions are treated with procyclidine IV/IM.

[CARD 36 - Type 1: Basic Q&A]
Q: What is the mechanism of domperidone and how does it differ from metoclopramide?
A: D2 antagonist (does NOT cross the BBB significantly) → peripheral prokinetic action only; antiemetic without CNS/extrapyramidal side effects.

[CARD 37 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Domperidone vs metoclopramide — which is safer in terms of CNS side effects?
A: Domperidone — does not cross the BBB, so causes no extrapyramidal side effects; however, domperidone prolongs QT interval; caution with other QT-prolonging drugs.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 8: ANTIEMETICS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 38 - Type 3: Mnemonic]
Q: What is the mnemonic for antiemetics by receptor class?
A: "5-HT3 Setrons, D2 MET/DOM, H1 Cyclizine, NK1 Aprepitant"

--- 5-HT3 ANTAGONISTS ---

[CARD 39 - Type 1: Basic Q&A]
Q: What is the mechanism of ondansetron?
A: Blocks 5-HT3 (serotonin) receptors in the gut and CTZ → ↓ vagal afferent stimulation → antiemetic.

[CARD 40 - Type 1: Basic Q&A]
Q: What are the 3 main indications for ondansetron?
A: Chemotherapy-induced nausea/vomiting (CINV), post-operative nausea/vomiting (PONV), radiotherapy-induced nausea.

[CARD 41 - Type 2: Cloze]
[c] Ondansetron [/c] causes QT interval prolongation — especially at higher doses or IV administration; avoid with other QT-prolonging drugs (e.g. haloperidol, domperidone, clarithromycin); ECG monitoring required.

[CARD 42 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What side effect of ondansetron requires ECG monitoring?
A: QT prolongation — particularly significant with IV ondansetron 32mg single dose (now withdrawn); avoid with other QT-prolonging agents.

--- D2 ANTAGONISTS (ANTIEMETICS) ---

[CARD 43 - Type 1: Basic Q&A]
Q: What is the mechanism of prochlorperazine as an antiemetic?
A: D2 receptor antagonist in the CTZ → antiemetic effect; also H1 and M1 blockade.

[CARD 44 - Type 1: Basic Q&A]
Q: What are the key indications for prochlorperazine?
A: Vertigo-associated nausea (Meniere's, labyrinthitis), PONV, general nausea — available as buccal tablet (Buccastem) for patients who cannot swallow.

--- H1 ANTIHISTAMINES (ANTIEMETICS) ---

[CARD 45 - Type 1: Basic Q&A]
Q: What is the mechanism of cyclizine as an antiemetic?
A: H1 antihistamine + anticholinergic → blocks vestibular and CTZ pathways → effective for motion sickness and vestibular nausea.

[CARD 46 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which antiemetics are safe in pregnancy?
A: Cyclizine (H1 antihistamine — first-line in early pregnancy), promethazine, metoclopramide (short-term); ondansetron used with caution (some concerns about cardiac defects).
[Trap: Assuming all antiemetics are safe in pregnancy is wrong — always check; cyclizine and promethazine are the safest options for pregnancy-related nausea.]

--- NK1 ANTAGONISTS ---

[CARD 47 - Type 1: Basic Q&A]
Q: What is the mechanism of aprepitant?
A: Blocks substance P at NK1 receptors in the CNS → prevents delayed CINV; part of triple antiemetic therapy for highly emetogenic chemotherapy (5-HT3 antagonist + dexamethasone + aprepitant).

[CARD 48 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is triple antiemetic therapy for highly emetogenic chemotherapy?
A: 5-HT3 antagonist (ondansetron) + dexamethasone + NK1 antagonist (aprepitant) — this combination covers acute and delayed CINV most effectively.

[CARD 49 - Type 2: Cloze]
[c] Aprepitant [/c] is a CYP3A4 inhibitor → increases dexamethasone levels; reduce dexamethasone dose by 50% when using with aprepitant in CINV prophylaxis.

--- OTHER ANTIEMETICS ---

[CARD 50 - Type 1: Basic Q&A]
Q: What is hyoscine (scopolamine) used for and how is it administered?
A: Motion sickness — transdermal patch applied behind the ear; anticholinergic mechanism; side effects include dry mouth, blurred vision, sedation.

[CARD 51 - Type 1: Basic Q&A]
Q: What is the role of dexamethasone as an antiemetic?
A: Potentiates 5-HT3 antagonists in CINV (part of triple therapy); mechanism not fully understood but highly effective as an adjunct.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 9: ANTIDIARRHOEALS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 52 - Type 3: Mnemonic]
Q: What is the mnemonic for loperamide?
A: "LOPE = LOng Poo Eliminator — but don't use in infection (prolongs it)"

[CARD 53 - Type 1: Basic Q&A]
Q: What is the mechanism of loperamide?
A: μ-opioid receptor agonist in the gut wall → ↓ peristalsis, ↑ anal sphincter tone, ↓ secretion; does NOT cross the BBB → no CNS opioid effects.

[CARD 54 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: When is loperamide safe and when must it NEVER be used?
A: Safe in traveller's diarrhoea (mild/watery, no blood/fever); NEVER use in bloody diarrhoea, suspected C. difficile, or invasive bacterial infection (Salmonella, E. coli O157) — can worsen infection, cause toxic megacolon.
[Trap: Prescribing loperamide for bloody diarrhoea or suspected C. difficile is dangerous — it can cause toxic megacolon and prolong infection.]

[CARD 55 - Type 2: Cloze]
[c] Loperamide [/c] at high doses causes cardiac arrhythmias and QT prolongation — a black box warning; loperamide misuse as an opioid substitute has caused deaths from cardiac toxicity.

[CARD 56 - Type 1: Basic Q&A]
Q: What is bismuth subsalicylate (Pepto-Bismol) used for and its key side effects?
A: Traveller's diarrhoea (prevention + treatment), H. pylori (quadruple therapy), nausea; side effects = black stools (harmless — bismuth sulfide, NOT GI bleed), black tongue, tinnitus (high doses), constipation.
[Trap: Black stools from bismuth are misidentified as GI bleeding — always ask about bismuth/Pepto-Bismol use when a patient reports black stools.]

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 10: LAXATIVES
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 57 - Type 3: Mnemonic]
Q: What is the mnemonic for laxative types?
A: BOSS = Bulk-forming, Osmotic, Stimulant, Stool Softeners

[CARD 58 - Type 1: Basic Q&A]
Q: What is the mechanism of bulk-forming laxatives (ispaghula husk/psyllium)?
A: Absorb water → ↑ stool bulk → stimulates peristalsis; must be taken with plenty of water to avoid intestinal obstruction.

[CARD 59 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is the danger of taking bulk-forming laxatives without adequate fluid?
A: Intestinal obstruction — bulk-forming agents swell with water; without adequate fluid intake they can form a solid plug and cause obstruction; always take with ≥250mL water.
[Trap: Prescribing ispaghula to a patient with inadequate fluid intake or dysphagia risks intestinal obstruction.]

[CARD 60 - Type 1: Basic Q&A]
Q: What is the mechanism of osmotic laxatives (lactulose, macrogol)?
A: Draw water into the bowel lumen by osmosis → ↑ stool water content → soften and promote evacuation.

[CARD 61 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is the special use of lactulose beyond constipation?
A: Hepatic encephalopathy — lactulose traps NH3 (ammonia) in the colon as NH4+ and promotes its excretion; ↓ blood ammonia → ↓ encephalopathy.

[CARD 62 - Type 2: Cloze]
[c] Lactulose [/c] causes bloating and flatulence because it is fermented by colonic bacteria to short-chain fatty acids and gas — a common side effect that patients often confuse with worsening GI disease.

[CARD 63 - Type 1: Basic Q&A]
Q: What is the mechanism of stimulant laxatives (senna, bisacodyl)?
A: Stimulate enteric nerve plexus → ↑ colonic motility; also ↓ water/electrolyte absorption from the colon.

[CARD 64 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which laxative is first-choice for opioid-induced constipation?
A: Stimulant laxative (senna) — NOT bulk-forming; opioids slow gut motility, so a stimulant is needed; bulk-forming agents do not address the motility defect and may cause worsening obstruction.
[Trap: Prescribing a bulk-forming laxative for opioid-induced constipation is wrong — stimulant laxatives (senna) are first-line.]

[CARD 65 - Type 1: Basic Q&A]
Q: What is the mechanism of stool softeners (docusate sodium)?
A: Anionic surfactant → lowers surface tension of stool → allows water and fat to penetrate → softens stool; used when straining must be avoided (e.g. post-MI, post-haemorrhoidectomy).

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 11: IBD DRUGS — AMINOSALICYLATES (5-ASA)
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 66 - Type 1: Basic Q&A]
Q: What is the mechanism of mesalazine (5-ASA)?
A: Reduces prostaglandin and leukotriene synthesis locally in the bowel mucosa → ↓ inflammation (local anti-inflammatory; mechanism not fully elucidated).

[CARD 67 - Type 1: Basic Q&A]
Q: What are the key indications for mesalazine (5-ASA)?
A: Induction and maintenance of remission in mild-to-moderate ulcerative colitis (UC); limited efficacy in Crohn's (mainly colonic Crohn's); colorectal cancer chemoprevention with long-term use.

[CARD 68 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: 5-ASA drugs (mesalazine, sulfasalazine) — which disease do they work best for?
A: Ulcerative colitis — 5-ASA drugs are first-line for UC induction and maintenance; they are less effective in Crohn's disease.
[Trap: Using 5-ASA as equivalent first-line treatment for Crohn's is wrong — they are primarily for UC; Crohn's requires different immunosuppression.]

[CARD 69 - Type 2: Cloze]
[c] Sulfasalazine [/c] causes reversible male infertility (oligospermia) because the sulfapyridine carrier molecule is toxic to sperm — use mesalazine instead in men who wish to conceive.
[Trap: Not counselling male patients on sulfasalazine about reversible infertility is a common HKMLE omission — this is exam-tested patient counselling.]

[CARD 70 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why should folate be supplemented with sulfasalazine?
A: Sulfasalazine inhibits folate absorption → folic acid 5mg daily must be co-prescribed (especially important in pregnancy and women of childbearing age).

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 12: IBD DRUGS — CORTICOSTEROIDS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 71 - Type 1: Basic Q&A]
Q: What is the role of corticosteroids in IBD?
A: Induction of remission in moderate-to-severe UC and Crohn's — NOT for long-term maintenance (significant systemic side effects); use oral prednisolone for acute flares.

[CARD 72 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why are steroids NOT used for IBD maintenance therapy?
A: Systemic side effects (osteoporosis, adrenal suppression, hyperglycaemia, HPA suppression) preclude long-term use; azathioprine or biologics are used for maintenance.
[Trap: Continuing prednisolone long-term for IBD maintenance is wrong — steroids are for short-term induction only; transition to steroid-sparing agents.]

[CARD 73 - Type 1: Basic Q&A]
Q: What is budesonide used for in IBD?
A: Ileocaecal Crohn's disease — topically active steroid with high first-pass hepatic metabolism → fewer systemic steroid side effects; also used in microscopic colitis.

[CARD 74 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Budesonide vs prednisolone in IBD — when is budesonide preferred?
A: Budesonide preferred for ileocaecal/right-sided Crohn's when wanting fewer systemic steroid side effects; does NOT work as well for extensive colitis (prednisolone needed).

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 13: IBD DRUGS — IMMUNOMODULATORS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 75 - Type 3: Mnemonic]
Q: What is the mnemonic for azathioprine?
A: "AZA = AZA waits 3 months before working = TPMT test first"

[CARD 76 - Type 1: Basic Q&A]
Q: What is the mechanism of azathioprine (AZA)?
A: Prodrug → converted to 6-mercaptopurine (6-MP) → inhibits purine synthesis → ↓ lymphocyte proliferation → immunosuppression.

[CARD 77 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What test must be done BEFORE starting azathioprine and why?
A: TPMT (thiopurine methyltransferase) enzyme activity — low TPMT activity → ↑ toxic 6-MP metabolites → severe myelosuppression; check activity first to dose appropriately.
[Trap: Starting azathioprine without checking TPMT is a patient safety error — low TPMT patients receiving standard doses get severe bone marrow suppression.]

[CARD 78 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: How long does azathioprine take to achieve full effect in IBD?
A: 3 months — do not switch drugs prematurely; use steroids to bridge while AZA takes effect.

[CARD 79 - Type 2: Cloze]
[c] Azathioprine [/c] causes early pancreatitis in up to 5% of patients — this is dose-independent and idiosyncratic; if pancreatitis occurs, stop permanently and do NOT re-challenge.

[CARD 80 - Type 1: Basic Q&A]
Q: What ongoing monitoring is required with azathioprine?
A: Monthly FBC (myelosuppression risk), LFTs, renal function; avoid live vaccines (immunosuppression).

[CARD 81 - Type 1: Basic Q&A]
Q: What is the mechanism of methotrexate (MTX) in IBD?
A: Inhibits dihydrofolate reductase → ↓ purine/pyrimidine synthesis → anti-inflammatory; used in Crohn's maintenance (especially after steroid dependence).

[CARD 82 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What are the 3 critical rules for methotrexate use in IBD?
A: 1. Teratogen (Category X) — must use contraception; 2. Co-prescribe folic acid 5mg weekly (different day to MTX); 3. Stop MTX 3 months before conception (both male and female patients).
[Trap: Prescribing methotrexate to a woman of childbearing age without contraception counselling is a serious HKMLE error — methotrexate is absolutely teratogenic.]

[CARD 83 - Type 1: Basic Q&A]
Q: What are the key side effects of methotrexate?
A: Hepatotoxicity (avoid alcohol, monitor LFTs), teratogenicity, myelosuppression, pulmonary toxicity (pneumonitis); folic acid 5mg weekly (different day) reduces toxicity.

[CARD 84 - Type 1: Basic Q&A]
Q: What is ciclosporin (cyclosporine) used for in IBD?
A: IV rescue therapy for severe acute UC before considering colectomy — calcineurin inhibitor → ↓ IL-2 → ↓ T-cell activation; bridge to azathioprine (not for long-term UC maintenance).

[CARD 85 - Type 1: Basic Q&A]
Q: What are the key side effects of ciclosporin?
A: Nephrotoxicity (most serious), hypertension, neurotoxicity, hirsutism, gingival hyperplasia.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 14: IBD DRUGS — BIOLOGICS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 86 - Type 3: Mnemonic]
Q: What is the mnemonic for IBD biologic classes?
A: FIAT = Full range: anti-TNF (Infliximab, Adalimumab), anti-Integrin (Vedolizumab), Anti-IL (Ustekinumab)

[CARD 87 - Type 1: Basic Q&A]
Q: What is the mechanism of infliximab and adalimumab?
A: Anti-TNF monoclonal antibodies → bind soluble and membrane-bound TNF-α → ↓ inflammatory cascade → ↓ mucosal inflammation.

[CARD 88 - Type 1: Basic Q&A]
Q: What are the indications for anti-TNF agents in IBD?
A: Moderate-to-severe Crohn's disease and UC failing conventional therapy (steroids + immunomodulators); fistulising Crohn's disease (infliximab).

[CARD 89 - Type 3: Mnemonic]
Q: What is the mnemonic for anti-TNF screening before starting therapy?
A: TITS = Tuberculosis (IGRA screening), Infections screen (hepatitis B, HIV), Trophoblastic (pregnancy test), Stress test heart (exclude HF — anti-TNF contraindicated in HF)

[CARD 90 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why must TB be screened for BEFORE starting anti-TNF therapy?
A: Anti-TNF agents suppress TNF-α, a key cytokine for TB granuloma formation — latent TB reactivates with devastating effect; IGRA (interferon-gamma release assay) must be done before starting.
[Trap: Starting anti-TNF without TB screening is a major patient safety error — always perform IGRA before initiation; treat latent TB first if positive.]

[CARD 91 - Type 2: Cloze]
[c] Anti-TNF agents (infliximab, adalimumab) [/c] are contraindicated in heart failure (NYHA class III-IV) because TNF-α normally has a cardioprotective role; anti-TNF therapy can worsen HF outcomes.

[CARD 92 - Type 1: Basic Q&A]
Q: What is the mechanism of vedolizumab?
A: Anti-integrin (anti-α4β7) monoclonal antibody → selectively blocks gut lymphocyte trafficking → gut-selective immunosuppression (does NOT suppress systemic immunity).

[CARD 93 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is the advantage of vedolizumab over anti-TNF agents in IBD?
A: Gut-selective (targets α4β7 integrin — gut-homing lymphocytes only) → lower risk of systemic infections including TB reactivation; preferred in patients with contraindications to anti-TNF.
[Trap: Assuming vedolizumab carries the same TB reactivation risk as anti-TNF agents is wrong — vedolizumab is gut-selective and has a lower systemic infection risk.]

[CARD 94 - Type 1: Basic Q&A]
Q: What is the mechanism of ustekinumab?
A: Anti-IL-12/IL-23 monoclonal antibody → ↓ Th1/Th17 pathway → ↓ inflammatory cytokine cascade; used for moderate-to-severe Crohn's disease.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 15: IBS DRUGS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 95 - Type 1: Basic Q&A]
Q: What is the mechanism of mebeverine?
A: Direct smooth muscle relaxant (blocks Na+/Ca2+ channels in gut smooth muscle) → ↓ intestinal spasm; NO anticholinergic side effects.

[CARD 96 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Mebeverine vs hyoscine butylbromide (Buscopan) for IBS — key difference?
A: Mebeverine has NO muscarinic side effects (not an anticholinergic — direct smooth muscle relaxant); hyoscine is anticholinergic → dry mouth, blurred vision, urinary retention.

[CARD 97 - Type 1: Basic Q&A]
Q: What is the mechanism of hyoscine butylbromide (Buscopan) in IBS?
A: Anticholinergic (M3 muscarinic antagonist) → reduces intestinal smooth muscle spasm; side effects include dry mouth, blurred vision, tachycardia, urinary retention.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 16: C. DIFFICILE MANAGEMENT
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 98 - Type 1: Basic Q&A]
Q: What antibiotics most commonly trigger C. difficile infection (CDI)?
A: Clindamycin (highest risk), broad-spectrum penicillins (co-amoxiclav), cephalosporins, fluoroquinolones — all disrupt the gut microbiome; PPIs also increase CDI risk.

[CARD 99 - Type 1: Basic Q&A]
Q: What is the first-line treatment for mild-moderate C. difficile?
A: Oral metronidazole (for mild) or oral vancomycin (for moderate-severe, first recurrence, or pregnant patients) — NOTE: oral vancomycin stays in the gut and is NOT absorbed systemically.
[Trap: IV vancomycin for C. difficile is wrong — it does not reach the gut lumen in therapeutic concentrations; must use ORAL vancomycin (same principle as the antibiotic deck).]

[CARD 100 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: First-line treatment for severe/recurrent C. difficile?
A: Oral fidaxomicin (preferred over vancomycin for recurrence) or oral vancomycin; for recurrent CDI: fidaxomicin or faecal microbiota transplant (FMT).

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
BONUS: HIGH-YIELD TRAP CARDS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 101]
Q: HKMLE Trap: Omeprazole is prescribed for a patient on clopidogrel after ACS stent. Problem?
A: Omeprazole inhibits CYP2C19 → reduces clopidogrel activation → ↓ antiplatelet effect → stent thrombosis risk; use pantoprazole instead.

[CARD 102]
Q: HKMLE Trap: Serology (IgG) is used to confirm H. pylori eradication. Correct?
A: No — antibodies remain positive for months; use urea breath test (UBT) or stool antigen test ≥4 weeks after treatment (and ≥2 weeks off PPI).

[CARD 103]
Q: HKMLE Trap: Sucralfate is prescribed with a PPI for stress ulcer prophylaxis. Problem?
A: Sucralfate requires acidic pH — the PPI raises gastric pH, abolishing sucralfate's mechanism; choose one or the other, not both together.

[CARD 104]
Q: HKMLE Trap: Misoprostol prescribed to a pregnant woman for NSAID gastroprotection. Danger?
A: Misoprostol causes uterine contractions → miscarriage/premature labour; absolutely contraindicated in pregnancy unless being used as an abortifacient.

[CARD 105]
Q: HKMLE Trap: Long-term metoclopramide prescribed for gastroparesis. What late complication may occur?
A: Tardive dyskinesia — potentially irreversible involuntary movements from chronic D2 blockade in basal ganglia; metoclopramide should not be used long-term (limit to 5 days in most cases).

[CARD 106]
Q: HKMLE Trap: Loperamide prescribed for diarrhoea in a patient with bloody stools and fever. Danger?
A: Invasive bacterial diarrhoea (or C. difficile) — loperamide stops gut motility → bacteria and toxins trapped → toxic megacolon risk; never use in bloody or febrile diarrhoea.

[CARD 107]
Q: HKMLE Trap: Bulk-forming laxative prescribed for opioid-induced constipation. First-line?
A: No — stimulant laxative (senna) is first-line for opioid-induced constipation; bulk-forming agents do not address the motility defect and may worsen obstruction.

[CARD 108]
Q: HKMLE Trap: Azathioprine started for IBD without checking TPMT. Risk?
A: Severe myelosuppression — low TPMT activity → accumulation of toxic 6-thioguanine nucleotides → bone marrow suppression; always check TPMT before starting.

[CARD 109]
Q: HKMLE Trap: Azathioprine is switched after 4 weeks for lack of effect in IBD. Correct?
A: No — azathioprine takes 3 months for full therapeutic effect; premature discontinuation leads to under-treatment; bridge with steroids while waiting.

[CARD 110]
Q: HKMLE Trap: Methotrexate prescribed for a female IBD patient who wants to conceive. What must be done?
A: Stop MTX 3 months before conception; it is absolutely teratogenic (Category X); prescribe folic acid 5mg weekly while on MTX; use alternative IBD therapy during conception/pregnancy.

[CARD 111]
Q: HKMLE Trap: Anti-TNF (infliximab) started for IBD without TB screening. Danger?
A: Latent TB reactivation — anti-TNF suppresses granuloma maintenance; always perform IGRA before starting; treat latent TB prophylactically before initiating anti-TNF.

[CARD 112]
Q: HKMLE Trap: Black stools in a patient taking Pepto-Bismol (bismuth). GI bleed?
A: No — bismuth subsalicylate turns stool black (bismuth sulfide); this is harmless; distinguish from melaena by history (Pepto-Bismol use, absence of other GI bleed features).

[CARD 113]
Q: HKMLE Trap: Tetracycline or ciprofloxacin taken together with antacids. Effect?
A: Chelation → ↓ antibiotic absorption by up to 90%; always separate antacids from tetracyclines, fluoroquinolones, and iron by at least 2 hours.

[CARD 114]
Q: HKMLE Trap: Sulfasalazine used for IBD in a man planning to start a family. What to counsel?
A: Reversible oligospermia (male infertility) — sulfasalazine's sulfapyridine component is spermotoxic; switch to mesalazine if fertility is a concern.

================================================================
END OF DECK — 114 CARDS TOTAL
================================================================

================================================================
HKMLE RHEUMATOLOGY PHARMACOLOGY — ANKI FLASHCARD DECK
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Generated from: Rheumatology 💊.pdf
================================================================

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SECTION 1: PARACETAMOL (ACETAMINOPHEN)
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 1 - Type 3: Mnemonic]
Q: What is the mnemonic for paracetamol?
A: "PARA = Pain + Afebrile control = no Antiplatelet effect = safe in stomach + pregnancy"

[CARD 2 - Type 1: Basic Q&A]
Q: What is the mechanism of paracetamol?
A: Inhibits prostaglandin synthesis in the CNS only (not peripheral tissues) → weak anti-inflammatory; does NOT inhibit platelets; exact mechanism possibly involves COX-3 inhibition.

[CARD 3 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Is paracetamol safe in pregnancy?
A: Yes — safe in all 3 trimesters (unlike NSAIDs); first-line analgesic in pregnancy; does NOT affect platelets or close the PDA.
[Trap: NSAIDs are contraindicated in 3rd trimester; paracetamol is safe throughout pregnancy.]

[CARD 4 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is the antidote for paracetamol overdose and when should it be given?
A: N-acetylcysteine (NAC) IV — replenishes glutathione; most effective if started within 8-10 hours of ingestion, but still give even if late (>10h); treat according to Rumack-Matthew nomogram.
[Trap: Waiting until LFTs are elevated before giving NAC is wrong — give NAC as soon as paracetamol OD is confirmed; delay worsens outcomes.]

[CARD 5 - Type 2: Cloze]
[c] Paracetamol overdose [/c] causes hepatotoxicity because toxic metabolite NAPQI accumulates when hepatic glutathione is depleted — NAC replenishes glutathione and converts NAPQI to a non-toxic form.

[CARD 6 - Type 1: Basic Q&A]
Q: What are the 4 clinical phases of paracetamol overdose?
A: Phase 1 (0-24h): N/V, malaise; Phase 2 (24-72h): RUQ pain, ↑ LFTs; Phase 3 (72-96h): hepatic failure, jaundice, coagulopathy, renal failure; Phase 4: recovery or death.

[CARD 7 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Who is at highest risk for NAPQI toxicity from paracetamol?
A: Chronic heavy alcohol users, malnourished/fasted patients (both deplete glutathione), patients on CYP-inducing drugs (↑ NAPQI production); staggered overdose is more dangerous than a single acute OD.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 2: NSAIDs (NON-SELECTIVE)
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 8 - Type 1: Basic Q&A]
Q: What is the mechanism of non-selective NSAIDs?
A: Inhibit both COX-1 and COX-2 → ↓ prostaglandin and thromboxane synthesis → ↓ inflammation, pain, fever; also inhibit platelet aggregation (reversible, except aspirin which is irreversible).

[CARD 9 - Type 1: Basic Q&A]
Q: Name 4 major contraindications to NSAIDs.
A: Active peptic ulcer/GI bleed, CKD (↓ renal prostaglandin → AKI), 3rd trimester pregnancy (premature PDA closure, oligohydramnios), aspirin-exacerbated asthma (AERD), concurrent anticoagulation (relative).

[CARD 10 - Type 2: Cloze]
[c] NSAIDs [/c] cause peptic ulcers by inhibiting COX-1 → ↓ prostaglandin E2/I2 → ↓ gastric mucus, bicarbonate, and mucosal blood flow → mucosal breakdown; also direct topical irritation.

[CARD 11 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Indomethacin — what special use does it have in neonatology?
A: Used to close patent ductus arteriosus (PDA) in premature neonates — inhibits PGE2 which keeps the PDA open; the same mechanism causes premature PDA closure in the 3rd trimester (why NSAIDs are contraindicated in late pregnancy).
[Trap: The same NSAID property that makes it therapeutic in premature babies causes fetal harm in the 3rd trimester — a classic HKMLE mechanistic trap.]

[CARD 12 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why are all NSAIDs avoided in CKD?
A: NSAIDs inhibit renal prostaglandins → ↓ renal afferent arteriole vasodilation → ↓ GFR → acute kidney injury; especially dangerous in pre-existing CKD, heart failure, or dehydration.

[CARD 13 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: NSAID + warfarin — what is the risk?
A: Doubled bleeding risk — NSAIDs inhibit platelet aggregation + cause GI mucosal damage; combined with anticoagulation, this significantly increases GI bleed risk; use paracetamol instead for analgesia.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 3: COX-2 SELECTIVE INHIBITORS (COXIBS)
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 14 - Type 3: Mnemonic]
Q: What is the mnemonic for COX-2 inhibitors?
A: "COX-2 = protects GI but COX-2 blocks PGI2 (prostacyclin) → Cardiovascular clot risk"

[CARD 15 - Type 1: Basic Q&A]
Q: What is the mechanism of COX-2 inhibitors (celecoxib)?
A: Selectively inhibit COX-2 only → ↓ inflammation without inhibiting COX-1 → preserves gastric mucosa and platelet function; but ↓ prostacyclin (PGI2) → ↑ thrombotic/CV risk.

[CARD 16 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is the key advantage of COX-2 inhibitors over non-selective NSAIDs?
A: Fewer GI ulcers/bleeds — BUT this GI advantage is lost if concurrent low-dose aspirin is given (aspirin causes GI irritation via COX-1 independently).
[Trap: Assuming COX-2 inhibitors retain GI benefit even with concurrent aspirin is wrong — the GI benefit is abolished by aspirin co-prescription.]

[CARD 17 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why was rofecoxib (Vioxx) withdrawn from the market?
A: Increased myocardial infarction risk — seminal pharmacovigilance case; class effect of all COX-2 inhibitors but rofecoxib was most pronounced.

[CARD 18 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why is celecoxib contraindicated in sulfonamide allergy?
A: Celecoxib contains a sulfonamide moiety — cross-reactivity causes hypersensitivity reactions in patients with sulfa allergy.
[Trap: Prescribing celecoxib to a patient with sulfa allergy (e.g. co-trimoxazole allergy) is a common error — always check sulfonamide allergy status before prescribing celecoxib.]

[CARD 19 - Type 1: Basic Q&A]
Q: Do COX-2 inhibitors affect platelet aggregation?
A: No — COX-2 inhibitors do NOT inhibit platelet COX-1; platelets are unaffected; they do NOT replace antiplatelet therapy.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 4: CONVENTIONAL DMARDs
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

--- METHOTREXATE (MTX) ---

[CARD 20 - Type 3: Mnemonic]
Q: What is the mnemonic for methotrexate monitoring?
A: "MTX = Must Take X-amount (folic acid), Must Test Xrays + LFTs monthly, Must eXclude pregnancy"

[CARD 21 - Type 1: Basic Q&A]
Q: What is the mechanism of methotrexate in rheumatology?
A: Inhibits dihydrofolate reductase (DHFR) → ↓ tetrahydrofolate → ↓ purine/pyrimidine synthesis → ↓ lymphocyte proliferation; also ↑ adenosine release → anti-inflammatory.

[CARD 22 - Type 1: Basic Q&A]
Q: What is methotrexate's role in RA?
A: First-line conventional DMARD (anchor drug) for RA; also used in psoriatic arthritis, psoriasis, JIA, SLE, Crohn's, ectopic pregnancy (high dose), choriocarcinoma.

[CARD 23 - Type 1: Basic Q&A]
Q: What are the 5 key side effects of methotrexate?
A: Hepatotoxicity (monitor LFTs), myelosuppression (monitor FBC), mucositis/oral ulcers, pneumonitis (MTX lung — dry cough, dyspnoea), teratogenicity (Category X).

[CARD 24 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why must folic acid be co-prescribed with methotrexate?
A: Folic acid 5mg weekly (different day to MTX) reduces toxicity (mucositis, myelosuppression, hepatotoxicity) without reducing efficacy; always co-prescribe.
[Trap: Giving folic acid on the SAME day as MTX reduces its efficacy — prescribe on a different day.]

[CARD 25 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: When must methotrexate be stopped before conception?
A: Stop MTX 3 months before conception (both male and female patients) — teratogenic; Category X; confirm serum drug levels undetectable before pregnancy.
[Trap: Stopping MTX 1 month before conception is insufficient — 3 months is required for both sexes.]

[CARD 26 - Type 2: Cloze]
[c] Methotrexate [/c] causes pneumonitis (MTX lung) presenting with dry cough and dyspnoea — an idiosyncratic reaction unrelated to dose; requires CXR + HRCT; stop MTX immediately and do NOT rechallenge.

[CARD 27 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is the dangerous interaction between MTX and NSAIDs/aspirin?
A: NSAIDs reduce renal clearance of MTX → ↑ MTX levels → ↑ toxicity (myelosuppression); avoid NSAIDs in patients on weekly low-dose MTX.

[CARD 28 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What monitoring is required for methotrexate in RA?
A: FBC + LFTs + renal function monthly for first 6 months, then 3-monthly; baseline CXR; use Metavir/liver biopsy if cumulative dose concern or elevated LFTs.

--- SULFASALAZINE (SSZ) ---

[CARD 29 - Type 1: Basic Q&A]
Q: What is the mechanism of sulfasalazine in RA?
A: Split in colon into 5-ASA (anti-inflammatory) + sulfapyridine (antimicrobial/anti-inflammatory) → ↓ cytokine production and lymphocyte function.

[CARD 30 - Type 1: Basic Q&A]
Q: What are the indications for sulfasalazine in rheumatology?
A: RA, seronegative spondyloarthropathies (ankylosing spondylitis, psoriatic arthritis, reactive arthritis), IBD (UC).

[CARD 31 - Type 2: Cloze]
[c] Sulfasalazine [/c] causes reversible male infertility (oligospermia) because the sulfapyridine component is toxic to sperm — reversible on stopping; switch to mesalazine in men wishing to conceive.

[CARD 32 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Is sulfasalazine safe in pregnancy?
A: Relatively safe — can be continued in pregnancy (unlike MTX and leflunomide); supplement with folic acid as sulfasalazine inhibits folate absorption.

[CARD 33 - Type 1: Basic Q&A]
Q: What are the key side effects of sulfasalazine?
A: Orange-yellow discolouration of urine (harmless — warn patient), reversible male infertility, rash, GI upset, myelosuppression (monitor FBC), rare hepatotoxicity.

--- HYDROXYCHLOROQUINE (HCQ) ---

[CARD 34 - Type 1: Basic Q&A]
Q: What is the mechanism of hydroxychloroquine (HCQ)?
A: Accumulates in lysosomes → raises intralysosomal pH → inhibits antigen presentation and inflammatory cytokine release (Toll-like receptor inhibition).

[CARD 35 - Type 1: Basic Q&A]
Q: What are the key indications for hydroxychloroquine?
A: SLE (mild-moderate; reduces flares, neonatal lupus, mortality), RA (mild; add-on), antimalarial prophylaxis.

[CARD 36 - Type 2: Cloze]
[c] Hydroxychloroquine [/c] causes bull's-eye maculopathy (retinopathy) due to cumulative dose-dependent deposition in the retina — irreversible; requires annual ophthalmology review after 5 years of use (or earlier if risk factors present).
[Trap: Not arranging annual ophthalmology screening for patients on long-term HCQ is a patient safety error — retinopathy is irreversible once established.]

[CARD 37 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Is hydroxychloroquine safe in pregnancy?
A: Yes — safest DMARD in pregnancy; continue throughout pregnancy in SLE patients (reduces disease flares, neonatal lupus risk, and fetal loss).
[Trap: Stopping HCQ in SLE during pregnancy is wrong — it should be continued as it reduces neonatal lupus and disease flares.]

[CARD 38 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What QT-related concern exists with hydroxychloroquine?
A: HCQ can prolong the QT interval — caution when co-prescribed with other QT-prolonging drugs (e.g. ondansetron, azithromycin, haloperidol).

--- LEFLUNOMIDE (LEF) ---

[CARD 39 - Type 3: Mnemonic]
Q: What is the mnemonic for leflunomide?
A: "LEFlunomide = LEFt the pregnancy behind (teratogen), LiFts blood pressure, LiFts LFTs"

[CARD 40 - Type 1: Basic Q&A]
Q: What is the mechanism of leflunomide?
A: Inhibits dihydroorotate dehydrogenase (DHODH) → ↓ pyrimidine synthesis → ↓ T and B lymphocyte proliferation.

[CARD 41 - Type 1: Basic Q&A]
Q: Key side effects of leflunomide?
A: Hepatotoxicity (monitor LFTs monthly x 6 months), hypertension, teratogenicity (Category X), diarrhoea, peripheral neuropathy, alopecia, rash.

[CARD 42 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why does leflunomide require cholestyramine washout before pregnancy?
A: Leflunomide's active metabolite (teriflunomide) has a t½ of up to 2 years — without washout, it persists; cholestyramine 8g TDS x 11 days is used to eliminate it rapidly before conception; confirm undetectable levels before pregnancy.
[Trap: Simply stopping leflunomide and waiting a few months is NOT sufficient — the very long active metabolite half-life requires active cholestyramine washout.]

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 5: CONVENTIONAL DMARD COMPARISON
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 43 - Type 3: Mnemonic]
Q: What is the mnemonic for DMARDs in pregnancy?
A: "HCQ = Happy (safe, continue), MTX/LEF = No way (both teratogenic, stop before conception)"

[CARD 44 - Type 1: Basic Q&A]
Q: Which conventional DMARDs are contraindicated in pregnancy?
A: Methotrexate (stop 3 months before) and leflunomide (cholestyramine washout required) — both are teratogenic; hydroxychloroquine and sulfasalazine are generally safe.

[CARD 45 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which DMARD has a unique side effect of orange urine?
A: Sulfasalazine — orange-yellow discolouration of urine and tears; harmless but must warn patient (they may mistake it for haematuria).

[CARD 46 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: DMARD monitoring summary — which DMARD requires ophthalmology review?
A: Hydroxychloroquine — annual ophthalmology review after 5 years; all other conventional DMARDs (MTX, SSZ, LEF) require FBC + LFT monitoring.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 6: BIOLOGIC DMARDs
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

--- ANTI-TNF AGENTS ---

[CARD 47 - Type 3: Mnemonic]
Q: What is the mnemonic for anti-TNF agents?
A: FAINT = Five anti-TNFs: Infliximab (IV), Adalimumab (SC), Etanercept (SC), Golimumab (SC), Certolizumab pegol (SC)

[CARD 48 - Type 1: Basic Q&A]
Q: What is the mechanism of anti-TNF agents?
A: Monoclonal antibodies (or fusion protein) that bind TNF-α → prevent TNF-α from binding its receptor → ↓ inflammatory cascade.

[CARD 49 - Type 1: Basic Q&A]
Q: What are the indications for anti-TNF agents in rheumatology?
A: RA (failing ≥2 conventional DMARDs), ankylosing spondylitis, psoriatic arthritis, psoriasis, IBD (Crohn's/UC — infliximab/adalimumab).

[CARD 50 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Pre-treatment screening before starting any biologic (anti-TNF)?
A: TITS = Tuberculosis (IGRA), Infections screen (hepatitis B, HIV), Trophoblastic (pregnancy test), Stress test (exclude NYHA III-IV heart failure — anti-TNF contraindicated in severe HF).
[Trap: Starting anti-TNF without TB IGRA screening is a major patient safety error — latent TB reactivates rapidly on TNF-α suppression.]

[CARD 51 - Type 2: Cloze]
[c] Anti-TNF agents [/c] are contraindicated in NYHA class III-IV heart failure because TNF-α has cardioprotective functions; anti-TNF therapy worsens cardiac outcomes in severe HF.

[CARD 52 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is etanercept and how does it differ from infliximab/adalimumab?
A: Etanercept is a TNF receptor fusion protein (not a monoclonal antibody) — it binds soluble TNF but NOT membrane-bound TNF; as a result it is LESS effective in IBD than infliximab/adalimumab.
[Trap: Using etanercept to treat Crohn's disease is wrong — etanercept does not work in IBD; use infliximab or adalimumab instead.]

[CARD 53 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which anti-TNF agent is safest in pregnancy?
A: Certolizumab pegol — does not cross the placenta (no Fc portion); can be used in pregnancy when treatment is necessary; etanercept and adalimumab also have relatively good safety data.

--- ANTI-IL-6: TOCILIZUMAB ---

[CARD 54 - Type 1: Basic Q&A]
Q: What is the mechanism of tocilizumab?
A: Monoclonal antibody against the IL-6 receptor → blocks IL-6 signalling → ↓ acute phase response, ↓ synovial inflammation.

[CARD 55 - Type 1: Basic Q&A]
Q: Key indications for tocilizumab?
A: RA (moderate-severe, after anti-TNF failure), cytokine release syndrome (CRS) from CAR-T therapy, giant cell arteritis (IV tocilizumab), COVID-19 cytokine storm (severe).

[CARD 56 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why does tocilizumab mask infection?
A: Tocilizumab suppresses IL-6 → ↓ CRP production and fever response — even severe infections may present with a normal CRP and no fever; always suspect infection in unwell patients on tocilizumab.
[Trap: A normal CRP does not exclude serious infection in a patient on tocilizumab — the drug directly suppresses the CRP response.]

[CARD 57 - Type 1: Basic Q&A]
Q: What are the key side effects of tocilizumab?
A: Infections (↑ risk), ↑ LFTs, hyperlipidaemia, neutropaenia, thrombocytopaenia, bowel perforation (especially with diverticulitis history), masks fever/CRP.

--- ANTI-IL-1: ANAKINRA ---

[CARD 58 - Type 1: Basic Q&A]
Q: What is the mechanism of anakinra?
A: Recombinant IL-1 receptor antagonist → blocks both IL-1α and IL-1β signalling → ↓ inflammation.

[CARD 59 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is the primary HKMLE indication for anakinra?
A: Adult-onset Still's disease (AOSD) — first-line biologic for AOSD; less used in RA now due to inferior efficacy compared to anti-TNF; also used in cryopyrin-associated periodic syndromes (CAPS) and refractory gout.

--- ANTI-CD20: RITUXIMAB ---

[CARD 60 - Type 3: Mnemonic]
Q: What is the mnemonic for rituximab?
A: "RiTUXimab = Removes T-less lymphocytes (B cells expressing CD20)"

[CARD 61 - Type 1: Basic Q&A]
Q: What is the mechanism of rituximab?
A: Chimeric anti-CD20 monoclonal antibody → B cell depletion → ↓ autoantibody production, ↓ B-cell-mediated inflammation.

[CARD 62 - Type 1: Basic Q&A]
Q: Indications for rituximab in rheumatology?
A: RA (after failure of ≥1 anti-TNF), ANCA-associated vasculitis (GPA/MPA — first-line biologic), SLE (refractory), lymphoma (oncology).

[CARD 63 - Type 2: Cloze]
[c] Rituximab [/c] causes progressive multifocal leukoencephalopathy (PML) due to reactivation of JC virus in immunocompromised patients — presents with progressive cognitive decline and focal neurological deficits; urgent MRI brain required.

[CARD 64 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why must hepatitis B status be checked before rituximab?
A: Rituximab causes B-cell depletion → hepatitis B reactivation (even in anti-HBc positive/anti-HBs positive patients); screen all patients and give prophylactic antiviral (tenofovir/entecavir) if HBsAg positive or core antibody positive.
[Trap: Checking only HBsAg without checking anti-HBc misses occult hepatitis B — check both; occult HBV can reactivate with rituximab.]

[CARD 65 - Type 1: Basic Q&A]
Q: How is rituximab administered and what premedication is required?
A: IV infusion every 6-12 months; premedicate with methylprednisolone IV + paracetamol + antihistamine before each infusion to reduce infusion reactions (first infusion has highest risk).

--- ANTI-CTLA-4: ABATACEPT ---

[CARD 66 - Type 1: Basic Q&A]
Q: What is the mechanism of abatacept?
A: CTLA-4-Ig fusion protein → binds CD80/CD86 on APCs → blocks CD28 co-stimulatory signal → prevents T-cell activation.

[CARD 67 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Abatacept — any specific side effect to know for HKMLE?
A: ↑ COPD exacerbations with IV abatacept — use SC form or alternative in COPD patients.

--- JAK INHIBITORS ---

[CARD 68 - Type 1: Basic Q&A]
Q: What is the mechanism of JAK inhibitors (tofacitinib, baricitinib, upadacitinib)?
A: Block Janus kinase (JAK1/JAK2/JAK3/TYK2) signalling → ↓ downstream STAT activation → ↓ expression of inflammatory cytokines.

[CARD 69 - Type 1: Basic Q&A]
Q: Indications for JAK inhibitors?
A: RA (after MTX failure; oral administration — convenient), psoriatic arthritis, ankylosing spondylitis, atopic dermatitis (upadacitinib), alopecia areata (baricitinib).

[CARD 70 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Key safety concerns with JAK inhibitors vs anti-TNF?
A: Higher risk of: venous thromboembolism (VTE — black box warning), herpes zoster reactivation, and potential increased cardiovascular events (especially in patients >65 or with CV risk factors); screen for TB before starting; avoid in active infection.
[Trap: Assuming JAK inhibitors have the same safety profile as anti-TNF agents is wrong — JAK inhibitors have additional VTE and herpes zoster risk beyond that of biologics.]

[CARD 71 - Type 2: Cloze]
[c] JAK inhibitors (tofacitinib, baricitinib) [/c] cause herpes zoster reactivation at higher rates than anti-TNF agents because JAK-STAT signalling is essential for antiviral immunity — vaccinate against herpes zoster before starting where possible.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 7: GOUT DRUGS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

--- ACUTE GOUT ---

[CARD 72 - Type 1: Basic Q&A]
Q: What are the 3 options for treating acute gout?
A: NSAIDs (e.g. indomethacin, naproxen — first-line if no contraindications), colchicine, or oral corticosteroids (prednisolone — when NSAIDs + colchicine contraindicated).

[CARD 73 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: When should urate-lowering therapy (ULT) be started in acute gout?
A: 2-4 weeks AFTER the acute attack resolves — starting ULT during an attack can prolong or worsen the flare; always co-prescribe colchicine or NSAID prophylaxis for at least 6 months when starting ULT.
[Trap: Starting allopurinol during an acute gout attack is wrong — it can paradoxically worsen and prolong the attack; wait 2-4 weeks after resolution.]

--- COLCHICINE ---

[CARD 74 - Type 1: Basic Q&A]
Q: What is the mechanism of colchicine?
A: Binds tubulin → inhibits microtubule polymerisation → ↓ neutrophil migration and activation → ↓ urate crystal phagocytosis and inflammatory response.

[CARD 75 - Type 1: Basic Q&A]
Q: What are the key indications for colchicine?
A: Acute gout (first-line alongside NSAIDs), prophylaxis when starting ULT (6 months), familial Mediterranean fever (FMF), pericarditis.

[CARD 76 - Type 2: Cloze]
[c] Colchicine [/c] causes diarrhoea as its most common side effect — diarrhoea is the clinical signal to stop or reduce the dose; at toxic doses, causes multi-organ failure (bone marrow suppression, respiratory failure, renal failure).

[CARD 77 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What drugs increase colchicine toxicity?
A: CYP3A4 inhibitors — clarithromycin, erythromycin, itraconazole, diltiazem, verapamil → ↑ colchicine levels → serious toxicity (GI, bone marrow suppression, neuromuscular toxicity); reduce colchicine dose or avoid combination.
[Trap: Prescribing clarithromycin to a patient on full-dose colchicine without dose adjustment can cause fatal colchicine toxicity.]

[CARD 78 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Is colchicine effective if given late in a gout attack?
A: No — colchicine is NOT effective if given more than 36-48 hours after attack onset; early administration is key.

--- ALLOPURINOL ---

[CARD 79 - Type 3: Mnemonic]
Q: What is the mnemonic for allopurinol?
A: "ALLO = ALLows Output of less uric acid (xanthine oxidase inhibitor)"

[CARD 80 - Type 1: Basic Q&A]
Q: What is the mechanism of allopurinol?
A: Competitive inhibitor of xanthine oxidase → ↓ conversion of hypoxanthine → xanthine → uric acid (↓ uric acid production).

[CARD 81 - Type 1: Basic Q&A]
Q: Indications for allopurinol?
A: First-line ULT for gout (overproducers AND underexcretors), uric acid nephrolithiasis, prevention of tumour lysis syndrome (TLS).

[CARD 82 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Allopurinol + azathioprine or 6-MP — what is the dangerous interaction?
A: Allopurinol inhibits xanthine oxidase which also metabolises azathioprine/6-MP → ↑ AZA/6-MP levels by ~4x → severe myelosuppression; reduce AZA/6-MP dose by 75% if combination is unavoidable, or switch to febuxostat.
[Trap: Prescribing allopurinol to a patient already on azathioprine without dose reduction is potentially fatal — this is a classic high-yield HKMLE drug interaction.]

[CARD 83 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: HLA-B*5801 and allopurinol — why is this important in Hong Kong?
A: HLA-B*5801 is strongly associated with severe allopurinol hypersensitivity (SJS/DRESS syndrome) in Han Chinese, Korean, and Thai populations — screen for HLA-B*5801 before starting allopurinol in these populations.
[Trap: Starting allopurinol without HLA-B*5801 screening in a Chinese patient is a patient safety error — the HKMLE specifically tests this for Hong Kong's population.]

[CARD 84 - Type 2: Cloze]
[c] Allopurinol [/c] can precipitate an acute gout flare when first started because rapidly lowering serum uric acid mobilises urate crystals from tissue deposits → joint inflammation; always start with colchicine/NSAID prophylaxis for at least 6 months.

[CARD 85 - Type 1: Basic Q&A]
Q: What are the uric acid targets with ULT in gout?
A: <360 µmol/L (<6 mg/dL) in non-tophaceous gout; <300 µmol/L (<5 mg/dL) in tophaceous gout.

--- FEBUXOSTAT ---

[CARD 86 - Type 1: Basic Q&A]
Q: What is the mechanism of febuxostat?
A: Non-purine selective inhibitor of xanthine oxidase (both oxidised and reduced forms) → ↓ uric acid synthesis.

[CARD 87 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: When is febuxostat preferred over allopurinol?
A: Allopurinol hypersensitivity/intolerance, mild-moderate CKD (febuxostat is predominantly hepatically metabolised — safer than allopurinol in CKD), or failure to reach uric acid target on allopurinol.
[Trap: Assuming febuxostat has no CV risk is wrong — febuxostat has a black box warning for increased cardiovascular events (MI, stroke, CV death); use with caution in patients with established CVD.]

[CARD 88 - Type 2: Cloze]
[c] Febuxostat [/c] shares the same dangerous interaction with azathioprine/6-MP as allopurinol — both are xanthine oxidase inhibitors; avoid combination or dramatically reduce AZA/6-MP dose.

--- URICOSURIC AGENTS (PROBENECID) ---

[CARD 89 - Type 1: Basic Q&A]
Q: What is the mechanism of probenecid?
A: Inhibits URAT1 and OAT urate transporters in the renal proximal tubule → ↓ urate reabsorption → ↑ uric acid excretion (uricosuric agent).

[CARD 90 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: When is probenecid contraindicated?
A: Uric acid nephrolithiasis/urolithiasis — increasing uric acid excretion into urine raises the risk of uric acid kidney stones further; also avoid in CKD (reduced efficacy as GFR <30 makes uricosuric action ineffective).
[Trap: Probenecid for gout in a patient with uric acid kidney stones is wrong — it increases urinary uric acid, worsening stone risk.]

[CARD 91 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Important drug interaction of probenecid?
A: Probenecid inhibits renal secretion of many drugs → ↑ levels of penicillin (used therapeutically for prolonged penicillin levels), methotrexate, NSAIDs, and some antivirals — monitor for toxicity.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 8: CORTICOSTEROIDS IN RHEUMATOLOGY
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 92 - Type 1: Basic Q&A]
Q: What is the role of corticosteroids in RA management?
A: Bridge therapy — used short-term to control flares while waiting for DMARDs to take effect (2-3 months); intra-articular steroids for mono-articular flares; NOT for long-term monotherapy.

[CARD 93 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Intra-articular steroid injection — key contraindication?
A: Suspected septic arthritis — never inject steroids into a possibly infected joint; must exclude infection first (aspirate and culture synovial fluid before injection).
[Trap: Injecting steroids into a joint with septic arthritis worsens infection dramatically — always exclude infection before intra-articular injection.]

[CARD 94 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why is high-dose prednisolone used in giant cell arteritis (GCA) and when?
A: Start high-dose prednisolone (40-60mg/day) IMMEDIATELY when GCA is clinically suspected — do NOT wait for temporal artery biopsy result; visual loss can occur rapidly and is irreversible if treatment is delayed.
[Trap: Waiting for temporal artery biopsy before starting steroids in GCA risks irreversible visual loss — treat first, biopsy within 2 weeks.]

[CARD 95 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is the role of corticosteroids in SLE management?
A: Short-term for acute flares (renal, CNS, haematological lupus); IV methylprednisolone pulse for severe organ-threatening SLE; aim to reduce/stop long-term steroids with disease-modifying agents (HCQ, azathioprine, mycophenolate).

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 9: SLE DRUGS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 96 - Type 1: Basic Q&A]
Q: What is the standard maintenance drug for ALL SLE patients (unless contraindicated)?
A: Hydroxychloroquine — reduces flares, prevents organ damage, safe in pregnancy; all SLE patients should be on HCQ unless contraindicated.
[Trap: Not prescribing HCQ to every SLE patient is a common omission — it is the backbone of SLE management at all stages.]

[CARD 97 - Type 1: Basic Q&A]
Q: What is mycophenolate mofetil (MMF) used for in SLE?
A: Lupus nephritis (induction and maintenance — preferred over azathioprine for induction of proliferative nephritis); also maintenance in other organ manifestations.

[CARD 98 - Type 2: Cloze]
[c] Mycophenolate mofetil (MMF) [/c] is teratogenic — Category D; must use effective contraception; stop 6 weeks before planned conception and switch to azathioprine for SLE during pregnancy.
[Trap: Continuing MMF during pregnancy for lupus nephritis is wrong — MMF is teratogenic; switch to azathioprine which is safer in pregnancy.]

[CARD 99 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which drug is used for refractory SLE or lupus nephritis as a biologic?
A: Belimumab (anti-BLyS/BAFF monoclonal antibody) — reduces SLE flares and organ damage in active SLE failing standard therapy; also voclosporin + MMF for active lupus nephritis.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 10: OSTEOPOROSIS IN RHEUMATOLOGY
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 100 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What osteoporosis prophylaxis should ALL patients starting long-term steroids receive?
A: Calcium + Vitamin D supplementation + bisphosphonate (alendronate) — all patients on ≥7.5mg prednisolone/day for ≥3 months should receive bone protection; assess FRAX score.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
BONUS: HIGH-YIELD TRAP CARDS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 101]
Q: HKMLE Trap: Methotrexate co-prescribed with an NSAID for RA. Danger?
A: NSAIDs reduce renal clearance of MTX → ↑ MTX levels → myelosuppression/mucositis toxicity; avoid NSAIDs in patients on weekly low-dose MTX.

[CARD 102]
Q: HKMLE Trap: Folic acid prescribed on the same day as methotrexate. Problem?
A: Folic acid directly competes with MTX and reduces its efficacy — prescribe folic acid 5mg on a DIFFERENT day from MTX; different-day co-prescription reduces toxicity without reducing efficacy.

[CARD 103]
Q: HKMLE Trap: Allopurinol started during an acute gout attack. Correct?
A: No — starting allopurinol during an acute attack prolongs and worsens the flare; wait 2-4 weeks after the attack resolves; always start prophylaxis (colchicine/NSAID) when initiating ULT.

[CARD 104]
Q: HKMLE Trap: Allopurinol prescribed to a patient already on azathioprine without dose adjustment. Danger?
A: Severe myelosuppression — allopurinol inhibits xanthine oxidase which metabolises AZA → 4x ↑ AZA toxicity; reduce AZA dose by 75% or switch to febuxostat.

[CARD 105]
Q: HKMLE Trap: Probenecid prescribed for gout in a patient with a history of uric acid kidney stones. Correct?
A: No — probenecid increases urinary uric acid excretion, worsening uric acid stone risk; use allopurinol (reduces uric acid production) instead.

[CARD 106]
Q: HKMLE Trap: Leflunomide stopped 1 month before planned conception. Sufficient?
A: No — active metabolite (teriflunomide) has t½ of up to 2 years; requires cholestyramine 8g TDS x 11 days washout followed by confirmed undetectable plasma levels before conception.

[CARD 107]
Q: HKMLE Trap: HCQ stopped during pregnancy in a patient with SLE. Correct?
A: No — HCQ should be CONTINUED throughout pregnancy in SLE; stopping increases flare risk and neonatal lupus risk; it is the safest DMARD in pregnancy.

[CARD 108]
Q: HKMLE Trap: TB IGRA not checked before starting infliximab for RA. Danger?
A: Latent TB reactivation — anti-TNF agents suppress granuloma maintenance; always perform IGRA and CXR before starting; treat latent TB with isoniazid first if IGRA positive.

[CARD 109]
Q: HKMLE Trap: Celecoxib prescribed to a patient with sulfonamide allergy. Correct?
A: No — celecoxib contains a sulfonamide moiety; cross-reactivity causes hypersensitivity; use a non-selective NSAID or paracetamol instead.

[CARD 110]
Q: HKMLE Trap: Intra-articular steroid injected into a hot, red, swollen knee without aspiration first. Danger?
A: Septic arthritis may be present — injecting steroids into an infected joint dramatically worsens the infection; always aspirate and culture synovial fluid before any steroid injection.

[CARD 111]
Q: HKMLE Trap: Allopurinol started in a Han Chinese patient without HLA-B*5801 screening. Risk?
A: Stevens-Johnson syndrome / DRESS — HLA-B*5801 is a major genetic risk factor for severe allopurinol hypersensitivity in Han Chinese, Korean, and Thai populations; HKMLE specifically tests this for Hong Kong.

[CARD 112]
Q: HKMLE Trap: Waiting for temporal artery biopsy before starting steroids in suspected GCA. Correct?
A: No — start high-dose prednisolone IMMEDIATELY when GCA is suspected; visual loss can occur rapidly and is irreversible; biopsy can still be performed within 2 weeks and remains positive after steroid initiation.

[CARD 113]
Q: HKMLE Trap: Normal CRP used to exclude serious infection in a patient on tocilizumab. Correct?
A: No — tocilizumab directly suppresses IL-6-mediated CRP production; CRP may be falsely normal even with life-threatening infection; clinical suspicion must override lab results.

[CARD 114]
Q: HKMLE Trap: Etanercept used to treat Crohn's disease. Will it work?
A: No — etanercept is a TNF fusion protein that does not bind membrane-bound TNF; it is ineffective in IBD; use infliximab or adalimumab (which bind both soluble and membrane-bound TNF) for Crohn's.

================================================================
END OF DECK — 114 CARDS TOTAL
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