What was created: 137 cards across 13 drug sections

================================================================
HKMLE CARDIOVASCULAR PHARMACOLOGY - ANKI FLASHCARD DECK
================================================================
Generated from: Cardio 💊.pdf (High-Yield HKMLE Notes)
137 Cards Total
================================================================

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 1: ACE INHIBITORS (-PRILS)
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[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 swelling 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.
[Trap: Angioedema is an ACEi class effect — ARBs can theoretically cause it too; in practice avoid both.]

[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 — 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).

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 2: ARBs (-SARTANS)
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[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.
[Trap: Older guidelines mentioned dual blockade for proteinuria — HKMLE expects you to know this 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.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 3: BETA-BLOCKERS (-OLOLS)
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[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), 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 safe in severe asthma — 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.

[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 — not all beta-blockers are interchangeable in HF.
[Trap: Not all beta-blockers reduce HF mortality — only these three are evidence-based.]

[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] mask hypoglycaemia symptoms in diabetics by blocking the adrenergic response (tachycardia, tremor) to low blood glucose.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 4: CALCIUM CHANNEL BLOCKERS (CCBs)
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 26 - Type 3: Mnemonic]
Q: What is the mnemonic to distinguish DHP vs Non-DHP CCBs?
A: DHP = "Dilate Peripheral vessels"; 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 — 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: Both drugs slow AV conduction — combined effect is additive and dangerous.]

[CARD 32 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which CCB is safe for hypertension in a patient with HFrEF?
A: Amlodipine only — non-DHPs (verapamil, diltiazem) are contraindicated in HFrEF (depress contractility).

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

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 5: 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 (hypo- for all four).

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

[CARD 40 - 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 41 - Type 1: Basic Q&A]
Q: What are the metabolic side effects of thiazides?
A: Hypokalaemia, hyperuricaemia (gout), hyperglycaemia, hyperlipidaemia, hypercalcaemia.

[CARD 42 - 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 have OPPOSITE effects on calcium — a classic HKMLE distinction.]

[CARD 43 - Type 1: Basic Q&A]
Q: What is the mechanism of spironolactone?
A: Aldosterone antagonist → blocks Na retention and K excretion in collecting duct.

[CARD 44 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which trial proved spironolactone reduces mortality in HFrEF?
A: RALES trial — spironolactone reduces mortality in HFrEF when added to ACEi + beta-blocker.

[CARD 45 - Type 2: Cloze]
[c] Spironolactone [/c] causes gynaecomastia because it blocks androgen receptors in addition to aldosterone receptors.

[CARD 46 - 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 no androgen side effects.

[CARD 47 - Type 1: Basic Q&A]
Q: What is the most important side effect of all potassium-sparing diuretics?
A: Hyperkalaemia — dangerous when combined with ACEi/ARB.

[CARD 48 - 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.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 6: NITRATES
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 49 - 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 50 - 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 51 - 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 52 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: A patient takes GTN and sildenafil together. What happens?
A: Potentially fatal hypotension — GTN + any PDE-5 inhibitor is absolutely contraindicated.
[Trap: The question may use trade names (Viagra, Cialis) — always recognise PDE-5 inhibitors and flag the GTN interaction.]

[CARD 53 - 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 54 - Type 1: Basic Q&A]
Q: Name 4 contraindications to nitrates.
A: PDE-5 inhibitors, HOCM, severe aortic stenosis, right ventricular infarction.

[CARD 55 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why are nitrates contraindicated in RV infarction?
A: RV infarction is preload-dependent — nitrate venodilation drops preload → severe hypotension.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 7: ANTIARRHYTHMICS (VAUGHAN-WILLIAMS)
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 56 - 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 blockers; II: Beta-blockers; III: K blockers; IV: Ca blockers.

[CARD 57 - Type 1: Basic Q&A]
Q: What is the mechanism of Class IA antiarrhythmics?
A: Block Na+ channels (slow phase 0) AND prolong repolarisation → risk of QT prolongation and Torsades de Pointes.

[CARD 58 - Type 2: Cloze]
[c] Procainamide [/c] causes drug-induced lupus (SLE-like syndrome) with long-term use.

[CARD 59 - Type 2: Cloze]
[c] Quinidine [/c] causes cinchonism (tinnitus, headache, visual disturbance) as its characteristic toxicity.

[CARD 60 - Type 1: Basic Q&A]
Q: What is the mechanism of Class IB antiarrhythmics (lidocaine)?
A: Block Na+ channels selectively in ischaemic tissue (shorten phase 3) — used for post-MI ventricular arrhythmias.

[CARD 61 - Type 1: Basic Q&A]
Q: What are the CNS side effects of lidocaine toxicity?
A: Nystagmus, seizures, confusion.

[CARD 62 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: When is flecainide (Class IC) contraindicated?
A: Structural heart disease (post-MI, LV dysfunction) — proarrhythmic in structural disease (CAST trial).
[Trap: Flecainide is safe for AF in structurally NORMAL hearts ("pill in pocket") — never give post-MI.]

[CARD 63 - Type 3: Mnemonic]
Q: What is the mnemonic for amiodarone organ toxicities?
A: THYROID LUNGS LIVER EYES SKIN = TFTs, PFTs/CXR, LFTs, corneal microdeposits, photodermatitis/slate-grey skin.

[CARD 64 - Type 1: Basic Q&A]
Q: What is amiodarone's primary mechanism?
A: Primarily Class III (K+ channel block → prolongs phase 3); also has Class I, II, and IV properties ("multi-class").

[CARD 65 - Type 1: Basic Q&A]
Q: Name 3 key indications for amiodarone.
A: AF (rhythm control), refractory VT/VF, WPW syndrome with AF.

[CARD 66 - 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 67 - 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.
[Trap: Always reduce warfarin dose and increase INR monitoring when starting amiodarone.]

[CARD 68 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: A patient on amiodarone develops digoxin toxicity with unchanged digoxin dose. Why?
A: Amiodarone inhibits P-glycoprotein and reduces renal digoxin clearance — reduce digoxin dose by ~50%.

[CARD 69 - Type 2: Cloze]
[c] Amiodarone [/c] causes both hypothyroidism AND hyperthyroidism because it contains iodine (37% by weight) and blocks T4→T3 conversion.

[CARD 70 - Type 1: Basic Q&A]
Q: What is the mechanism of adenosine?
A: Activates A1 receptors → hyperpolarises AV node → transiently blocks AV conduction.

[CARD 71 - Type 1: Basic Q&A]
Q: Name 2 indications for adenosine.
A: First-line for acute SVT termination; diagnostic tool to unmask atrial flutter waves.

[CARD 72 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why is adenosine contraindicated in WPW + AF?
A: Blocking the AV node forces ALL conduction down the accessory pathway → extremely fast ventricular rate → VF.
[Trap: This is a life-threatening mistake — in WPW + AF, use flecainide or DC cardioversion instead.]

[CARD 73 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What drugs antagonise adenosine?
A: Caffeine and theophylline block A1 receptors — higher adenosine doses needed in these patients.

[CARD 74 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: How should adenosine be administered?
A: Rapid IV bolus into a large/antecubital vein — half-life is ~10 seconds, so slow administration fails.

[CARD 75 - 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.

[CARD 76 - 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 77 - Type 2: Cloze]
[c] Digoxin toxicity [/c] can cause ANY arrhythmia — bradycardia, heart block, VT, or VF — making ANY new arrhythmia in a digoxin patient suspect for toxicity.

[CARD 78 - Type 3: Mnemonic]
Q: What is the mnemonic for digoxin toxicity precipitants?
A: DIAL = Diuretics (hypokalaemia), Impaired renal function, Amiodarone, Low Mg.

[CARD 79 - 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 levels.
[Trap: Patient on furosemide + digoxin is HIGH RISK — diuretic causes hypokalaemia → digoxin toxicity.]

[CARD 80 - 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 81 - Type 1: Basic Q&A]
Q: Name 3 contraindications to digoxin.
A: HOCM, WPW + AF, AV block.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 8: STATINS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 82 - Type 1: Basic Q&A]
Q: What is the mechanism of statins?
A: Block HMG-CoA reductase → ↓ hepatic cholesterol synthesis → upregulate LDL receptors → ↓ LDL.

[CARD 83 - 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 84 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which combination most commonly causes statin-induced rhabdomyolysis?
A: Simvastatin + gemfibrozil — gemfibrozil inhibits CYP3A4 → statin accumulates → rhabdomyolysis.
[Trap: Fenofibrate is the safer fibrate alternative if co-prescription is needed.]

[CARD 85 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Post-MI statin use — when is it indicated?
A: Always — regardless of baseline LDL. Statins stabilise plaques via anti-inflammatory effects, not just lipid lowering.

[CARD 86 - Type 1: Basic Q&A]
Q: Name the two highest-potency statins.
A: Rosuvastatin and Atorvastatin.

[CARD 87 - Type 1: Basic Q&A]
Q: Name 2 contraindications to statins.
A: Pregnancy, active liver disease.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 9: ANTIPLATELET DRUGS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 88 - 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 89 - Type 1: Basic Q&A]
Q: What is the mechanism of clopidogrel?
A: Irreversibly blocks P2Y12 ADP receptor → inhibits platelet aggregation.

[CARD 90 - Type 1: Basic Q&A]
Q: What is the mechanism of ticagrelor vs clopidogrel?
A: Ticagrelor reversibly blocks P2Y12 (clopidogrel is irreversible); ticagrelor is preferred in NSTEMI/STEMI.

[CARD 91 - Type 2: Cloze]
[c] Ticagrelor [/c] causes dyspnoea as a unique side effect — it is not bronchospasm and does not indicate lung disease.
[Trap: Do NOT stop ticagrelor for dyspnoea alone unless severe — this is NOT an asthma attack.]

[CARD 92 - 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 for 12 months post-ACS or PCI.

[CARD 93 - Type 1: Basic Q&A]
Q: When should prasugrel be avoided?
A: Prior stroke/TIA, age >75, weight <60 kg — higher bleeding risk in these groups.

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

[CARD 94 - 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 95 - Type 1: Basic Q&A]
Q: How is warfarin reversed urgently vs non-urgently?
A: Urgently: FFP or PCC (prothrombin complex concentrate); Non-urgently: Vitamin K (slow onset, 6-12h).

[CARD 96 - Type 2: Cloze]
[c] Warfarin [/c] is the ONLY anticoagulant appropriate for mechanical heart valves — DOACs are contraindicated in this setting.

[CARD 97 - Type 1: Basic Q&A]
Q: Name 3 drugs that potentiate warfarin (increase INR).
A: Amiodarone, metronidazole, fluconazole (all inhibit CYP2C9).

[CARD 98 - Type 1: Basic Q&A]
Q: Name 2 drugs that reduce warfarin effect (decrease INR).
A: Rifampicin, carbamazepine (CYP enzyme inducers).

[CARD 99 - Type 1: Basic Q&A]
Q: What is the mechanism of UFH and how is it reversed?
A: Activates antithrombin III → inactivates IIa (thrombin) and Xa. Reversed by protamine sulfate.

[CARD 100 - Type 1: Basic Q&A]
Q: What is the mechanism of LMWH (enoxaparin) vs UFH?
A: LMWH mainly inhibits Factor Xa (less thrombin effect vs UFH); partially reversed by protamine.

[CARD 101 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: A patient on heparin develops a drop in platelets and new thrombosis. Diagnosis and management?
A: Heparin-induced thrombocytopaenia (HIT) — STOP all heparin, switch to argatroban or fondaparinux. NEVER give platelets.
[Trap: Giving platelets in HIT is paradoxically thrombogenic and can trigger life-threatening clots.]

[CARD 102 - Type 1: Basic Q&A]
Q: Name the 2 DOAC types and their mechanisms.
A: Anti-Xa: rivaroxaban, apixaban; Anti-IIa (direct thrombin inhibitor): dabigatran.

[CARD 103 - 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 104 - 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 105 - Type 3: Mnemonic]
Q: What is the mnemonic for post-MI secondary prevention?
A: ABCDE = Aspirin + P2Y12 (DAPT), Beta-blocker, Cholesterol (statin), DAPT + ACEi/ARB, Exercise/Eplerenone (if HF post-MI).

[CARD 106 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: When should oxygen NOT be given in ACS?
A: Do not give if SpO2 ≥94% — routine oxygen in normoxic ACS patients may increase infarct size.

[CARD 107 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why is morphine used cautiously in NSTEMI?
A: Morphine delays gastric motility → slows absorption of oral antiplatelets (e.g. ticagrelor) → may worsen outcomes.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 12: HEART FAILURE DRUGS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 108 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which HF drugs have proven MORTALITY BENEFIT in HFrEF?
A: ACEi/ARB, Beta-blocker (bisoprolol/carvedilol/metoprolol), Spironolactone/Eplerenone, Sacubitril-valsartan, SGLT2 inhibitors.
[Trap: Furosemide and digoxin = SYMPTOM RELIEF only — no mortality benefit.]

[CARD 109 - 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 reduce mortality.

[CARD 110 - Type 2: Cloze]
[c] Sacubitril/valsartan (ARNI) [/c] replaces ACEi in HFrEF when a patient remains symptomatic on ACEi + beta-blocker + aldosterone antagonist.

[CARD 111 - 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 BP).

[CARD 112 - Type 1: Basic Q&A]
Q: What are the indications for ivabradine in HF?
A: HFrEF with HR >70 bpm, sinus rhythm, on maximum tolerated beta-blocker dose.

[CARD 113 - Type 1: Basic Q&A]
Q: What is the unique visual side effect of ivabradine?
A: Phosphenes — transient visual bright flashes.

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

[CARD 114 - 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 115 - Type 2: Cloze]
[c] Hydralazine [/c] causes drug-induced lupus with long-term use (same as procainamide and isoniazid).

[CARD 116 - Type 3: Mnemonic]
Q: What is the mnemonic for drugs causing drug-induced lupus?
A: SHIPS = Sulfonamides, Hydralazine, Isoniazid, Procainamide, Statins (rare).

[CARD 117 - Type 1: Basic Q&A]
Q: What is the mechanism of sodium nitroprusside?
A: Releases NO → ↓ both preload AND afterload (venous + arterial dilation).

[CARD 118 - Type 1: Basic Q&A]
Q: What is the serious toxicity of prolonged sodium nitroprusside infusion?
A: Cyanide (thiocyanate) toxicity.

[CARD 119 - Type 1: Basic Q&A]
Q: Name 2 key indications for sodium nitroprusside.
A: Hypertensive emergency (IV only); aortic dissection.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
BONUS: KEY TRAP CARDS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 120]
Q: HKMLE Trap: Patient on furosemide + digoxin develops toxicity. Why?
A: Furosemide → hypokalaemia → K+ and digoxin compete for Na+/K+ ATPase → digoxin toxicity at normal levels.

[CARD 121]
Q: HKMLE Trap: Patient with WPW + AF is given adenosine. What happens?
A: AV node blocked → all conduction down accessory pathway → extremely rapid ventricular rate → VF.

[CARD 122]
Q: HKMLE Trap: Flecainide prescribed to a post-MI patient with AF. What is the danger?
A: Flecainide is proarrhythmic in structural heart disease — contraindicated post-MI (CAST trial).

[CARD 123]
Q: HKMLE Trap: Platelets are transfused in a patient with HIT. What is wrong?
A: Never give platelets in HIT — paradoxically thrombogenic; worsens clotting, not bleeding.

[CARD 124]
Q: HKMLE Trap: ARB started in a patient with bilateral renal artery stenosis. What happens?
A: Acute kidney injury — same mechanism as ACEi; both contraindicated in bilateral RAS.

[CARD 125]
Q: HKMLE Trap: Patient with mechanical heart valve needs anticoagulation. Can you use a DOAC?
A: No — DOACs are contraindicated in mechanical heart valves. Warfarin is the only option.

[CARD 126]
Q: HKMLE Trap: Patient with HFrEF is given verapamil for rate control. What is the concern?
A: Non-DHP CCBs (verapamil, diltiazem) are contraindicated in HFrEF — they depress contractility further.

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

[CARD 127 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Name 4 cardiac drugs UNSAFE in pregnancy.
A: ACEi, ARBs (renal agenesis/oligohydramnios), warfarin (teratogenic 1st trimester), statins (teratogenic).

[CARD 128 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which cardiac drugs are SAFE in pregnancy?
A: Methyldopa (1st-line HTN), hydralazine, labetalol, heparin/LMWH (don't cross placenta).

[CARD 129 - 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.

================================================================
END OF DECK — 129 CARDS
================================================================

1. Copy the text above into a .txt file
2. In Anki, use File → Import or manually create cards using the Q/A format
3. For cloze cards (Type 2), use the Cloze note type and replace [c]...[/c] with {{c1::...}}

================================================================
HKMLE ANTIBIOTICS & ANTIFUNGALS — ANKI FLASHCARD DECK
160 Cards Total
================================================================

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
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]
Q: Which antibiotic class inhibits folate synthesis (step 1)?
A: Sulfonamides (inhibit dihydropteroate synthase).

[CARD 7 - Type 1]
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]
Q: What is the mechanism of penicillins?
A: Bind PBPs → inhibit transpeptidation → ↓ cell wall cross-linking → bactericidal (time-dependent killing).

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

[CARD 11 - Type 1]
Q: What is the drug of choice for MSSA infections?
A: Flucloxacillin.
[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 patient with EBV given ampicillin develops a maculopapular rash. Is this a true penicillin allergy?
A: No — ampicillin rash in EBV is a non-allergic drug-virus interaction; do NOT label the patient as penicillin-allergic.
[Trap: Classic HKMLE trap — the patient can safely receive penicillins in the future.]

[CARD 14 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is the actual 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 ~1-2%.]

[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 cholestatic hepatotoxicity — classic in elderly males on prolonged courses.

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

[CARD 17 - Type 1]
Q: Which penicillin combination covers Pseudomonas?
A: Piperacillin-tazobactam (Tazocin).

[CARD 18 - Type 1]
Q: What is the role of clavulanate in co-amoxiclav?
A: β-lactamase inhibitor — protects amoxicillin from degradation, broadening coverage to 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]
Q: What is the gold standard surgical prophylaxis cephalosporin?
A: 1st generation — cefazolin (IV) or cefalexin (oral).

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

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

[CARD 23 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which cephalosporin covers MRSA?
A: Only ceftaroline (5th generation) — no other cephalosporin covers MRSA.
[Trap: 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 covers Enterococcus; use penicillin or vancomycin.

[CARD 25 - Type 1]
Q: What unique side effect does ceftriaxone cause in children?
A: Biliary sludge/pseudolithiasis (precipitates in bile).

[CARD 26 - Type 1]
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]
Q: What does carbapenem coverage exclude?
A: NOT MRSA, NOT Stenotrophomonas (covers gram+, gram-, anaerobes, Pseudomonas).

[CARD 29 - Type 2: Cloze]
[c] Imipenem [/c] causes seizures more than other carbapenems; meropenem is preferred for CNS/meningitis infections.

[CARD 30 - Type 1]
Q: Why is imipenem always combined with cilastatin?
A: Cilastatin prevents renal dehydropeptidase-I from metabolising imipenem (and reduces 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) — what do you treat with?
A: Colistin/polymyxin B or ceftazidime-avibactam — classic HKMLE MDR scenario.

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

[CARD 33 - Type 1]
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.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 5: GLYCOPEPTIDES — VANCOMYCIN
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[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]
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).

[CARD 38 - Type 1]
Q: What is the coverage of vancomycin?
A: Gram-positive only — MRSA, MSSA, Enterococcus, Streptococcus; oral form stays in gut (C. difficile only).

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

[CARD 40 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Oral vancomycin — will it treat MRSA bacteraemia?
A: No — oral vancomycin is NOT absorbed; it only treats C. difficile in the gut. IV vancomycin is needed for systemic MRSA.
[Trap: Oral vs IV vancomycin = completely different indications — classic HKMLE distinction.]

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

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

[CARD 43 - Type 1]
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]
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]
Q: Why do aminoglycosides NOT work against anaerobes?
A: They require oxygen for active uptake into bacteria — no O2 = no 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 most other drug-induced ototoxicity.]

[CARD 49 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Two drug combinations that increase aminoglycoside toxicity?
A: Aminoglycosides + 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 weakness and can trigger respiratory failure.

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

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

[CARD 53 - Type 1]
Q: What is the role of gentamicin in endocarditis?
A: Synergy with β-lactams or vancomycin for Enterococcus and Streptococcus endocarditis.

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

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

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

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

[CARD 57 - Type 1]
Q: Which macrolide is given as a single 1g dose for Chlamydia?
A: Azithromycin (long tissue half-life — single dose achieves sustained tissue levels).

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

[CARD 59 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which macrolide is teratogenic and must be avoided in pregnancy?
A: Clarithromycin — 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) — use erythromycin base instead.

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

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

[CARD 63 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Clarithromycin + simvastatin — what is the risk?
A: Rhabdomyolysis — CYP3A4 inhibition 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]
Q: What is the mechanism of fluoroquinolones?
A: Inhibit DNA gyrase (gram-negative) and Topoisomerase IV (gram-positive) → bactericidal (concentration-dependent).

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

[CARD 67 - Type 2: Cloze]
[c] Fluoroquinolones [/c] cause Achilles tendon rupture — highest risk in elderly patients on concurrent corticosteroids or with renal failure.
[Trap: Classic HKMLE scenario = elderly + 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: Always check theophylline levels when starting ciprofloxacin — classic HKMLE drug interaction.]

[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 — does not reach therapeutic levels in urine.
[Trap: Common wrong answer is moxifloxacin for UTI — use ciprofloxacin or levofloxacin instead.]

[CARD 70 - Type 1]
Q: Which fluoroquinolone has the best anti-pseudomonal activity?
A: Ciprofloxacin.

[CARD 71 - Type 1]
Q: Which fluoroquinolones are "respiratory quinolones"?
A: Levofloxacin and moxifloxacin — better gram-positive and atypical coverage for CAP.

[CARD 72 - Type 3: Mnemonic]
Q: What is the mnemonic for antibiotics most likely to cause C. difficile?
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 (DOC), Acne, C. pylori (historical), Young children avoid (<8), Cross BBB, Light sensitivity, Esophageal irritation

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

[CARD 75 - Type 1]
Q: Name 4 organisms where doxycycline is drug of choice.
A: Rickettsia (RMSF — DOC!), Chlamydia (2nd line), Lyme disease (Borrelia), Brucellosis.

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

[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; separate by 2-3 hours.

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

[CARD 80 - Type 1]
Q: What rare CNS side effect do tetracyclines cause?
A: Pseudotumour cerebri (benign intracranial hypertension — headache, papilloedema, ↑ ICP).

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

[CARD 81 - Type 3: Mnemonic]
Q: What is the mnemonic for metronidazole?
A: "METRO = Must avoid alcohol, Then DNA damaged (anaerobes), Reduces warfarin clearance (CYP inhibition), Obese bugs/protozoa killed"

[CARD 82 - Type 1]
Q: What is the mechanism of metronidazole?
A: Prodrug activated by bacterial nitroreductases → DNA strand breaks → bactericidal.

[CARD 83 - Type 1]
Q: What organisms does metronidazole cover?
A: Obligate anaerobes (Bacteroides fragilis, Clostridium) and protozoa (Giardia, Entamoeba, Trichomonas) — NO aerobic bacteria.

[CARD 84 - Type 2: Cloze]
[c] Metronidazole [/c] causes a disulfiram-like reaction with alcohol (flushing, vomiting, hypotension) — also triggered by alcohol-containing mouthwashes.

[CARD 85 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Metronidazole + warfarin — effect?
A: ↑ INR — metronidazole inhibits CYP2C9 → potentiates warfarin → bleeding risk.
[Trap: Classic HKMLE interaction — always check INR when starting metronidazole in a warfarin patient.]

[CARD 86 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: C. difficile — mild/moderate vs severe treatment?
A: Mild/moderate = oral metronidazole or oral vancomycin; Severe = oral vancomycin or fidaxomicin.

[CARD 87 - Type 1]
Q: Why must metronidazole always be combined with another antibiotic in mixed infections?
A: Metronidazole does NOT cover aerobic bacteria — must be paired with a broad-spectrum agent.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 11: LINEZOLID
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 88 - 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 89 - Type 1]
Q: What is the mechanism of linezolid?
A: Binds unique site on 50S (23S rRNA-peptidyl transferase centre) → prevents 70S initiation complex formation → bacteriostatic.

[CARD 90 - Type 1]
Q: What is the coverage of linezolid?
A: Gram-positive only — MRSA, VRE, drug-resistant Streptococcus.

[CARD 91 - 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 — classic HKMLE drug interaction.]

[CARD 92 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why is linezolid preferred over daptomycin for MRSA pneumonia?
A: Daptomycin is inactivated by pulmonary surfactant — it cannot treat lung infections; use linezolid for MRSA pneumonia.
[Trap: Common wrong answer is daptomycin for MRSA lung infection — always use linezolid.]

[CARD 93 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is the unique pharmacokinetic advantage of linezolid?
A: 100% oral bioavailability — oral = IV efficacy; allows step-down to oral without loss of efficacy.

[CARD 94 - Type 1]
Q: What haematological side effect requires weekly FBC monitoring with linezolid >2 weeks?
A: Myelosuppression — thrombocytopaenia most common.

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

[CARD 95 - Type 1]
Q: What is the mechanism of clindamycin?
A: Binds 50S ribosome → blocks translocation → bacteriostatic.

[CARD 96 - Type 1]
Q: What is clindamycin's anaerobic niche vs metronidazole?
A: Clindamycin covers anaerobes ABOVE the diaphragm (aspiration pneumonia, dental); metronidazole preferred for below-diaphragm anaerobes.

[CARD 97 - 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.
[Trap: While many antibiotics cause C. diff, clindamycin is the classic highest-risk answer.]

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

[CARD 98 - Type 1]
Q: What is the mechanism of co-trimoxazole?
A: Sequential double block of folate synthesis — sulfamethoxazole inhibits step 1 (dihydropteroate synthase); trimethoprim inhibits step 2 (dihydrofolate reductase) → synergistic bactericidal effect.

[CARD 99 - Type 1]
Q: What is the primary indication for co-trimoxazole in HIV patients?
A: PCP (Pneumocystis jirovecii pneumonia) prophylaxis and treatment — first-line.

[CARD 100 - Type 2: Cloze]
[c] Co-trimoxazole [/c] causes Stevens-Johnson syndrome (SJS/TEN) — a severe blistering skin reaction from the sulfonamide component.

[CARD 101 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: A patient on TMP-SMX and ACEi develops hyperkalaemia. Why?
A: Trimethoprim blocks K+ excretion in the collecting duct (amiloride-like ENaC block) — combined with ACEi, hyperkalaemia can be severe and dangerous.
[Trap: TMP-SMX hyperkalaemia is a classic trap — especially dangerous in patients on ACEi/ARBs/spironolactone.]

[CARD 102 - Type 1]
Q: Name 3 contraindications to co-trimoxazole.
A: Severe renal impairment, pregnancy (folate antagonism — give folic acid if must use), G6PD deficiency (haemolysis).

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

[CARD 103 - Type 3: Mnemonic]
Q: What is the mnemonic for antifungal targets?
A: "EEE" = Ergosterol binding (polyenes/amphotericin B), Ergosterol synthesis inhibition (azoles), Exoskeleton/cell wall glucan (echinocandins)

[CARD 104 - Type 3: Mnemonic]
Q: What is the mnemonic for amphotericin B?
A: "Ampho-TERRIBLE = Terrible side effects but Terrific spectrum"

[CARD 105 - Type 1]
Q: What is the mechanism of amphotericin B?
A: Binds ergosterol in fungal cell membrane → forms pores → K+ leakage → cell death (fungicidal).

[CARD 106 - Type 1]
Q: What is the broad-spectrum coverage of amphotericin B?
A: Candida, Aspergillus, Cryptococcus, Mucor, Histoplasma, Coccidioides, Blastomyces, Leishmaniasis.

[CARD 107 - Type 1]
Q: Name 3 major side effects of amphotericin B.
A: "Shake and bake" (infusion rigors/fever), nephrotoxicity (hypokalaemia, hypomagnesaemia, renal tubular acidosis), anaemia (↓ EPO).

[CARD 108 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: How do you reduce amphotericin B nephrotoxicity?
A: Use liposomal amphotericin B (AmBisome) — same efficacy, much less nephrotoxicity; preferred in renal impairment.

[CARD 109 - Type 1]
Q: How do you premedicate before amphotericin B infusion?
A: Paracetamol + antihistamine + hydrocortisone; monitor and replace K+ and Mg2+ throughout treatment.

[CARD 110 - 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 required, Ergosterol synthesis blocked"

[CARD 111 - Type 1]
Q: What is the mechanism of azole antifungals?
A: Inhibit fungal CYP51 (lanosterol 14α-demethylase) → ↓ ergosterol synthesis → fungistatic.

[CARD 112 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Does fluconazole cover Aspergillus?
A: NO — fluconazole has NO activity against Aspergillus; use voriconazole for invasive aspergillosis.
[Trap: Most tested azole coverage gap on HKMLE — fluconazole only covers Candida and Cryptococcus.]

[CARD 113 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: First-line treatment for invasive aspergillosis?
A: Voriconazole (IV or oral).

[CARD 114 - Type 1]
Q: What unique visual side effect does voriconazole cause?
A: Visual disturbances — photopsia (flashes), hallucinations; unique to voriconazole among antifungals.

[CARD 115 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which azole is contraindicated in heart failure?
A: Itraconazole — negative inotropic effect (↓ cardiac contractility); contraindicated in HF.
[Trap: Only itraconazole has this cardiac contraindication — other azoles do not.]

[CARD 116 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which antifungals cover Mucormycosis?
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 — classic HKMLE coverage gap.]

[CARD 117 - Type 1]
Q: Which azole is used for Cryptococcal meningitis maintenance/consolidation?
A: Fluconazole (after amphotericin B + flucytosine induction phase).

[CARD 118 - Type 2: Cloze]
[c] All azoles [/c] inhibit CYP3A4 → raise warfarin (↑ INR), statin (rhabdomyolysis), and tacrolimus/cyclosporin (nephrotoxicity) levels — monitor closely.

[CARD 119 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why must posaconazole be taken with food?
A: Posaconazole requires a fatty meal for adequate absorption — TDM also required.

[CARD 120 - Type 3: Mnemonic]
Q: What is the mnemonic for echinocandins?
A: "Echinocandins = Echo = They WALL off fungi (inhibit β-1,3-glucan cell wall synthesis)"

[CARD 121 - Type 1]
Q: What is the mechanism of echinocandins?
A: Inhibit β-1,3-glucan synthase → ↓ fungal cell wall synthesis.

[CARD 122 - Type 1]
Q: What does echinocandin coverage EXCLUDE?
A: NOT Cryptococcus, NOT Mucor — covers Candida (including azole-resistant) and Aspergillus (not first-line).

[CARD 123 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: First-line antifungal for invasive candidiasis in ICU?
A: Echinocandin (caspofungin or micafungin) — especially in haemodynamically unstable or azole-exposed patients.

[CARD 124 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Are echinocandins available orally?
A: No — IV only; no oral formulation available for any echinocandin.

[CARD 125 - Type 1]
Q: What is the mechanism of flucytosine?
A: Converted to 5-FU inside fungal cells → inhibits DNA/RNA synthesis.

[CARD 126 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: When is flucytosine used and why never alone?
A: Flucytosine is used in combination for Cryptococcal meningitis (+ amphotericin B, 2-week induction) — monotherapy causes rapid resistance.

[CARD 127 - Type 1]
Q: What toxicities require monitoring with flucytosine?
A: Myelosuppression (leucopenia, thrombocytopaenia) and hepatotoxicity — monitor FBC and LFTs.

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

[CARD 128]
Q: Metronidazole + warfarin — effect and mechanism?
A: ↑ INR — metronidazole inhibits CYP2C9 → ↓ warfarin breakdown → bleeding risk.

[CARD 129]
Q: Metronidazole + alcohol — what happens?
A: Disulfiram-like reaction (flushing, vomiting, hypotension) — acetaldehyde accumulates; also triggered by alcohol mouthwashes.

[CARD 130]
Q: Ciprofloxacin + theophylline — effect and mechanism?
A: ↑ Theophylline toxicity — ciprofloxacin inhibits CYP1A2 → ↓ theophylline metabolism.

[CARD 131]
Q: Rifampicin + warfarin/OCP/ART/tacrolimus — what happens?
A: ↓ Efficacy of all co-drugs — rifampicin is a potent CYP450 inducer → accelerates metabolism.
[Trap: Rifampicin reduces OCP efficacy — missed contraception is a classic HKMLE scenario.]

[CARD 132]
Q: Fluconazole + warfarin — effect?
A: Significantly ↑ INR — fluconazole inhibits CYP2C9 → ↓ warfarin breakdown.

[CARD 133]
Q: Linezolid + SSRIs — what is the risk?
A: Serotonin syndrome — linezolid's MAO-inhibiting activity + serotonergic drug = dangerous combination.

[CARD 134]
Q: Clarithromycin + simvastatin — risk and mechanism?
A: Rhabdomyolysis — CYP3A4 inhibition raises statin levels → myotoxicity.

[CARD 135]
Q: Aminoglycosides + furosemide — what is the risk?
A: Additive ototoxicity — both independently toxic to cochlea/vestibular system.

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

[CARD 136 - Type 3: Mnemonic]
Q: What is the mnemonic for antibiotics safe in pregnancy?
A: "SAFE MOM" = Penicillins, Azithromycin, Few cephalosporins, Erythromycin base, Metronidazole (avoid T1)

[CARD 137 - Type 3: Mnemonic]
Q: What is the mnemonic for antibiotics to avoid in pregnancy?
A: "FCAT" = Fluoroquinolones, Cotrimoxazole (T1), Aminoglycosides (streptomycin), Tetracyclines

[CARD 138 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which antibiotics are safe throughout pregnancy?
A: Penicillins (all), cephalosporins, erythromycin BASE, azithromycin, clindamycin.

[CARD 139 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why is trimethoprim avoided in 1st trimester?
A: Folate antagonist → risk of neural tube defects in T1; give folic acid supplementation if must be used.

[CARD 140 - Type 2: Cloze]
[c] Chloramphenicol [/c] causes Grey Baby Syndrome near term — neonatal cardiovascular collapse due to inability to metabolise the drug.

[CARD 141 - Type 1]
Q: Why is nitrofurantoin avoided near term?
A: Risk of haemolytic anaemia in the neonate due to immature glutathione pathways (G6PD-like vulnerability).

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

[CARD 142 - Type 1]
Q: First-line IV treatment for MRSA bacteraemia?
A: Vancomycin IV (trough 15-20 µg/mL for bacteraemia/endocarditis).

[CARD 143 - Type 1]
Q: First-line for community MRSA skin/soft tissue infections?
A: Doxycycline or TMP-SMX (co-trimoxazole).

[CARD 144 - Type 1]
Q: First-line antibiotics for Pseudomonas aeruginosa?
A: Piperacillin-tazobactam, ceftazidime, cefepime, meropenem, or ciprofloxacin (context-dependent).

[CARD 145 - Type 1]
Q: Treatment for ESBL gram-negative infection?
A: Meropenem (or ertapenem if Pseudomonas not a concern).

[CARD 146 - Type 1]
Q: Treatment for severe C. difficile?
A: Oral vancomycin or fidaxomicin (fidaxomicin preferred — lower recurrence rate).

[CARD 147 - Type 1]
Q: Three-phase treatment of Cryptococcal meningitis?
A: Induction: amphotericin B + flucytosine (2 weeks) → Consolidation: fluconazole (8 weeks) → Maintenance: fluconazole.

[CARD 148 - Type 1]
Q: First-line treatment for atypical pneumonia (Mycoplasma, Chlamydia)?
A: Macrolide (azithromycin) or doxycycline or levofloxacin.

[CARD 149 - Type 1]
Q: Drug of choice for Legionella pneumonia?
A: Levofloxacin or azithromycin.

[CARD 150 - Type 1]
Q: First-line for invasive candidiasis in haemodynamically unstable/ICU patient?
A: Echinocandin (caspofungin or micafungin).

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

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

[CARD 152]
Q: HKMLE Trap: Fluconazole prescribed for invasive aspergillosis. What is wrong?
A: Fluconazole has NO activity against Aspergillus — use voriconazole (first-line).

[CARD 153]
Q: HKMLE Trap: Daptomycin given for MRSA pneumonia. What is the problem?
A: Daptomycin is inactivated by pulmonary surfactant — cannot treat lung infections; use linezolid for MRSA pneumonia.

[CARD 154]
Q: HKMLE Trap: Oral vancomycin prescribed for MRSA bacteraemia. Will it work?
A: NO — oral vancomycin is not absorbed; IV vancomycin is required for systemic MRSA.

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

[CARD 156]
Q: HKMLE Trap: Moxifloxacin prescribed for complicated UTI. What is wrong?
A: Moxifloxacin has negligible urinary excretion — use ciprofloxacin or levofloxacin for UTI.

[CARD 157]
Q: HKMLE Trap: Patient starts ciprofloxacin while on theophylline — what must you do?
A: Check theophylline levels — CYP1A2 inhibition can cause life-threatening theophylline toxicity.

[CARD 158]
Q: HKMLE Trap: Flucytosine given alone for Cryptococcal meningitis. What is the problem?
A: Flucytosine monotherapy = rapid resistance — always combine with amphotericin B.

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

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

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

• Type 1 & Type 4 cards: Use the Basic note type — paste Q/A directly
• Type 2 (Cloze) cards: Use Cloze note type — replace [c]...[/c] with {{c1::...}}
• Type 3 (Mnemonic) cards: Use Basic note type

================================================================
HKMLE EMERGENCY & TOXICOLOGY — ANKI FLASHCARD DECK
143 Cards Total
================================================================

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
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]
Q: What are the classic features of the sympathomimetic toxidrome?
A: ↑HR, ↑BP, dilated pupils, ↑temp, ↑sweating, agitation, seizures, hyperthermia. Causes: cocaine, amphetamines, MDMA.

[CARD 4 - Type 1]
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]
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]
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 SLUDGE features in cholinergic vs respiratory depression in opioid.]

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

[CARD 10 - Type 1]
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?
A: Serotonin syndrome = fast onset (hours), clonus/hyperreflexia, serotonergic drugs; NMS = slow onset (days), lead-pipe rigidity, markedly ↑CK, caused by antipsychotics.
[Trap: Both have hyperthermia and rigidity — key distinctions are onset speed, cause, and rigidity type.]

[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]
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]
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 LIAP as its specific failures.]

[CARD 16 - Type 1]
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]
Q: Name 3 contraindications to activated charcoal.
A: Reduced GCS/unprotected airway (aspiration risk), caustic ingestion (acid/alkali), intestinal obstruction/absent bowel sounds.

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

[CARD 18 - Type 1]  Q: Antidote for paracetamol OD?  A: N-Acetylcysteine (NAC).
[CARD 19 - Type 1]  Q: Antidote for opioid OD?  A: Naloxone (competitive μ-opioid receptor antagonist).
[CARD 20 - Type 1]  Q: Antidote for benzodiazepine OD?  A: Flumazenil (competitive GABA-A receptor antagonist).
[CARD 21 - Type 1]  Q: Antidotes for organophosphate poisoning?  A: Atropine (muscarinic block) + Pralidoxime (AChE reactivation).
[CARD 22 - Type 1]  Q: Antidote for TCA and salicylate OD?  A: Sodium bicarbonate.
[CARD 23 - Type 1]  Q: Antidote for warfarin OD?  A: Vitamin K (non-urgent) + PCC/FFP (urgent).
[CARD 24 - Type 1]  Q: Antidote for heparin OD?  A: Protamine sulfate.
[CARD 25 - Type 1]  Q: Antidote for dabigatran OD?  A: Idarucizumab.
[CARD 26 - Type 1]  Q: Antidote for rivaroxaban/apixaban OD?  A: Andexanet alfa.
[CARD 27 - Type 1]  Q: Antidote for digoxin toxicity?  A: Digoxin-specific Fab fragments (DigiFab).
[CARD 28 - Type 1]  Q: Preferred antidote for cyanide poisoning?  A: Hydroxocobalamin 5g IV.
[CARD 29 - Type 1]  Q: Antidote for carbon monoxide poisoning?  A: 100% high-flow O2; hyperbaric O2 for indications (COHb >25%, pregnancy, LOC, cardiac/neuro features).
[CARD 30 - Type 1]  Q: Antidote for methanol and ethylene glycol?  A: Fomepizole (inhibits alcohol dehydrogenase).
[CARD 31 - Type 1]  Q: Antidote for iron OD?  A: Deferoxamine.
[CARD 32 - Type 1]  Q: Antidote for lead poisoning?  A: DMSA (succimer) or EDTA.
[CARD 33 - Type 1]  Q: Antidote for methotrexate toxicity?  A: Leucovorin (folinic acid).
[CARD 34 - Type 1]  Q: Drug for serotonin syndrome?  A: Cyproheptadine (5-HT2A antagonist) + cooling + BZDs for agitation.
[CARD 35 - Type 1]  Q: Drug for malignant hyperthermia and NMS?  A: Dantrolene (blocks ryanodine receptor → ↓ Ca2+ release → ↓ muscle rigidity) ± bromocriptine for NMS.
[CARD 36 - Type 1]  Q: Role of calcium gluconate in hyperkalaemia?  A: Membrane stabilisation (cardiac protection) — does NOT lower serum K+.

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

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

[CARD 38 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Should you fully wake the patient up with naloxone in opioid OD?
A: No — titrate naloxone to restore BREATHING only; full reversal precipitates acute withdrawal (agitation, vomiting, pulmonary oedema).
[Trap: "Full reversal of consciousness" is the wrong endpoint — the correct endpoint is adequate respiration.]

[CARD 39 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why does methadone OD require naloxone infusion rather than single dose?
A: Naloxone t½ ~1h is much shorter than methadone t½ (24-36h) — re-narcotisation occurs after each single 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 OD — does naloxone reverse the seizures?
A: No — tramadol seizures are serotonergic/noradrenergic, not opioid-mediated; treat with benzodiazepines.

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

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

[CARD 43 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: When should flumazenil NEVER be given?
A: Suspected TCA overdose — removes BZD protection → TCA seizures emerge → fatal status epilepticus.
[Trap: #1 flumazenil trap on HKMLE — BZDs are protective in TCA OD; flumazenil kills.]

[CARD 44 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why is flumazenil dangerous in BZD-dependent patients?
A: Precipitates acute BZD withdrawal → seizures.

[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]
Q: What is the mechanism of NAC in paracetamol OD?
A: Glutathione precursor → replenishes hepatic glutathione → detoxifies NAPQI (toxic CYP2E1 metabolite).

[CARD 47 - Type 1]
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, ↑INR; Phase 3 (72-96h): peak hepatotoxicity, jaundice, renal failure; Phase 4: recovery or death.

[CARD 48 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Within what window is NAC most effective — and should it be withheld if the patient presents late?
A: Most effective within 8-10 hours — but NEVER withhold NAC for late presentation; it still reduces hepatic failure risk.
[Trap: Withholding late NAC is wrong — late presentation is not a contraindication.]

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

[CARD 50 - Type 2: Cloze]
[c] NAC (N-acetylcysteine) [/c] causes anaphylactoid reactions (urticaria, flushing, bronchospasm) — NOT IgE-mediated; slow the infusion and give antihistamine; do NOT permanently stop NAC.
[Trap: Stopping NAC permanently for a reaction is dangerous — always restart after managing the reaction.]

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

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

[CARD 52 - Type 1]
Q: What is the mechanism of organophosphate toxicity?
A: Irreversibly inhibit acetylcholinesterase → ACh accumulates → muscarinic + nicotinic + CNS effects.

[CARD 53 - 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: HR or miosis reversal are wrong endpoints — dry secretions/clear chest is the only correct answer.]

[CARD 54 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why must pralidoxime be given early?
A: Must be given before "ageing" (irreversible covalent bonding of OP to AChE after several hours) — delayed pralidoxime is ineffective.

[CARD 55 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Should pralidoxime be given for carbamate poisoning?
A: No — carbamates reversibly inhibit AChE (no ageing); use atropine only; pralidoxime is not needed and may be harmful.
[Trap: Common wrong answer — pralidoxime is for organophosphates only, not carbamates.]

[CARD 56 - Type 1]
Q: What are the nicotinic effects of organophosphate poisoning?
A: Muscle fasciculations → paralysis (including respiratory muscles), tachycardia (can mask bradycardia).

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

[CARD 57 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: TCA OD + QRS >120ms — immediate treatment?
A: Sodium bicarbonate IV (target pH 7.45-7.55) — narrows QRS and prevents VT/VF.
[Trap: Phenytoin worsens Na-channel blockade in TCA — use BZDs for seizures, NaHCO3 for arrhythmia.]

[CARD 58 - 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 59 - Type 2: Cloze]
[c] Sodium bicarbonate [/c] is used in salicylate poisoning to alkalinise the urine (target urine pH 7.5-8) → traps ionised salicylate in tubular lumen → increased renal excretion.

[CARD 60 - Type 1]
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 61 - 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 62 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What two drugs must NEVER be given in TCA OD?
A: Flumazenil (fatal seizures) and physostigmine (worsens arrhythmias).
[Trap: Both seem logical as antidotes in a sedated/confused patient — both are dangerous in TCA OD.]

[CARD 63 - Type 1]
Q: What is used to treat seizures in TCA OD?
A: Benzodiazepines (diazepam/lorazepam) — NOT phenytoin (worsens Na-channel blockade).

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 10: SALICYLATE OVERDOSE
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 64 - Type 3: Mnemonic]
Q: What is the mnemonic for salicylate toxicity?
A: SALE = Salicylates cause: Acidosis (metabolic), Lungs (NCPE), Ears (tinnitus), Early alkalosis (initial respiratory alkalosis)

[CARD 65 - Type 1]
Q: What is the classic ABG pattern in salicylate poisoning?
A: Mixed respiratory alkalosis (early, from direct respiratory centre stimulation) + metabolic acidosis (late, from lactic acid + salicylate).

[CARD 66 - Type 1]
Q: Indications for haemodialysis in salicylate poisoning?
A: Severe poisoning, renal failure, pulmonary oedema, neurological features, salicylate >700mg/L.

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

[CARD 67 - Type 1]
Q: What is the therapeutic window for lithium?
A: 0.4-1.0 mmol/L; >1.5 mild; >2.0 moderate; >2.5 severe toxicity.

[CARD 68 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Name 4 drugs/situations that raise lithium to toxic levels.
A: NSAIDs, ACEi/ARBs, thiazide diuretics, dehydration — all increase renal tubular reabsorption of lithium.
[Trap: NSAIDs are the classic exam interaction — ibuprofen for pain can rapidly push lithium to toxic levels.]

[CARD 69 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Does activated charcoal work for lithium?
A: No — lithium is in LIAP; use IV 0.9% NaCl (↑ renal Li excretion) and haemodialysis for severe toxicity.

[CARD 70 - Type 1]
Q: When is haemodialysis indicated in lithium toxicity?
A: Lithium >2.5-3.0 mmol/L with neurological features.

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

[CARD 71 - Type 1]
Q: What is the most common arrhythmia in digoxin toxicity, and what is pathognomonic?
A: Bradycardia + AV block most common; bidirectional VT is pathognomonic of digoxin toxicity.

[CARD 72 - Type 1]
Q: What is the "digoxin effect" on ECG (not toxicity)?
A: Down-sloping ST depression — "reverse tick / hockey stick" pattern.

[CARD 73 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why is calcium contraindicated in digoxin toxicity?
A: Hypercalcaemia mimics digoxin effect → worsens toxicity → "stone heart" (irreversible cardiac contracture); absolutely contraindicated.
[Trap: Even in hyperkalaemia, calcium cannot be given if the patient has digoxin toxicity — this is a classic HKMLE management trap.]

[CARD 74 - Type 3: Mnemonic]
Q: What is the mnemonic for digoxin toxicity management?
A: "K up, Mg up, Ca down, DigiFab for life-threatening" = correct K+ and Mg2+, avoid calcium, give DigiFab for severe arrhythmias.

[CARD 75 - Type 3: Mnemonic]
Q: What is the mnemonic for hyperkalaemia management?
A: C-BIG-K-Drop = Calcium (stabilise heart), Bicarbonate, Insulin + Glucose, Kayexalate, Dialysis (definitive)

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

[CARD 76 - Type 1]
Q: Key features of theophylline toxicity?
A: Severe N/V, refractory seizures, tachyarrhythmias, hypokalaemia, hyperglycaemia.

[CARD 77 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: How do you manage theophylline toxicity seizures?
A: Benzodiazepines (NOT phenytoin — ineffective); multi-dose activated charcoal; haemodialysis if severe.

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

[CARD 78 - Type 1]
Q: Toxic metabolite of methanol vs ethylene glycol?
A: Methanol → formic acid (blindness); Ethylene glycol → oxalic acid (renal failure + calcium oxalate crystals in urine).

[CARD 79 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: High anion gap metabolic acidosis + elevated osmolar gap — what is the diagnosis?
A: Methanol or ethylene glycol poisoning until proven otherwise.
[Trap: Anion gap alone is non-specific — osmolar gap elevation is the key distinguishing feature from other causes of HAGMA.]

[CARD 80 - Type 1]
Q: What is the mechanism of fomepizole?
A: Inhibits alcohol dehydrogenase → blocks conversion of methanol/ethylene glycol to toxic metabolites.

[CARD 81 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Unique symptom distinguishing methanol from ethylene glycol?
A: Visual disturbance → blindness (formic acid damages optic nerve) — specific to methanol; ethylene glycol causes renal failure, not visual loss.

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

[CARD 82 - Type 1]
Q: Why does pulse oximetry give a falsely normal reading in CO poisoning?
A: Pulse oximetry cannot distinguish oxyhaemoglobin from carboxyhaemoglobin → SpO2 appears normal; always order ABG with co-oximetry.
[Trap: Normal SpO2 does NOT exclude CO poisoning — the most tested investigation trap on HKMLE.]

[CARD 83 - Type 1]
Q: Mechanism of CO toxicity?
A: CO binds Hb with 250x affinity vs O2 → ↓ O2 carrying capacity + left-shifts O2-Hb curve + inhibits cytochrome c oxidase (mitochondrial).

[CARD 84 - Type 1]
Q: Indications for hyperbaric O2 in CO poisoning?
A: COHb >25%, any CO exposure in pregnancy (any level), loss of consciousness, cardiac/neurological features.

[CARD 85 - 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 86 - Type 1]
Q: Mechanism of cyanide toxicity?
A: Binds cytochrome c oxidase (complex IV) → blocks mitochondrial electron transport → histotoxic hypoxia → lactic acidosis despite adequate O2.

[CARD 87 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why is hydroxocobalamin preferred over sodium nitrite in smoke inhalation?
A: Smoke inhalation = co-existing CO; sodium nitrite induces methemoglobinaemia → further reduces O2 carrying capacity → dangerous with concurrent CO poisoning.
[Trap: Classic HKMLE scenario — always use hydroxocobalamin for house fire/smoke inhalation cyanide poisoning.]

[CARD 88 - Type 2: Cloze]
[c] Hydroxocobalamin [/c] causes 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 89 - Type 3: Mnemonic]
Q: What is the mnemonic for malignant hyperthermia management?
A: "STOP sux/volatile → DANTROLENE" — stop the trigger immediately, give dantrolene 2.5mg/kg IV.

[CARD 90 - Type 1]
Q: What triggers malignant hyperthermia?
A: Volatile anaesthetics (halothane, sevoflurane, desflurane) and suxamethonium.

[CARD 91 - Type 1]
Q: Mechanism of dantrolene?
A: Blocks ryanodine receptor → inhibits SR Ca2+ release → reduces skeletal muscle contraction and rigidity.

[CARD 92 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: MH vs NMS — trigger and onset?
A: MH: triggered by sux/volatile anaesthetics, onset minutes in OR, masseter spasm, extreme hyperthermia. NMS: triggered by antipsychotics (↓ dopamine), onset hours-days, lead-pipe rigidity, ↑CK.

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

[CARD 93 - Type 3: Mnemonic]
Q: What is the mnemonic for anaphylaxis management?
A: SAFE = Stop trigger, Adrenaline (IM) FIRST, Fluid resuscitation, Extra drugs (antihistamine/steroids adjuncts only)

[CARD 94 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is the FIRST treatment for anaphylaxis?
A: Adrenaline 0.5mg IM (1:1000) into anterolateral thigh — antihistamines and steroids are adjuncts, NOT first-line.
[Trap: Antihistamine first is the classic wrong answer — it treats urticaria only, not airway or cardiovascular collapse.]

[CARD 95 - Type 1]
Q: What are the 3 receptor effects of adrenaline in anaphylaxis?
A: α1 (vasoconstriction → reverses hypotension/angioedema), β1 (↑HR/CO), β2 (bronchodilation + ↓ mast cell mediator release).

[CARD 96 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: When is IV adrenaline used in anaphylaxis?
A: Only for refractory anaphylaxis or cardiac arrest — IM is safe and standard; IV risks severe hypertension and arrhythmias.
[Trap: IV adrenaline for standard anaphylaxis is NOT correct answer — IM is the right route.]

[CARD 97 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Patient on beta-blockers has refractory anaphylaxis. What do you add?
A: Glucagon — bypasses β-receptor blockade by stimulating cAMP independently.

[CARD 98 - Type 1]
Q: Why are corticosteroids given in anaphylaxis?
A: To prevent biphasic reaction (recurrence up to 72h later) — adjunct only; take hours to act.

[CARD 99 - Type 1]
Q: How long must patients be observed after anaphylaxis?
A: 4-6 hours minimum — biphasic reaction can occur up to 72 hours later.

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

[CARD 100 - Type 3: Mnemonic]
Q: What is the mnemonic for RSI induction agent selection?
A: "Haemodynamic instability = Etomidate; Asthma/bronchospasm = Ketamine; ICU/elective = Propofol"

[CARD 101 - Type 1]
Q: Mechanism and key property of ketamine?
A: NMDA receptor antagonist → dissociative anaesthesia; sympathomimetic (↑HR, ↑BP), bronchodilator — ideal for asthma and haemodynamic instability.

[CARD 102 - Type 1]
Q: What unique side effect of ketamine requires co-prescribing midazolam?
A: Emergence reactions (hallucinations, dissociation on recovery).

[CARD 103 - Type 1]
Q: Mechanism and key advantage of etomidate?
A: GABA-A potentiation (imidazole) — most haemodynamically stable induction agent; preferred for IHD/elderly.

[CARD 104 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Important endocrine side effect of etomidate?
A: Adrenal suppression (↓ cortisol for 24-48h after a single dose) — controversial in sepsis.

[CARD 105 - Type 2: Cloze]
[c] Propofol [/c] causes hypotension (vasodilation + ↓ CO) and is contraindicated in haemodynamic instability; Propofol Infusion Syndrome (lactic acidosis + multi-organ failure) occurs with high-dose prolonged infusions.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 20: RSI — NEUROMUSCULAR BLOCKERS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 106 - 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 107 - Type 2: Cloze]
[c] Suxamethonium [/c] raises serum K+ by 0.5-1 mmol/L — fatal in patients with hyperkalaemia, burns after 24h, crush injury, prolonged immobility, or denervating conditions (spinal cord injury, Guillain-Barré).
[Trap: Suxamethonium is safe in ACUTE burns within the first 24 hours — the K+ risk starts AFTER 24h due to upregulation of extrajunctional ACh receptors.]

[CARD 108 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What triggers malignant hyperthermia in the OR?
A: Suxamethonium + volatile anaesthetics — treat immediately with dantrolene (stop trigger first).

[CARD 109 - Type 1]
Q: How is rocuronium reversed?
A: Sugammadex — encapsulates rocuronium → excreted renally; cannot reverse suxamethonium.

[CARD 110 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: "Cannot intubate, cannot oxygenate" after rocuronium — what is the rescue?
A: Sugammadex IV immediately → reverses rocuronium → patient regains spontaneous breathing.
[Trap: Suxamethonium CANNOT be reversed — if you cannot intubate after sux, there is no pharmacological rescue.]

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

[CARD 111 - Type 3: Mnemonic]
Q: What is the mnemonic for cardiac arrest drugs?
A: "AAA + MCS" = Adrenaline (all rhythms), Amiodarone (shockable after 3rd shock), Magnesium (TdP), Calcium (specific indications), Sodium bicarb (specific indications)

[CARD 112 - Type 3: Mnemonic]
Q: What is the dosing mnemonic for cardiac arrest drugs?
A: "1mg Adrenaline every 3-5 min; 300mg Amiodarone after 3rd shock; 150mg after 5th; Magnesium 2g IV for TdP"

[CARD 113 - Type 1]
Q: When is adrenaline given in VF/pVT vs PEA/asystole?
A: VF/pVT: after 3rd shock; PEA/asystole: as soon as IV/IO access obtained.

[CARD 114 - Type 1]
Q: Drug of choice for Torsades de Pointes (TdP)?
A: Magnesium sulfate 2g IV over 15 minutes.
[Trap: Amiodarone is NOT first-line for TdP — it prolongs QT and can worsen TdP; magnesium is the answer.]

[CARD 115 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: When is calcium gluconate given in cardiac arrest?
A: Hyperkalaemic arrest, hypocalcaemic arrest, CCB OD arrest, hypermagnesaemia — but NEVER in digoxin toxicity.

[CARD 116 - Type 3: Mnemonic]
Q: What is the mnemonic for reversible causes of cardiac arrest?
A: 4H4T = Hypoxia, Hypovolaemia, Hypo/hyperK+ + metabolic, Hypothermia + Thrombosis (PE/MI), Tension pneumothorax, Tamponade, Toxins

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 22: HAEMODIALYSIS INDICATIONS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 117 - Type 1]
Q: Name 5 toxins requiring haemodialysis for elimination.
A: Lithium, Ethylene glycol, Aspirin (salicylate), Salicylate, Theophylline — also methanol.
[Trap: Activated charcoal is NOT an alternative to dialysis for lithium — charcoal does not adsorb it.]

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

[CARD 118] Q: HKMLE Trap: Mixed TCA + BZD OD → flumazenil given. What happens?
A: Flumazenil removes BZD protection → TCA seizures emerge → fatal status epilepticus.

[CARD 119] Q: HKMLE Trap: Naloxone given to fully wake up an opioid OD patient. What is the risk?
A: Acute opioid withdrawal (agitation, vomiting, hypertension, pulmonary oedema) — titrate to restore breathing only.

[CARD 120] Q: HKMLE Trap: SpO2 99% in a house fire victim — does this exclude CO poisoning?
A: No — pulse oximetry reads COHb as O2Hb → falsely normal; always order ABG with co-oximetry.

[CARD 121] Q: HKMLE Trap: Activated charcoal for lithium OD. Will it help?
A: No — lithium is NOT adsorbed by charcoal (LIAP); use IV saline + haemodialysis.

[CARD 122] Q: HKMLE Trap: Calcium gluconate given for hyperkalaemia in a digoxin toxicity patient. What is the danger?
A: Calcium potentiates digoxin toxicity → worsens arrhythmias → "stone heart"; absolutely contraindicated.

[CARD 123] Q: HKMLE Trap: Phenytoin given for TCA overdose seizures. What is the problem?
A: Phenytoin worsens Na-channel blockade in TCA OD → worsens arrhythmias; use benzodiazepines.

[CARD 124] Q: HKMLE Trap: Suxamethonium given 3 days after severe burns. What is the danger?
A: Massive K+ efflux → fatal hyperkalaemia → VF (extrajunctional ACh receptors upregulated after 24h of burns).

[CARD 125] Q: HKMLE Trap: Pralidoxime given for carbamate insecticide poisoning. Is it appropriate?
A: No — carbamates reversibly inhibit AChE without ageing; atropine only is correct.

[CARD 126] Q: HKMLE Trap: Anaphylaxis treated with chlorphenamine first. What is the error?
A: Antihistamine treats urticaria only — does NOT treat airway or cardiovascular collapse; adrenaline IM FIRST.

[CARD 127] Q: HKMLE Trap: "Cannot intubate, cannot oxygenate" after rocuronium. What is the rescue?
A: Sugammadex IV immediately — reverses rocuronium → spontaneous breathing restored (impossible with suxamethonium).

[CARD 128] Q: HKMLE Trap: Sodium nitrite + thiosulfate given to house fire victim with cyanide poisoning. What is the danger?
A: Sodium nitrite induces methemoglobinaemia — dangerous with co-existing CO poisoning; use hydroxocobalamin instead.

[CARD 129] Q: HKMLE Trap: NAC stopped permanently because the patient developed urticaria and flushing. Is this correct?
A: No — NAC reactions are anaphylactoid, NOT allergic; slow infusion + antihistamine; never permanently stop NAC.

================================================================
END OF DECK — 129+ CARDS TOTAL
================================================================

================================================================
HKMLE CNS PHARMACOLOGY — ANKI FLASHCARD DECK
146 Cards Total
================================================================

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
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

[CARD 2 - Type 1]
Q: Mechanism of SSRIs?
A: Block serotonin (5-HT) reuptake transporter → ↑ synaptic serotonin.

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

[CARD 4 - Type 1]
Q: Most common SSRI side effect?
A: Sexual dysfunction (↓ libido, anorgasmia, delayed ejaculation).

[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: Washout is NOT the same both ways — MAOI → SSRI = 2 weeks; fluoxetine → MAOI = 5 weeks (long t½).]

[CARD 7 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: How long does an antidepressant take to work — and what must patients be told?
A: 2-4 weeks — patients must continue the drug even with no initial benefit.

[CARD 8 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which SSRI is preferred in pregnancy?
A: Fluoxetine — longest half-life, fewest discontinuation symptoms, most safety data.
[Trap: Paroxetine is the SSRI to AVOID in pregnancy — most discontinuation symptoms and highest teratogenicity concern.]

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

[CARD 10 - Type 1]
Q: Which SSRI is used for bulimia nervosa?
A: Fluoxetine (only SSRI licensed for bulimia).

[CARD 11 - Type 1]
Q: Black box warning for SSRIs?
A: Increased suicidal ideation in patients ≤24 years — monitor closely in the first weeks.

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

[CARD 12 - Type 1]
Q: Mechanism of SNRIs?
A: Block both serotonin AND noradrenaline reuptake.

[CARD 13 - Type 1]
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
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[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]
Q: Mechanism of TCAs?
A: Block 5-HT + noradrenaline reuptake; also block muscarinic, histamine, and α1 receptors.

[CARD 18 - Type 1]
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]
Q: Name 4 contraindications to TCAs.
A: Recent MI, arrhythmias, narrow-angle glaucoma, prostatic hypertrophy.

[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).
[Trap: Never 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 2: Cloze]
[c] MAOIs [/c] cause hypertensive crisis with tyramine-rich foods (cheese, red wine, cured meats) because MAO normally breaks down tyramine in the gut — inhibition allows tyramine to enter circulation → massive noradrenaline release.

[CARD 23 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Washout when switching from fluoxetine to an MAOI?
A: 5 weeks (fluoxetine's very long t½ means serotonin levels remain elevated long after stopping).
[Trap: Other SSRIs only need 2 weeks washout — the 5-week rule is unique to fluoxetine.]

[CARD 24 - Type 1]
Q: Which MAOI has fewer dietary restrictions and why?
A: Moclobemide — reversible MAO inhibitor (RIMA); tyramine displaces it from MAO so the interaction is less dangerous.

[CARD 25 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Pethidine + MAOI — what happens?
A: Serotonin syndrome — absolutely contraindicated; use morphine instead.

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

[CARD 26 - Type 1]
Q: Mechanism and key features of mirtazapine?
A: α2 antagonist + 5-HT2/5-HT3 antagonist → weight gain + sedation, NO sexual dysfunction — good for elderly/underweight depressives.

[CARD 27 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Bupropion — what is its main seizure risk?
A: Lowers seizure threshold — avoid in bulimia, anorexia, and epilepsy; also used for smoking cessation and depression.

[CARD 28 - Type 2: Cloze]
[c] Trazodone [/c] causes priapism (prolonged painful erection) as a rare but characteristic side effect — requires urgent urological management.

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

[CARD 29 - Type 3: Mnemonic]
Q: What distinguishes typical vs atypical antipsychotics?
A: "Typical = D2 block (motor side effects); Atypical = D2 + 5-HT2 block (less EPS, more metabolic)"

[CARD 30 - Type 3: Mnemonic]
Q: What is the mnemonic for EPS timeline?
A: "Acutely Agitated Patients Take Drugs" = Acute dystonia (hours-days) → Akathisia (days-weeks) → Parkinsonism (weeks-months) → Tardive dyskinesia (months-years)

[CARD 31 - Type 1]
Q: Acute dystonia treatment?
A: IM procyclidine or benztropine (anticholinergic).

[CARD 32 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Patient on haloperidol can't sit still and is restless. Diagnosis and treatment?
A: Akathisia — reduce dose, add propranolol or benzodiazepine; do NOT increase antipsychotic.
[Trap: Akathisia is often misidentified as worsening psychosis or anxiety — increasing the antipsychotic makes it worse.]

[CARD 33 - Type 2: Cloze]
[c] Tardive dyskinesia [/c] causes oro-facial movements (lip smacking, tongue protrusion) appearing months-years after antipsychotic use — it can be irreversible; stop drug if possible.

[CARD 34 - Type 1]
Q: Treatment for antipsychotic-induced Parkinsonism?
A: Anticholinergics (procyclidine, benztropine) or reduce dose/switch to atypical.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 7: NMS
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 35 - 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 36 - Type 1]
Q: Treatment for NMS?
A: Stop antipsychotic immediately; supportive care; dantrolene (muscle relaxant); bromocriptine (D2 agonist).

[CARD 37 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: NMS vs serotonin syndrome — key clinical differences?
A: NMS = lead-pipe rigidity, slow onset (days), normal/small pupils, high CK, antipsychotic cause; serotonin syndrome = clonus/hyperreflexia, rapid onset (hours), dilated pupils, diarrhoea, serotonergic drug cause.
[Trap: Both have hyperthermia — muscle tone type and speed of onset are the key differentiators.]

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

[CARD 38 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which antipsychotic is for treatment-resistant schizophrenia?
A: Clozapine — after failure of 2 antipsychotics; weekly FBC mandatory for first 18 weeks (then monthly) for agranulocytosis.
[Trap: Clozapine is NOT first-line — reserved for treatment-resistant schizophrenia only.]

[CARD 39 - Type 2: Cloze]
[c] Clozapine [/c] causes agranulocytosis in ~1-2% of patients — FBC monitored weekly for 18 weeks then monthly; neutropenia = stop immediately.

[CARD 40 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Aripiprazole mechanism — what is unique?
A: Partial D2 agonist (not a pure antagonist) — stabilises dopamine pathways; least metabolic side effects.
[Trap: Common wrong answer is "D2 antagonist" — aripiprazole is a PARTIAL agonist, an exam-tested distinction.]

[CARD 41 - Type 1]
Q: Which atypical antipsychotic causes the most metabolic syndrome?
A: Olanzapine — highest risk of weight gain, diabetes, dyslipidaemia.

[CARD 42 - Type 1]
Q: Which atypical antipsychotic is most useful for bipolar depression?
A: Quetiapine.

[CARD 43 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which antipsychotic is safe for psychosis in Parkinson's disease?
A: Quetiapine or clozapine (least D2 blockade) — all others worsen Parkinson's motor symptoms.
[Trap: Never give haloperidol, risperidone, or olanzapine to a Parkinson's patient.]

[CARD 44 - Type 2: Cloze]
[c] Risperidone [/c] causes the most hyperprolactinaemia of atypical antipsychotics (galactorrhoea, amenorrhoea, sexual dysfunction) and causes EPS at high doses.

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

[CARD 45 - Type 1]
Q: Mechanism of benzodiazepines?
A: Positive allosteric modulator at GABA-A receptor → ↑ frequency of Cl- channel opening → CNS depression.

[CARD 46 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: First-line treatment for status epilepticus?
A: IV lorazepam (or rectal/buccal diazepam) → phenytoin/levetiracetam → phenobarbitone.

[CARD 47 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why is diazepam preferred over lorazepam for alcohol withdrawal management?
A: Diazepam has long-acting active metabolites (t½ days) → provides smooth taper, prevents withdrawal seizures and delirium tremens.
[Trap: Lorazepam is for acute withdrawal seizures; diazepam is for the overall withdrawal management.]

[CARD 48 - Type 1]
Q: Contraindications to benzodiazepines?
A: Sleep apnoea, severe respiratory depression, pregnancy (cleft palate risk), myasthenia gravis.

[CARD 49 - Type 2: Cloze]
[c] BZD + opioid combination [/c] carries a black box warning for additive respiratory depression — avoid unless necessary with close monitoring.

[CARD 50 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Limitations of flumazenil for BZD reversal?
A: Short-acting (t½ ~1h) → re-sedation can occur; does NOT reverse respiratory depression from other drugs; precipitates seizures in BZD-dependent patients.

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

[CARD 51 - Type 1]
Q: Mechanism of Z-drugs (zolpidem, zopiclone, zaleplon)?
A: Same GABA-A site as BZDs but selective for α1 subunit → more hypnotic, less anxiolytic/anticonvulsant.

[CARD 52 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Are Z-drugs safer than BZDs for dependence?
A: No — similar dependence potential; short-term use only (2-4 weeks max, per NICE).
[Trap: Z-drugs are commonly thought to be "safer" — this is false for dependence risk.]

[CARD 53 - Type 1]
Q: Mechanism and key limitation of buspirone for GAD?
A: 5-HT1A partial agonist; no dependence/sedation — but delayed onset (2-4 weeks); cannot abort acute anxiety, no cross-tolerance with BZDs.
[Trap: Buspirone cannot replace BZDs acutely — it takes weeks to work and does not prevent BZD withdrawal seizures.]

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

[CARD 54 - Type 3: Mnemonic]
Q: What is the mnemonic for AED mechanisms?
A: "Sodium Blocks Fits, Calcium Crushes Absence, GABA Guards neurons"

[CARD 55 - Type 3: Mnemonic]
Q: What is the mnemonic for AED seizure type matching?
A: Absence = Ethosuximide; Myoclonic = Valproate; Focal = Carbamazepine

[CARD 56 - Type 3: Mnemonic]
Q: What is the mnemonic for valproate toxicity?
A: HALT = Hepatotoxicity, Alopecia, Liver failure, Teratogen (neural tube defects)

[CARD 57 - Type 1]
Q: Mechanism of sodium valproate?
A: ↑ GABA, ↓ Na+ channels, ↓ T-type Ca2+ channels → broad spectrum (all seizure types including absence).

[CARD 58 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Most important contraindication to valproate?
A: Women of childbearing age — highest teratogen risk of all AEDs; neural tube defects, spina bifida, neurodevelopmental delay; avoid unless no alternative.

[CARD 59 - Type 1]
Q: Mechanism of carbamazepine?
A: Blocks voltage-gated Na+ channels.

[CARD 60 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which seizure types does carbamazepine WORSEN?
A: Absence and myoclonic seizures — never use carbamazepine for these.
[Trap: Carbamazepine is often chosen as a "broad AED" — it is NOT broad spectrum.]

[CARD 61 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Carbamazepine in Asian patients — what must you check?
A: HLA-B*1502 allele (common in Han Chinese, Vietnamese, Thai) — associated with severe Stevens-Johnson syndrome; screen before prescribing.

[CARD 62 - Type 2: Cloze]
[c] Carbamazepine [/c] is a potent CYP450 inducer — reduces efficacy of warfarin, OCP, and many other drugs by accelerating their metabolism.

[CARD 63 - Type 3: Mnemonic]
Q: What is the mnemonic for phenytoin side effects?
A: GANG = Gingival hyperplasia, Ataxia, Nystagmus (toxicity), coarse facies + hirsutism (also megaloblastic anaemia, teratogen)

[CARD 64 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: What is special about phenytoin pharmacokinetics?
A: Zero-order (saturation) kinetics — small dose increases cause disproportionately large rises in plasma levels; narrow therapeutic window (10-20 µg/mL).
[Trap: Most drugs follow first-order kinetics — phenytoin's zero-order kinetics means doubling the dose can triple or quadruple blood levels → toxicity.]

[CARD 65 - Type 1]
Q: Signs of phenytoin toxicity in order?
A: Nystagmus (earliest) → ataxia/diplopia → dysarthria → sedation → seizures.

[CARD 66 - Type 1]
Q: Mechanism of lamotrigine?
A: Blocks voltage-gated Na+ channels.

[CARD 67 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Lamotrigine + valproate — what are the two risks?
A: Valproate inhibits lamotrigine glucuronidation → doubles lamotrigine levels; combined use greatly increases SJS risk → titrate lamotrigine VERY slowly.
[Trap: Rapid titration of lamotrigine (especially with valproate) is the most common cause of drug-induced SJS.]

[CARD 68 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Safest AED in pregnancy?
A: Lamotrigine (lowest risk among older AEDs); levetiracetam increasingly preferred; BOTH require dose increases in pregnancy (levels drop).

[CARD 69 - Type 1]
Q: Mechanism of levetiracetam?
A: Binds SV2A synaptic vesicle protein → broad spectrum (focal, generalised, myoclonic); renally cleared, minimal drug interactions.

[CARD 70 - Type 1]
Q: Mechanism of ethosuximide and what is it used for?
A: Blocks T-type Ca2+ channels in thalamus → ONLY for pure absence (petit mal) seizures.
[Trap: Ethosuximide only treats absence — if the patient also has tonic-clonic seizures, use valproate instead.]

[CARD 71 - Type 2: Cloze]
[c] Topiramate [/c] causes weight LOSS (unlike most AEDs), cognitive dulling ("Dope-amax"), and kidney stones (carbonic anhydrase inhibition) — used for focal/generalised seizures and migraine prophylaxis.

[CARD 72 - Type 1]
Q: First-line AED for focal (partial) seizures?
A: Carbamazepine, lamotrigine, or levetiracetam.

[CARD 73 - Type 1]
Q: Drug of choice for pure absence seizures?
A: Ethosuximide (pure absence) or valproate (if mixed with tonic-clonic).
[Trap: Carbamazepine and phenytoin can WORSEN absence — never use for pure absence seizures.]

[CARD 74 - Type 1]
Q: First-line drugs for myoclonic seizures?
A: Valproate, levetiracetam, or clonazepam.
[Trap: Carbamazepine and phenytoin worsen myoclonic epilepsy — never use for juvenile myoclonic epilepsy.]

[CARD 75 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Folic acid dose for women on AEDs pre-conception?
A: 5mg/day (NOT standard 400mcg) — higher dose required for all women on AEDs to protect against neural tube defects.
[Trap: Standard 400mcg is insufficient for women on AEDs — 5mg/day is the correct HKMLE answer.]

[CARD 76 - Type 1]
Q: Which AED causes fetal hydantoin syndrome?
A: Phenytoin — cleft palate, digit defects, developmental delay.

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

[CARD 77 - 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)

[CARD 78 - Type 1]
Q: Why is carbidopa combined with levodopa?
A: Carbidopa blocks peripheral dopa decarboxylase → ↓ peripheral conversion to dopamine → more L-DOPA crosses BBB + reduced nausea/hypotension.
[Trap: Carbidopa does NOT cross BBB — it only reduces peripheral side effects, not central dopamine effects.]

[CARD 79 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: On-off phenomenon in Parkinson's disease?
A: Motor fluctuations with long-term levodopa — "on" (drug works) alternates with "off" (wears off, immobility); managed by adding COMT inhibitors, MAO-B inhibitors, or dopamine agonists.

[CARD 80 - Type 2: Cloze]
[c] Levodopa [/c] causes dyskinesias (involuntary writhing movements) at high doses after years of therapy — this is dopamine overstimulation, not disease progression.

[CARD 81 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Dopamine agonists — what impulse control side effect must you warn about?
A: Pathological gambling, hypersexuality, binge eating — a characteristic and frequently tested dopamine agonist side effect.

[CARD 82 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Selegiline (MAO-B inhibitor) + pethidine — what happens?
A: Serotonin syndrome — absolutely contraindicated; also avoid SSRIs with selegiline.

[CARD 83 - Type 1]
Q: Mechanism of COMT inhibitors (entacapone, tolcapone)?
A: Block COMT → ↓ peripheral levodopa breakdown → more L-DOPA enters brain; given WITH every levodopa dose.

[CARD 84 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why is tolcapone more dangerous than entacapone?
A: Tolcapone causes hepatotoxicity (requires LFT monitoring) — entacapone preferred.

[CARD 85 - Type 1]
Q: Anticholinergics in Parkinson's — who should avoid them?
A: Elderly patients — confusion, falls, urinary retention; useful in younger patients with tremor-predominant PD.

[CARD 86 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Amantadine's unique indication in Parkinson's disease?
A: Reducing levodopa-induced dyskinesias in late/advanced PD — this is its unique niche.

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

[CARD 87 - 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 88 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Only AChEI approved for severe Alzheimer's disease?
A: Donepezil — licensed for mild, moderate, AND severe AD; others are mild-moderate only.

[CARD 89 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which AChEI is approved for Parkinson's disease dementia?
A: Rivastigmine — also inhibits BuChE; available as transdermal patch; only AChEI with this specific indication.

[CARD 90 - Type 2: Cloze]
[c] Donepezil [/c] can cause bradycardia via cholinergic cardiac stimulation — monitor closely in patients with sick sinus syndrome or heart block.

[CARD 91 - Type 1]
Q: Mechanism of memantine?
A: Non-competitive NMDA receptor antagonist → blocks glutamate excitotoxicity → used for moderate-severe AD.

[CARD 92 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Antipsychotics in Lewy body dementia — what is the risk?
A: Severely contraindicated — even small doses cause severe irreversible Parkinsonism and can be fatal; use AChEIs for behavioural symptoms instead.
[Trap: AChEIs are USEFUL in Lewy body dementia — the trap is giving antipsychotics for behavioural symptoms.]

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

[CARD 93 - 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 94 - Type 3: Mnemonic]
Q: What is the mnemonic for opioid overdose triad?
A: RMP = Respiratory depression, Miosis (pinpoint pupils), coma

[CARD 95 - Type 1]
Q: Which opioid side effect does tolerance NOT develop to?
A: Constipation — always prescribe laxatives with opioids.
[Trap: Tolerance develops to sedation and nausea but NEVER to constipation.]

[CARD 96 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why does morphine accumulate in renal failure?
A: Active metabolite M6G (morphine-6-glucuronide) is renally cleared — accumulates in CKD → prolonged toxicity; use fentanyl or oxycodone instead.

[CARD 97 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why is codeine dangerous in ultra-rapid CYP2D6 metabolisers?
A: Codeine → morphine via CYP2D6; ultra-rapid metabolisers convert too much → morphine toxicity; avoid in children post-tonsillectomy (multiple deaths).
[Trap: Poor metabolisers get NO analgesia from codeine; ultra-rapid metabolisers get toxicity — both extremes are tested.]

[CARD 98 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why is tramadol more dangerous than a simple opioid?
A: Tramadol is a weak μ agonist + SNRI → lowers seizure threshold + serotonin syndrome risk with SSRIs; seizures NOT reversed by naloxone.

[CARD 99 - Type 2: Cloze]
[c] Pethidine (meperidine) [/c] causes seizures via norpethidine — avoid in renal failure and in Parkinson's patients on MAO-B inhibitors (serotonin syndrome).

[CARD 100 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Why does methadone require cardiac monitoring?
A: Prolongs QT interval → risk of Torsades de Pointes; also unpredictable long t½ (24-36h).

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

[CARD 101 - Type 1]
Q: Mechanism of triptans (sumatriptan)?
A: 5-HT1B/1D agonist → vasoconstriction of meningeal vessels + ↓ CGRP neuropeptide release → aborts migraine.

[CARD 102 - Type 1]
Q: 3 contraindications to triptans?
A: IHD, uncontrolled hypertension, hemiplegic migraine.

[CARD 103 - Type 1]
Q: First-line migraine prophylaxis?
A: Propranolol (β-blocker) — avoid in asthma; alternatives: amitriptyline, topiramate, valproate.

[CARD 104 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Newest class of migraine preventives for refractory cases?
A: CGRP monoclonal antibodies (erenumab, fremanezumab) — injection site reactions and constipation.

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
SECTION 16: SUBSTANCE MISUSE
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

[CARD 105 - Type 1]
Q: Mechanism of disulfiram?
A: Blocks ALDH → acetaldehyde accumulates → flushing, nausea, headache, hypotension if alcohol consumed.

[CARD 106 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Which drug causes the same reaction as disulfiram with alcohol?
A: Metronidazole — also inhibits ALDH → same acetaldehyde syndrome.
[Trap: The disulfiram reaction is not unique to disulfiram — metronidazole is the classic exam trap drug.]

[CARD 107 - Type 1]
Q: Mechanism of acamprosate?
A: GABA agonist / NMDA antagonist → reduces craving; started after detox in abstinent patients.

[CARD 108 - Type 1]
Q: Naltrexone use in addiction medicine?
A: Opioid receptor antagonist — reduces alcohol craving (mechanism unclear) AND prevents opioid relapse; oral or monthly injection.

[CARD 109 - Type 4: HKMLE Pearl]
Q: HKMLE Pearl: Most effective single agent for smoking cessation?
A: Varenicline (partial α4β2 nicotinic ACh receptor agonist) — more effective than NRT or bupropion; neuropsychiatric warning (depression, suicidal ideation).

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

[CARD 110 - Type 1]
Q: Causes: serotonin syndrome vs NMS?
A: SS = excess serotonin (SSRI + MAOI, SSRI + tramadol, SSRI + linezolid); NMS = antipsychotics (dopamine blockade) or sudden DA drug withdrawal.

[CARD 111 - Type 1]
Q: Muscle tone in SS vs NMS?
A: SS = clonus, hyperreflexia, myoclonus; NMS = lead-pipe rigidity.

[CARD 112 - Type 1]
Q: Pupils in SS vs NMS?
A: SS = dilated (mydriasis); NMS = normal or small.

[CARD 113 - Type 1]
Q: CK level in SS vs NMS?
A: SS = normal or mildly elevated; NMS = markedly elevated (rhabdomyolysis).

[CARD 114 - Type 1]
Q: 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 115] Q: HKMLE Trap: SSRI stopped suddenly — patient develops dizziness, electric shock sensations, flu-like symptoms. What is this?
A: SSRI discontinuation syndrome (NOT relapse) — taper slowly; worst with paroxetine (shortest t½).

[CARD 116] Q: HKMLE Trap: Ethosuximide prescribed for absence + tonic-clonic seizures. What is wrong?
A: Ethosuximide only treats pure absence — no effect on tonic-clonic; use valproate for mixed generalised epilepsy.

[CARD 117] Q: HKMLE Trap: Carbamazepine prescribed for juvenile myoclonic epilepsy. What is the problem?
A: Carbamazepine worsens myoclonic and absence seizures — use valproate or levetiracetam.

[CARD 118] Q: HKMLE Trap: Phenytoin dose increased from 250mg to 300mg — patient develops nystagmus and ataxia. Why?
A: Zero-order kinetics — small dose increase causes disproportionately large plasma level rise → toxicity.

[CARD 119] Q: HKMLE Trap: Haloperidol prescribed for psychosis in a Parkinson's patient. What is the danger?
A: Severely worsens motor symptoms — use quetiapine or clozapine only.

[CARD 120] Q: HKMLE Trap: Antipsychotic continued as patient develops high fever, lead-pipe rigidity, elevated CK. What must you do?
A: Stop the antipsychotic immediately — this is NMS; continuing it can be fatal.

[CARD 121] Q: HKMLE Trap: 25-year-old woman with epilepsy started on valproate. What must be done first?
A: Counsel on teratogenicity risks, document discussion, ensure effective contraception (PREVENT programme), consider alternative AED.

[CARD 122] 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; use AChEIs instead.

[CARD 123] Q: HKMLE Trap: Z-drugs prescribed long-term as "safer" alternative to BZDs. What is wrong?
A: Z-drugs have similar dependence potential to BZDs — maximum 2-4 weeks only.

[CARD 124] Q: HKMLE Trap: Standard 400mcg folic acid prescribed to a woman on carbamazepine planning pregnancy. What is the correct dose?
A: 5mg/day folic acid — standard 400mcg is insufficient for women on AEDs.

================================================================
END OF DECK — 124 CARDS (+ 22 section cards = 146 TOTAL)
================================================================

HKMLE ENDOCRINE PHARMACOLOGY — ANKI FLASHCARD DECK

SECTION 1: INSULIN

SECTION 2: METFORMIN

SECTION 3: SULFONYLUREAS

SECTION 4: SGLT2 INHIBITORS (GLIFLOZINS)

SECTION 5: GLP-1 RECEPTOR AGONISTS

SECTION 6: DPP-4 INHIBITORS (GLIPTINS)

SECTION 7: THIAZOLIDINEDIONES (TZDs)

SECTION 8: DIABETES DRUG QUICK-SELECT

SECTION 9: THYROID DRUGS

SECTION 10: CORTICOSTEROIDS

SECTION 11: ADRENAL INSUFFICIENCY

SECTION 12: BISPHOSPHONATES

SECTION 13: DENOSUMAB

SECTION 14: CALCITONIN & TERIPARATIDE

SECTION 15: DESMOPRESSIN (DDAVP)

SECTION 16: SOMATOSTATIN ANALOGUES & PITUITARY DRUGS

BONUS: HIGH-YIELD TRAP CARDS

• Insulin (9 cards) — types, IV rules, hypokalaemia/DKA
• Metformin (8 cards) — CRASH mnemonic, lactic acidosis, B12
• Sulfonylureas (5 cards) — mechanism, gliclazide vs glibenclamide
• SGLT2 inhibitors (8 cards) — FUNGUS mnemonic, euglycaemic DKA, periop hold
• GLP-1 agonists (6 cards) — MTC/MEN2 CI, weight loss, CVD trials
• DPP-4 inhibitors (5 cards) — linagliptin renal exception, saxagliptin HF
• TZDs (5 cards) — HF contraindication, rosiglitazone, bladder cancer
• Diabetes quick-select (6 cards) — scenario-based drug choice
• Thyroid drugs (17 cards) — PTU vs carbimazole in pregnancy, BIIP mnemonic, thyroid storm, levothyroxine pearls
• Corticosteroids (9 cards) — STEROIDS mnemonic, potency table, HPA suppression
• Adrenal insufficiency (5 cards) — HISS mnemonic, sick day rules, periop cover
• Bisphosphonates (9 cards) — BONE SNAP + STOP EAT mnemonics, ONJ, acute phase reaction
• Denosumab (4 cards) — CKD preference, rebound fractures
• Calcitonin & Teriparatide (5 cards) — tachyphylaxis, anabolic mechanism paradox
• Desmopressin (5 cards) — central vs nephrogenic DI, water intoxication
• Somatostatin & Pituitary drugs (8 cards) — octreotide, cabergoline, GnRH agonists, pegvisomant
• Bonus Trap cards (11 cards)

HKMLE RESPIRATORY PHARMACOLOGY — ANKI FLASHCARD DECK

SECTION 1: SHORT-ACTING β2 AGONISTS (SABAs)

SECTION 2: LONG-ACTING β2 AGONISTS (LABAs)

SECTION 3: SHORT-ACTING MUSCARINIC ANTAGONISTS (SAMAs)

SECTION 4: LONG-ACTING MUSCARINIC ANTAGONISTS (LAMAs)

SECTION 5: INHALED CORTICOSTEROIDS (ICS)

SECTION 6: COMBINED INHALERS (ICS + LABA)

SECTION 7: THEOPHYLLINE

SECTION 8: MONTELUKAST (LTRA)

SECTION 9: MAST CELL STABILISERS (CROMOLYN)

SECTION 10: BIOLOGICS

SECTION 11: TB DRUGS — "RIPE" REGIMEN

SECTION 12: PNEUMONIA ANTIBIOTICS

SECTION 13: INHALER DEVICES

SECTION 14: ASTHMA STEP-UP THERAPY

SECTION 15: COPD DRUG MANAGEMENT

SECTION 16: DRUGS TO AVOID IN ASTHMA

BONUS: HIGH-YIELD TRAP CARDS

• SABAs (6 cards) — mechanism, hypokalaemia, overuse signal
• LABAs (5 cards) — black box, MART, formoterol vs salmeterol
• SAMAs/ipratropium (5 cards) — ED adjunct, anticholinergic SE, glaucoma CI
• LAMAs/tiotropium (3 cards) — once-daily COPD, asthma add-on
• ICS (8 cards) — mouth rinse, budesonide in pregnancy, no acute use, dysphonia
• Combined inhalers (2 cards) — Symbicort MART vs Seretide
• Theophylline (8 cards) — CANT mnemonic, narrow TI, drug interactions, smokers
• Montelukast (7 cards) — dual indication, neuropsychiatric black box, EGPA, AERD
• Cromolyn (3 cards) — prophylaxis only, no acute use
• Biologics (9 cards) — omalizumab vs mepolizumab biomarker selection
• TB RIPE (18 cards) — regimen, all 4 drug mechanisms, B6/isoniazid, ethambutol eyes, rifampicin CYP, latent TB, MDR-TB, pregnancy
• CAP/HAP antibiotics (11 cards) — CURB-65, atypical cover, Legionella, HAP organisms
• Inhaler devices (6 cards) — child <8 MDI+spacer, acute = nebuliser, DPI flow
• Asthma step-up (6 cards) — Steps 1-5 complete
• COPD management (6 cards) — O2 88-92% target, triple therapy, steroids
• Drugs to avoid in asthma (4 cards) — BANNS mnemonic, SAFE in pregnancy, Samter's triad
• Bonus trap cards (11 cards)

HKMLE GI PHARMACOLOGY — ANKI FLASHCARD DECK

SECTION 1: PROTON PUMP INHIBITORS (PPIs)

SECTION 2: H2 RECEPTOR ANTAGONISTS

SECTION 3: H. PYLORI ERADICATION

SECTION 4: ANTACIDS

SECTION 5: SUCRALFATE

SECTION 6: MISOPROSTOL

SECTION 7: PROKINETICS

SECTION 8: ANTIEMETICS

SECTION 9: ANTIDIARRHOEALS

SECTION 10: LAXATIVES

SECTION 11: IBD DRUGS — AMINOSALICYLATES (5-ASA)

SECTION 12: IBD DRUGS — CORTICOSTEROIDS

SECTION 13: IBD DRUGS — IMMUNOMODULATORS

SECTION 14: IBD DRUGS — BIOLOGICS

SECTION 15: IBS DRUGS

SECTION 16: C. DIFFICILE MANAGEMENT

BONUS: HIGH-YIELD TRAP CARDS

• PPIs (8 cards) — PPI CHOB mnemonic, timing, pantoprazole + clopidogrel, hypomagnesaemia, C. diff risk, rebound
• H2 blockers (5 cards) — cimetidine anti-androgen + CYP inhibitor
• H. pylori eradication (5 cards) — PAC/PBMT mnemonics, UBT vs serology
• Antacids (4 cards) — aluminium/magnesium side effects, chelation rule
• Sucralfate (4 cards) — acidic pH requirement, administration timing, drug interactions
• Misoprostol (5 cards) — PGE1 mechanism, pregnancy CI, PPI vs misoprostol
• Prokinetics (6 cards) — metoclopramide EPS/tardive dyskinesia, procyclidine treatment, domperidone QT
• Antiemetics (13 cards) — 5-HT3/D2/H1/NK1 by receptor, triple CINV therapy, pregnancy-safe antiemetics, QT prolongation
• Antidiarrhoeals (5 cards) — loperamide CI in bloody diarrhoea, bismuth black stool
• Laxatives (9 cards) — BOSS mnemonic, lactulose in hepatic encephalopathy, opioid constipation = stimulant first
• IBD 5-ASA (5 cards) — UC first-line, sulfasalazine infertility + folate
• IBD corticosteroids (4 cards) — induction only, budesonide for ileocaecal Crohn's
• IBD immunomodulators (11 cards) — AZA TPMT + 3-month wait, pancreatitis, MTX teratogen + folic acid, ciclosporin rescue
• IBD biologics (9 cards) — FIAT mnemonic, TITS screening, vedolizumab gut-selectivity, anti-TNF + HF
• IBS drugs (3 cards) — mebeverine vs hyoscine
• C. difficile (3 cards) — triggers, oral vancomycin, FMT
• Bonus trap cards (14 cards)

HKMLE RHEUMATOLOGY PHARMACOLOGY — ANKI FLASHCARD DECK

SECTION 1: PARACETAMOL

SECTION 2: NSAIDs (NON-SELECTIVE)

SECTION 3: COX-2 INHIBITORS (COXIBS)

SECTION 4: CONVENTIONAL DMARDs — METHOTREXATE

SECTION 4: CONVENTIONAL DMARDs — SULFASALAZINE

SECTION 4: CONVENTIONAL DMARDs — HYDROXYCHLOROQUINE

SECTION 4: CONVENTIONAL DMARDs — LEFLUNOMIDE

SECTION 5: DMARD COMPARISON IN PREGNANCY

SECTION 6: BIOLOGIC DMARDs

SECTION 7: GOUT DRUGS

SECTION 8: CORTICOSTEROIDS IN RHEUMATOLOGY

SECTION 9: SLE DRUGS

SECTION 10: OSTEOPOROSIS IN RHEUMATOLOGY

BONUS: HIGH-YIELD TRAP CARDS

• Paracetamol (7 cards) — PARA mnemonic, NAC antidote, NAPQI phases, risk factors
• NSAIDs non-selective (6 cards) — COX-1/2 mechanism, renal/GI/PDA risks, indomethacin in PDA
• COX-2 inhibitors (6 cards) — celecoxib sulfa allergy, rofecoxib withdrawal, GI benefit lost with aspirin
• MTX (9 cards) — MTX mnemonic, folic acid timing, 3-month pre-conception stop, pneumonitis, NSAID interaction
• Sulfasalazine (5 cards) — male infertility, orange urine, folate, pregnancy safety
• Hydroxychloroquine (5 cards) — bull's-eye maculopathy, annual ophthalmology, safe in pregnancy, QT
• Leflunomide (4 cards) — LEF mnemonic, cholestyramine washout, long half-life
• DMARD comparison (3 cards) — HCQ/MTX/LEF pregnancy mnemonic
• Biologic DMARDs (22 cards) — anti-TNF (TITS screening, HF CI, etanercept vs infliximab), tocilizumab (masks CRP), anakinra (AOSD), rituximab (PML, HBV reactivation), abatacept, JAK inhibitors (VTE + zoster)
• Gout drugs (20 cards) — acute vs chronic treatment, colchicine timing, CYP3A4 interaction, allopurinol mechanism + HLA-B*5801 + AZA interaction, febuxostat (CKD + CV risk), probenecid (stone CI)
• Corticosteroids in rheumatology (3 cards) — bridge therapy, septic arthritis CI, GCA emergency
• SLE drugs (3 cards) — HCQ for all, MMF + pregnancy switch
• Osteoporosis (1 card) — steroid-induced osteoporosis prophylaxis
• Bonus traps (14 cards)