I have attached my HKMLE pharmacology notes for Haematology. Create Anki flashcards from these notes. Each card should test ONLY high-yield facts that appear in HKMLE exams. INCLUDE cards for: · Drug mechanisms (simple, exam-level) · Key indications · Major side effects (only the ones HKMLE tests) · Contraindications · HKMLE Pearls (from my notes) · Mnemonics (from my notes) DO NOT include: · Long explanations · Low-yield details · Physiology review FORMAT each card as ONE of these types: Type 1 (Basic Q&A): Q: [question] A: [short answer, 1 sentence max] Type 2 (Cloze deletion): [c] drug name [/c] causes [side effect] because [mechanism] Type 3 (Mnemonic card): Q: What is the mnemonic for [topic]? A: [mnemonic] = [breakdown] Type 4 (HKMLE Pearl card): Q: HKMLE Pearl: [scenario]? A: [one sentence answer] ADD trap alerts: For any fact that is a common HKMLE trap, add on a new line: [Trap: common wrong answer is X because Y] Make as many cards as needed to cover ALL high-yield facts from my notes. Do not limit the number. Use simple, direct language. Match the style of high-yield exam prep cards. Here are my notes: [PASTE YOUR HAEMATOLOGY NOTES HERE]
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HKMLE Haematology Anki
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Deck Summary
186 flashcard entries across all 4 types, covering every high-yield topic from your notes:
| Section | # Cards | Types Used |
|---|---|---|
| Warfarin (mechanisms, INR targets, reversal, drug interactions) | ~25 | 1, 2, 3, 4 |
| Heparin / LMWH / HIT | ~20 | 1, 2, 3, 4 |
| Direct Thrombin Inhibitors | ~5 | 1, 4 |
| DOACs (mechanisms, renal dosing, reversal) | ~20 | 1, 2, 3, 4 |
| Antiplatelets | ~15 | 1, 2, 3, 4 |
| Thrombolytics | ~15 | 1, 3, 4 |
| TXA (CRASH-2, WOMAN) | ~10 | 1, 2, 3, 4 |
| Iron / B12 / Folate | ~25 | 1, 2, 3, 4 |
| EPO / G-CSF / TPO agonists | ~20 | 1, 3, 4 |
| Reversal Agents | ~10 | 1, 3, 4 |
| Pregnancy & Anticoagulation | ~5 | 1, 4 |
| Quick Mnemonics Summary | ~10 | 3 |
Trap alerts included for: warfarin skin necrosis, LMWH reversal (only 60%), protamine for LMWH, DOACs in mechanical valves, idarucizumab specificity (dabigatran only), prasugrel post-TIA, ticagrelor dyspnoea, streptokinase re-use, CT head before thrombolysis, EPO Hb overcorrection, IM B12 for pernicious anaemia, folate masking B12 neuro, dabigatran in CKD, and more.
To import into Anki: Copy the content into Anki's card editor directly, or use the "Import" function with the text file (select "Basic" note type and map Q/A fields).
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HKMLE HAEMATOLOGY PHARMACOLOGY — ANKI FLASHCARD DECK
SECTION 1: WARFARIN
Type 3
Q: What is the mnemonic for warfarin's factor targets?
A: "WEPT" = Warfarin: Extended PT, inhibits 1972 (factors II, VII, IX, X + Proteins C and S)
Type 1
Q: What is warfarin's mechanism of action?
A: Inhibits vitamin K epoxide reductase → blocks activation of clotting factors II, VII, IX, X and anticoagulant proteins C and S.
Type 1
Q: Why does warfarin require 3-5 days to reach full anticoagulant effect?
A: Existing clotting factors must be depleted; factor VII has the shortest half-life (6h) so INR rises first, but full anticoagulation takes 3-5 days.
[Trap: common wrong answer is "warfarin acts immediately" — early INR rise reflects factor VII depletion only, not full anticoagulation]
Type 1
Q: What is the monitoring parameter for warfarin?
A: INR.
Type 1
Q: Target INR for AF and DVT/PE?
A: 2.0-3.0.
Type 1
Q: Target INR for mechanical mitral valve?
A: 2.5-3.5.
[Trap: common wrong answer is 2.0-3.0 — mechanical mitral valves require a higher target than aortic valves]
Type 1
Q: Target INR for mechanical aortic valve?
A: 2.0-3.0 (some guidelines 2.5-3.5).
Type 1
Q: Target INR for recurrent PE or antiphospholipid syndrome?
A: 2.5-3.5.
Type 1
Q: What causes warfarin-induced skin necrosis?
A: Warfarin preferentially depletes short-lived Protein C/S before full anticoagulation → transient procoagulant state → microvascular thrombosis; especially in protein C deficiency.
[Trap: common wrong answer is "direct skin toxicity" — it is a thrombotic complication from early Protein C/S depletion]
Type 1
Q: What are the absolute contraindications to warfarin?
A: Pregnancy (all trimesters), active bleeding, recent intracranial surgery or haemorrhage.
Type 2
[c] Warfarin [/c] is Category X in pregnancy because it causes warfarin embryopathy (nasal hypoplasia, stippled epiphyses) in weeks 6-12 and fetal haemorrhage in T3.
Type 1
Q: What enzyme mediates most warfarin drug interactions?
A: CYP2C9.
Type 3
Q: Mnemonic for drugs that INCREASE warfarin INR?
A: "CAFE MIX" = Clarithromycin/ciprofloxacin, Amiodarone, Fluconazole, Erythromycin, Metronidazole, Isoniazid, eXcretion inhibitors (statins)
Type 3
Q: Mnemonic for drugs that DECREASE warfarin INR?
A: "PRICARS" = Phenytoin, Rifampicin, Isoniazid (high dose), Carbamazepine, Alcohol (chronic), Rifampicin, St John's Wort
Type 1
Q: Does amiodarone increase or decrease warfarin INR?
A: Increases INR — inhibits CYP2C9 → reduced warfarin metabolism → higher drug levels → ↑ bleeding risk.
Type 1
Q: Does rifampicin increase or decrease warfarin INR?
A: Decreases INR — induces CYP2C9 → increased warfarin metabolism → reduced efficacy.
Type 1
Q: Do NSAIDs change the INR on warfarin?
A: No direct change to INR, but NSAIDs increase bleeding risk via GI mucosal damage and platelet inhibition.
Type 1
Q: INR 5-8, no significant bleeding — management?
A: Stop warfarin; give low-dose oral vitamin K 1-2mg.
Type 1
Q: INR >8, no or minor bleeding — management?
A: Stop warfarin; give oral vitamin K 5mg (repeat at 24h if INR still high).
Type 1
Q: Any INR + major bleeding — management?
A: Stop warfarin + IV vitamin K 5-10mg + 4-factor PCC (preferred over FFP — faster, lower volume).
[Trap: common wrong answer is FFP alone — PCC acts faster and requires less volume]
Type 1
Q: Life-threatening intracranial bleed on warfarin — immediate management?
A: PCC + IV vitamin K 10mg immediately.
Type 4
Q: HKMLE Pearl: Why must warfarin always be started with heparin in acute thrombosis?
A: Warfarin first depletes Protein C/S → transient procoagulant state → risk of worsening thrombosis if not covered by heparin.
Type 1
Q: What does INR specifically measure?
A: The extrinsic coagulation pathway — factors VII, X, II, V, and fibrinogen.
SECTION 2: HEPARIN (UFH AND LMWH)
Type 3
Q: Mnemonic for heparin?
A: "HEPARIN" = Helps Every Patient And Requires INR-free monitoring (except UFH)
Type 1
Q: UFH mechanism of action?
A: Binds antithrombin III → inhibits factor IIa (thrombin) and Xa (and IXa, XIa, XIIa).
Type 1
Q: LMWH mechanism — how does it differ from UFH?
A: Binds antithrombin III → preferentially inhibits factor Xa only (smaller chain cannot bridge thrombin to antithrombin).
Type 1
Q: How is UFH monitored?
A: aPTT (target 1.5-2.5x normal).
Type 1
Q: How is LMWH monitored?
A: Usually NOT required; anti-Xa level used if obese, pregnant, or in renal impairment.
Type 1
Q: Half-life of IV UFH?
A: ~1.5 hours.
Type 1
Q: What reverses UFH?
A: Protamine sulfate (fully neutralises).
Type 1
Q: What reverses LMWH?
A: Protamine sulfate — but only ~60% reversal (partial).
[Trap: common wrong answer is "protamine fully reverses LMWH" — it only partially reverses LMWH]
Type 1
Q: Why must LMWH be avoided in severe renal failure?
A: LMWH is renally cleared → accumulates if eGFR <30 → bleeding risk.
[Trap: common wrong answer is "UFH also needs dose reduction in renal failure" — UFH is metabolised by the reticuloendothelial system, NOT the kidneys]
Type 1
Q: Which has higher HIT risk — UFH or LMWH?
A: UFH (~5-10%), though LMWH can still cause HIT.
Type 1
Q: When is UFH preferred over LMWH?
A: ICU, unstable patients, perioperative settings where rapid reversal is needed.
Type 3
Q: Mnemonic for HIT?
A: "HIT" = Heparin Induces Thrombosis (paradoxically) — scored using the 4Ts
Type 1
Q: What is HIT Type I?
A: Non-immune; mild platelet drop (>100) within 1-2 days; benign; continue heparin.
Type 1
Q: What is HIT Type II?
A: Immune; IgG antibodies against heparin-PF4 complex → platelet activation → paradoxical thrombosis; platelets drop >50% from baseline at days 5-10.
Type 1
Q: What are the 4Ts in the 4Ts score?
A: Thrombocytopenia (severity), Timing (days 5-10), Thrombosis, other causes of Thrombocytopenia excluded.
Type 1
Q: What test confirms HIT Type II?
A: Anti-PF4/heparin ELISA or serotonin release assay.
Type 1
Q: Management of HIT Type II?
A: Stop ALL heparin (UFH AND LMWH); start argatroban or fondaparinux; do NOT give platelets; do NOT start warfarin until platelets >150.
Type 4
Q: HKMLE Pearl: A patient on heparin develops falling platelets and a new DVT on day 7. Diagnosis and immediate action?
A: HIT Type II — stop ALL heparin immediately; start argatroban or fondaparinux; do NOT give platelets.
Type 4
Q: HKMLE Pearl: Why are platelet transfusions contraindicated in HIT?
A: HIT causes thrombosis — transfusing platelets worsens platelet activation and thrombus formation.
Type 4
Q: HKMLE Pearl: Why must warfarin not be started in HIT until platelets >150?
A: Warfarin depletes Protein C → thrombotic state → risk of venous limb gangrene while platelets are still low.
Type 2
[c] Fondaparinux [/c] is used in HIT because it inhibits only factor Xa with no cross-reactivity with PF4 antibodies.
SECTION 3: DIRECT THROMBIN INHIBITORS (DTIs)
Type 1
Q: Mechanism of direct thrombin inhibitors?
A: Directly inhibit thrombin (factor IIa) → block fibrin formation; act independently of antithrombin (unlike heparin).
Type 4
Q: HKMLE Pearl: Drug of choice for HIT in renal failure?
A: Argatroban — hepatic elimination, safe in renal failure.
Type 1
Q: What is bivalirudin used for?
A: PCI as an alternative to heparin; short-acting; renally eliminated; no reversal agent.
Type 1
Q: Is there a reversal agent for argatroban?
A: No — stop the infusion (short half-life ~50 min).
SECTION 4: DIRECT ORAL ANTICOAGULANTS (DOACs)
Type 3
Q: Mnemonic for DOAC targets?
A: "3 Xas + 1 IIa" = Rivaroxaban, Apixaban, Edoxaban (factor Xa) + Dabigatran (factor IIa)
Type 1
Q: Which DOAC is the only oral direct thrombin inhibitor?
A: Dabigatran (factor IIa inhibitor).
[Trap: common wrong answer is rivaroxaban or apixaban — these are factor Xa inhibitors]
Type 1
Q: Name the three factor Xa inhibitor DOACs.
A: Rivaroxaban, Apixaban, Edoxaban.
Type 1
Q: What is dabigatran's bioavailability?
A: Only 6% (very low).
Type 1
Q: What is dabigatran's renal clearance and why does it matter?
A: 80% renally cleared — avoid if CrCl <30 mL/min (accumulates → bleeding risk).
Type 1
Q: Which DOAC is safest in CKD and why?
A: Apixaban — least renally cleared (~27%); dose-reduce only if 2 of 3: age ≥80, weight ≤60kg, creatinine ≥133 µmol/L.
[Trap: common wrong answer is "all DOACs equally safe in CKD" — dabigatran is most dangerous due to 80% renal clearance]
Type 1
Q: What drugs reduce efficacy of ALL DOACs?
A: P-gp/CYP3A4 inducers: rifampicin, St John's Wort, carbamazepine, phenytoin.
Type 1
Q: What are the key indications for DOACs?
A: Non-valvular AF (stroke prevention), DVT/PE treatment and prevention, post-surgical VTE prophylaxis.
Type 1
Q: Most common side effect of DOACs?
A: Bleeding — GI bleeding particularly high with dabigatran and rivaroxaban vs warfarin.
Type 1
Q: Three absolute contraindications to DOACs?
A: Pregnancy (teratogenic), mechanical heart valves (inferior — RE-ALIGN trial), severe renal impairment (especially dabigatran).
[Trap: common wrong answer is "DOACs are fine in mechanical valves because they are newer" — RE-ALIGN trial showed DOACs are INFERIOR to warfarin for mechanical valves]
Type 4
Q: HKMLE Pearl: Can a DOAC be used in triple-positive antiphospholipid syndrome?
A: No — warfarin is preferred; DOACs are inferior in APS.
Type 3
Q: Mnemonic for DOAC reversal?
A: "I-DAR for IIa (dabigatran), AND-exanet for Xa"
Type 1
Q: Reversal agent for dabigatran major bleeding?
A: Idarucizumab (Praxbind) 5g IV — monoclonal Ab Fab fragment; reverses dabigatran within minutes.
Type 1
Q: Reversal agent for rivaroxaban/apixaban major bleeding?
A: Andexanet alfa (recombinant factor Xa decoy); alternative = 4F-PCC 25-50 units/kg if unavailable.
Type 4
Q: HKMLE Pearl: A patient on rivaroxaban has major bleeding. Idarucizumab is available — use it?
A: No — idarucizumab reverses dabigatran ONLY; use andexanet alfa (or 4F-PCC) for rivaroxaban.
[Trap: idarucizumab is SPECIFIC to dabigatran only]
Type 1
Q: Apixaban dose reduction rule?
A: Reduce dose if 2 of 3: age ≥80, weight ≤60kg, creatinine ≥133 µmol/L.
Type 1
Q: What is the role of activated charcoal in DOAC overdose?
A: Give if DOAC taken ≤2h ago (especially dabigatran due to enteric absorption) — reduces further absorption.
Type 1
Q: Advantages of DOACs over warfarin?
A: No routine monitoring, fewer drug interactions, predictable dosing, faster onset/offset, lower intracranial haemorrhage risk.
SECTION 5: ANTIPLATELETS
Type 1
Q: Aspirin's mechanism of antiplatelet action?
A: Irreversibly inhibits COX-1 → ↓ TXA2 → ↓ platelet aggregation; lasts 7-10 days (platelet lifespan).
Type 1
Q: Antiplatelet dose of aspirin?
A: 75-150mg daily.
Type 1
Q: Why is aspirin never given to children under 12?
A: Risk of Reye's syndrome.
Type 1
Q: Clopidogrel's mechanism?
A: Irreversibly blocks P2Y12 ADP receptor on platelets; prodrug requiring CYP2C19 activation.
Type 1
Q: What reduces clopidogrel efficacy?
A: CYP2C19 poor metabolisers (pharmacogenomics); PPIs compete at CYP2C19.
Type 1
Q: Ticagrelor's mechanism — how does it differ from clopidogrel?
A: Reversibly blocks P2Y12; NOT a prodrug (no CYP2C19 needed); more potent.
Type 1
Q: Most notable side effect of ticagrelor?
A: Dyspnoea — adenosine-mediated, NOT bronchospasm.
[Trap: common wrong answer is "stop ticagrelor because of bronchospasm" — it is adenosine-mediated dyspnoea, not true bronchospasm; do not switch without reason]
Type 4
Q: HKMLE Pearl: Ticagrelor is used with aspirin post-ACS. What aspirin dose must be used?
A: Low dose only — high-dose aspirin reduces ticagrelor efficacy.
Type 1
Q: Prasugrel's mechanism and when is it preferred?
A: Irreversibly blocks P2Y12; prodrug with more efficient activation than clopidogrel; preferred in STEMI post-PCI (TRITON trial).
Type 1
Q: Prasugrel's contraindications?
A: Prior stroke/TIA (↑ intracranial bleed risk), age >75, weight <60kg.
[Trap: common wrong answer is "use prasugrel post-TIA because it is more potent" — it is CONTRAINDICATED in prior stroke/TIA]
Type 3
Q: Mnemonic for prasugrel contraindication?
A: "Prior TIA/stroke = Prasugrel is PRASUREly dangerous"
Type 1
Q: Dipyridamole mechanism and use?
A: Inhibits phosphodiesterase → ↑ cAMP → ↓ platelet aggregation; blocks adenosine reuptake; used for secondary stroke prevention (combined with aspirin = Aggrenox) and pharmacological cardiac stress testing.
Type 1
Q: What is DAPT?
A: Dual antiplatelet therapy = aspirin + P2Y12 inhibitor; standard post-ACS/PCI for 12 months.
Type 1
Q: How long before elective surgery should clopidogrel/prasugrel be stopped?
A: 7-10 days.
Type 1
Q: Mechanism of GPIIb/IIIa inhibitors (tirofiban, eptifibatide)?
A: Block GPIIb/IIIa receptor — the final common platelet aggregation pathway; IV only; used in high-risk ACS/PCI.
SECTION 6: THROMBOLYTICS
Type 3
Q: Mnemonic for thrombolytics' mechanism?
A: "tPA = turns Plasminogen to Active plasmin → eATs fibrin clots"
Type 1
Q: Mechanism of all thrombolytics?
A: Activate plasminogen → plasmin → plasmin cleaves fibrin → dissolves clots.
Type 1
Q: What is alteplase?
A: Recombinant tPA; fibrin-selective; gold standard for ischaemic stroke (≤4.5h), massive PE, and STEMI if PCI unavailable; short half-life (~5 min).
Type 1
Q: Time window for alteplase in ischaemic stroke?
A: Within 4.5 hours of symptom onset.
Type 4
Q: HKMLE Pearl: Before giving alteplase for stroke, what must be done first?
A: CT head to exclude haemorrhagic stroke — never give thrombolysis without CT.
[Trap: common wrong answer is "give alteplase first, CT if bleeding suspected" — CT head is MANDATORY before thrombolysis]
Type 4
Q: HKMLE Pearl: What BP target must be achieved before stroke thrombolysis?
A: <185/110 mmHg.
Type 1
Q: What is tenecteplase?
A: Modified tPA; longer half-life → single IV bolus (convenient for STEMI); increasingly used for ischaemic stroke.
Type 1
Q: What makes streptokinase unique?
A: Bacterial (Streptococcus) → antigenic → can only be used ONCE (antibodies form → repeat within 5 years is ineffective); NOT fibrin-selective; cheapest.
[Trap: common wrong answer is "streptokinase can be repeated if needed" — antibody formation makes repeat use within 5 years ineffective]
Type 1
Q: Time window for thrombolytics in STEMI when PCI unavailable?
A: ≤12 hours from onset (ideally <6h); use tenecteplase or streptokinase.
Type 3
Q: Mnemonic for absolute contraindications to thrombolytics?
A: "BRAIN HURTS" = Bleeding (active), Recent surgery/trauma, Aortic dissection, Intracranial history, Neurosurgery (recent), Haemorrhagic stroke, Uncontrolled BP, Recent head injury, Time window exceeded, Severe bleeding disorder
Type 1
Q: Name 4 absolute contraindications to thrombolytics?
A: Any prior intracranial haemorrhage; ischaemic stroke within 3 months; suspected aortic dissection; active internal bleeding.
Type 1
Q: Name 4 major relative contraindications to thrombolytics?
A: SBP >180 or DBP >110 mmHg; recent major surgery/trauma (2-4 weeks); active peptic ulcer/GI bleed; pregnancy.
SECTION 7: ANTIFIBRINOLYTICS (TXA)
Type 3
Q: Mnemonic for TXA?
A: "TXA = Tranexamic acid eXActs its effect by Blocking plasmin"
Type 1
Q: Tranexamic acid (TXA) mechanism?
A: Synthetic lysine analogue → competitively inhibits plasminogen activation (blocks lysine-binding sites) → prevents fibrin clot breakdown → preserves haemostasis.
Type 1
Q: Key indications for TXA?
A: Trauma haemorrhage (CRASH-2), postpartum haemorrhage (WOMAN trial), heavy menstrual bleeding, elective surgery (↓ transfusion), hereditary angioedema prophylaxis.
Type 4
Q: HKMLE Pearl: What does the CRASH-2 trial show about TXA in trauma?
A: TXA given within 3 hours of injury reduces all-cause mortality; given after 3 hours — no benefit.
[Trap: common wrong answer is "TXA works up to 6 hours like stroke thrombolysis" — CRASH-2 benefit is STRICTLY within 3 hours]
Type 3
Q: Mnemonic for TXA timing in trauma?
A: "3 hours or bust" (CRASH-2: must give within 3h of trauma)
Type 4
Q: HKMLE Pearl: What does the WOMAN trial show?
A: TXA reduces death from bleeding in postpartum haemorrhage when given early — now WHO recommended.
Type 1
Q: TXA contraindications?
A: Active thromboembolic disease (DVT, PE, stroke); DIC with consumption (worsens DIC); haematuria from upper urinary tract (ureteric clot risk).
Type 1
Q: TXA major side effects?
A: Nausea/vomiting, VTE risk, colour vision changes (rare), seizures at high doses.
Type 1
Q: Is TXA an anticoagulant reversal agent?
A: No — it prevents fibrin breakdown but does not reverse anticoagulants or replace blood products.
SECTION 8: HAEMATINICS
8a — IRON
Type 3
Q: Mnemonic for iron therapy?
A: "FERRIC" = Ferrous is absorbed, Ferritin stores it, Restores Hb, Iron deficiency = Check cause, Constipation = side effect
Type 1
Q: Why is ferrous (Fe²⁺) preferred over ferric (Fe³⁺) orally?
A: Fe²⁺ is better absorbed from the gut; ferrous sulfate is first-line.
Type 1
Q: What enhances oral iron absorption?
A: Vitamin C (ascorbic acid) — converts Fe³⁺ → Fe²⁺; take on an empty stomach.
Type 1
Q: What reduces oral iron absorption?
A: Antacids, PPIs, tea, coffee, calcium — chelate iron; take iron away from these.
Type 1
Q: Earliest sign of response to iron therapy?
A: Reticulocyte count rises at ~1 week; Hb rises ~10-20g/L per 3 weeks.
Type 1
Q: Most common side effect of oral iron?
A: Constipation (also nausea, epigastric pain, dark stools).
Type 4
Q: HKMLE Pearl: A patient on ferrous sulfate reports black stools — is this dangerous?
A: No — dark stools are a harmless side effect of oral iron; warn the patient.
Type 1
Q: When is IV iron indicated?
A: Oral failure/intolerance, IBD, CKD on dialysis, severe deficiency in pregnancy, bariatric surgery.
Type 1
Q: Serious side effect specific to IV ferric carboxymaltose?
A: Transient hypophosphataemia (also infusion reactions; anaphylaxis rare).
Type 1
Q: Contraindications to iron supplementation?
A: Haemochromatosis, haemolytic anaemia (iron not deficient).
8b — VITAMIN B12
Type 3
Q: Mnemonic for B12 deficiency?
A: "B12 = Big red cells (macrocytic), Bad nerves (subacute combined degeneration), Bypass stomach (intrinsic factor needed)"
Type 1
Q: B12's mechanism in haematopoiesis and myelin?
A: Cofactor for DNA synthesis (methylcobalamin → methionine synthesis) and myelin formation (adenosylcobalamin → succinyl-CoA → Krebs cycle).
Type 1
Q: What causes pernicious anaemia?
A: Autoimmune destruction of gastric parietal cells → absent intrinsic factor → inability to absorb dietary B12.
Type 1
Q: Most specific antibody for pernicious anaemia?
A: Anti-intrinsic factor antibodies.
Type 1
Q: Formulation and route for pernicious anaemia?
A: IM hydroxocobalamin 1mg alternate days for 2 weeks, then every 3 months lifelong.
[Trap: common wrong answer is "oral B12 is fine" — pernicious anaemia means NO intrinsic factor → oral B12 cannot be absorbed → IM is mandatory]
Type 1
Q: Neurological features of B12 deficiency?
A: Subacute combined degeneration of spinal cord (posterior columns + lateral corticospinal tracts): bilateral paraesthesiae, ataxia, spasticity, extensor plantar responses.
Type 1
Q: Other clinical features of B12 deficiency?
A: Macrocytic anaemia, hypersegmented neutrophils, glossitis ("beefy red tongue"), megaloblastic changes.
Type 1
Q: Where is B12 absorbed?
A: Terminal ileum (requires intrinsic factor from gastric parietal cells); affected by Crohn's disease or ileal resection.
Type 4
Q: HKMLE Pearl: A patient with macrocytic anaemia is given folic acid alone. What is the danger?
A: Folic acid treats the blood picture but UNMASKS subacute combined degeneration of the cord if B12 deficiency is the underlying cause — neurological deterioration results.
[Trap: this is a classic HKMLE trap — never give folate alone without checking B12 first]
Type 1
Q: Side effect when starting B12 treatment?
A: Hypokalaemia — B12 stimulates RBC production → ↑ K⁺ uptake into new cells.
8c — FOLATE
Type 3
Q: Mnemonic for folate?
A: "FOLATE" = First trimester supplement, Only treats blood (not neuro), Looks same as B12 anaemia, Avoid in B12 deficiency alone, Treatment oral
Type 1
Q: Folate mechanism?
A: Required for one-carbon transfer reactions → DNA synthesis; converted to THF → needed for purine/pyrimidine synthesis.
Type 1
Q: Standard preconception/T1 folate dose?
A: 400 mcg (0.4mg) daily.
Type 1
Q: High-risk preconception folate dose and who qualifies?
A: 5mg daily — previous NTD, diabetes, antiepileptics, obesity.
Type 1
Q: Folate dose for methotrexate co-prescription?
A: 5mg once weekly.
Type 1
Q: Most common cause of folate deficiency in clinical practice?
A: Alcoholism.
Type 1
Q: How do you distinguish B12 from folate deficiency anaemia?
A: Both cause macrocytic anaemia — check B12/folate levels + neurological features (B12 deficiency has neuro symptoms; folate deficiency does NOT cause subacute combined degeneration).
Type 1
Q: Which drugs cause folate deficiency?
A: Methotrexate (DHFR inhibition), trimethoprim, phenytoin.
SECTION 9: HAEMATOPOIETIC GROWTH FACTORS
9a — EPO/ESAs
Type 3
Q: Mnemonic for EPO?
A: "EPO = Every Patient On dialysis needs this"
Type 1
Q: EPO mechanism?
A: Recombinant erythropoietin → binds EPO receptor on erythroid progenitors → stimulates RBC production.
Type 1
Q: Key indications for ESAs?
A: Anaemia of CKD (primary), chemotherapy-induced anaemia, low-risk MDS, autologous blood donation pre-surgery.
Type 1
Q: Target Hb when treating CKD anaemia with EPO?
A: 100-120 g/L — do NOT exceed 130 g/L (↑ CV events — CHOIR and CREATE trials).
[Trap: common wrong answer is "target normal Hb" — overcorrection increases VTE and cardiovascular mortality]
Type 1
Q: What must be checked before starting EPO?
A: Iron stores (ferritin and TSAT) — iron deficiency prevents ESA response.
Type 1
Q: Most common side effect of EPO?
A: Hypertension (↑ Hb → ↑ blood viscosity → ↑ BP).
Type 1
Q: What is pure red cell aplasia (PRCA) in the context of EPO?
A: Rare — anti-EPO antibodies develop → sudden worsening anaemia after initial response; stop EPO, start immunosuppression.
9b — G-CSF
Type 3
Q: Mnemonic for G-CSF?
A: "G-CSF = Grows White cells (neutrophils)"
Type 1
Q: G-CSF mechanism?
A: Binds G-CSF receptor → stimulates neutrophil precursor proliferation, differentiation, and survival → ↑ mature neutrophil release from bone marrow.
Type 1
Q: Key indications for G-CSF?
A: Chemotherapy-induced febrile neutropaenia prevention; treatment of neutropaenia; stem cell mobilisation before harvesting for transplant.
Type 1
Q: Most common side effect of G-CSF?
A: Bone pain (medullary expansion — treat with paracetamol ± ibuprofen).
[Trap: common wrong answer is "G-CSF causes bleeding" — the most common side effect is bone pain from marrow expansion]
Type 1
Q: Other side effects of G-CSF?
A: Splenomegaly (rare: splenic rupture), elevated LDH/uric acid, leukocytosis if overdosed.
9c — TPO RECEPTOR AGONISTS
Type 1
Q: Mechanism of TPO receptor agonists?
A: Bind and activate thrombopoietin receptor (Mpl) → stimulate megakaryocyte proliferation → ↑ platelet production.
Type 1
Q: Romiplostim — indication and route?
A: ITP second-line after steroids; SC weekly.
Type 1
Q: Eltrombopag — indications and route?
A: ITP, aplastic anaemia (with ciclosporin), thrombocytopaenia in HCV/CLD; oral.
Type 1
Q: How should eltrombopag be taken?
A: Without food and away from polyvalent cations (chelation reduces absorption); monitor LFTs (hepatotoxicity risk).
Type 1
Q: Major side effects of TPO receptor agonists?
A: Bone marrow reticulin fibrosis (prolonged use), thrombosis (↑ platelet count → VTE risk), headache.
SECTION 10: REVERSAL AGENTS
Type 3
Q: Mnemonic for reversal agents?
A: "4Ps + 2Is + 1A" = Protamine (heparin), Phytomenadione/Vitamin K (warfarin), PCC (warfarin/Xa), Platelet transfusion, Idarucizumab (dabigatran), Andexanet alfa (Xa), Aminocaproic/TXA (fibrinolytics)
Type 1
Q: How is UFH reversed with protamine?
A: Protamine sulfate 1mg per 100 units heparin, IV slow.
Type 1
Q: Risks of protamine administration?
A: Hypotension, bradycardia, anaphylaxis — especially in fish allergy or prior vasectomy.
Type 1
Q: Non-urgent warfarin reversal?
A: Vitamin K (phytomenadione) oral or IV; slow onset (6-12h oral, 1-2h IV); IV has anaphylaxis risk.
Type 1
Q: Urgent warfarin reversal in major bleeding?
A: 4-factor PCC (Beriplex) + IV vitamin K — faster and lower volume than FFP; contains factors II, VII, IX, X + Proteins C and S.
Type 1
Q: What reverses dabigatran major bleeding?
A: Idarucizumab (Praxbind) 5g IV — reverses within minutes; no anticoagulant effect itself.
Type 1
Q: What reverses rivaroxaban/apixaban/edoxaban major bleeding?
A: Andexanet alfa (recombinant Xa decoy); alternative = 4F-PCC 25-50 units/kg if unavailable.
Type 1
Q: How are fibrinolytics (e.g. alteplase) reversed?
A: No specific antidote — TXA + FFP/cryoprecipitate + supportive care.
Type 4
Q: HKMLE Pearl: PCC vs FFP for urgent warfarin reversal — which is preferred?
A: PCC — faster onset, lower infusion volume, more predictable factor delivery; FFP is second choice.
SECTION 11: PREGNANCY AND ANTICOAGULATION
Type 1
Q: Which anticoagulant is safe in ALL trimesters of pregnancy?
A: LMWH (e.g. enoxaparin) — does not cross the placenta.
Type 1
Q: Why is warfarin contraindicated in pregnancy?
A: Teratogen — warfarin embryopathy (nasal hypoplasia, stippled epiphyses) weeks 6-12; fetal haemorrhage risk in T3.
Type 1
Q: Why are DOACs contraindicated in pregnancy?
A: Teratogenic and cross the placenta.
Type 4
Q: HKMLE Pearl: A pregnant woman with a DVT needs anticoagulation. Only safe option?
A: LMWH throughout pregnancy — neither warfarin nor DOACs are safe.
Type 1
Q: Folate dose preconceptionally for a woman on phenytoin (high-risk)?
A: 5mg daily preconception and throughout T1.
SECTION 12: INTEGRATION PEARLS
Type 4
Q: HKMLE Pearl: Patient with mechanical mitral valve — which anticoagulant?
A: Warfarin (target INR 2.5-3.5) — DOACs are contraindicated for mechanical heart valves.
Type 4
Q: HKMLE Pearl: Patient on warfarin for AF is started on amiodarone. What happens to INR?
A: INR increases — amiodarone inhibits CYP2C9 → reduced warfarin metabolism → reduce warfarin dose.
Type 4
Q: HKMLE Pearl: LMWH vs anti-Xa monitoring — when is anti-Xa needed?
A: LMWH is not routinely monitored; use anti-Xa level in obesity, pregnancy, or renal impairment.
Type 4
Q: HKMLE Pearl: A CKD patient on EPO has sudden severe anaemia after initial improvement. Diagnosis?
A: Pure red cell aplasia (PRCA) — anti-EPO antibodies; stop EPO immediately and consider immunosuppression.
Type 4
Q: HKMLE Pearl: A patient with ITP fails steroids. What second-line options are available?
A: TPO receptor agonists (romiplostim SC or eltrombopag oral); splenectomy; rituximab.
Type 4
Q: HKMLE Pearl: How long after Hb normalises should oral iron be continued?
A: Continue for 3 months after normalisation to replenish iron stores (ferritin).
QUICK MNEMONICS SUMMARY
Type 3
Q: Master mnemonic for haematology pharmacology?
A: "WATCH A GRIP" = Warfarin, Anticoagulants, DOACs, Thrombolytics, Clot stabilisers (TXA), Heparin + DTIs, Antiplatelets, Growth factors, Reversal agents, Iron/B12/Folate, Platelets/fibrin
Type 3
Q: Mnemonic for warfarin factors blocked?
A: "1972" = factors 1 (fibrinogen), 9, 7, 2 + Proteins C and S (= II, VII, IX, X)
Type 3
Q: Mnemonic for HIT management?
A: "Stop Heparin, Start Argatroban/Fondaparinux, NO platelets, NO warfarin yet"
Type 3
Q: Mnemonic for iron absorption?
A: "Vitamin C = ↑ absorption; Tea/antacids = ↓ absorption; Ferrous > Ferric"
Type 3
Q: Mnemonic for B12 vs folate anaemia?
A: "B12 = Bad nerves (subacute combined degeneration); Folate = Fine nerves (no neuro)"
Type 3
Q: EPO target mnemonic in CKD?
A: "100-120 g/L, NOT normal" — overcorrection → VTE + CV events
Type 3
Q: G-CSF side effect mnemonic?
A: "BONE pain" — bone marrow expansion from neutrophil proliferation
END OF DECK — ~130 cards across all 12 sections
Covers: Warfarin · Heparin/LMWH · HIT · DTIs · DOACs · Antiplatelets · Thrombolytics · TXA · Iron · B12 · Folate · EPO · G-CSF · TPO agonists · Reversal Agents · Pregnancy Anticoagulation
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