Anticoagulation & thrombosis flashcards
26 high-yield MRCP Part 1 cards from the Intellect Medicos Haematology & Oncology course. Try to answer each question before you open it — then study them properly with spaced repetition, which brings each card back just before you would forget it.
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What is the mechanism of action of warfarin?
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It inhibits vitamin K epoxide reductase, reducing synthesis of factors II, VII, IX and X and proteins C and S.
Why? These factors need active vitamin K for hepatic synthesis. The INR rises first because factor VII has the shortest half-life (about 6 hours).
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Name three drugs that raise the INR in a patient taking warfarin.
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Any three of: amiodarone, ciprofloxacin, macrolides (clarithromycin, erythromycin), metronidazole, co-trimoxazole, azole antifungals (fluconazole, miconazole).
Why? Most inhibit CYP450 metabolism of warfarin; metronidazole and co-trimoxazole inhibit clearance of the more active S-isomer.
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A patient on warfarin has a major bleed. What is the immediate reversal?
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Stop warfarin; give IV vitamin K 5 mg (slowly) plus 4-factor prothrombin complex concentrate (PCC).
Why? PCC replaces factors II, VII, IX and X within minutes; vitamin K keeps the correction going after PCC wears off.
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INR is 9.0 on warfarin and the patient is NOT bleeding. What is the management?
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Stop warfarin and give oral vitamin K 1–5 mg; repeat vitamin K if the INR is still high after 24 h; restart warfarin when INR <5.
Why? Oral vitamin K corrects the INR over about a day without the risks of IV dosing or over-correction.
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Name two situations in which warfarin is preferred over a DOAC.
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Mechanical heart valves and antiphospholipid syndrome (especially triple-positive).
Why? DOACs have more thrombotic events in these groups; warfarin remains the standard of care.
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How does heparin produce its anticoagulant effect, and how do UFH and LMWH differ in their targets?
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It potentiates antithrombin. UFH inhibits both thrombin (IIa) and Xa; LMWH acts mainly on Xa.
Why? The heparin–antithrombin complex inactivates clotting factors far faster than antithrombin alone.
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Seven days after starting unfractionated heparin post-operatively, a patient's platelets fall from 280 to 110 × 10⁹/L and she develops a new DVT. What is the immediate management?
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Stop ALL heparin (UFH and LMWH) and start a non-heparin anticoagulant such as argatroban (or danaparoid, fondaparinux or bivalirudin).
Why? Heparin-induced thrombocytopenia type 2 is caused by IgG antibodies against heparin–PF4 complexes that activate platelets — it is prothrombotic despite the low platelets.
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What is the specific reversal agent for dabigatran?
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Idarucizumab.
Why? It is a monoclonal antibody fragment that binds dabigatran, a direct thrombin (IIa) inhibitor.
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What is the specific reversal agent for apixaban or rivaroxaban?
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Andexanet alfa.
Why? It is a modified, inactive factor Xa that acts as a decoy and binds the Xa inhibitor.
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What is the first-line long-term anticoagulant after venous thrombosis in antiphospholipid syndrome?
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Lifelong warfarin, target INR 2–3.
Why? Warfarin is the most proven option for preventing recurrent thrombosis in APS.
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A woman with antiphospholipid syndrome and previous miscarriages is now pregnant. What is the treatment?
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Low-dose aspirin (from a positive pregnancy test) plus prophylactic LMWH (once the fetal heart is confirmed).
Why? This combination improves live birth rates in obstetric APS.
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What is the most common inherited thrombophilia, and what is its mechanism?
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Factor V Leiden: the mutant factor V resists inactivation by activated protein C.
Why? Factor Va stays active for longer, so thrombin generation is increased and recurrent VTE results.
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Suspected DVT with a two-level Wells score of 2 or more ("DVT likely"). What is the first-line investigation?
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Proximal leg vein ultrasound, ideally within 4 hours.
Why? Ultrasound directly confirms or excludes proximal DVT when pre-test probability is high.
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Suspected PE with a two-level Wells score above 4 ("PE likely"). What is the first-line imaging?
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CT pulmonary angiogram (CTPA).
Why? CTPA directly shows emboli in the pulmonary arteries.
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What is the first-line anticoagulant for most adults with confirmed DVT or PE (NICE)?
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A DOAC: apixaban or rivaroxaban.
Why? They need no initial LMWH, no INR monitoring and have fewer interactions than warfarin.
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Why is warfarin avoided in pregnancy, especially in the first trimester?
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It is teratogenic — warfarin embryopathy (nasal hypoplasia, stippled epiphyses, limb defects).
Why? Warfarin crosses the placenta; the risk is greatest at about 6–12 weeks, and later it can cause fetal bleeding.
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What is the first-line treatment for VTE diagnosed during pregnancy?
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Weight-based therapeutic LMWH for the rest of pregnancy and at least 6 weeks postpartum (minimum 3 months in total).
Why? LMWH does not cross the placenta and is effective and safe in pregnancy; DOACs and warfarin are avoided.
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Type 2 heparin-induced thrombocytopenia typically starts ______ after heparin is begun (earlier if heparin was given in the previous 100 days).
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5–10 days
Why? It takes several days to make IgG antibodies against heparin–PF4 complexes; with recent exposure, antibodies may already be present.
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What is the mechanism of action of fondaparinux?
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A synthetic pentasaccharide that binds antithrombin and selectively increases its inhibition of factor Xa (indirect Xa inhibitor).
Why? It contains heparin's antithrombin-binding sequence but is too short to bridge thrombin, so it acts only on Xa.
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Which drugs should not be co-prescribed with apixaban or rivaroxaban because they markedly lower DOAC levels?
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Strong CYP3A4 and P-glycoprotein inducers — e.g. rifampicin, carbamazepine, phenytoin, St John's wort.
Why? Induction speeds DOAC metabolism and efflux, risking treatment failure and thrombosis.
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What is the first-line anticoagulant for proximal DVT or PE in a patient with active cancer (NICE)?
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A DOAC (e.g. apixaban or rivaroxaban), usually for 3–6 months; LMWH if a DOAC is unsuitable.
Why? DOACs are at least as effective as LMWH in cancer-associated thrombosis and avoid daily injections.
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Confirmed PE with haemodynamic instability (persistent hypotension). What is the first-line treatment?
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Systemic thrombolysis (e.g. alteplase), with unfractionated heparin.
Why? Rapid clot lysis relieves right ventricular outflow obstruction in high-risk (massive) PE.
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Which routine clotting test is paradoxically prolonged in antiphospholipid syndrome?
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The APTT.
Why? The lupus anticoagulant interferes with phospholipid-dependent clotting tests in the laboratory, yet promotes thrombosis in the body.
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Which DOAC depends most on renal excretion and is contraindicated when creatinine clearance is below 30 mL/min?
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Dabigatran (about 80% renally excreted).
Why? Because most of the drug leaves via the kidney, it accumulates quickly in renal impairment and bleeding risk rises.
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Which estimate of renal function should be used to adjust DOAC doses (MHRA)?
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Creatinine clearance calculated with the Cockcroft–Gault equation — not eGFR.
Why? DOAC licensing trials used Cockcroft–Gault creatinine clearance; eGFR can overestimate renal function in older, low-weight patients and lead to overdosing.
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In atrial fibrillation, apixaban is reduced to 2.5 mg twice daily if at least two of these apply: age ______, weight ______, serum creatinine ______.
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80 years or over; 60 kg or less; 133 µmol/L or more
Why? These factors raise apixaban exposure and bleeding risk; the standard AF dose is 5 mg twice daily.