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Antiplatelets, Anticoagulants and Thrombolysis Quiz
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Which statement best explains why a single low dose of aspirin produces a prolonged antiplatelet effect?
- A Aspirin blocks the platelet P2Y12 receptor, which takes several days to be replaced You picked ✕
- B Aspirin has a long plasma half-life, so active drug stays in the blood for several days You picked ✕
- C Aspirin irreversibly inhibits cyclo-oxygenase-1 in platelets, and platelets cannot synthesise new enzyme You picked ✓
- D Aspirin is stored inside platelets and released slowly over the following week You picked ✕
- E Aspirin reversibly inhibits cyclo-oxygenase-2 in endothelial cells, reducing prostacyclin production You picked ✕
Correct!
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The answer is C: Aspirin irreversibly inhibits cyclo-oxygenase-1 in platelets, and platelets cannot synthesise new enzyme
Explanation
Why C is correct
See Aspirin. Option C is correct because aspirin irreversibly acetylates (attaches an acetyl chemical group to) cyclo-oxygenase-1 (COX-1) in platelets. COX-1 makes thromboxane A2, the main chemical that makes platelets stick together, so blocking it reduces platelet aggregation. A platelet is a cell fragment with no nucleus, so it cannot make new COX-1 enzyme. The platelet therefore stays inhibited for its whole life of about 7 to 10 days, even though the drug itself leaves the plasma quickly (a half-life of around 20 minutes). New platelets arrive from the bone marrow each day and are not blocked, so the effect wears off gradually as the platelet population is replaced. The antiplatelet dose is much lower than the analgesic dose, typically 75 mg daily for long-term use. Aspirin is used for secondary prevention after myocardial infarction, stroke or TIA. The main adverse effects are stomach bleeding and ulcers, caused by loss of the protective effect of prostaglandins on the stomach lining. A useful way to remember it is that the drug is gone in minutes but the platelet is blocked for its life.
- Target: aspirin irreversibly acetylates COX-1 in platelets.
- Effect: less thromboxane, so less platelet aggregation.
- Duration: platelets cannot make new enzyme, so they stay blocked for their life of about 7 to 10 days.
Why the other options are incorrect
- A. Aspirin blocks the platelet P2Y12 receptor, which takes several days to be replaced: Blocking the P2Y12 receptor is the action of clopidogrel, ticagrelor and prasugrel, not aspirin. Aspirin acts on cyclo-oxygenase. Your answer
- B. Aspirin has a long plasma half-life, so active drug stays in the blood for several days: Aspirin has a short plasma half-life of around 20 minutes. The long effect is because the platelet enzyme is permanently blocked, not because the drug stays in the blood. Your answer
- D. Aspirin is stored inside platelets and released slowly over the following week: Aspirin is not stored and released. The effect is a permanent chemical change to the platelet enzyme that cannot be reversed in a cell with no nucleus. Your answer
- E. Aspirin reversibly inhibits cyclo-oxygenase-2 in endothelial cells, reducing prostacyclin production: Aspirin inhibits COX-2 as well as COX-1, but it does so irreversibly, not reversibly. Reduced prostacyclin from endothelial cells would also favour clotting, and it does not explain a prolonged antiplatelet effect. Your answer
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More questions from this set. Start the quiz to answer them and see each explanation.
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1
Which of the following oral anticoagulants directly inhibits thrombin (factor IIa)?
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2
Which drug acts by irreversibly acetylating cyclo-oxygenase-1 in platelets, leading to reduced thromboxane A2 production?
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