Aspirin inhibits platelet aggregation irreversibly. The reason the antiplatelet effect of a single low dose outlasts aspirin's plasma half-life of ~20 minutes is:
- A Aspirin metabolite (salicylate) continues to inhibit COX-1 in platelets
- B Aspirin binds to plasma albumin, providing a depot for slow-release onto platelets
- C Platelets are anucleate and cannot synthesize new COX-1; inhibition persists for the platelet lifespan (~7–10 days) ✓
- D Aspirin upregulates thromboxane synthetase, which paradoxically reduces TXA2
Correct answer: C. Platelets are anucleate and cannot synthesize new COX-1; inhibition persists for the platelet lifespan (~7–10 days)
Explanation
Aspirin acetylates the active-site serine of COX-1 irreversibly; because mature circulating platelets are anucleate, they cannot synthesize replacement COX-1 protein, so the inhibition persists for the entire 7–10 day platelet lifespan. The short plasma half-life of aspirin (15–20 minutes for the parent drug) is clinically irrelevant to antiplatelet duration. Only ~10% of the platelet pool is renewed each day from COX-competent megakaryocytes, so antiplatelet effect wanes gradually.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
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