Aspirin irreversibly inhibits cyclooxygenase (COX) in platelets. The antiplatelet effect of a single 100 mg aspirin dose lasts for the platelet's lifetime (~10 days) because:
- A Aspirin is slowly excreted by the kidneys, maintaining plasma levels
- B The acetyl group covalently modifies platelet membrane lipids, permanently blocking thromboxane release
- C Anucleate platelets cannot synthesise new COX enzyme, so inhibition persists for platelet lifespan ✓
- D Aspirin upregulates prostacyclin synthesis, which counteracts platelet aggregation indefinitely
Correct answer: C. Anucleate platelets cannot synthesise new COX enzyme, so inhibition persists for platelet lifespan
Explanation
Aspirin covalently acetylates the serine-530 residue of COX-1 (and COX-2), irreversibly inactivating the enzyme. Because platelets are anucleate, they cannot synthesise new COX protein; thus, the inhibition persists for the entire platelet lifespan (~10 days). Nucleated vascular endothelial cells recover COX-2 activity within hours, allowing prostacyclin synthesis to resume — this differential recovery underpins aspirin's selective antiplatelet effect at low doses.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
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