Aspirin Mechanism — MFDS Part 1 MCQ

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ModeratePhysiologyAspirin MechanismMFDS Part 1

Low-dose aspirin inhibits platelet thromboxane A2 production for the lifespan of the platelet. This antiplatelet effect results principally from irreversible acetylation of which enzyme?

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Correct answer: B — Cyclooxygenase-1 (COX-1)

Explanation lettering: E = shown as A · A = shown as B · D = shown as C · B = shown as D · C = shown as E

A is correct. Aspirin irreversibly acetylates platelet cyclooxygenase-1 (COX-1), preventing formation of prostaglandin H2 and thereby reducing thromboxane A2 synthesis, platelet activation and aggregation. Platelets are anucleate and cannot synthesise replacement COX-1, so inhibition persists for their lifespan, approximately 7–10 days. COX-2 is not the principal cyclooxygenase isoform responsible for platelet thromboxane production. Phospholipase A2 acts upstream by releasing arachidonic acid from membrane phospholipids. Thromboxane synthase acts downstream by converting prostaglandin H2 to thromboxane A2 but is not aspirin's acetylated target. Lipoxygenase generates leukotrienes and related mediators rather than thromboxane.

Reference: Huczek Z et al. Aspirin and fibrin clot modulation in vascular pharmacology: Fibrinogen acetylation, disease context, and translational uncertainty. 2026. https://pubmed.ncbi.nlm.nih.gov/42437624/