What is the effect of aspirin on platelets and its clinical use?

• A. Reversibly inhibits COX-2, reducing inflammation.
• B. Irreversibly inhibits COX-1, reducing thromboxane A2 and platelet aggregation; used in cardiovascular risk prevention; GI bleeding risk.
• C. Inhibits platelet production in the bone marrow.
• D. Increases platelet aggregation.

Answer: (B)

Aspirin’s effect on platelets comes from irreversibly inhibiting COX-1 in platelets, which blocks the production of thromboxane A2, a substance that promotes platelet activation and clumping. Because platelets don’t have a nucleus, they can’t replace COX-1 once it’s acetylated, so the anti-platelet effect lasts for the platelet’s entire lifespan (about 7–10 days). This lasting reduction in platelet aggregation is why low-dose aspirin is used to prevent cardiovascular events in people at risk. At the same time, blocking thromboxane and other prostaglandins can increase the risk of GI bleeding, since prostaglandins help protect the stomach lining. The other ways described don’t fit aspirin’s main action on platelets: it doesn’t reversibly inhibit COX-1 in a rapid, short-lived way for this purpose, it doesn’t stop platelet production in the bone marrow, and it doesn’t increase platelet aggregation.