Aspirin action

• A. Prev ents platelet aggregation and inhibits prostaglandin synthesis
• B. Increases platelet aggregation
• C. Inhibits angiotensin converting enzyme
• D. Blocks beta-adrenergic receptors

Answer: (C)

Aspirin works by irreversibly inhibiting the cyclooxygenase enzyme in platelets, which stops the production of thromboxane A2 and prostaglandins from arachidonic acid. The loss of thromboxane A2 prevents platelet aggregation, giving aspirin its antiplatelet effect. The reduction in prostaglandin synthesis also explains anti-inflammatory effects and some GI side effects. Because platelets are anucleate and cannot make new enzymes, this effect lasts for the platelets’ lifespan (about 7–10 days). Endothelial cells can recover COX activity, which helps limit overall disruption of prostacyclin balance with proper dosing.

The other statements don’t fit aspirin’s action: it does not increase platelet aggregation, it does not inhibit angiotensin-converting enzyme, and it does not block beta-adrenergic receptors.