How does aspirin reduce thrombosis risk?

• A. Increases plasminogen activation.
• B. Irreversibly inhibits COX-1 (and to a lesser extent COX-2) in platelets, decreasing thromboxane A2 production and platelet aggregation.
• C. Inhibits ADP receptor P2Y12.
• D. Blocks fibrinogen binding to GPIIb/IIIa.

Answer: (C)

Aspirin lowers thrombosis risk by irreversibly inhibiting COX-1 in platelets, which cuts down the production of thromboxane A2, a key molecule that promotes platelet activation and aggregation. Because platelets have no nucleus, they can’t make new COX-1, so the inhibitory effect persists for the lifespan of the platelet, reducing the tendency for platelets to clump together. Endothelial cells can still synthesize new COX enzymes and produce prostacyclin (PGI2), which helps oppose platelet activation, so the overall effect favors less clot formation, especially with low-dose aspirin that mainly affects platelets.

The other options describe different antiplatelet or fibrinolytic actions that are not how aspirin works: increasing plasminogen activation would enhance clot breakdown rather than prevent formation; inhibiting the ADP receptor P2Y12 is the mechanism of drugs like clopidogrel; blocking fibrinogen binding to GPIIb/IIIa is how GP IIb/IIIa inhibitors work.