Aspirin affects platelet function by interfering with platelet metabolism of:

Aspirin affects platelet function by interfering with platelet metabolism of:

• A. Lipids
• B. Cyclooxygenase
• C. Carbohydrates
• D. Nucleic acids

Answer: (B)

Aspirin’s antiplatelet effect comes from blocking the cyclooxygenase enzyme in platelets, which normally converts arachidonic acid into thromboxane A2, a key trigger of platelet activation and aggregation. By acetylating cyclooxygenase, aspirin irreversibly stops TXA2 production. Since platelets lack a nucleus, they can’t synthesize new cyclooxygenase, so the inhibition lasts for the life of the platelet (about 7–10 days), giving a lasting decrease in platelet aggregation. The other options don’t fit because aspirin doesn’t broadly disrupt lipid, carbohydrate, or nucleic acid metabolism in platelets; it specifically targets the cyclooxygenase pathway that leads to thromboxane A2.

Aspirin’s antiplatelet effect comes from blocking the cyclooxygenase enzyme in platelets, which normally converts arachidonic acid into thromboxane A2, a key trigger of platelet activation and aggregation. By acetylating cyclooxygenase, aspirin irreversibly stops TXA2 production. Since platelets lack a nucleus, they can’t synthesize new cyclooxygenase, so the inhibition lasts for the life of the platelet (about 7–10 days), giving a lasting decrease in platelet aggregation. The other options don’t fit because aspirin doesn’t broadly disrupt lipid, carbohydrate, or nucleic acid metabolism in platelets; it specifically targets the cyclooxygenase pathway that leads to thromboxane A2.