Aspirin impairs platelet function by which mechanism?

Aspirin impairs platelet function by which mechanism?

• A. Impairs von Willebrand factor via GPIb/IX/V receptor
• B. Decreased amounts of arachidonic acid
• C. Inactivating cyclooxygenase which blocks thromboxane A2
• D. Inactivation of ADP and phospholipase A2

Answer: (C)

Aspirin works by irreversibly inhibiting cyclooxygenase-1 in platelets, which stops the conversion of arachidonic acid into prostaglandin H2 and, subsequently, thromboxane A2. Thromboxane A2 is a powerful promoter of platelet activation and aggregation, so blocking its production reduces platelet function. Because platelets lack nuclei, they cannot synthesize new cyclooxygenase, so the effect lasts for the platelets’ lifespan (about 7–10 days) until new platelets are made. Endothelial cells can produce new cyclooxygenase and prostacyclin, but the net result still favors reduced platelet aggregation. The other options don’t fit aspirin’s action: it doesn’t directly affect von Willebrand factor or GPIb/IX/V, it doesn’t deplete arachidonic acid, and it doesn’t inactivate ADP or phospholipase A2.

Aspirin works by irreversibly inhibiting cyclooxygenase-1 in platelets, which stops the conversion of arachidonic acid into prostaglandin H2 and, subsequently, thromboxane A2. Thromboxane A2 is a powerful promoter of platelet activation and aggregation, so blocking its production reduces platelet function. Because platelets lack nuclei, they cannot synthesize new cyclooxygenase, so the effect lasts for the platelets’ lifespan (about 7–10 days) until new platelets are made. Endothelial cells can produce new cyclooxygenase and prostacyclin, but the net result still favors reduced platelet aggregation. The other options don’t fit aspirin’s action: it doesn’t directly affect von Willebrand factor or GPIb/IX/V, it doesn’t deplete arachidonic acid, and it doesn’t inactivate ADP or phospholipase A2.