Prostacyclin and thromboxane A2 exert opposing effects on hemostasis. Their opposing actions depend chiefly on their differing sites of production because:

• A Platelets lack cyclooxygenase-1 and use only cyclooxygenase-2
• B Thromboxane A2 is degraded within seconds whereas prostacyclin persists for hours
• C Endothelium expresses prostacyclin synthase while platelets express thromboxane synthase ✓
• D Aspirin irreversibly inhibits prostacyclin synthase but not thromboxane synthase

Explanation

Both mediators derive from the same prostaglandin endoperoxide intermediates PGH2, but platelets contain thromboxane synthase yielding TXA2, a vasoconstrictor and platelet aggregator, while endothelial cells contain prostacyclin synthase yielding PGI2, a vasodilator and inhibitor of aggregation. Low-dose aspirin spares endothelial COX-2 because endothelial cells can resynthesize the enzyme, preserving PGI2 while permanently disabling platelet TXA2 synthesis.

Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.