Aspirin at 75 mg daily inhibits platelet aggregation selectively while sparing prostacyclin production by vascular endothelium. The pharmacological basis for this selectivity is:

• A Anucleate platelets cannot resynthesise cyclooxygenase, whereas endothelial cells can ✓
• B Endothelial COX-1 has a different active site structure than platelet COX-1
• C Low-dose aspirin undergoes presystemic acetylation of platelets in portal blood
• D Prostacyclin synthase is resistant to aspirin

Explanation

Aspirin irreversibly acetylates a serine residue of COX-1. Platelets are anucleate and cannot synthesise new enzyme, so a single dose suppresses thromboxane B2 production for their 7 to 10 day lifespan. Endothelial cells have nuclei and resynthesise COX within hours, restoring prostacyclin output. Presystemic exposure in portal blood contributes to this selectivity but the core explanation is irreversible inhibition plus absent platelet protein synthesis, making A the best answer.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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