Aspirin 81 mg inhibits platelet COX-1 irreversibly, while COX-1 in gastric mucosa is also inhibited. However, gastric mucosa recovers faster than platelets. Why?
- A Gastric mucosal cells have higher COX-2 expression to compensate for COX-1 loss
- B Enteric coating of aspirin reduces bioavailability to gastric mucosa but not to platelets
- C Gastric mucosal cells are nucleated, can synthesise new COX-1 protein within hours; anucleate platelets cannot and must wait for new platelet release (~7–10 days) ✓
- D Acetyl group is deacetylated rapidly in gastric mucosa, restoring COX activity faster
Correct answer: C. Gastric mucosal cells are nucleated, can synthesise new COX-1 protein within hours; anucleate platelets cannot and must wait for new platelet release (~7–10 days)
Explanation
Aspirin irreversibly acetylates the serine residue (Ser530) of COX-1. Nucleated gastric mucosal cells can transcribe and synthesise new COX-1 protein within hours, restoring prostaglandin synthesis and mucosal protection. Anucleate platelets lack this ability and depend on new platelet release from megakaryocytes, which takes 7–10 days, explaining the lasting antiplatelet effect versus faster gastric recovery.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.