Paper I
2018 February (2010 Scheme) · 40 marks · 120 min

Question

Rationale of using low dose aspirin in post myocardial infarction.

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Answer

Low-dose aspirin irreversibly inhibits COX-1 in platelets (which lack nuclei and cannot resynthesize the enzyme), blocking thromboxane A2 synthesis and platelet aggregation for the lifespan of the platelet (~7–10 days) with a single small dose. At low doses, this antiplatelet effect is achieved while relatively sparing vascular endothelial COX-mediated prostacyclin (PGI2) synthesis (which itself inhibits platelet aggregation and is desirable to preserve). This makes low-dose aspirin effective for secondary prevention of recurrent myocardial infarction/thrombotic events, by reducing platelet-mediated thrombus formation on the injured/atherosclerotic coronary endothelium.

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