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Pathology · Haematology: aspirin and platelet function
Sample itemA 50-year-old woman on daily low-dose aspirin has frequent nosebleeds and easy bruising. Platelet count, PT and aPTT are normal, but bleeding time is prolonged. Which mechanism accounts for this?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
B. Irreversible acetylation of platelet cyclooxygenase-1
Aspirin irreversibly acetylates COX-1 in platelets. Platelets cannot make new enzyme, so thromboxane A2 production is lost for the life of the platelet, impairing aggregation and prolonging bleeding time.
Option by option
A. Blockade of the platelet ADP receptor by a thienopyridine
ADP receptor blockade is the action of clopidogrel and related drugs, not aspirin.
B. Irreversible acetylation of platelet cyclooxygenase-1 (correct)
Correct. Platelet COX-1 acetylation abolishes thromboxane A2 synthesis for the platelet's lifespan.
C. Inhibition of vitamin K epoxide reductase
Vitamin K epoxide reductase inhibition is the action of warfarin, which prolongs the PT.
D. Neutralisation of thrombin by antithrombin
Neutralising thrombin through antithrombin is the action of heparin, which prolongs the aPTT.
Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.
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