Aspirin produces its characteristic platelet defect through irreversible acetylation of cyclooxygenase-1. Which laboratory finding best reflects this defect?

• A Absent platelet aggregation with arachidonic acid and diminished second-wave aggregation with ADP and epinephrine ✓
• B Prolonged aPTT with normal bleeding time
• C Absent ristocetin-induced platelet agglutination
• D Normal aggregation with all agonists but prolonged PT

Explanation

COX-1 inhibition blocks conversion of arachidonic acid to thromboxane B2 within platelets. Aggregation studies therefore show absent response to arachidonate and loss of the secondary wave with weak agonists such as ADP and epinephrine, since TxA2 normally amplifies their signal. Because aspirin acetylates COX irreversibly and anucleate platelets cannot resynthesize the enzyme, the effect lasts the platelet lifespan of 7 to 10 days. Coagulation times remain normal.

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.