If a patient exhibits prolonged bleeding times despite normal platelet count after taking a new medication, which mechanism of platelet aggregation is most likely inhibited?

💡 Explanation

Platelet aggregation requires fibrinogen bridging via glycoprotein IIb/IIIa receptors; therefore, inhibiting this interaction prevents proper clot formation, because the receptor binding is blocked. Thromboxane A2 synthesis, vWF binding and degranulation initiate aggregation, rather than mediate the final crosslinking.

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