Glanzmann thrombasthenia specifically involves deficiency of which platelet receptor?

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Multiple Choice

Glanzmann thrombasthenia specifically involves deficiency of which platelet receptor?

Explanation:
Glanzmann thrombasthenia is defined by deficiency of the platelet receptor GPIIb/IIIa (integrin αIIbβ3), the receptor that binds fibrinogen (and von Willebrand factor) to bridge platelets together during aggregation. When this receptor is absent or dysfunctional, platelets cannot aggregate in response to most stimuli, so a patient bleeds easily despite having normal platelet counts and normal initial adhesion to exposed subendothelium. A helpful diagnostic clue is that ristocetin-induced platelet aggregation remains normal, because that pathway relies on the GPIb-IX-V complex for adhesion, not GPIIb/IIIa–mediated aggregation. Other receptors like GPIb-IX-V (defective in Bernard-Soulier), GPV, or integrin alpha2beta1 (a collagen receptor) do not explain the aggregation defect seen in Glanzmann thrombasthenia.

Glanzmann thrombasthenia is defined by deficiency of the platelet receptor GPIIb/IIIa (integrin αIIbβ3), the receptor that binds fibrinogen (and von Willebrand factor) to bridge platelets together during aggregation. When this receptor is absent or dysfunctional, platelets cannot aggregate in response to most stimuli, so a patient bleeds easily despite having normal platelet counts and normal initial adhesion to exposed subendothelium. A helpful diagnostic clue is that ristocetin-induced platelet aggregation remains normal, because that pathway relies on the GPIb-IX-V complex for adhesion, not GPIIb/IIIa–mediated aggregation. Other receptors like GPIb-IX-V (defective in Bernard-Soulier), GPV, or integrin alpha2beta1 (a collagen receptor) do not explain the aggregation defect seen in Glanzmann thrombasthenia.

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