Platelet Aggregation — MFDS Part 1 MCQ

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HardPhysiologyPlatelet AggregationMFDS Part 1

Following vascular injury, initial platelet tethering and collagen-mediated activation are intact. However, inside-out signalling cannot generate the high-affinity receptor state required for fibrinogen-dependent bridging between adjacent platelets. Which platelet glycoprotein receptor is defective?

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Correct answer: B — GPIIb/IIIa

The correct answer is **GPIIb/IIIa**, also termed integrin alphaIIb beta3. Platelet activation produces an inside-out conformational change that increases its ligand affinity. Fibrinogen can then bind GPIIb/IIIa on adjacent platelets, producing platelet aggregation and stabilising the primary haemostatic plug. GPIb instead binds von Willebrand factor and is particularly important for initial platelet capture under high shear. GPIa/IIa is integrin alpha2 beta1 and supports stable adhesion to collagen. GPVI is principally a collagen-signalling receptor that drives platelet activation and release of secondary mediators. GPV forms part of the GPIb-IX-V complex but is not the principal receptor responsible for fibrinogen-mediated platelet aggregation.

Reference: Shen R, Xu R, Lei H, Fan D. Platelet-Collagen Interactions in Hemostatic Mechanisms. Advances in Healthcare Materials. 2026;15(26):e71326. https://pubmed.ncbi.nlm.nih.gov/42251479/