Glanzmann thrombasthenia is a quantitative or qualitative deficiency of platelet glycoprotein IIb/IIIa (GPIIb/IIIa, integrin alphaIIbbeta3). The primary function of GPIIb/IIIa after platelet activation is:

• A Binding von Willebrand factor to mediate platelet adhesion to subendothelial collagen
• B Binding fibrinogen and von Willebrand factor to mediate platelet-platelet aggregation ✓
• C Binding ADP to amplify the platelet activation signal
• D Binding thromboxane A2 to initiate arachidonic acid release

Explanation

GPIIb/IIIa (integrin alphaIIbbeta3) is the most abundant platelet surface receptor and mediates platelet-to-platelet aggregation (the primary hemostatic plug). Upon platelet activation by ADP, thrombin, or collagen, inside-out signaling converts GPIIb/IIIa from a low-affinity to a high-affinity state, allowing binding of fibrinogen (which crosslinks adjacent platelets) and vWF. Glanzmann thrombasthenia: absent/dysfunctional GPIIb/IIIa causes failure of aggregation with normal adhesion (GPIb-vWF interaction is intact). Bernard-Soulier syndrome: deficient GPIb-IX-V causes impaired platelet adhesion to vWF.

Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.