A clot retraction defect is most likely due to

• A. Lack of platelet receptor glycoprotein Ib
• B. Lack of platelet receptor glycoprotein IIb/IIIa
• C. Insufficient ADP in dense bodies
• D. Absence of von Willebrand factor

Answer: (B)

Clot retraction happens when platelets pull on the fibrin network using their contractile machinery, and this process depends on platelets being able to form stable links between each other through fibrinogen bridges. The receptor that mediates these fibrinogen bridges is GPIIb/IIIa on the platelet surface. If this receptor is absent or nonfunctional, platelets can’t crosslink via fibrinogen, so the platelets can’t generate the pulling forces needed to retract the clot effectively. This is classic for a defect in GPIIb/IIIa, as seen in Glanzmann thromboasthenia, where clot retraction is impaired despite other platelet functions being variably affected.

Lack of GPIb would disrupt initial platelet adhesion to von Willebrand factor, not the retraction mechanism itself. Absence of von Willebrand factor causes a broader defect in primary hemostasis rather than a focused retraction issue. Insufficient ADP in dense bodies impairs platelet activation and aggregation but doesn’t specifically explain a failure of the contraction-driven retraction process mediated by GPIIb/IIIa–fibrinogen interactions.