Further evaluation shows decreased von Willebrand factor activity in the patient's serum. This protein normally binds to which of the following?

Question

Further evaluation shows decreased von Willebrand factor activity in the patient's serum.  This protein normally binds to which of the following?

Quizplus · Accepted Answer

11ec160b_3afc_57af_9249_d58fcc7d33d2_MD0001_00 von Willebrand factor (vWF) serves 2 important roles in hemostasis: vWF promotes platelet adhesion at sites of vascular injury by binding to and crosslinking platelet glycoproteins (primarily GpIb) with exposed collagen underneath damaged endothelium. vWF also enhances platelet aggregation, particularly under conditions of high shear stress (such as in small vessels). vWF functions as a protective carrier protein for factor VIII that increases its plasma half-life. In the absence of vWF, factor VIII is rapidly degraded in the circulation via proteolytic inactivation. (Choice B) A hemostatic fibrin polymer is the end result of the coagulation cascade. Fibrin also plays a role in inflammation and coagulation regulation. (Choice C) Prostacyclin functions both as an inhibitor of platelet aggregation and a vasodilator. (Choice D) Protein C is a vitamin K-dependent anticoagulant activated by bound thrombin in the presence of endothelial thrombomodulin. Protein C acts together with protein S to inactivate the activated forms of factors V and VIII, which are necessary for the production of thrombin. (Choice E) Thrombin is produced from prothrombin by activated factor X. Thrombin, in turn, converts fibrinogen to fibrin. Thrombin also activates factors V, VIII, and XIII. Educational objective: von Willebrand factor (vWF) functions as a promoter of platelet adhesion at sites of vascular injury by binding platelet glycoproteins to subendothelial collagen on injured blood vessel walls. It also acts as a protective carrier protein for circulating factor VIII. __________ References: Platelet adhesive dynamics. Part II: high shear-induced transient aggregation via GPIba-vWF-GPIba bridging. (http://www.ncbi.nlm.nih.gov/pubmed/18515386) The role of von Willebrand factor in thrombus formation. (http://www.ncbi.nlm.nih.gov/pubmed/17493665)

Further Evaluation Shows Decreased Von Willebrand Factor Activity in the Patient's