Platelet Plug Formation: Adhesion

Platelets (thrombocytes) are small, anucleate fragments of megakaryocytes that adhere to exposed collagen of damaged endothelium, get activated, and aggregate to form a platelet plug (Fig. 1). Formation of the platelet plug is referred to as primary hemostasis because it is the first response to bleeding. In a normal adult, there are 150,000–450,000 platelets per μl of blood. They have a life span of up to 10 days, after which they are taken up by the liver and spleen and destroyed. Clinical laboratory tests to measure platelet number and activity are available.

Figure 35.20 Size comparison of platelets, erythrocytes, and a leukocyte.
Adhesion
Adhesion of platelets to exposed collagen at the site of vessel injury is mediated by the protein von Willebrand factor (VWF). VWF binds to collagen, and platelets bind to VWF via glycoprotein Ib (GPIb), a component of a membrane receptor complex (GPIb–V–IX) on the platelet surface (Fig. 2). Binding to VWF stops the forward movement of platelets. [Note: Deficiency in the receptor for VWF results in Bernard-Soulier syndrome, a disorder of decreased platelet adhesion.] VWF is a glycoprotein that is released from platelets. It also is made and secreted by endothelial cells. In addition to mediating the binding of platelets to collagen, VWF also binds to and stabilizes FVIII in the blood. Deficiency of VWF results in von Willebrand disease (VWD), the most common inherited coagulopathy. VWD results from decreased binding of platelets to collagen and a deficiency in FVIII (due to increased degradation). Platelets can also bind directly to collagen via the membrane receptor glycoprotein VI (GPVI). Once adhered, platelets get activated. [Note: Damage to the endothelium also exposes FIII, initiating the extrinsic pathway of blood clotting and activation of FX .]

Figure 2: Binding of platelets via the glycoprotein Ib receptor (GPIb) to von Willebrand factor (VWF). VWF is bound to the exposed collagen at a site of injury.