Nov 01, 2010
Hemostasis has three stages: platelet plug formation (primary hemostasis), platelet plug stabilization with cross-linked fibrin (secondary hemostasis), and clot breakdown (fibrinolysis).
Under normal conditions, platelets adhere to damaged subendothelium through the interaction of various ligands and receptors. After platelets adhere, they change shape to facilitate cross-bridging, which leads to platelet activation. Platelet activation involves the release and synthesis of agonists (adenosine diphosphate, serotonin, epinephrine, platelet-activating factor, and thromboxane A2) from the platelets, which recruit additional platelets and promote further adhesion and activation.1Platelet activation can also occur independently of aggregation in the presence of thrombin. Thrombin is a potent platelet activator, and inflammation may trigger thrombin production and circulation and lead to widespread platelet activation.2 The activated platelet membranes provide a framework for the assembly of coagulation factors and catalyze fibrinogen's conversion to fibrin.1
Initiation involves the exposure of tissue factor to blood after endothelial damage. Circulating activated factor VII then binds to tissue factor, leading to activation of the common pathway and a small amount of thrombin production. The small amount of thrombin produced by this reaction is then free to activate platelets as well as start the amplification phase.
In the propagation phase, fibrinogen is cleaved into fibrin, which is further cross-linked by factor XIII, resulting in stable thrombus formation.2 Many of these processes occur on the activated platelet surface.