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Physiology of hemostasis
Abstract
Background
Hemostasis is a physiologic process involving platelets, coagulation and fibrinolysis proteins, and blood vessels that maintain blood in the fluid state under normal conditions but rapidly form a blood clot at sites of injury. Intact endothelial cells lining the blood vessels prevent activation of platelets and coagulation factors. When an injury occurs, platelets and coagulation factors form a blood clot to prevent hemorrhage. Blood clots must be limited to the site of injury to prevent intravascular clotting; therefore coagulation and platelet activation is highly regulated. This chapter sets the stage for discussions of pathophysiology and laboratory testing in subsequent chapters.
Content
This chapter describes the basic roles and interactions of platelets, coagulation factors, and blood vessels/endothelium in hemostasis. Blood vessels contract to slow down bleeding, and the subendothelial matrix provides stimuli for platelet adhesion and coagulation. Primary hemostasis refers to the platelets’ response at the site of injury that results in a platelet plug. The plasma coagulation cascade is initiated by tissue factor exposed at the injury site and is propagated by a complex cascade of reactions resulting in a fibrin clot on top of the platelet plug. Fibrinolysis cleaves the fibrin clot into soluble fragments and begins the healing process. Endothelial cells participate in the regulation of hemostasis through secretion of molecules and complex interactions on the endothelial surface. Basic molecular mechanisms and cell interactions involved in the regulation of primary hemostasis, plasma coagulation, and fibrinolysis are described below.
Hemostasis
Hemostasis is the mechanism of preventing excessive exsanguination after a traumatic injury. The mechanism leads to the production of a hemostatic plug at the site of an injury and the eventual dissolution of the blood clot to allow healing. It is well recognized that the process may hypofunction, leading to a bleeding diathesis, or it may hyperfunction, leading to formation of a potentially life-threatening blood clot in a blood vessel (thrombosis). For purposes of discussion, hemostasis is often divided into three contributing components: (1) platelets, (2) plasma proteins, and (3) blood vessels. These contributors do not act separately but are simultaneously activated and mutually dependent on one another. Primary hemostasis results in an initial platelet plug, then coagulation produces a fibrin meshwork that forms the clot, and finally, fibrinolysis breaks the clot up so healing can continue. In order to prevent widespread thrombosis and bleeding, numerous mechanisms keep coagulation and fibrinolysis localized to the site of injury. Localization of coagulation is facilitated by the platelet, serving as the template for coagulation, and by the inactivation of any circulating activated factors in downstream capillary beds. Similarly, the fibrin clot provides binding sites for many of the fibrinolytic enzymes, and excess circulating profibrinolytic enzymes are neutralized and cleared.
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