There are three components of hemostasis: primary, secondary, and fibrinolysis. The primary hemostasis has two parts that is the interaction between platelets and endothelial cells, which are the vascular part and the platelet plug. In the vascular part, there is a production of factor VIII and von Willebrands factor by endothelial cells. There is also a vascular spasm that is stimulated by sympathetic nerves that causes constriction of smooth muscles. The second part of the primary hemostasis is the platelet plug, which has three different parts: adhesion, aggregation, and secretion.
Adhesion is the platelets attaching to the subendothelial collagen. Aggregation is the platelets sticking together. Secretion of thromboxane, platelet phospholipids, von Willebrands factor, and platelet dervided growth factor all help form the platelet plug. Thromboxane causes vasoconstriction and further platelet aggregation. Platelet phospholipids help to stimulate and amplify coagulation cascade. Von Willebrands factor is needed for the coagulation cascade to occur. Platelet dervided growth factor is for neovascularization. The secondary hemostasis includes the formation of fibrin to stabilize the primary hemostatic plug.
It requires soluble coagulation factors and cofactors, which depends on whether it is an extrinsic or intrinsic pathway. Extrinsic pathways require a tissue factor for activation and it reacts specifically to factor VII. Intrinsic pathways have all components necessary available in the blood (factors XII, XI, IX, VIII). These factors are produced by the liver and endothelium/platelets and are activated by contact with collagen, endotoxin platelet products, and other negatively charged substances. When the intrinsic and extrinsic pathways converge, it is called the common pathway.
The final product is a stable fibrin clot which seals larger blood vessel defects, such as my hanging finger. The last step of hemostasis is the fibrinolysis. During fibrinolysis, plasminogen that is present in the plasma and platelet membranes are activated into plasmin within the clot when it binds to fibrin. This bound plasmin hydrolyzes fibrin producing fibrin degradation products. Fibrin degradation products have anticoagulant activity, which blocks thrombin and inhibits platelets from sticking to each other. Eventually the fibrin degradation products are cleared by the liver.