I truly must not have understood this concept when I studied it. I kick myself now for selling my book. Would you say that, following the definitions given below, that extrinsic hemostasis is the same as primary hemostasis and that intrinsic hemostasis is the same as secondary hemostasis. This question can be for anyone who wishes to answer. i'm having very little luck finding good websites to answer my questions...
Primary hemostasis is characterized by vascular contraction, platelet adhesion and formation of a soft aggregate plug. It begins immediately after endothelial disruption. Injury causes temporary local contraction of vascular smooth muscle. Vasoconstriction slows blood flow, enhancing platelet adhesion and activation.
Adhesion occurs when circulating von Willebrand factor(vWf) attaches to the subendothelium. Next, glycoproteins on the platelet surface adhere to the "sticky" von Willebrand factor(vWf). Platelets collect across the injured surface. These platelets are then "activated" by contact with collagen. Collagen-activated platelets form pseudopods which stretch out to cover the injured surface and bridge exposed fibers. The collagen-activated platelet membranes expose receptors which bind circulating fibrinogen to their surfaces. Fibrinogen has many platelet binding sites. An aggregation of platelets and fibrinogen build up to form a soft plug. Platelet aggregation occurs about 20 seconds after injury.
Primary hemostasis is short lived. The immediate post injury vascular constriction abates quickly. If flow is allowed to increase, the soft plug could be sheared from the injured surface, possibly creating emboli.
Secondary hemostasis is responsible for stabilizing the soft clot and maintaining vasoconstriction. Vasoconstriction is maintained by platelet secretion of serotonin, prostaglandin and thromboxane. The soft plug is solidified through a complex interaction between platelet membrane, enzymes, and coagulation factors.
Coagulation factors are produced by the liver and circulate in an inactive form until the coagulation cascade is initiated. The cascade occurs in steps. The completion of each step activates another coagulation factor in a chain reaction which leads to the conversion of fibrinogen to fibrin.