Factor VI, Nonexistent
Factor VII, Proconvertin or Stable Factor
This is activated by tissue thromboplastin, which in turn activates factor X. It is a vitamin K-dependent factor.
Factor VIII, Antihemophilic
This cofactor is used for the cleavage of factor X-Xa by IXa. Factor VIII is described as VIII/vWF:VIII:C active portion, measured by clotting, VIII:Ag is the antigenic portion, vWF:Ag measures antigen that binds to endothelium for platelet function; it is deficient in hemophilia A.
Factor IX, Plasma Thromboplastin Component
A component of the thromboplastin generating system, it influences amount as opposed to rate. It is deficient in hemophilia B, also known as Christmas disease. It is sex linked and vitamin K-dependent.
Factor X, Stuart-Prower
Final common pathway merges to form conversion of prothrombin to thrombin, activity also related to factors VII and IX. It is vitamin K-dependent and can be independently activated by Russell's viper venom.
Factor XI, Plasma Thromboplastin Antecedent
Essential to intrinsic thromboplastin generating of the cascade, it has increased frequency in the Jewish population. Bleeding tendencies vary, but there is the risk of postoperative hemorrhage.
Factor XII, Hageman factor
This surface contact factor is activated by collagen. Patients do not bleed but have a tendency to thrombosis.
Factor XIII, Fibrin Stabilizing Factor
In the presence of calcium, this transaminase stabilizes polymerized fibrin monomers in the initial clot. This is the only factor that is not found in circulating plasma.
This surface contact factor is activated by kallikrein.
Prekallikrein, Fletcher Factor
This is a surface contact activator, in which 75% is bound to HMWK.
Physiological Coagulation (In Vivo)
The original theory of coagulation used a cascade or waterfall theory. This description depicted the generation of thrombin by the soluble coagulation factors and the initiation of coagulation. This theory identified two starting points for the generation of thrombin: the initiation of the Intrinsic pathway with factor XII and surface contact, and the extrinsic pathway with factor VIIa and tissue factor. These two pathways meet at the common pathway, where they both generate factor Xa from X, leading to a common pathway of thrombin from prothrombin and the conversion of fibrinogen to fibrin. This process holds true under laboratory conditions (Fig. 15.5). The discovery of a naturally occurring inhibitor of hemostasis, tissue factor pathway inhibitor (TFPI), is able to block the activity of the tissue factor VIIa complex, soon after it becomes active.14
Revised Coagulation Cascade: In Vivo Vessel injury
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