Vitamin K-Dependent Proteins in Blood Clotting

The extrinsic pathway, which is initiated by thromboplastin released from injured tissues and the protease proconvertin (Factor VII). 

The intrinsic pathway, which is initiated by the activation of Factor XII as a result of adsorption onto collagen, platelet membranes, or (under laboratory conditions) glass. 

FactorX can also be activated by kallikrein - in turn prekallikrein is activated to kallikrein by activated Factor XII, thus prolonging the initial contact activation of Factor XII. 

The intrinsic pathway is involved in the clotting of blood in glass tubes and in the undesirable intravascular clotting that results in thrombosis. Control of the clotting mechanism is thus central to hemostasis to avoid bothhemorrhage and thrombosis. 

The cascade is not a simple linear one. The concerted action of activated Factors Vlll and fX is required in the intrinsic pathway for the activation of Factor X. The rate of prothrombin activation by activated Factor X alone is inadequate to meet physiological needs an additional protein, proaccelerin or Factory, is also required. In addition to prothrombin. Factors VII, IX, and X contain y-carboxyglutamate and hence are vitamin K-dependent, as are three 

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