Coagulation factor vitamin

Aquilante, C.L. et al. Influence of coagulation factor, vitamin K epoxide reductase complex subunit 1, and cytochrome P450 2C9 gene polymorphisms on warfarin dose requirements. Clin Pharmacol Ther 2006, 79 291-302. 

Coagulation Factors II, III, VII, IX, X, XI, and Xlla fragments, thrombin, and plasmin are classified as serine proteases because each possesses a serine residue with neighboring histidine and asparagine residues at its enzymatically active site (Table 3). Factors II, VII, IX, and X, Protein C, Protein S, and Protein Z are dependent on the presence of vitamin K [84-80-0] for their formation as biologically functionally active procoagulant glycoproteins. 

Warfarin exerts its anticoagulant effect by inhibiting the production of the vitamin K-dependent coagulation factors... 

The levels of vitamin K-dependent coagulation factors are physiologically low in neonates. Absence of vitamin K impairs y-carboxylation, and the inactive precursors of factors II, VII, IX, and X accumulate in the plasma, unable to bind calcium and cell membranes. Consequently, the precursor levels may decline further, impairing coagulation and potentially leading to VKDB. 

In the future, this test may be replaced by the proteins induced by vitamin K antagonists absence (PIVKA) concentrations in serum. PIVKAs are coagulation factor precursors, normally not detectable in blood but released into the... 

The most commonly used oral anticoagulant drug in the U.S. is warfarin. It acts by altering vitamin K so that it is unavailable to participate in synthesis of vitamin K-dependent coagulation factors in the liver (coagulation factors II, VII, IX, and X). Because of the presence of preformed clotting factors in the blood, the full antithrombotic effect of warfarin therapy may require 36 to 72 h. 

Answer D. Phenyl hydantoins decrease the activity of vitamin K, which is required for the y-carboxylation of coagulation factors (11, VII, IX, X), as well as proteins C and S. 

The table also lists important globulins in blood plasma, with their mass and function. The a- and p-globulins are involved in the transport of lipids (lipoproteins see p. 278), hormones, vitamins, and metal ions. In addition, they provide coagulation factors, protease inhibitors, and the proteins of the complement system (see p. 298). Soluble antibodies (immunoglobulins see p. 300) make up the y-globulin fraction. 

Vitamin K (phylloquinone) and similar substances with modified side chains are involved in carboxylating glutamate residues of coagulation factors in the liver (see p. 290). The form that acts as a cofactor for carboxylase is derived from the vitamin by enzymatic reduction. Vitamin K antagonists (e. g., coumarin derivatives) inhibit this reduction and consequently carboxylation as well. This fact is used to inhibit blood coagulation in prophylactic treatment against thrombosis. Vitamin K deficiency occurs only rarely, as the vitamin is formed by bacteria of the intestinal flora. 

Hepatic injury Serious liver injury (eg, cirrhosis) may enhance the anticoagulant effect of lepirudin caused by coagulation defects secondary to reduced generation of vitamin K-dependent coagulation factors. 

Warfarin Vitamin Kj Stimulates coagulation factor synthesis... 

Mechanism of Action A fat-soluble vitamin that promotes hepatic formation of coagulation factors II, VII, IX, and X. Therapeutic Effect Essential for normal clotting of blood. 

Coumarins are competitive inhibitors of vitamin K, which is required for the formation in the liver of the amino acid, gamma-carboxyglutamic acid. This is necessary for the synthesis of prothrombin and factors VII, IX and X (Figure 17.1). After starting treatment the anticoagulant effect is delayed until the concentration of normal coagulation factors falls (36-72 h). The effects can be reversed by vitamin K (slow maximum effect only after 3-6 h) or by whole blood or plasma (fast). Gut bacteria synthesise vitamin K and thus are an important source of this vitamin. Consequently, antibiotics can cause excessive prolongation of the prothrombin time in patients otherwise adequately controlled on warfarin. 

Inhibits the synthesis of vitamin K-dependent coagulation factors, leading to sequential depression of Factors VII, IX, X, and II... 

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