Which coagulation factors require vitamin k

Thrombocytopenia causes more severe issues with blood clotting as the platelet plug will not be able to form or activate the coagulation cascade.

Learning Objectives Describe the role of vitamin K in hemostasis. Key Points Vitamin K is involved in the synthesis of many factors of the coagulation cascade. Vitamin K is antagonized inhibited by the anticoagulant drug warfarin.

Calcium and phospholipids are needed to activate tenase, which converts prothrombin to thrombin. Both calcium and vitamin K are needed to synthesize Protein C, an anticoagulant that prevents excessive coagulation after the coagulation cascade occurs. Deficiency of any of these clotting cofactors will cause an impaired ability for blood to coagulate, which can contribute to excessive bleeding and hemorrhage.

There are also useful clinical and laboratory implications involved. The occurrence of venous thrombosis at a young age is important. Similarly, important is the observation that venous thrombosis may be present in a family in association with decreased prothrombin activity as seen in dysprothrombinemias.

It remains now to be seen whether other clotting factors, for example, FX and Protein Z, might show similar features. The sol to gel transformation of blood is still, after so many years, a material for study. These studies on the prothrombin complex have further shown the complexity of the relation existing among clotting factors.

The prothrombin complex could be envisaged as one of the homeostatic mechanisms in blood coagulation. No grant number, only secretarial support. This article does not contain any study with human participants performed by any of the authors.

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Keywords: prothrombin complex, vitamin K, bleeding, thrombosis. Classification Vitamin K-dependent coagulation proteins should be divided today into 1 conditions associated only with bleeding FX ; 2 those associated with both bleeding and thrombosis FII, FVII, and FIX ; 3 those associated only with thrombosis, protein C and protein S ; and, finally, 4 those probably associated with neither bleeding nor thrombosis protein Z 9 ; Table 1.

Table 1. Open in a separate window. Table 2. Conditions not Associated With Bleeding and Thrombosis: Protein Z Deficiency Belongs to This Group Protein Z deficiency Protein Z deficiency should also be mentioned here, since a few sporadic observations or articles have suggested but not proven the possibility that this factor plays a role in blood coagulation.

References 1. Hemostasis and Thrombosis: basic principles and clinical practice. Thrombosis of abdominal aorta in congenital afibrinogenemia: case report and review of literature.

Wada Y, Lord ST. Dusart syndrome: a new concept of the relationship between fibrin clot architecture and fibrin clot degradability: hypofibrinolysis related to an abnormal clot structure.

Thrombosis from a prothrombin mutation conveying antithrombin resistance. Perry DJ. Factor VII Deficiency. Br J Haematol. Congenital bleeding disorders of the vitamin K-dependent clotting factors. Vitam Horm. Congenital deficiencies and abnormalities of prothrombin. Blood Coagul Fibrinolysis. Eur J Haematol. Associated prothrombotic conditions are probably responsible for the occurrence of thrombosis in almost all patients with congenital FVII deficiency.

Critical review of the literature. J Thromb Thrombolysis. Complex history of the discovery and characterization of congenital factor X deficiency. Semin Thromb Hemost. Uprichard J, Perry DJ.

Factor X deficiency. Blood Rev. In , it was demonstrated that the mutation ArgLeu in exon 8 of FIX was associated with the appearance of a thrombophilic state and venous thrombosis. Both these mutations are type 2 defects, namely, they show low activity but normal or near-normal FVII antigen.

Both are quinone derivatives. The structure of vitamin K 1 is depicted below. Vitamin K serves as an essential cofactor for a carboxylase that catalyzes carboxylation of glutamic acid residues on vitamin K-dependent proteins. The key vitamin K-dependent proteins include:. These proteins have in common the requirement to be post-translationally modified by carboxylation of glutamic acid residues forming gamma-carboxyglutamic acid in order to become biologically active.