Search results
Results from the WOW.Com Content Network
The deficiency leads to decreased activity in the intrinsic pathway (F-IX) factors, monitored by PTT, and the extrinsic pathway (F-VII) which PT monitors. However, factor VII has the shortest half-life of all the factors carboxylated by vitamin K; therefore, when deficient, it is the PT that rises first, since the activated Factor VII is the ...
Factor VII deficiency is a bleeding disorder characterized by a lack in the production of Factor VII (FVII) (proconvertin), a protein that causes blood to clot in the coagulation cascade. After a trauma factor VII initiates the process of coagulation in conjunction with tissue factor (TF/factor III) in the extrinsic pathway. [citation needed]
The action of the factor is impeded by tissue factor pathway inhibitor (TFPI), which is released almost immediately after initiation of coagulation. Factor VII, which was discovered around 1950, is vitamin K-dependent and produced in the liver. Use of warfarin or similar anticoagulants decreases hepatic synthesis of FVII. [citation needed]
To avoid a vitamin K deficiency, eat foods high in vitamin K1, including leafy green veggies, broccoli, edamame, pumpkin, and pomegranate juice and those high in vitamin K2, including dark-meat ...
If the mixing study shows correction and no prolongation with incubation, factor deficiency should be looked for, starting with VIII and IX. Vitamin K-dependent and nonvitamin K–dependent factors should be considered to rule out vitamin K deficiency, or accidental or surreptitious warfarin ingestion.
Vitamin K is an essential factor to the hepatic gamma-glutamyl carboxylase that adds a carboxyl group to glutamic acid residues on factors II, VII, IX and X, as well as Protein S, Protein C and Protein Z. In adding the gamma-carboxyl group to glutamate residues on the immature clotting factors, Vitamin K is itself oxidized.
Factor VII has a short half-life and the carboxylation of its glutamate residues requires vitamin K. The prothrombin time can be prolonged as a result of deficiencies in vitamin K, warfarin therapy, malabsorption, or lack of intestinal colonization by bacteria (such as in newborns). In addition, poor factor VII synthesis (due to liver disease ...
The availability of reduced vitamin K is of importance for activation vitamin K 2,3-epoxide. The reduction of vitamin K epoxide is then responsible for the carboxylation of glutamic acid residues in some blood-clotting proteins, including factor VII, factor IX, and factor X. [5] [7] VKORC1 is of therapeutic interest both for its role in ...