<P> Supplemental vitamin K (for which oral dosing is often more active than injectable dosing in human adults) reverses the vitamin K deficiency caused by warfarin, and therefore reduces the intended anticoagulant action of warfarin and related drugs . Sometimes small amounts of vitamin K are given orally to patients taking warfarin so that the action of the drug is more predictable . The proper anticoagulant action of the drug is a function of vitamin K intake and drug dose, and due to differing absorption must be individualized for each patient . The action of warfarin and vitamin K both require two to five days after dosing to have maximum effect, and neither warfarin or vitamin K shows much effect in the first 24 hours after they are given . </P> <P> The newer anticoagulants dabigatran and rivaroxaban have different mechanisms of action that do not interact with vitamin K, and may be taken with supplemental vitamin K . </P> <P> The three synthetic forms of vitamin K are vitamins K (menadione), K, and K, which are used in many areas, including the pet food industry (vitamin K) and to inhibit fungal growth (vitamin K). </P> <P> The MK - 4 form of vitamin K is produced by conversion of vitamin K in the testes, pancreas, and arterial walls . While major questions still surround the biochemical pathway for this transformation, the conversion is not dependent on gut bacteria, as it occurs in germ - free rats and in parenterally - administered K in rats . In fact, tissues that accumulate high amounts of MK - 4 have a remarkable capacity to convert up to 90% of the available K into MK - 4 . There is evidence that the conversion proceeds by removal of the phytyl tail of K to produce menadione as an intermediate, which is then condensed with an activated geranylgeranyl moiety (see also prenylation) to produce vitamin K in the MK - 4 (menatetrenone) form . </P>

Where is vitamin k produced in the body