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Vitamin K is a family of structurally similar, fat-soluble vitamers found in foods and marketed as dietary supplements. [1] The human body requires vitamin K for post-synthesis modification of certain proteins that are required for blood coagulation ("K" from Danish koagulation, for "coagulation") or for controlling binding of calcium in bones and other tissues. [2]
4-Hydroxycoumarins are a class of vitamin K antagonist (VKA) anticoagulant drug molecules. Chemically, they are derived from coumarin by adding a hydroxy group at the 4 position to obtain 4-hydroxycoumarin , then adding a large aromatic substituent at the 3-position (the ring-carbon between the hydroxyl and the carbonyl).
See warfarin for a more detailed discovery history. Identified in 1940, dicoumarol became the prototype of the 4-hydroxycoumarin anticoagulant drug class . Dicoumarol itself, for a short time, was employed as a medicinal anticoagulant drug, but since the mid-1950s has been replaced by its simpler derivative warfarin , and other 4 ...
Another enzyme, Vitamin K epoxide reductase (VKORC), reduces vitamin K back to its active form. Vitamin K epoxide reductase is pharmacologically important as a target of anticoagulant drugs warfarin and related coumarins such as acenocoumarol, phenprocoumon, and dicumarol. These drugs create a deficiency of reduced vitamin K by blocking VKORC ...
The term "vitamin K antagonist" is a misnomer, as the drugs do not directly antagonise the action of vitamin K in the pharmacological sense, but rather the recycling of vitamin K. Vitamin K is required for the proper production of certain proteins involved in the blood clotting process.
A 20-year-old female college student presented with abdominal pain and blood in urine. She was tested for warfarin, a common anticoagulant also used in some rodenticides, which returned a negative result. Vitamin K and fresh plasma were administered to treat symptoms. Three weeks later, she returned with bleeding into her calf, and was ...
Gamma-glutamyl carboxylase is an enzyme that catalyzes the posttranslational modification of vitamin K-dependent proteins. Many of these vitamin K-dependent proteins are involved in coagulation so the function of the encoded enzyme is essential for hemostasis. [ 5 ]
VKAs diminish vitamin K levels in the body and inhibit the synthesis of vitamin K dependent clotting factors. [27] Thus, by inhibiting vitamin K, a key element by which the body produces clots, the risk of prolonged bleeding increases. [28] Traditionally, vitamin K has been used as a reversal agent for VKAs.
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