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[50] [51] Other adverse effects of warfarin are associated with depletion of vitamin K, which can lead to inhibition of G1a proteins and growth arrest-specific gene 6, which can lead to increased risk of arterial calcification and heart valve, especially if too much Vitamin D is present.
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.
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).
Warfarin is indicated for the prophylaxis and treatment of venous thrombosis and its extension, pulmonary embolism; [9] prophylaxis and treatment of thromboembolic complications associated with atrial fibrillation and/or cardiac valve replacement; [9] and reduction in the risk of death, recurrent myocardial infarction, and thromboembolic events such as stroke or systemic embolization after ...
Lengyel M (December 2004). "[Warfarin or acenocoumarol is better in the anticoagulant treatment of chronic atrial fibrillation?]". Orvosi Hetilap. 145 (52): 2619– 2621. PMID 15724697. Ufer M (2005). "Comparative pharmacokinetics of vitamin K antagonists: warfarin, phenprocoumon and acenocoumarol". Clinical Pharmacokinetics. 44 (12): 1227– 1246.
In enzymology, a vitamin-K-epoxide reductase (warfarin-sensitive) (EC 1.17.4.4) is an enzyme that catalyzes the chemical reaction 2-methyl-3-phytyl-1,4-naphthoquinone + oxidized dithiothreitol ⇌ {\displaystyle \rightleftharpoons } 2,3-epoxy-2,3-dihydro-2-methyl-3-phytyl-1,4-naphthoquinone + 1,4-dithiothreitol
Prior to the introduction of direct factor Xa inhibitors, vitamin K antagonists such as warfarin were the only oral anticoagulants for over 60 years, and together with heparin have been the main blood thinners in use. People admitted to hospital requiring blood thinning were started on an infusion of heparin infusion, which thinned blood ...
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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