![]() ![]() Respiratory disorders such as tracheal or tracheobronchial calcification.Skin disorders with rashes, dermatitis (including bullous eruptions), pruritus, and alopecia.Gastrointestinal disorders including nausea, vomiting, diarrhea, taste aversions, abdominal pain, flatulence, and bloating.Hepatobiliary diseases including hepatitis and increased liver enzymes – the use of coumadin with ticlopidine at the same time has been linked to cholestatic hepatitis.Immune system disorders such as hypersensitivity/allergic responses including urticaria and anaphylactic reactions.Bruising that appears without a known cause.Vomiting blood or a substance that resembles coffee grounds.Joint pain, stiffness, or edema might occur especially after an injury.Bleeding, including menstrual bleeding that is heavier than usual.Metabolite excretion is a type of urinary excretion. Only a small amount of coumadin is eliminated unaltered in the urine. Up to 92 percent of the orally delivered dose is retrieved in urine, according to studies with radiolabeled drugs. R-coumadin has a half-life of 37 to 89 hours, while S-coumadin has a half-life of 21 to 43 hours. Because the clearance of R-coumadin is half that of S-coumadin and the volumes of distribution are identical, R-coumadin has a longer half-life than S-coumadin. 2C9 is most likely the main type of human liver P-450 that regulates coumadin’s anticoagulant action in vivo.Ĭoumadin has a terminal half-life of roughly one week following a single dose however, the effective half-life ranges from 20 to 60 hours, with a mean of about 40 hours. The isozymes of the cytochrome P-450 family that are involved in the metabolism of coumadin 2C9, 2C19, 2C8, 2C18, 1A2, and 3A4 are among them. Dehydrocoumadin, two Di stereoisomer alcohols, 4′-, 6-, 7-, 8-, and 10-hydroxycoumadin are among the coumadin metabolites that have been discovered. The majority of the metabolites are expelled primarily in the urine, but also in the bile to a lesser proportion. ![]() The anticoagulant action of coumadin alcohols is quite low. Coumadin is metabolized stereo selectively by hepatic microsomal enzymes (cytochrome P-450) to inactive hydroxylated metabolites (predominant pathway) and reduced metabolites by reductases (coumadin alcohols). Coumadin is almost totally eliminated through metabolism. ![]()
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