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Pharmacology: Pharmacodynamics: Heparin inhibits reactions that lead to the clotting of blood and the formation of fibrin clots in vitro and in vivo. Heparin acts at multiple sites in the normal coagulation system. Small amounts of heparin in combination with anti-thrombin III (heparin cofactor) can inhibit thrombosis by inactivating activated Factor X and inhibiting the conversion of prothrombin to thrombin. Clotting time is prolonged by full therapeutic doses of heparin; in most cases, it is not measurably affected by low doses of heparin. Peak plasma levels of heparin are achieved 2 to 4 hours following subcutaneous administration, although there are considerable individual variations. Heparin does not have fibrinolytic activity, therefore it will not lyse existing clots.
Pharmacokinetics: Heparin is not absorbed from the gastrointestinal tract. It is extensively bound to plasma proteins following intravenous or subcutaneous injection. It does not cross the placenta and not excreted in breast milk. The half-life of heparin depends on the dose and route of administration as well as the method of calculation and is subject to wide inter- and intra-individual variation; a range of 1 to 6 hours with an average of 1.5 hours. It may be slightly prolonged in renal impairment, decreased in patients with pulmonary embolism, and either increased or decreased in patients with liver disorder. Heparin is taken up by the reticuloendothelial system. It is excreted in the urine, mainly as metabolites, although, following administration of large doses, up to 50% may excreted unchanged.
