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Coagulation defects

Antihemophilic factor [9001-28-9] (AHF) is a protein found in normal plasma that is necessary for clot formation. It is needed for transformation of prothrombin to thrombin. Administration of AHF by injection or infusion can temporarily correct the coagulation defect present in patients with hemophilia. Antihemophilic factor VIII (Alpha Therapeutic) has been approved by the FDA as replacement therapy in patients with hemophilia B to prevent bleeding episodes, and also during surgery to correct defective hemostasis (178). [Pg.311]

Hepatic injury Serious liver injury (eg, cirrhosis) may enhance the anticoagulant effect of lepirudin caused by coagulation defects secondary to reduced generation of vitamin K-dependent coagulation factors. [Pg.149]

Hematologic effects Aspirin interferes with hemostasis. Avoid use if patients have severe anemia, history of blood coagulation defects, or take anticoagulants. Long-term therapy To avoid potentially toxic concentrations, warn patients on long-term therapy not to take other salicylates (nonprescription analgesics, etc). Salicylism Salicylism may require dosage adjustment. [Pg.914]

O. Smithies, B.H. Koller, T.M. Coffman, Coagulation defects and altered hemodynamic responses in mice lacking receptors for thromboxane A2,J. Clin. Invest. 102(1998) 1994. [Pg.654]

Vision and hearing alterations, seizures, liverfailure, coagulation defects, multiple organ failure, and sepsis maybe noted. [Pg.73]

Adverse effects include nausea, vomiting, headache, fever, abdominal pain, hyperglycemia leading to coma, hypersensitivity, renal damage, coagulation defects, thrombosis, CNS depression or hyperexcitability and acute haemorrhagic pancreatitis. [Pg.378]

Clinical pharmacology Activated factor IX in combination with activated factor VIII activates factor X. This results ultimately in the conversion of prothrombin to thrombin. Thrombin then converts fibrinogen to fibrin, and a clot can be formed. Factor IX is the specific clotting factor deficient in patients with hemophilia B and in patients with acquired factor IX deficiencies. The administration of Coagulation Factor IX (Recombinant) increases plasma levels of factor IX and can temporarily correct the coagulation defect in these patients. [Pg.145]

Coagulation defects have been noted with severe hypothermia. These defects include platelet dysfunction, increased fibrinolytic activity, and decreased enzymatic activity necessary for clotting to occur (48,49). However, even mild surface cooling may produce a reversible platelet defect (48,50,51). Mild hypothermia typically reduces metabolism and hepatic clearance of various anesthetic agents and other medications (52). This must be taken into consideration when formulating an anesthetic plan for the hypothermic patient. [Pg.109]

Allergic disorders, pregnancy and lactation - manufacturers advise to avoid use, coagulation defects, renal, hepatic and cardiac impairment, the elderly, epilepsy, parkinsonism, psychiatric disturbance... [Pg.262]

Renal, hepatic and cardiac impairment including cardiac failure, LV dysfunction, dehydration, hypertension, oedema and patients with risk factors for developing heart disease, the elderly, in coagulation defects... [Pg.263]

Diclofenac is contraindicated in those with a history of hypersensitivity to aspirin or another NSAID, severe heart failure, patients with previous or active peptic ulceration, or porphyria. It should be avoided in pregnancy. It should be used with caution in patients with allergic disorders, renal, hepatic and cardiac impairment, the elderly, in lactation and in those with coagulation defects. [Pg.267]

Thrombocytopenia Prolonged hypoglycemia Lactic acidosis Fatal Acidosis Infertility Hypodiyroidism Coagulation defects Wididrawal syndrome Neonatal bleeding, deadi Hypodiermia Behavioral changes Retarded development Neonatal depression Wididrawal symptoms Wididrawal syndrome... [Pg.247]

A review of 253 cases of Budd-Chiari syndrome found COC use to be the presumed cause in 9% of patients [29]. There appears to be a correlation between the development of BCS and the oestrogenic component of COCs [12]. Obstruction of the hepatic and portal veins has been documented and has been attributed to the thrombotic effects of the COCs however, the affected women may have had an underlying coagulation defect [16]. Budd-Chiari patients should be advised not to use COCs, as such patients have a demonstrated haematological tendency to form thrombi, and oestrogen-containing contraceptives may increase the risk of recurrent thrombosis [2]. [Pg.285]

Frozen fresh plasma is used in cases of higher blood losses (>50%), or even earlier if necessary (e.g. in the presence of concomitant coagulation defects), (s. p. 346)... [Pg.351]

Vitamin E is considered nontoxic at levels up to 3200 mg/day. It has not been found to be teratogenic, mutagenic, or carcinogenic at doses below 1 g/kg of body weight. Vitamin E can heighten the effect of vitamin K deficiency (coagulation defect) or anticoagulation therapy. A recent study, however, indicates that it may be the oxidation product a-tocoquinone that causes the effect (46). [Pg.148]

Albumin can inhibit platelet aggregation (6). In addition, coagulation defects can result from dilution after albumin administration (6). [Pg.54]

Important susceptibility factors include age, endogenous coagulation defects, thrombocytopenia, hypertension, cerebrovascular disease, thyroid disease, renal insufficiency, liver disease, tumors, cerebrovascular disease, alcoholism, a history of gastrointestinal bleeding (peptic ulcer disease alone without past bleeding is not associated with an increased risk of bleeding), and an inability to adhere to the regimen. [Pg.985]

Hemin (hematin), an exogenous source of heme, is used to treat acute intermittent porphyria and other hepatic porphyrias. It is generally well tolerated in the recommended doses, although thrombophlebitis, coagulation defects, circnlatory collapse, and occasional renal insnffi-ciency have been reported (1). [Pg.1588]

CNS depression or hyperexcitability acute hemorrhagic pancreatitis coagulation defects, thrombosis renal damage hepatic damage... [Pg.396]

Acquit coagulation defects are more common, and may be due to liver disease (since bile is required for absorption of vitamin K), dietary deficiency of vitamin K, or ingesUon of oral anticoagulant agents. Most of these can be treated by giving vitamin K and its congeners, menadiol sodium phosphate or phytomenadione. [Pg.138]

Use caution with patients with coagulation defects. [Pg.130]

Toxic effects due to formation of hydrochlorous and hydrochloric acid when comes into contact with water in body tissue, causing tissue necrosis and coagulation defects... [Pg.317]

D2. Davidson, E., Howard, A. N., and Gresham, G. A., The nature of the coagulation defect in rats fed diets which produce thrombosis or experimental atherosclerosis. Bril. J. Exptl. Pathol. 43, 166-171 (1962). [Pg.219]


See other pages where Coagulation defects is mentioned: [Pg.148]    [Pg.253]    [Pg.76]    [Pg.150]    [Pg.149]    [Pg.769]    [Pg.779]    [Pg.14]    [Pg.402]    [Pg.583]    [Pg.240]    [Pg.612]    [Pg.342]    [Pg.343]    [Pg.988]    [Pg.2567]    [Pg.2971]    [Pg.1086]    [Pg.1788]   
See also in sourсe #XX -- [ Pg.109 , Pg.135 ]




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