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Coagulation factor prothrombin

Fibrinogen -i These factors are usually referred Prothrombin J to by their common names. Tissue factor -i These factors are usually not re-Ca + J ferred to as coagulation factors. [Pg.600]

It is believed that heparin acts by neutralizing a number of active blood coagulation factors, thus disrupting the transformation of prothrombin into thrombin. Heparin is used to prevent thrombo-formation in myocardial infarctions, thrombosis, and embolism, for maintaining liquid conditions in the blood in artificial blood drcnlation and hemodialysis. Synonyms of this drug are arteven, hepalen, leparan, Uquemin, panheprin, vetren, and many others. [Pg.325]

Inhibition of synthesis of prothrombin and coagulation factors Vll, IX, and X Inhibition of platelet aggregation in vitro Activation of plasminogen... [Pg.101]

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]

Controls were a sample of 723 postmenopausal women without MI who were matched to cases by age, calendar year, and hypertension status. The main outcome measure was risk of hrst nonfatal MI based on current use of HRT and the presence or absence of coagulation factor V Leiden and prothrombin 20210 G A variants among cases and controls, stratihed by hypertension. [Pg.395]

Coumarins are competitive inhibitors of vitamin K, which is required for the formation in the liver of the amino acid, gamma-carboxyglutamic acid. This is necessary for the synthesis of prothrombin and factors VII, IX and X (Figure 17.1). After starting treatment the anticoagulant effect is delayed until the concentration of normal coagulation factors falls (36-72 h). The effects can be reversed by vitamin K (slow maximum effect only after 3-6 h) or by whole blood or plasma (fast). Gut bacteria synthesise vitamin K and thus are an important source of this vitamin. Consequently, antibiotics can cause excessive prolongation of the prothrombin time in patients otherwise adequately controlled on warfarin. [Pg.260]

Quantification of coagulation factors is notoriously difficult, because of the interrelations among the various components of the coagulation cascade, the broad range of normal values, and considerable inter-laboratory variability (52). This variability is illustrated by a WHO study of users of combined oral contraceptives, conducted on several continents, which showed statistically significant differences among clinical centers in prothrombin time, fibrin plate lysis, plasminogen, and activated partial thromboplastin time (SEDA-16, 464). Effects also vary between different populations, users of different doses, users of different products, and tests performed at different periods of the medication cycle (63,69). [Pg.218]

Freeze-dried concentrates of plasma containing prothrombin, factors IX and X, and varied amounts of factor VII (Proplex, etc) are commercially available for treating deficiencies of these factors (Table 34-3). Each unit of factor IX per kilogram of body weight raises its activity in plasma 1.5%. Heparin is often added to inhibit coagulation factors activated by the manufacturing process. However, addition of heparin does not eliminate all thromboembolic events. [Pg.781]

Schematic view of the role of coagulation factor Xa in arterial thrombosis. After endothelial injury, platelets adhere to the subendothelial matrix. The procoagulant activity of the arterial clot can be attributed to the formation of the prothrombinase complex on the platelet surface which cleaves prothrombin and produces thrombin. Thrombin subsequently acts as a strong agonist of further platelet aggregation. Schematic view of the role of coagulation factor Xa in arterial thrombosis. After endothelial injury, platelets adhere to the subendothelial matrix. The procoagulant activity of the arterial clot can be attributed to the formation of the prothrombinase complex on the platelet surface which cleaves prothrombin and produces thrombin. Thrombin subsequently acts as a strong agonist of further platelet aggregation.
Compounds with vitamin K activity (Table 6.2) are required in our diets for y-carboxyglutamate biosynthesis (Table 4.1). This amino acid is produced from certain protein glutamyl residues by carboxylation. Proteins that contain y-carboxyglutamate are blood prothrombin and coagulation factors VII, IX, and X (see Chapter 7). Other proteins of this type are osteocalcin from bone and several kidney and muscle calcium-binding proteins. [Pg.144]

Ca Ca2+ 800 mg Coagulation factors, e.g., prothrombin Important second messenger in hormone action and the visual process... [Pg.146]


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See also in sourсe #XX -- [ Pg.180 ]




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