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Clotting factors, deficiency

Recessively inherited coagulation disorders (RICDs) refer to relatively rare deficiencies in factor II, V, VII, and X-XIII resulting in either decreased clotting factor production or production of a dysfunctional molecule with reduced activity.19 The clinical severity of bleeding varies and generally is poorly correlated with the factor blood levels. Table 64-6 illustrates these clotting factor deficiencies and some of their characteristics. [Pg.994]

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]

There is growing evidence that desmopressin can be used safely in pregnant women and no adverse effects have been reported in either mothers with diabetes insipidus or their babies (71), or in women with clotting factor deficiencies (72). However, the manufacturers advise that it should be used with caution in women with bleeding disorders, who require high doses. [Pg.483]

The other factor deficiencies are rare genetic disorders. Mutations in the gene for the respective clotting factors results in impaired functionality or production of the factor (Table 64-7). [Pg.994]

Several substances that contribute to the blood coagulation process are formed in the liver. These include fibrinogen, prothrombin, and several of the blood clotting factors (II, VII, IX, and X). Deficiency in any of these substances leads to impaired blood coagulation. [Pg.296]

Hypercoagulable states include malignancy activated protein C resistance deficiency of protein C, protein S, or antithrombin factor VIII or XI excess antiphospholipid antibodies and other situations. Estrogens and selective estrogen receptor modulators have been linked to venous thrombosis, perhaps due in part to increased serum clotting factor concentrations. Although a thrombus can form in any part of the venous circulation, the majority of thrombi begin in the lower extremities. Once formed, a venous... [Pg.176]

The most important adverse effect is bleeding. With coumarins, this can be counteracted by giving vitamin Ki. Coagulability of blood returns to normal only after hours or days, when the liver has resumed synthesis and restored sufficient blood levels of clotting factors. In urgent cases, deficient factors must be replenished directly (e.g., by transfusion of whole blood or of prothrombin concentrate). [Pg.144]

Figure 8.2 A developing blood clot is shown in this picture. A blood clot is made of platelets, membrane fragments of a bone marrow cell, and a network of insoluble proteins, particularly fibrin generated from a precursor protein, fibrinogen, through the work of a cascade of protein clotting factors. Several bleeding disorders result from inherited deficiencies in clotting proteins. Figure 8.2 A developing blood clot is shown in this picture. A blood clot is made of platelets, membrane fragments of a bone marrow cell, and a network of insoluble proteins, particularly fibrin generated from a precursor protein, fibrinogen, through the work of a cascade of protein clotting factors. Several bleeding disorders result from inherited deficiencies in clotting proteins.
In normal individuals phytonadione and the menaquinones have no activity while in vitamin K deficiency the vitamin promotes the hepatic biosynthesis of factor II (prothrombin), factor VII, factor IX and factor X. Vitamin K functions as an essential cofactor for the enzymatic activation of precursors of these vitamin K dependent clotting factors. The quinone structure of the active form of vitamin K, i.e. reduced vitamin K or hydroquinone. [Pg.476]

Male Insomnia, chills, decreased libido, hepatic dysfunction, nausea, diarrhea, prostatic hyperplasia (elderly), iron deficiency anemia, suppression of clotting factors... [Pg.844]

Therapeutically, vitamin K is used in prophylaxis and treatment of deficiency of clotting factor due to dietary deficiency of vitamin K, chronic antimicrobial therapy, malabsorption syndrome, obstructive jaundice, liver diseases such as cirrhosis and hepatitis, in neonates to prevent or treat haemorrhagic disease of new born to counteract the overdosing of oral anticoagulants... [Pg.241]

B. Indications and use BeneFix is intended for the prevention and control of excessive, potentially life-threatening bleeding in patients with hemophilia B, including control and prevention of bleeding in the surgical setting. Patients with hemophilia B, also known as Christmas disease, are unable to form blood clots adequately because of a deficiency or defect in clotting factor IX. Treatment with factor IX products corrects the defect temporarily. [Pg.144]

Indications Treatment of classical hemophilia (hemophilia A) in which there is a demonstrated deficiency of activity of the plasma clotting factor, factor VIII... [Pg.149]

Treatment of classic hemophilia (hemophilia A) in which there is a demonstrated deficiency of activity of the plasma clotting factor FVIII (Compared to Kogenate, some patients who developed inhibitors on study with Kogenate-FS continued to manifest a clinical response when inhibitor titers were less than 10 Bethesda units (BU) per ml). [Pg.571]

Vitamin K (menadione, menaquinone, and phyloquinone) are responsible for they-car-boxylation of glutamate residues in clotting factors and other proteins. A deficiency of vitamin K is seen in newborns but is rare in adults it causes bleeding. The vitamin has little toxicity. [Pg.502]

The most obvious effect of a deficiency in vitamin K in animals is delayed blood clotting, which has been traced to a decrease in the activity of prothrombin and of clotting factors VII, IX, and X (Chapter 12, Fig. 12-17). Prothrombin formed by the liver in the absence of vitamin K lacks the ability to chelate calcium ions essential for the binding of prothrombin to phospholipids and to its activation to thrombin. The structural differences between this abnormal protein and the normal prothrombin have been pinpointed at the N terminus of the 560 residue glycoprotein.e f Tryptic peptides from the N termini differed in electrophoretic mobility. As detailed in Chapter 12, ten residues within the first 33, which were identified as glutamate residues by the sequence analysis on normal prothrombin, are actually y-carboxyglutamate (Gla). The same amino acid is present near the N termini of clotting factors VII, IX, and X. [Pg.821]

Deficiencies in vitamin K and the related synthesis of the vitamin K-dependent clotting factors are treated by administering exogenous vitamin K.20 Various commercial forms of this vitamin are available for oral or parenteral (intramuscular or subcutaneous) administration. Specifically, individuals with a poor diet, intestinal disease, or impaired intestinal absorption may require vitamin K to maintain proper hemostasis. [Pg.357]

Vitamin K deficiency (necessary for synthesizing clotting factors)... [Pg.38]


See other pages where Clotting factors, deficiency is mentioned: [Pg.994]    [Pg.994]    [Pg.149]    [Pg.122]    [Pg.13]    [Pg.294]    [Pg.707]    [Pg.1251]    [Pg.120]    [Pg.994]    [Pg.994]    [Pg.149]    [Pg.122]    [Pg.13]    [Pg.294]    [Pg.707]    [Pg.1251]    [Pg.120]    [Pg.376]    [Pg.602]    [Pg.693]    [Pg.132]    [Pg.334]    [Pg.191]    [Pg.283]    [Pg.150]    [Pg.421]    [Pg.255]    [Pg.756]    [Pg.768]    [Pg.769]    [Pg.98]    [Pg.136]    [Pg.356]    [Pg.357]    [Pg.357]    [Pg.361]    [Pg.38]   
See also in sourсe #XX -- [ Pg.26 ]




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