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See Fibrinogen |
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See Prothrombin |
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Hypoprothrombinemia; Prothrombin deficiency. A very rare disorder of blood clotting resulting from a deficiency of prothrombin. It is inherited as an autosomal recessive trait (both parents are carriers). Acquired Factor II deficiency is common and results from Vitamin K deficiency, severe liver disease, and therapeutic use of anticoagulant drugs. MEDLINEplus |
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G to A substitution at the position 20210 in the 3' untranslated region of the prothrombin gene that leads to an increased risk of thrombosis. |
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See Thromboplastin, Tissue Factor |
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Calcium |
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Labile Factor |
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An inherited disorder that causes abnormal blood clotting, resulting from a deficiency of the plasma protein Factor V. The disease is similar to hemophilia, except bleeding into joints is less common. Bleeding can occur almost anywhere in the body, and death from hemorrhage has occurred with this disorder. MEDLINEplus |
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Substitution of Gln for Arg in the 506 position of the factor V gene. This results in resistance to APC and risk of thrombosis. |
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Stable Factor |
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Extrinsic factor deficiency. An inherited disorder that causes abnormal blood clotting caused by an inherited deficiency of Factor VII, an important clotting protein. MEDLINEplus |
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Antihemophilic Factor (AHF); antihemophilic globulin (AHG); antihemophilic factor A, Factor VIII:C. A protein substance in blood plasma that participates in and is essential for the blood-clotting process. Most cases of hemophilia are caused by a deficiency of this factor. |
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Hemophilia A; Classical hemophilia. A hereditary disease found only in males characterized by excessive bleeding due to delayed clotting, even after minor injury, caused by a deficient activity of plasma protein factor VIII. MEDLINEplus |
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Plasma thromboplastin component (PTC); Christmas factor; antihemophilic factor B. |
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Hemophilia B; Christmas disease. A hereditary blood coagulation disorder caused by a deficiency of a plasma protein factor IX. The disorder is caused by an inherited sex-linked recessive trait with the defective gene located on the X chromosome. Females carry two copies of the X chromosome, so if the factor IX gene on one chromosome is defective, the other can compensate. Males, however, carry only one X chromosome, so if the factor IX gene on that chromosome is defective, they have the disease. Females with one defective factor IX gene are carriers of this trait. Fifty percent of the male offspring of female carriers will have the disease, and 50% of their female offspring will be carriers. All female children of a male hemophiliac will be carriers of the trait. MEDLINEplus |
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Stuart factor; Prower factor; Stuart-Prower factor. |
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Stuart-Prower deficiency. A rare inherited disorder that causes abnormal blood clotting resulting from a deficiency of the plasma protein Factor X. MEDLINEplus |
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Plasma thromboplastin antecedent (PTA); antihemophilic factor C |
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See Hageman factor; surface factor; contact factor |
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An inherited disorder that causes prolonged clotting (coagulation) of blood in a test tube without a clinical bleeding tendency, and results from a deficiency of the plasma protein factor XII. It is not associated with abnormal bleeding, and is a rare disorder. MEDLINEplus |
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Fibrin stabilizing factor (FSF); fibrin stabilizing enzyme; fibri-nase |
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A white insoluble protein formed from the precursor fibrinogen by the proteolytic activity of thrombin and precipitated as a tangle of threads when blood clots. |
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FDPs; FSPs; Fibrin split products; Fibrin breakdown products. The measurement of FDPs provides a direct indication of the activity of the fibrinolytic (clot-dissolving) system. When plasmin dissolves fibrinblood clots, FDPs are formed. These degradation products, which have an anticoagulant effect and inhibit clotting, can be measured. When they are present in large amounts, they indicate increased fibrinolysis, or clot breakdown, as occurs in DIC and primary fibrinolytic disorders. MEDLINEplus |
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Serum fibrinogen; Plasma fibrinogen; Factor I. Fibrinogen is a protein synthesized by the liver used in the blood to form a clot. It circulates in the blood as a soluble protein and when the clotting process is triggered, the soluble fibrinogen is converted to insoluble fibrin, the major protein that maintains integrity of the clot. It is cleaved (broken) by the enzyme thrombin to form fibrinpeptides (short protein fragments) during normal coagulation. MEDLINEplus |
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Assay for fibrinogen concentration - measured by the rate at which fibrinogen is converted to fibrin by the action of thrombin. |
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The process by which a fibrin clot (blood clot) breaks down, caused by the action of several enzymes. Fibrinolysis occurs continuously and naturally in the body, with continuing formation and dissolution of clots in equilibrium. However, the rate of fibrinolysis can be abnormally high because of stressors like intense exercise, inadequate oxygenation of tissues, low blood sugar, and bacterial infections. Primary fibrinolysis occurs as an "original" condition; secondary fibrinolysis develops because of another disorder, medications, or other causes. In some cases, doctors may wish to speed up the rate of fibrinolysis. For example, when an abnormal "clot" forms in the coronary artery vessels, leading to a heart attack, man-made fibrinolytics such as tPA, streptokinase or retavase may be given intravenously to attempt to break up the culprit clot, if catheterization facilities are not readily available. MEDLINEplus |
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A molecular marker of thrombosis. Fibrinopeptide A and B are produced by the cleavage of fibrinogen by thrombin. Fibrinopeptide levels are an early indication of clot formation. |
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Prekallikrein |
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Fibrinopeptide a |
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The relative proportions of different foods that make up a nutritious, well-balanced diet. MEDLINEplus |
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See Fibrin degradation products |