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  2. Factor V Leiden - Wikipedia

    en.wikipedia.org/wiki/Factor_V_Leiden

    Factor V Leiden is an autosomal dominant genetic condition that exhibits incomplete penetrance, i.e. not every person who has the mutation develops the disease. The condition results in a factor V variant that cannot be as easily degraded by activated protein C. The gene that codes the protein is referred to as F5.

  3. Thrombocythemia - Wikipedia

    en.wikipedia.org/wiki/Thrombocythemia

    High platelet counts can occur in patients with polycythemia vera (high red blood cell counts), and is an additional risk factor for complications. [ citation needed ] A very small number of people report symptoms of erythromelalgia , a burning sensation and redness of the extremities that resolves with cooling, or aspirin or both.

  4. Protein S deficiency - Wikipedia

    en.wikipedia.org/wiki/Protein_S_deficiency

    Human Chr 3. In terms of the cause of protein S deficiency it can be in inherited via autosomal dominance.A mutation in the PROS1 gene triggers the condition. The cytogenetic location of the gene in question is chromosome 3, specifically 3q11.1 [6] [7] Protein S deficiency can also be acquired due to vitamin K deficiency, treatment with warfarin, liver disease, kidney disease, chemotherapy ...

  5. Coagulopathy - Wikipedia

    en.wikipedia.org/wiki/Coagulopathy

    Coagulopathy (also called a bleeding disorder) is a condition in which the blood's ability to coagulate (form clots) is impaired. [1] This condition can cause a tendency toward prolonged or excessive bleeding (bleeding diathesis), which may occur spontaneously or following an injury or medical and dental procedures.

  6. Heparin-induced thrombocytopenia - Wikipedia

    en.wikipedia.org/wiki/Heparin-induced...

    Up to 8% of patients receiving heparin are at risk to develop HIT antibodies, but only 1–5% on heparin will progress to develop HIT with thrombocytopenia and subsequently one-third of them may develop arterial or venous thrombosis. [1] After vascular surgery, 34% of patients receiving heparin developed HIT antibodies without clinical symptoms ...

  7. Thrombophilia - Wikipedia

    en.wikipedia.org/wiki/Thrombophilia

    The combination activates factor X to factor Xa and factor IX to factor IXa. Factor Xa (in the presence of factor V ) activates prothrombin into thrombin. Thrombin is a central enzyme in the coagulation process: it generates fibrin from fibrinogen , and activates a number of other enzymes and cofactors ( factor XIII , factor XI , factor V and ...

  8. Quebec platelet disorder - Wikipedia

    en.wikipedia.org/wiki/Quebec_platelet_disorder

    These proteins include platelet factor V, von Willebrand factor, fibrinogen, thrombospondin-1, and osteonectin. [3] There is also a quantitative deficiency in the platelet protein multimerin 1 . Furthermore, upon QPD platelet activation, uPA can be released into forming clots and accelerate clot lysis, resulting in delayed-onset bleeding (12 ...

  9. Protein C deficiency - Wikipedia

    en.wikipedia.org/wiki/Protein_C_deficiency

    Primary prophylaxis with low-molecular weight heparin, heparin, or warfarin is often considered in known familial cases. Anticoagulant prophylaxis is given to all who develop a venous clot regardless of underlying cause. [6] Studies have demonstrated an increased risk of recurrent venous thromboembolic events in patients with protein C deficiency.