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  2. Hypoprothrombinemia - Wikipedia

    en.wikipedia.org/wiki/Hypoprothrombinemia

    Hypoprothrombinemia can be the result of a genetic defect, may be acquired as the result of another disease process, or may be an adverse effect of medication.For example, 5-10% of patients with systemic lupus erythematosus exhibit acquired hypoprothrombinemia due to the presence of autoantibodies which bind to prothrombin and remove it from the bloodstream (lupus anticoagulant ...

  3. 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.

  4. Factor V - Wikipedia

    en.wikipedia.org/wiki/Factor_V

    14067 Ensembl ENSG00000198734 ENSMUSG00000026579 UniProt P12259 O88783 RefSeq (mRNA) NM_000130 NM_007976 RefSeq (protein) NP_000121 NP_032002 Location (UCSC) Chr 1: 169.51 – 169.59 Mb Chr 1: 163.98 – 164.05 Mb PubMed search Wikidata View/Edit Human View/Edit Mouse Coagulation factor V (Factor V), also less commonly known as proaccelerin or labile factor, is a protein involved in ...

  5. 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 ...

  6. 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 ...

  7. Platelet storage pool deficiency - Wikipedia

    en.wikipedia.org/wiki/Platelet_storage_pool...

    Platelet storage pool deficiency is a family of clotting disorders characterized by deficient granules in platelets. Individuals with these disorders have too few or abnormally functioning alpha granules , delta granules , or both alpha and delta granules and are therefore unable to form effective clots, which leads to prolonged bleeding.

  8. 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.

  9. Activated protein C resistance - Wikipedia

    en.wikipedia.org/wiki/Activated_protein_C_resistance

    APC resistance is the inability of protein C to cleave Factor Va and/or Factor VIIIa, which allows for longer duration of thrombin generation and may lead to a hypercoagulable state. This may be hereditary or acquired. [4] The best known and most common hereditary form is Factor V Leiden, which is responsible for more than 95% of cases. [5]