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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 ...
The reference range for prothrombin time depends on the analytical method used, but is usually around 12–13 seconds (results should always be interpreted using the reference range from the laboratory that performed the test), and the INR in absence of anticoagulation therapy is 0.8–1.2.
Prothrombinase assembly begins with the binding of factor Xa and factor Va to negatively charged phospholipids on plasma membranes. Activated factor Xa and factor Va bind to the plasma membranes of a variety of different cell types, including monocytes, platelets, and endothelial cells. [9]
Clotting time is a general term for the time required for a sample of blood to form a clot, or, in medical terms, coagulate.The term "clotting time" is often used when referring to tests such as the prothrombin time (PT), activated partial thromboplastin time (aPTT or PTT), activated clotting time (ACT), thrombin time (TT), or Reptilase time.
Low levels of platelets in turn may lead to prolonged or excessive bleeding. It is the most common coagulation disorder among intensive care patients and is seen in a fifth of medical patients and a third of surgical patients.
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 ...
Hypoproteinemia is a condition where there is an abnormally low level of protein in the blood. There are several causes that all result in edema once serum protein levels fall below a certain threshold.
Protein C is vitamin K-dependent. Patients with Protein C deficiency are at an increased risk of developing skin necrosis while on warfarin. Protein C has a short half life (8 hour) compared with other vitamin K-dependent factors and therefore is rapidly depleted with warfarin initiation, resulting in a transient hypercoagulable state.