Factor V Leidan and mutations of the prothrombin gene are the two most common genetic causes of hypercoagulability.
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|length of the surgical procedure type of operation hip or knee surgery related to subsequent state of hypercoagulability
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A point mutation in the gene encoding Factor V can lead to a hypercoagulability disorder called Factor V Leiden.
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Hypercoagulability can be promoted by increased platelet count, enhanced platelet aggregation, increased protein S count, and a decrease in coagulation inhibiters like antithrombin.
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It is important to consider May Thurner syndrome in patients who have no other obvious reason for hypercoagulability and who present with left lower extremity thrombosis.
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This causes an increase in hematocrit, serum total protein, blood viscosity and, as a result of increased concentration of coagulation factors, it causes orthostatic hypercoagulability.
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Factor V Leiden is a variant ( mutated form ) of human factor V ( one of several substances that helps blood clot ) that causes an increase in blood clotting ( hypercoagulability ).
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The three major mechanisms for such an imbalance are enumerated in Virchow's triad : alterations in normal blood flow, injury to the blood vessel wall, and alterations in the constitution of blood ( hypercoagulability ).
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Hypercoagulability states as a pre-existing condition in pregnancy include both acquired ones, such as antiphospholipid antibodies, and congenital ones, including factor V Leiden, prothrombin mutation, proteins C and S deficiencies, and antithrombin III deficiency.
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The basics are these : Virhow's Triad states that any mix of hypercoagulability ( a state that makes the blood more likely to clot ), venous stasis ( blood sitting in a vein not really moving ) and vascular damage ( injury to the inside wall of the veins, in this case ) increases the risk of the formation of a blood clot, or thrombus.
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