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Generally speaking the risk for thrombosis increases over the life course of individuals, depending on life style factors like smoking, diet, and physical activity, the presence of other diseases like cancer or autoimmune disease, while also platelet properties change in aging individuals which is an important consideration as well.
Various risk factors contribute to VTE, including genetic and environmental factors, though many with multiple risk factors never develop it. [57] [58] Acquired risk factors include the strong risk factor of older age, [5] which alters blood composition to favor clotting. [59] Previous VTE, particularly unprovoked VTE, is a strong risk factor. [60]
The last category, alterations in the constitution of blood, [6] has numerous possible risk factors such as hyperviscosity, coagulation factor V Leiden mutation, coagulation factor II G2021A mutation, deficiency of antithrombin III, protein C or S deficiency, nephrotic syndrome, changes after severe trauma or burn, cancer, late pregnancy and ...
While venous thrombosis of the legs is the most common form, venous thrombosis may occur in other veins. These may have particular specific risk factors: [5] Cerebral venous sinus thrombosis, cavernous sinus thrombosis and jugular vein thrombosis: thrombosis of the veins of the brain and head
The risk depends on the types of hormones used, the dose of estrogen, and the presence of other thrombophilic risk factors. [28] Various mechanisms, such as deficiency of protein S and tissue factor pathway inhibitor, are said to be responsible. [29] Obesity has long been regarded as a risk
Studies of the pathophysiologic mechanisms for the increased risk of Venous thrombosis embolism or VTE after long-distance travel have not produced consistent results, but venous stasis appears to play a major role; other factors specific to air travel may increase coagulation activation, particularly in passengers with individual risk factors ...
The coagulation factors are generally enzymes called serine proteases, which act by cleaving downstream proteins. The exceptions are tissue factor, FV, FVIII, FXIII. [28] Tissue factor, FV and FVIII are glycoproteins, and Factor XIII is a transglutaminase. [27] The coagulation factors circulate as inactive zymogens. The coagulation cascade is ...
The three factors have been further refined to include circulatory stasis, vascular wall injury, and hypercoagulable state, all of which contribute to increased risk for venous thromboembolism and other cardiovascular diseases. [4] Virchow's triad describes the pathogenesis of thrombus formation: [7] [8]
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