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In healthy people, there is a physiological balance between procoagulant factors on the one hand and anticoagulant and fibrinolytic factors on the other side. A variety of genetic and acquired factors and environmental influences can shift this balance to coagulant side. This leads to the pathological formation of thrombi in veins such. B. deep vein thrombosis (DVT), in arteries (eg. As myocardial infarction, ischemic stroke) or in the ventricles. Thrombi can obstruct blood flow at the site of their origin or are carried away by the blood stream and embolize distant vessels (z. B. pulmonary embolism, embolic stroke). Etiology The genetic changes that increase the risk of venous thromboembolism include, Factor V Leiden, which confer resistance to activated protein C (APC) gives prothrombin 20210 gene mutation deficiency of protein C deficiency of protein S deficiency of protein Z antithrombin iii deficiency also causes acquired increase the risk of venous and arterial thrombosis (see table: acquired causes of thromboembolism). Other diseases or environmental factors can also increase the risk of thrombosis, especially when genetic changes are present. Acquired causes of thromboembolism cause Note antiphospholipid autoimmune disease with an increased risk of venous or arterial thrombi atherosclerosis increases with pre-existing stenosis When atherosclerotic plaque rupture, the risk of arterial thrombi Higher risk patients, they give the “Expose” – from or tissue factor. Therefore, the coagulation is activated, and there is local to a Platelet adhesion and aggregation and thrombosis. Malignant tumors (promyelocytic leukemia; lung, breast, prostate, pancreatic, gastric and colon tumors) Activation of the coagulation can both via secretion of a factor X-activating protease, on the expression / exposure of tissue factor on the tumor cell surface, or respectively. Heparin-induced thrombocytopenia is related to the platelet aggregation and an increased risk for thrombosis in connection hyperhomocysteinemia Cause By folic acid, vitamin B12 or vitamin B6 deficiency infection (severe;., For example, sepsis) increases the risk of venous thrombosis increases the expression / exposure of tissue factor by monocytes and macrophages Oral contraceptives, estrogen containing low risk with low-dose regimens common in patients who have a genetic predisposition for venous thromboembolism, and smoking women Tissue damage by trauma or surgery Venous congestion through surgery, orthopedic or paralytic immobilization-induced, heart failure, pregnancy and About Wicht symptoms and discomfort Common manifestations of a thrombotic disorder include unexplained deep vein thrombosis DVT and pulmonary embolism (PE). Superficial thrombophlebitis may also develop. Other sequences can include arterial thrombosis (z. B. stroke or mesenteric ischemia cause). The symptoms depend on the location of the clot; as in the following examples: chest pain and shortness of breath: possible pulmonary embolism sensation of heat, redness and swelling of the legs: DVT weakness / numbness one side of the body, problems with speech and problems with balance and walking: possible ischemic stroke abdominal pain: possible mesenteric Women may have a history of multiple miscarriages. Diagnosis The diagnoses are discussed elsewhere in the MSD Manual in accordance with the localization of the thrombus (z. B. deep vein thrombosis, pulmonary embolism, ischemic stroke. Predisposing factors predisposing factors should always be considered. In some cases, are leading to thrombosis causes obviously (z. B. recent surgery or recent trauma, prolonged immobilization, malignant tumors, generalized atherosclerosis). If a predisposing factor is not clear, further investigations should be carried out, particularly in patients with venous thrombosis in family history more than a previous venous thrombosis venous or arterial thrombosis aged under 50 Unusual localization of venous n thrombosis (eg. B. cavernous sinus, mesenteric veins) with spontaneous deep venous thrombosis have a predisposing factor, more than half of all patients. The studies for predisposing hereditary factors, specific samples to measure the amount or activity of physiological anticoagulants in plasma and search for specific genetic defects as follows: coagulation test of the lupus anticoagulant clotting test of resistance to activated protein C (APC) gene test the Factor V Leiden genetic test the prothrombin gene mutation (G20210A) function test of the antithrombin function test for the protein C function test of the protein S antigen assay of the total and free present protein S measure homocysteine ??levels in the plasma immunoassay of antiphospholipid treatment the treatment is in accordance with the localization of the thrombus elsewhere in MSDManu al discussed.