Thrombosis requires three main conditions:
(1) vascular endothelial cell injury
Endothelial cells have prevent blood in intravascular coagulation function: (1) it is a single layer of membrane barrier, the blood clotting factors, platelet and can promote the blood coagulation in subcutaneous collagen isolated; Potassium can secrete TM, which is a glycoprotein coated on the surface of the intima and can bind to thrombin to control thrombin. Chemotherapy synthesis of prostacyclin can inhibit platelet aggregation. The secretion of adenosine diphosphate converts the ADP released by platelets, which has a strong effect on platelet aggregation, into adenine nucleotide, which is anti-aggregation; (5) the endothelial cells of the surface of the cell membrane containing heparin sample molecules (heparan sulphate), it has to promote antithrombin Ⅲ role; Q 2 macroglobulin can inhibit the chain reaction of coagulation factor activation. The production of a fibrinolytic enzyme activator factor in succinylase has the effect of promoting fibrinolysis. S all landowners to make proteins, it can coordinated APC inhibit blood coagulation factor a and Ⅷ Ⅴ a. Due to the above factors, platelet and clotting factor activation beyond physiological limits cannot occur without endovascular injury.
Endothelial cell injury in the exposed skin collagen, this is very important to activate platelet and blood coagulation factor Ⅻ. After endothelial injury, first activate platelet is in contact with the platelet collagen, following the clotting chain reaction after start to generate thrombin, and continues to be the platelet activation and release of ADP and thromboxane A2, comes along with blood stream in local being activated platelets. Fibronectin in the intradermal connective tissue also helps blood cells and fibrinogen adhere to exposed vascular walls. In addition, the subendothelial generated by platelets and endothelial cells of thrombin sensitive protein (thrombospondin, TSP) and fibrinogen large molecules such as protein and fiber connection, make the blood and vessel wall adhesion. Platelet activation plays a central role in triggering clotting.
Platelet activation is an important mechanism to complete the initial hemostasis directly. The initial hemostasis occurs within a few seconds of vascular injury, mainly involving blood vessels and platelets. Because of vascular endothelial cell damage, exposure, subcutaneous tissue elements in circulating platelets adhesion with the vessel wall, and the resulting platelet aggregation and release reaction, eventually platelet thrombus formation, to complete the initial hemostatic function. After activation of platelets, deformation, adhesion, aggregation, release and other reactions occur.
(2) changes in blood flow status
Within the normal velocity and the normal flow of blood, red blood cells and white blood cells in the center axis of the blood flow (axial), platelet, outer layer is the slow flow more red, and white blood cells, the outside is a layer of plasma edge (flow), isolated from the rest of the visible part of the blood and vessel wall, prevent platelets from contact with lining. When the blood flow is slow or the blood flow produces a whirlpool, the platelet can enter the side flow, increasing the chance of contact with the intima of the blood vessel, and the possibility of platelet sticking to the intima is inevitably increased. In addition, when the blood flow is slow and the blood flow generates whirlpools, the activated clotting factor and thrombin can locally reach the concentration required for the coagulation process, which is easy to start the coagulation process.
Easier than arteries venous thrombosis, in addition to blood stream is slow factors, also for vein venous flap, flap venous blood flow not only within the slowly, and a vortex, so often venous thrombosis in valve capsule as the starting point; In addition, unlike arteries, veins do not relax with the beating of the heart. The venous wall is thin and easy to be compressed. When blood flows through the capillaries into the veins, the blood becomes more viscous. The blood flow to the inside your heart and arteries, not easy to form the blood clots, but there was a spiral blood flow to the moderate, also can have thrombosis, such as mitral stenosis, blood stream is slow and left atrium appear when blood flow within the aneurysm in swirling flow, then all easy concurrent thrombosis.
(3) increased coagulation of blood
Increased coagulability of the blood refers to the high coagulation state of the blood caused by increased platelets and coagulants in the blood, or decreased activity of the fibrinolytic system. High coagulation can be classified as hereditary and acquired.
Hereditary hypercoagulation is seen in hereditary thrombosis. Hereditary thrombolysis refers to the existence of anticoagulant protein, coagulant factor, fibrinolytic protein and other genetic defects in the body, with a high tendency of thrombosis. Common genetic Yi Shuan disease include protein C deficiency syndrome, protein S defects, antithrombin defects, factor Ⅴ Leiden mutation disease (also known as activated protein C resistance disease) and thrombin original G20210A mutation. The main clinical manifestation of hereditary thrombosis is thrombosis, especially venous thrombosis.
Acquired hypercoagulation is seen in patients with advanced cancer, DIC, severe trauma, burns, hemorrhagic shock, pregnancy-induced hypertension, coronary atherosclerosis, hyperlipidemia, smoking and obesity. The increased coagulability of DIC is due to the activation of coagulation factor induced by a series of factors. Especially pancreatic cancer patients with adanced tumor and bronchogenic carcinoma, gastric cancer, breast cancer, its blood coagulability increase system is due to the cancer cells release the coagulation factors, such as tissue factor, promote clotting factor A (procoagulant A) etc. After severe trauma, burn, hemorrhagic shock and hemorrhagic shock, the blood is concentrated and coagulant substances are activated. In addition, a pregnancy, after surgery, postpartum, high fat diet, smoking, high coagulation state caused by coronary atherosclerosis because thrombocytosis or enhanced platelet viscosity increase blood coagulability.
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