(1) the process of thrombosis
When there is damage blood vessels, collagen and tissue factor are exposed to the flow of blood, activating thrombosis, exposed collagen trigger platelet aggregation and activation, and exposed tissue factor is start the generation of thrombin, which not only convert fibrinogen to fibrin, but also activated platelets. Activation of platelet deformation and spread out to cover the defect part of the endothelium, and began to take off the particles, thus will raise to have other platelet adhesion of platelets, platelet through its various GP Ⅱ b/Ⅲ a receptor and fibrinogen bridge combined with micro and platelet aggregation. Starts at initial activation of platelet adhesion, adhesion of blood platelet release of active substances further around the platelet activation, the activation of platelets continue to release reaction including alpha particle, dense particle contents, lysozyme, etc. Thrombus formation and growth as the platelet adhesion, aggregation and activation of platelet thrombus has gradually formed, the platelet adhesion, activation of local damage, platelet activation through its receptor (GP Ⅱ b/Ⅲ a receptor, thromboxane receptor and thrombin receptor) is activated at the same time, through between platelet and platelet fibrinogen solid connection mutually, and form a small particles around on platelet aggregation, which can further catalytic production of thrombin, if the reaction occurs in the blood flow faster artery injury, local blood flow to generate thrombin was washed away, not easy to form in local high concentration. This low concentration of thrombin binds to thrombin receptors on platelets, activating platelets and forming platelet thrombus. On the downstream side of the platelet thrombus, blood flow to form vortex, thrombin there gathered easily and achieve high concentration, high concentrations of thrombin on fibrinogen and make its degradation of fibrin, to stabilize the platelet thrombus, and start the blood coagulation system, eventually forming blood fibrinogen network, red thrombus formation, become the tail arterial thrombosis.
Type of thrombus
1. Classification by composition of thrombus formation:
(1) palethrombus: composed of platelets and white blood cells. Occurs at a site of rapid blood flow (such as an artery or ventricle) or at a time of rapid blood flow at the time of thrombosis (such as the beginning of a venous mixed thrombus). Microscopically, white thrombus is mainly composed of a number of coralline platelet trabeculae with many neutrophils attached to its surface, forming the leukocyte boundary layer. A reticular network of cellulose formed between platelet trabeculae due to the action of activated clotting factors. The unaided eye is grayish white, the surface is rough and wavy, the quality is hard, and is closely connected with the vascular wall.
(2) redthrombus: it is made up of fibrin and red blood cells. It occurs after the blood flow is extremely slow or even stops, and its formation process is the same as the process of external coagulation. Therefore, red thrombus occurs when the mixed thrombus gradually increases and blocks the lumen. After local blood flow stops, it often forms the tail of continuous thrombus. Microscopically, the cellulosic mesh is filled with blood cells as normal as blood. The naked eye is dark red. Fresh red clots are moist and elastic, and old red clots become dry, brittle, inelastic, and prone to fall off and cause embolism due to absorption of water.
(3) mixedthrombus: the main part (body part) of the continuous thrombus of the vein is red and white striped layer by layer, that is, mixedthrombus. Its formation process is: predominantly trabecular platelet thrombus growth so that blood flow to the downstream vortex formation, thus generating another is given priority to with platelet thrombus, in between blood coagulation, thrombosis be given priority to with red blood cells. If carried out alternately, it is a mixed thrombus. In mitral stenosis and atrial fibrillation, spherical thrombus can form in the left atrium. Both the thrombus and the thrombus within the aneurysm have alternating layers of gray, white and reddish brown, called laminar thrombus, which is also a mixed thrombus.
(4) hyaline thrombus: it is composed of modified proteins. This kind of thrombus occurs in small blood vessels of microcirculation, which can only be seen under microscope.
2. Classification by site of thrombus formation
(1) arterial thrombosis: white thrombus is often used as the head and red thrombus as the tail. Arterial thrombosis due to arterial blood pressure is high, fast speed, rapid flow of clotting factor interactions, thus thrombin also not easy to accumulate in local achieve effective concentration, so the coagulation process is dependent on the plaques in the arteries burst parts firm adhesion of platelets as reaction platform, so in the process of platelet in arterial thrombosis plays an important role. When atherosclerotic plaque ruptures, platelets adhere to the exposed collagen and vWF factor, and platelets accumulate locally to form white thrombus. At the same time, coagulation factor is activated by tissue factor, which induces coagulation cascade reaction. Formed at the beginning of the reaction, partial thrombin by continual flow away, not easy to form a high concentration of thrombin in local, so also is not easy to form red blood clots, along with the increasing of white blood clots, the local slow blood flow and thrombus distal turbulence in white, in the white blood clots the telecentric end of the high concentration of thrombin formation, its soluble fibrinogen into insoluble fibrin, fibrin network red blood cells to form blood clots, thus arterial thrombosis in the head for white blood clots, tail to red blood clots. Thrombus formed at the rupture of plaque can enter plaque fissures and vascular cavities. The current application of intravascular ultrasound and blood vessels, according to a study by the mirror cavity which is formed by the most artery atheromatous plaque rupture for non occlusive thrombus, may not have any clinical symptoms, blood clots lead to artery atheromatous plaque expansion machine.
(2) venous thrombosis: usually red thrombus. Venous blood flow velocity is slow, thrombin and other coagulation factors in local accumulation form high concentrations, and easy to stick, so the vein thrombosis is mainly composed of thrombin fibrinogen degradation generates fibrin, fibrin and blood cells form mixed thrombus. Congenital absence of antithrombin, protein C deficiency, lack of protein S, malignant tumor, congenital heart disease, birth control pills, nephrotic syndrome and for antiphospholipid antibody syndrome, long-term lie in bed, hand surgery, obesity and varicose veins are all factors of venous thrombosis. Due to the slow flow of blood through veins, individuals with high coagulation tend to form a high concentration of thrombin in veins, which leads to the formation of red thrombus by fibrin network of blood cells.
(3) atrioventricular thrombus: red thrombus; Red blood clots occur in atrial fibrillation due to blood flow disorders and the formation of eddy currents to activate the coagulation process.
(4) microvascular thrombosis: cell thrombus and transparent thrombus. A clear thrombus or cellular thrombus is formed in the microvessels, which often leads to organ failure.
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