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PostSubject: increased concentration   Fri Apr 06, 2007 2:49 pm

Haemorrhagic syndrome - state or group of states, the hallmark of which is increased bleeding in the form of bleeding from the mucous membranes nose, a haemorrhage in the skin and joints, and gastrointestinal bleeding, etc. Bleeding is the result of pathology : 1. Platelets; 2. Out blood; 3. The walls of blood vessels. Closing blood-set consecutive reactions involving platelets, factors plasma and tissues and generates fibrina bunch at the damage to the receptacle. Damage to the vessel resulted in a number of processes : 1-reduction damaged receptacle; 2-leukocyte accumulation in the lesions; 3-activation of liquidation; 4-activation reaction fibrinolysis. Indeed down blood is divided into three main stages : 1) formation of enzyme активирующего протромбин; 2) making protrombina in trombin influenced enzyme aguirutego protrombin; 3) making fibrinoguena in fibrin by 821-828. Closing blood can be either within the receptacle, and therefore it is an internal closure within and outside the receptacle. Phasing out the dish called back outside and active coagulation factors, are mainly from damaged tissue. Domestic down a free from the influence of tissue damage, and how that might seem strange blood sworachiwauschayasa on the surface of glass or inside the tubes down to the identical Inland out. Inside out is when blood contact with the negatively charged surfaces. The undamaged vessel out there, in contact with blood negatively charged surfaces endotelia, as well as collagen or phospholipids. Negative charges, collagen or cures trigger factor XII (Hageman factor), which in turn activates XI factor. Then activated factor XI in the presence of ions Ca2 + and phospholipids is the active factor IX (factor Christmasa). Factor IX is a complex with factor VIII (antigemofiliceski factor), ions Ca2 + and activates factor X (factor Stewart). Active X factor interacts with the activated V factor ions Ca2 + and phospholipids and the result is an enzyme, aguiruty protrombin. The response has been similar, both in domestic and in external closure. Looking back is influenced by factors evolved from damaged tissue. The starting point of external phase is the interaction factor III (tissue factor) in the presence of ions Ca2 + and phospholipids with factor VIII (prokonvertinom), which leads to the activation of factor X (Stewart factor). The reaction is similar to the reaction that flows with an internal closure. Phase out the same place as in the domestic and the external phase, in which factor II (протромбин) reacts with V and X factors and leads to the formation of 821-828. The third phase phase is to translate фибриногена in fibrin by 821-828. Trombin enzyme 20:1; Resulting fibrin monomer in the presence of ions Ca2 + and factor XIII (fibrinstabilizirut th factor) is a dense thread in the form of insoluble bunch. The resulting modules (clot) compressed (packed), making liquid - whey. The seals, called retrakciei greater role platelets. Given the shortage of platelets retraktion process is not happening. The fact is that platelets contain sokratitionay protein-trombostenin, which declined in collaboration with the ATF. Blood clot is not constant and, after some time, he dissolves or stabilizing. The lysis transformation инактивного predecessor in the by the factor XII . Problems first round fibrinolizina on a feedback of the global XII factor in the process of decomposing enzyme. Fibrinolizin destroys network of thread fibrina and leads to the disintegration bunch. Inside the strikes a balance between education trombov and lizisom. Thus, in response to the introduction of a natural factor preventing out-heparin, in the blood is increased concentration profibrinolizina. It is likely that this process is responsible for the maintenance of normal blood flow in capillaries, preventing mikrotrombov education.

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