Overview of Hemostasis

Plasma coagulation factors interact to produce thrombin, and thrombin converts fibrinogen to fibrin. Fibrin enhances blood clots by radiating from the tampon and fixing the tampon

In the intrinsic pathway, factor XII, high molecular weight kininogen, prekallikrein and activated factor XI (factor XIa) interact to produce factor IX to factor IXa. Factor IXa is then bound to factor VIIIa and procoagulant phospholipids (present on the surface of activated platelets and tissue cells) to form a complex of activator X. In the extrinsic pathway, factor VIIa and tissue factor (TF) directly activate factor X (factor VIIa / tissue factor complex also activates factor IX - figure: coagulation pathway table: blood coagulation Reaction components).

Activation of endogenous or extrinsic pathways activates a common pathway leading to the formation of fibrin clots. Common path activation involves three steps:

Calcium ions are required for most thrombin generation reactions (calcium chelators [eg citrate, ethylenediamine tetraacetic acid] are used as anticoagulants in vitro). In the absence of vitamin K synthesis factor, vitamin K-dependent coagulation factors (Factors II, VII, IX and X) usually do not bind to the phospholipid surface via calcium bridges and play a role in blood clotting.

Although the coagulation pathway helps to understand the mechanism and laboratory evaluation of coagulopathy, in vivo coagulation is mainly done by external routes. People with genetic defects of factor XII, high molecular weight kininogen or prekallikrein have no bleeding abnormality. People with genetic factor XI deficiency have mild to moderate bleeding disorders. In vivo, factor XI (intrinsic pathway factor) is activated when a small amount of thrombin is produced. Factor IX can be activated by factor XIa and factor Vila / tissue factor complex

In vivo, the initiation of the extrinsic pathway occurs when vascular injury brings blood into contact with tissue factor on the cell wall surrounding the vessel wall and around the vessel wall. Contact with this tissue factor produces a Factor Vila / tissue factor complex that activates factor X and factor IX. Factor IXa binds to its cofactor VIIIa on the surface of the phospholipid membrane to produce additional factor Xa. Factor X activation of factor VIIa / tissue factor and factor IXa / factor VIIa complex is necessary for normal hemostasis. This requirement for factor VIII and factor IX suggests that wholly exogenous coagulation pathway is caused by factor VIIa / tissue factor complex, why hemophilia type A (factor VIII deficiency) or type B (IX factor deficiency ) Will cause bleeding.

Haemorrhagic diseases are characterized by increased bleeding sensitivity (also known as bleeding sensitivity). They are caused by platelet disease (primary hemostasis disorder), coagulopathy (secondary hemostasis disorder), or in some cases a combination of the two. Coagulopathy can be classified as general or even endogenous or extrinsic defects, depending on the particular pathway of the diseased coagulation cascade. Hemorrhagic disease is hereditary or acquired. Clinical features of hereditary and acquired diseases may overlap, but mucosal cutaneous bleeding (eg, nasal bleeding, ecchymosis bleeding, gastrointestinal bleeding) is more relevant to platelet disease, and potential Infiltration into the space muscle bleeding) is a characteristic of coagulation disorder.

Hemostasis or hemostasis is the process of stopping bleeding. In other words, blood stays in the damaged blood vessel (the opposite of hemostasis is bleeding). This is the first stage of wound healing. This involves blood coagulation, which changes from liquid to gel. Complete blood vessels are at the center of the tendency to delay the formation of blood clots. Endothelial cells of intact blood vessels use heparin-like molecules and thrombomodulin to prevent blood coagulation and to prevent platelet aggregation by nitric oxide and prostacyclin. When endothelial damage occurs, endothelial cells stop secretion of coagulation and aggregation inhibitors, but secrete von Willebrand factor which stops bleeding after injury. Hemostasis has three main steps: 1) vasoconstriction, 2) temporary occlusion of platelet embolism, 3) blood coagulation, or formation of a fibrin clot. These processes seal the holes until the tissue is repaired