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:Coagulation is the thickening or congealing of any liquid into solid clots. This article is about a specific medical usage of the term with reference to human blood's mechanisms for forming scabs over wounds.

The coagulation of human blood is a fairly complex process by which blood becomes solid clots. It is an important part of hemostasis where a damaged blood vessel is ultimately covered by a fibrin clot to stop hemorrhage. Disorders in coagulation can lead to increased hemorrhage on the one side and thrombosis and embolism on the other.

1 In brief

Ordinarily coagulation is initiated within seconds after an injury occurs when platelets form a plug at the site of injury. This is called primary hemostasis. Following this, various plasma components, called clotting factors respond (in a complex cascade) to form fibrin strands which strengthen the platelet plug.

The use of adsorbent chemicals, such as zeolite, and other hemostatic agent s is also being explored for use in sealing severe injuries quickly.

2 Primary hemostasis

Primary hemostasis is initiated when platelets adhere, using a specific platelet collagen receptor glycoprotein Ia/IIa, to collagen fibers in the vascular endothelium. This adhesion is mediated by von Willebrand factor (vWF), which forms links between the platelet glycoprotein Ib/IX/X and collagen fibrils.

The platelets are then activated and release the contents of their granules in to the plasma, this inturn activates other platelets and white blood cells. They undergo a change in their shape which exposes a phospholipid surface for those coagulation factors that require it. Fibrinogen, which links adjacent platelets by forming links via the glycoprotein IIb/IIIa.In addition, thrombin activates platelets.

3 Secondary hemostasis

3.1 The coagulation cascade

The coagulation cascade of secondary hemostasis has two pathways, the Contact Activation pathway (formally known as the Intrinsic Pathway) and the Tissue Factor pathway (formally known as the Extrinsic pathway) that lead to fibrin formation. It was previously thought that the coagulation cascade consisted of two pathways of equal importance joined to a common pathway. It is now known that the primary pathway for the initiation of blood coagulation is the Tissue Factor pathway. The pathways are a series of reactions, in which a zymogen of a serine proteaseIn biochemistry, a serine proteases or serine endopeptidases (newer name) are a class of peptidases which are characterised by the presence of a serine residue in the active domain of the enzyme. Serine proteases participate in a wide range of functions i and its glycoprotein co-factor are activated to become active components that then catalyze the next reaction in the cascade. Coagulation factors are generally indicated by Roman numerals, with a lowercase a appended to indicate an active form, ultimately resulting in cross-linked fibrin.

The coagulation factors are serine proteaseIn biochemistry, a serine proteases or serine endopeptidases (newer name) are a class of peptidases which are characterised by the presence of a serine residue in the active domain of the enzyme. Serine proteases participate in a wide range of functions is except FVIII and FV which are glycoproteins., which act by cleaving other proteins. Factor XIII is a transglutaminaseTransglutaminases are a family of enzymes that catalyze the formation of a covalent bond between a free amine group (e. protein- or peptide-bound lysine) and the gamma-carboxamid group of protein- or peptide bound glutamine. Transglutaminase is now produc. Protein C is a serine protease.

The coagulation cascade can be summarised as follows:

  1. Tissue Factor pathway: the main role of the tissue factor pathway is to generate a "thrombin burst". Thrombin being the single most important constituent of the coagulation cascade in terms of its feedback activation roles. FVIIa circulates in a higher amount than any other activated coagulation factor and following damage to the blood vessel endothelium Tissue Factor (TF) is released, this then forms a complex with FVIIa (TF-FVIIa) this activates FIX and FX. FVII itself is activated by thrombin, FXIa, plasmin, FXII and FXa. The activation of FXa by TF-FVIIa is almost immediately inhibited by tissue factor pathway inhibitor (TFPI). FXa and its co-factor FVa form the prothombinase complex which activates prothrombin to thrombin. Thrombin then activates other components of the coagulation cascade including FV, FVII (which activates FXI which in turn activates FIX) and activates and releases FVIII from being bound to vWF. FVIIIa is the co-factor of FXIa and together they form the "tenase" complex which activates FX and so the cycle continues.
  2. Contact Activation pathway: formation of the primary complex on collagen by high molecular weight kininogen (HMWK), prekallikrein and FXII (Hageman factor), prekallikrein is converted to kallikrein and FXII becomes FXIIa. FXIIa converts FXI into FXIa. FXI is also activated by FVIIa. Factor IX is in turn activated by FXIa which with its co-factor FVIIIa form the tenase complex which activates FX to FXa. The minor role that the contact activation pathway has in initiating clot formation can be illustrated by the fact that patients with severe deficiencies of FXII, HMWK and prekallikrein do not have a bleeding disorder.
  3. Thrombin Thrombin has a large array of functions. Its primary role is the conversion of fibrinogen to fibrin, the building block of a haemostatic plug. In addition, it activates Factors VIII and V and their inhibitor protein C (in the presence of thrombomodulin ), and it activates Factor XIII, which forms covalent bonds that crosslink the fibrin polymers that form from activated monomers.

Following activation by the contact factor or tissue factor pathways the coagulation cascade is maintained in a prothrombotic state by the continued activation of FVIII and FIX to form the tenase complex, until it is down regulated by the anticoagulant pathways.



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