Intrinsic And Extrinsic Pathway Of Blood Clotting Pdf

intrinsic and extrinsic pathway of blood clotting pdf

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When platelets are activated, they acquire enhanced capacity to catalyze interaction between activated coagulation on factors [Hirsh J, et al, ]. These factors circulated in the form of inactive precursors zymogens. Rupture of the atherosclerotic plaque leads to activation of the coagulation cascade: each zymogen is converted into an activated coagulation factor, which in turn activates the next zymogen in the sequence. This process culminates in the generation of thrombin, an enzyme that converts the soluble protein fibrinogen to insoluble fibrin, forming a blood clot.

16.5D: Coagulation

Coagulation is the process by which a blood clot forms to reduce blood loss after damage to a blood vessel. Several components of the coagulation cascade, including both cellular e. The role of the cellular and protein components can be categorized as primary hemostasis the platelet plug and secondary hemostasis the coagulation cascade. The coagulation cascade is classically divided into three pathways: the contact also known as the intrinsic pathway, the tissue factor also known as the extrinsic pathway , and the common pathway. Both the contact pathway and the tissue factor feed into and activate the common pathway. Hemostasis can either be primary or secondary.

Factor VII, the protease that initiates the normal blood clotting cascade, circulates in the blood in both its proenzyme factor VII and its activated factor VIIa forms. No clotting occurs, however, because neither form of the protein has any catalytic activity when free in solution. Blood clotting is normally initiated when tissue factor TF , an intrinsic plasma membrane protein, is exposed to the blood by injury to the wall of a blood vessel. TF is then able to bind factor VIIa from plasma, and possibly also factor VII, to form complexes capable of catalyzing the conversion of factor X, from plasma, into its activated form, factor Xa. Factor Xa catalyzes the conversion of additional factor VII molecules to their activated form, increasing the amount of tissue factor:factor VIIa complex available at the site of injury, accelerating the generation of factor Xa, and allowing the activation of factor IXa as well. This process is self-limiting because as levels of factor Xa increase, tissue factor:factor VIIa complexes become trapped in the form of catalytically inactive heterotetramers with factor Xa and the protein TFPI tissue pathway factor inhibitor.

Negreva, K. Vitlianova, R. Background: Clinical interest in the haemostasis profile of patients with paroxysmal atrial fibrillation PAF , and in particular, in blood coagulation is significant. It is known that blood coagulation is activated in two pathways: extrinsic and intrinsic. Regardless of the activation method, the coagulation cascade ends with a final common pathway, in which the activated factor X FX is central to the prothrombin complex, responsible for the conversion of prothrombin factor II F II to thrombin that converts fibrinogen into fibrin. Materials and methods: 51 non-anticoagulated patients 26 men, 25 women; mean age

Intrinsic pathway of blood coagulation

Platelets are key players in hemostasis , the process by which the body seals a ruptured blood vessel and prevents further loss of blood. Although rupture of larger vessels usually requires medical intervention, hemostasis is quite effective in dealing with small, simple wounds. There are three steps to the process: vascular spasm, the formation of a platelet plug, and coagulation blood clotting. Failure of any of these steps will result in hemorrhage —excessive bleeding. When a vessel is severed or punctured, or when the wall of a vessel is damaged, vascular spasm occurs. In vascular spasm , the smooth muscle in the walls of the vessel contracts dramatically. This smooth muscle has both circular layers; larger vessels also have longitudinal layers.

Blood coagulation refers to the process of forming a clot to stop bleeding. Coagulation is a complicated subject and is greatly simplified here for the student's understanding. To stop bleeding, the body relies on the interaction of three processes: Primary hemostasis involves the first two processes. Vasoconstriction is the body's first response to injury in the vascular wall. When injury occurs, vessel walls constrict, causing reduced blood flow to the site of injury.

Coagulation , also known as clotting , is the process by which blood changes from a liquid to a gel , forming a blood clot. It potentially results in hemostasis , the cessation of blood loss from a damaged vessel, followed by repair. The mechanism of coagulation involves activation, adhesion and aggregation of platelets , as well as deposition and maturation of fibrin. Coagulation begins almost instantly after an injury to the endothelium lining a blood vessel. Exposure of blood to the subendothelial space initiates two processes: changes in platelets, and the exposure of subendothelial tissue factor to plasma factor VII , which ultimately leads to cross-linked fibrin formation.

The Internet Stroke Center

All the components necessary for the clotting process to proceed are found in the blood. As such, the proteins required for such clotting to take place are part of the intrinsic pathway of blood coagulation. This pathway involves a series of proteins, protein cofactors, and enzymes, which interact in reactions that take place on membrane surfaces. These reactions are initiated by tissue injury and result in the formation of a fibrin clot Figure 1.



Coagulation clotting is the process by which blood changes from a liquid to a gel, forming a clot. It potentially results in hemostasis , the cessation of blood loss from a damaged vessel, followed by repair. The mechanism of coagulation involves activation, adhesion, and aggregation of platelets along with deposition and maturation of fibrin. Disorders of coagulation can result in bleeding hemorrhage or bruising or obstructive clotting thrombosis. The coagulation cascade of secondary hemostasis has two initial pathways which lead to fibrin formation:. The primary pathway for the initiation of blood coagulation is the tissue factor extrinsic pathway. The pathways are a series of reactions, in which a zymogen inactive enzyme precursor of a serine protease and its glycoprotein co-factor are activated to become active components that then catalyze the next reaction in the cascade, ultimately resulting in cross-linked fibrin.

The Blood Coagulation Process. Coagulation can be initiated by either of two distinct pathways. Regardless of whether the Extrinsic or Intrinsic pathway starts coagulation, completion of the process follows a common pathway. Both pathways are required for normal hemostasis and there are positive feedback loops between the two pathways that amplify reactions to produce enough fibrin to form a lifesaving plug. Deficiencies or abnormalities in any one factor can slow the overall process, increasing the risk of hemorrhage. The coagulation factors are numbered in the order of their discovery.

Coagulation Cascade

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