Extrinsic And Intrinsic Pathway Of Blood Coagulation Pdf
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- 16.5D: Coagulation
- A mathematical model for in vitro coagulation of blood: role of platelet count and inhibition
The article also illustrates the appropriateness of monitoring treatment in specialist units to maintain the level of anticoagulation within the very narrow margin that allows prevention of thrombosis without causing bleeding complications. All thrombotic processes have their origin in the dysfunction or rupture of the vascular endothelium, leading to release of tissue factor, which initiates the process of coagulation, and of collagen and von Willebrand factor, which initiates adhesion and activation of platelets. Alteration of the homeostatic balance between prothrombotic and antithrombotic factors during anticoagulation therapy can result in insufficient inhibition of coagulation thrombosis or the occurrence of bleeding due to excessive antithrombotic treatment. The interpretation of the coagulation process described by MacFarlane 2 in the "MacFarlane cascade" has been of use for many years in beginning to understand the complex problem of thrombus formation.
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. At this point the intinsic pathway, as an independent source of activated factor X, is thought to become critical for the continuation of clot formation Broze ; Mann et al.
Natalya M. Ananyeva, Diana V. Kouiavskaia, Midori Shima, Evgueni L. Saenko; Intrinsic pathway of blood coagulation contributes to thrombogenicity of atherosclerotic plaque. Blood ; 99 12 : —
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 Enzyme-linked immunoassays and kinetic enzyme tests were used.
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 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. Primary hemostasis refers to platelet plug formation, which forms the primary clot.
The intrinsic pathway consists of factors I, II, IX, X, XI, and XII. Respectively, each one is named, fibrinogen, prothrombin, Christmas factor, Stuart-Prower factor, plasma thromboplastin, and Hageman factor. The extrinsic pathway consists of factors I, II, VII, and X. Factor VII is called stable factor.
A mathematical model for in vitro coagulation of blood: role of platelet count and inhibition
A mechanistic model including the role of platelets is proposed for clot formation and growth in plasma in vitro. Initiation of clot formation is by the addition of tissue factor, and initiation via the intrinsic pathway is neglected. Activation of zymogens follows the extrinsic pathway cascade and reactions on platelet membranes are included. Platelet activation occurs due to thrombin and also due to other activated platelets. The model predictions matched existing data for thrombin production in synthetic plasma.
A cell-based model of coagulation and its implications. The concept of a coagulation cascade describes the biochemical interactions of the coagulation factors, but it is flawed as a model of the in vivo hemostatic process. Hemostasis requires both platelet and fibrin plug formation at the site of vessel injury and that the procoagulant substances activated in this process remain at the site of injury.
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.