Coagulation Cascade SIMPLEST EXPLANATION The Extrinsic and Intrinsic Pathway of HEMOSTASIS

>> YOUR LINK HERE: ___ http://youtube.com/watch?v=LVYmV5mK6QI

GET LECTURE HANDOUTS and other DOWNLOADABLE CONTENT FROM THIS VIDEO • SUPPORT US ON PATREON OR JOIN HERE ON YOUTUBE. • / medsimplified • • Coagulation (also known as 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 are disease states which can result in bleeding (hemorrhage or bruising) or obstructive clotting (thrombosis).[1] • LIKE ON FACEBOOK : • • The coagulation factors are generally serine proteases (enzymes), which act by cleaving downstream proteins. There are some exceptions. For example, FVIII and FV are glycoproteins, and Factor XIII is a transglutaminase.[7] The coagulation factors circulate as inactive zymogens. The coagulation cascade is therefore classically divided into three pathways. The tissue factor and contact activation pathways both activate the final common pathway of factor X, thrombin and fibrin • Tissue factor pathway (extrinsic)[edit] • The main role of the tissue factor pathway is to generate a thrombin burst , a process by which thrombin, the most important constituent of the coagulation cascade in terms of its feedback activation roles, is released very rapidly. FVIIa circulates in a higher amount than any other activated coagulation factor. The process includes the following steps:[7] • Following damage to the blood vessel, FVII leaves the circulation and comes into contact with tissue factor (TF) expressed on tissue-factor-bearing cells (stromal fibroblasts and leukocytes), forming an activated complex (TF-FVIIa). • TF-FVIIa activates FIX and FX. • FVII is itself activated by thrombin, FXIa, FXII and FXa. • The activation of FX (to form FXa) by TF-FVIIa is almost immediately inhibited by tissue factor pathway inhibitor (TFPI). • FXa and its co-factor FVa form the prothrombinase complex, which activates prothrombin to thrombin. • Thrombin then activates other components of the coagulation cascade, including FV and FVIII (which activates FXI, which, in turn, activates FIX), and activates and releases FVIII from being bound to vWF. • FVIIIa is the co-factor of FIXa, and together they form the tenase complex, which activates FX; and so the cycle continues. ( Tenase is a contraction of ten and the suffix -ase used for enzymes.) • Contact activation pathway (intrinsic)[edit] • The contact activation pathway begins with 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. Factor XIa activates FIX, 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. Instead, contact activation system seems to be more involved in inflammation.[7] • Final common pathway[edit] • The division of coagulation in two pathways is mainly artificial, it originates from laboratory tests in which clotting times were measured after the clotting was initiated by glass (intrinsic pathway) or by thromboplastin (a mix of tissue factor and phospholipids). In fact thrombin is present from the very beginning, already when platelets are making the plug. Thrombin has a large array of functions, not only the conversion of fibrinogen to fibrin, the building block of a hemostatic plug. In addition, it is the most important platelet activator and on top of that 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.[7] • 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 • SUBSCRIBE • / @medsimplified • WATCH AGAIN • • Coagulation Cascade SIMPLEST EXPLANAT... • ~-~~-~~~-~~-~ • CHECK OUT NEWEST VIDEO: Nucleic acids - DNA and RNA structure • • Nucleic acids - DNA and RNA structure • ~-~~-~~~-~~-~

#############################

New on site