BMS 460 Lecture : Hemostasis, coagulation cascade, bleeding disorders, hematologic abnormalities, anemia, anemia of chronic disease, iron deficiency anemia, thalassemia
27 Apr 2014
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Polymerization fibrin and platelet aggregates form a solid, permanent plug to prevent any further hemorrhage. Once activated, the coagulation cascade must be restricted to the local site of vascular injury to prevent clotting of the entire vascular tree. At this stage, counter-regulatory mechanisms (e. g. , tissue plasminogen activator. [t-pa]) are set into motion to limit the hemostatic plug to the site of injury. Fibrinolytic cascade modulates the size of the final clot. Endothelial cells secrete tissue plasminogen activator (t-pa), which is most active when bound to fibrin. t-pa converts plasminogen (a circulating zymogen secreted by liver) into active plasmin, which breaks down fibrin and interferes with polymerization. The resulting fibrin degradation products also act as anticoagulants. Other pas include urokinase (plasma and tissues) and streptokinase (bacterial infections). Freely circulating plasmin is inactivated by alpah2-plasmin inhibitor. Initial step is formation of platelet plug to stop bleeding from damaged vessel. Then, fibrin clot is stabilized by activated factor xiiia, which cross-links fibrin strands.
