Examples of fibrin in the following topics:
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- As part of the process, the body deposits fibrin onto injured tissues.
- The fibrin acts like a glue to seal the injury and builds the fledgling adhesion, said at this point to be fibrinous.
- In many cases however, the production or activity of these enzymes are compromised because of injury and the fibrinous adhesion persists.
- Fibrinous adhesions are causes of early postoperative obstruction which settles down within 3–5 days.
- The majority of fibrinous adhesions will disappear in due course.
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- The main enzyme in primary fibrinolysis is plasmin, a proteolytic enzyme that degrades fibrin mesh.
- Plasminogen cannot cleave fibrin and circulates in the bloodstream.
- Following fibrin degradation by plasmin, old activated platelets from the platelet plug are phagocytized and destroyed by macrophages.
- Plasmin operates on a negative feedback process because it is reduced when the fibrin clot is fully degraded.
- Fibrinolytic drugs include synthesized tissue plasminogen activator and streptokinase, a bacterial enzyme that has degrades fibrin directly.
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- It takes approximately sixty seconds until the first fibrin strands begin to intersperse among the wound.
- After several minutes, the platelet plug is completely formed by fibrin.
- Thrombin facilitates the conversion of a soluble plasma protein called fibrinogen into long, insoluble fibers or threads of the protein, fibrin.
- Fibrin threads wind around the platelet plug at the damaged area of the blood vessel, forming an interlocking network of fibers and a framework for the clot.
- This temporary fibrin clot can form in less than a minute and slows blood flow before platelets attach.
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- Several components of the coagulation cascade, including both cellular (e.g. platelets) and protein (e.g. fibrin) components, are involved in blood vessel repair.
- Secondary hemostasis refers to the coagulation cascade, which produces a fibrin mesh to strengthen the platelet plug.
- Thrombin then cleaves fibrinogen into fibrin, which forms the mesh that binds to and strengthens the platelet plug, finishing coagulation and thus hemostasis.
- It also activates more factor V, which later acts as an anticoagulant with inhibitor protein C, and factor XIII, which covalently bonds to fibrin to strengthen its attachment to the platelets.
- Plasmin: generated by proteolytic cleavage of plasminogen, a potent fibrinolytic that degrades fibrin and destroys clots.
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- Platelets also contain adhesive proteins that allow them to adhere to fibrin mesh and the vascular endothelium, as well as to a microtubule and microfilament skeleton that extends into filaments during platelet activation.
- The adhesive surface proteins of platelets allow them to accumulate on the fibrin mesh at an injury site to form a platelet plug that clots the blood.
- During coagulation, they release factors that increase local platelet aggregation (thromboxane A), mediate inflammation (serotonin), and promote blood coagulation through increasing thrombin and fibrin (thromboplastin).
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- Fibrinogen generates fibrin when activated by the coagulant thrombin, which forms a mesh that clots blood with the assistance of a platelet plug.
- Normally, anticoagulants and fibrinolytics in the plasma, such as plasmin and heparin, break up fibrin clots and inactivate thrombin.
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- The coagulation factors include factor V and VIII, which are involved in the coagulation cascade that converts fibrinogen into fibrin mesh after platelet plug formation.
- The completed plug will cover the damaged components of the endothelium and will stop blood from flowing out of it, but if the wound is large enough, blood will not coagulate until the fibrin mesh from the coagulation cascade is produced, which strengthens the platelet plug.
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- These factors cause the fibrin mesh to contract by forming twists and knots that condense the size of the clot.
- Following clot retraction, a separate process called fibrinolysis occurs which degrades the fibrin of the clot while macrophages consume the expended platelets, thus preventing possible thromboembolism.
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- Calcium mediates the binding of the tenase enzyme complexes (via the terminal
gamma-carboxy residues on FXa and FIXa) to the phospholipid surfaces
expressed by platelets, which in turn activates prothrombin to produce thrombin, which then produces fibrin from fibrinogen.
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- Movat stain (black = nuclei, elastic fibers; yellow = collagen, reticular fibers; blue = ground substance, mucin; bright red = fibrin; red = muscle).