• Monday May 25,2020

fibrin

Fibrin is a non-water-soluble, high molecular weight protein that forms during clotting by enzymatic action of thrombin from fibrinogen (coagulation factor I). The medical specialties are histology and biochemistry.

What is fibrin?

When coagulating, fibrin is formed by the action of thrombin from fibrinogen. It forms soluble fibrin, also called fibrin monomers, which polymerizes by means of calcium ions and factor XIII to a Fibrinnetz. Fibrin molecules impede blood flow in a pathological process. Fibrinolysin dissolves the resulting blood clots.

Fibrin is a protein and an important body-own substance, which is responsible for the blood coagulation. It is caused by the action of the coagulation enzymes prothrombin and fibrinogen, which are formed in the liver. Fibrin consists of fibrous molecules that crosslink with each other through a fine lattice. Fibrin lattices are an indispensable prerequisite for blood clotting. The medical terminology also uses the terms plasma pulp, blood pulp and globular plasma protein (serum proteins, blood proteins).

Anatomy & Construction

There is no ready-made fibrin in the blood, only the soluble precursor fibrinogen. Normally, the solid and liquid components of the blood do not readily separate. When the blood leaves the body, long fibrin fibers are created, which spin the blood cells into a lump in the form of a blood cake. This process is indispensable for a regularly functioning blood coagulation.

The exiting platelets stick to the fibrin fibers of the wound edges. After a bleeding time of about three minutes, enough platelets are stuck together at the site of injury to form a blood plug that will stop the bleeding. Through the network of the resulting fibrin threads, the graft receives the necessary strength. Fibrin causes blood clotting due to its ability to cross-link polymerization (reactions that lead to the formation of molecular substances). So fibrin belongs to the blood coagulation factors. These substances cause blood clotting after injury and stop bleeding. There are various blood coagulation factors, which are designated by the numbers I to XIII. Fibrinogen is the most important coagulation factor I.

The blood clotting in the body runs cascade-like. To stop bleeding and cause blood clotting, fibrinogen is converted to fibrin. This forms chainlike structures that stabilize the blood clot. The fibrinogen forms the uncrosslinked precursor of fibrin. Two small peptides (fibrinopeptides), which convert it into monomeric fibrin, are split off from this after an injury during blood coagulation under the action of the serine protease thrombin. Subsequently, the polymeric fibrin forms from this covalent cross-linking involving calcium (calcium ions) and blood coagulation (factor XIII). As a result, a fibrin scaffold is formed, with which platelets, erythrocytes and leukocytes stick together and lead to thrombus formation.

Plasmin allows the subsequent breakdown of fibrin (fibrinolysis). Fibrinogen is one of the acute phase proteins that may indicate inflammation in the body. The human body has thirteen coagulation factors: factor I fibrinogen, factor II prothrombin, factor III tissue thrombokinase, factor IV calcium, factor V proaccelerin, factor VI corresponds to the activated factor V, factor VII proconvertin, factor VIII hemophilia A factor is absent Hemophiliacs, factor IX Hemophilia - B factor, factor X Stuard power factor, factor XI Rosenthal factor, factor XII Hagemann factor, factor XIII Fibrin stabilizing factor. This classification is not identical with the order of activation in the blood clotting.

The reaction steps are carried out in different ways depending on the injury. The coagulation factors are aligned so that they undergo exactly matched fibrin production steps when activated in a chain reaction.

Function & Tasks

The coagulation system protects the organism against bleeding by quickly arresting the bleeding of smaller vessels. The endogenous plasma plasma protein helps in this process and acts like an adhesive. Not only in the case of injuries caused by external influences, which are immediately noticeable, a normally intact vascular system is endangered.

Regularly in the human body the smallest vessels are injured or leaked, for example due to impact or inflammation. The arterial vascular system is constantly under pressure. For this reason, even the smallest vascular lesions are suitable for causing bleeding out of the vessel. To prevent this process, the coagulation system seals these leaking vessels from the inside out. The coagulation mechanism proceeds in several stages by controlling the blood plasma substances in the form of coagulation factors (I to XIII). Three reactions form a chain reaction. The vascular reaction restricts blood loss through the narrowing of the affected blood vessel.

The Trombozytenpfropf causes the haemostasis by a short-term vascular occlusion. Long-term vascular occlusion occurs through the formation of a fibrous network of fibrin. In the liver, the coagulation proteins prothrombin are formed as a precursor of thrombin and fibrinogen as a precursor of fibrin. These two substances enter the blood plasma. The blood plasma is transformed with the help of the enzymes blood thrombokinase, tissue thrombokinase and calcium ions in prothrombin. This becomes thrombin and fibrinogen becomes fibrin. Fibrin forms the tissue network essential to hemostasis and helps to stop bleeding.

Diseases

If the human coagulation system no longer works properly, severe disturbances occur, which severely restrict the blood circulation. Depending on the underlying disorder, excessive blood thickening can lead to the formation of blood clots such as thrombosis and embolism. A heavy blood dilution causes an increased bleeding tendency or life-threatening bleeding.

The cause may be inherited as well as disorders of platelets or coagulation factors. Occasionally, coagulation problems also appear as a symptom of other coagulation system-independent ailments or conditions, such as an injury. Fibrinogen is determined in suspected various diseases if the patient has an excessive bleeding tendency (hemorrhagic diathesis) or a tendency to clot formation (thrombosis).

Furthermore, the fibrin determination is carried out during treatment with streptokinase (extracellular protein, antigen) or urokinase (plasminogen activator, enzyme of peptidases) to dissolve a blood clot (fibrinolytic therapy) for monitoring purposes and in diseased activation of blood coagulation (consumption coagulopathy). The value is determined from the blood plasma.


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