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Disseminated Intravascular Coagulation Essay

1753 words - 7 pages

To stop the blood flow after damage, body uses three ways to maintain hemostasis; vascular spasm, platelet plug formation, and coagulation. Coagulation is an important process to prevent loss of blood when blood vessels are cut or damaged. Blood clot is a plug of platelet reinforce with the mesh of fibrin. However, a person with Disseminated intravascular coagulation, DIC, the blood clots have formed throughout the blood vessels when does not necessary. It leads to organ damages due to blocked blood vessels; furthermore, it leads to life-threatening bleeding due to wasting clotting factors and platelets when they are needed.
According to Marieb and Hoehn, to do the blood clot, the enzyme, thrombin, and clotting factors are required. The clotting factors are represented with Roman numerals. There are thirteen different types of clotting factors. There are two ways to initiate the blood clot; the extrinsic pathway and intrinsic pathway. With the extrinsic pathway, the faster coagulation occurred in outer tissues. With the cut, cells get damaged, and more tissue factors, TF, are produced on the surface protein. This TF then binds to factor VII, form TF/VIIa complex, and it substrates into factor IX and factor X. With the intrinsic pathway slower but broader coagulation occurred within the damaged vessels. Factor XII is regularly circulates in the blood, but when the blood vessel gets cut, the blood flow into the tissue space. The collagens in the tissue activate the factor XII. This activated factor XIIa trigger factor XI which then activates factor IX, and factor X. The factor X from both of the pathways binds and activates factor V. This combination is called as prothrombinase because it converts prothrombin, factor II, to thrombin, factor IIa. Thrombin helps fibrinogen, factor I to form fibrin, and it activates Factor XIII and bind with calcium which converts the soluble fibrin into an insoluble clot.
There are four main mechanisms which lead to DIC. First, increased in thrombin generation leads to DIC. When endothelial layers of the blood vessels get damaged, or tissue get damaged, or with inflammatory or with a disease such as sepsis, thrombin produced by the tissue factor are amplified. According to Massimo,Lippi,Manzato, when monocytes and macrophages are stimulated by the endotoxemia such as Gram-negative sepsis, intestinal infarction, increased synthesis and release of tissue factor, procoagulant molecule promote clotting. “Bacterial endotoxins can also directly activate factor XII” (Massimo,Lippi,Manzato). The increases of the tissue factors, activated factor XII and thrombin then stimulate the massive amount of the fibrinogen and the fibrin mesh then will formed to enhance the coagulation. Another way that tissue factors can in amplified is through polymorphonuclear leukocytes, PMNs. These leukocytes actually synthesize the small amount of the tissue factor due to transferring leukocytes to activated platelets on a collagen surface....

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