Disseminated Intravascular Coagulation Essay

I decided to write my paper about the coagulation system, including congest formation, but mainly about Disseminated Intravascular Coagulation. Disseminated Intravascular Coagulation, also known as DIC, is a pathological energizing of blood coagulumting mechanisms that may happen in response to a variety of diseases, or illnesses. However, DIC, is most commonly sight in severe sepsis and septic shock. DIC is not a specific illness, quite it is a complication or an effect of the progression of other illnesses or diseases. (Porth, 2011). When the body becomes inju scarlet, certain proteins in your blood become activated and live on to the injury site to help stop bleeding and control hemostasis. haemostasia is the normal process of sealing off a blood vas to prevent blood loss and exhaust. It is abnormal when it fails to appropriately clot the blood, or when this clotting is insufficient to stop the bleeding. Following an injury, there is an immediate watercraft spasm that prom otes vasoconstriction, which tries to diminish the blood flow.Collagen from the damaged site, releases blood platelets which adhere to the damaged vessel, and there, they permit degranulation and release cytoplasmic granules, ADP, Thromboxane A2, and Serotonin which is a vasoconstrictor. The ADP then attracts much platelets to the area, and the Thromboxane A2 promotes platelet aggregation, degranulation, and even more than vasoconstriction. This process promotes the formation of a platelet plug. The damaged tissue now releases part III (3), which, with the aid of Ca++, will activate Factor VII (7), which initiates the extrinsic mechanism of clotting. Factor XII (12), which comes from active platelets, will activate Factor XI (11), which initiates the inhering mechanism. Both active Factors VII (7), and active Factors XI (11), promote a cascade-like reaction, eventu exclusivelyy activating Factor X (10). Activating Factor X (10), along with Factor III (3), V (5), Ca++, and Plat elet Thromboplastic Factor, all activate prothrombin.Prothrombin activator converts prothrombin to thrombin.Thrombin converts fibrinogen to fibrin. Fibrin initially forms a tolerant mesh, but then Factor XIII, (13) causes the formation of cross link-like structures, which convert fibrin into denser fibers. Platelets and red blood cells become caught up in this mesh of fiber, and the end ensue is the formation of a blood clot. (Liebman, et al, 2008). Disseminated Intravascular Coagulation, as stated earlier, leads to the formation of olive-sized blood clots inside the blood vessels, and may occur in 30-50% of patients with sepsis. It develops in an estimated 1% of all hospitalized patients. DIC occurs at all ages and in all races, and no particular sex predisposition has been noted. (Matsuda, 1996).As stated above, that massive activation of the cascade-like reaction as a normal clotting mechanism, now causes a generation of microthrombi to release that make vessels occlude and le ads to tissue ischemia. All these clot formations devour the available coagulation proteins and platelets. They become depleted and severe bleed may result. The common bleeding sites are the mouth, nose and venipuncture sites. There is vast bruising, and multiple organ failure. Laboratory findings show the PT and APTT are normally very prolonged and the fibrinogen level is markedly reduced. High levels of fibrin abjection products are noted. There is severe thrombocytopenia.The only effective treatment is reversing the primal cause. Platelets may be transfused if counts are less than 5-10,000/mm and massive hemorrhage is occurring. Fresh frozen plasma can also be administered in an attempt to replenish the coagulation factors, though these are only pro tem measures and may result in an increased development of even more thrombi. The prognosis varies depending on the cause and extent of the intravascular thrombosis. For patients with DIC, regardless of the cause, it is often sad , and amidst 10% and 50% of these patients will die. DIC with sepsis has a significantly higher govern of death than DIC that is associated with trauma.ReferencesLeibman, H.A., Weitz, I.C. Disseminated intravascular coagulation. InHoffman, R., Benz, E.J., Shattil, S.S., et al, eds. HematologyBasic Principles and Practice. 5th ed. Philadelphia, Pa Saunders, Elsevier, Churchill, Livingstone 2008 132. Matsuda, T. clinical aspects of DIC-disseminated intravascular coagulation. Pol Journal of Pharmacology.Jan-Feb 199648(1)73-5. Medline. Porth Mattson, C. 2011. Essentials of Pathophysiology. (3rd ed.). Philadelphia, PaLippincott, Williams, and Wilkins. Schafer, A. I. Hemorrhagic disordersdisseminated intravascular coagulation, liver failure, and vitamin K deficiency. InGoldman, L., Ausiello D. eds. Cecil Medicine. 23rd ed. Philadelphia, Pa Saunders, Elsevier, Churchill, Livingstone 2008chap 181.