Coagulopathy Consumption

Consumptive coagulopathies, or disseminated intravascular coagulation syndrome (DIC syndrome), is one of the types of coagulopathies and is a pathological condition characterized by an acute disorder of hemostasis caused by insufficient production of physiological blood coagulation factors and platelet aggregation while maintaining normal levels of fibrinolysis system factors.

Consumer coagulopathy affects the function of multiple coagulation factors, including factors XI, XII, IX, and X, as well as protein C, thrombomodulin, platelet activation, and complement. The degree of hemostatic impairment depends on the duration of bleeding and the general condition of the patient.

DIC often occurs as a result of acute tissue injury, such as massive blood loss from trauma, internal bleeding, sepsis, or surgical trauma in patients with surgery, organ infarction, or traumatic brain injury. During the syndrome, components that promote blood clotting bind to products such as vicinate factors and tissue factors. At this stage of DIC syndrome, hemolysis

Coagulopathy of Consumption is a systemic disorder of hemostasis that occurs in people as a result of prolonged and frequently repeated damage to the vascular wall with increased bleeding. Consumptive coagulopathy is classified in the medical community as a syndrome with a high risk of mortality because, against the background of a sharp decrease in thromboplastin, a person loses a lot of blood due to numerous small hemorrhages throughout the body. The syndrome is most often observed in patients with HIV infection and has recently spread significantly among people infected with the hepatitis B virus.

Absorption coagulopathy in humans develops under the influence of viral pathogens and cytokines produced by the body itself during viral inflammation. Viruses are “blamed” for increasing the synthesis of anticoagulant proteins (exclusively antithrombin-III). Firstly, more prothrombinase-producing cells and antithrombin-activated plasminogens are produced, which are actively involved in the process of prolonging all blood coagulation factors, including the anticoagulant itself - antithrombin. And secondly, a huge number of viral “antithrombotic” proteins appear that participate in the processes of fibrinolysis, that is, in the breakdown of blood clots. Plasma coagulation factors are also activated with the formation of large blood clots. This is the pathogenesis scheme for the condition of patients with consumption coagulopathy.