62. Vascular shock: definition, etiology, pathogenesis, pathological anatomy.

Vascular shock is a shock caused by a decrease in vascular tone. Its subspecies are septic, neurogenic, anaphylactic. Septic shock occurs as a result of human infection with a bacterial infection (sepsis, peritonitis, gangrenous process). In septic shock, DIC syndrome is most pronounced, because bacterial endotoxins have a direct effect on the blood clotting system. Neurogenic shock is most often manifested after injury to the spinal cord or medulla oblongata. Anaphylactic shock is a severe allergic reaction that occurs within the first 2-15 minutes after the allergen enters the body. The development of anaphylactic shock is based on hypersensitivity of the reagin type, due to the fixation of IgE on blood basophils and tissue basophils. There is a significant expansion of the resistive vessels. There is a violation of microcirculation, see pathological anatomy in the general question about SHOCK (it is the same).

63. Infectious-toxic shock: etiology, pathogenesis, pathological anatomy.

Infectious toxic shock (synonym bacterial, bacteriotoxic shock) is a shock resulting from the action of microorganisms and their toxins. It is a relatively common type of shock, inferior in frequency to cardiogenic and hypovolemic shock. Etiology: Infectious and toxic shock most often develops in infections that are accompanied by bacteremia, for example, meningococcemia, typhoid fever, leptospirosis. At the same time, it can occur in severe flu, hemorrhagic fevers, rickettsiosis. Much less often, it can be caused by some protozoa, for example, malarial plasmodia and fungi. Pathogenesis: A large number of microbial toxins enter the bloodstream (the destruction of bacterial cells during antibiotic therapy can contribute to this). This leads to a sharp release of cytokines, adrenaline and other biologically active substances. Initially, under the action of biologically active substances, a spasm of arterioles and postcapillary venules occurs. This leads to the opening of arteriovenous shunts. The blood discharged through the shunts does not perform a transport function, which leads to tissue ischemia and metabolic acidosis. Next, histamine is released, while the sensitivity of blood vessels to adrenaline decreases. As a result, arteriole paresis occurs, while the postcapillary venules are in a state of increased tone. Blood is deposited in the capillaries, which leads to the release of its liquid part into the intercellular space.

Often, infectious and toxic shock is accompanied by DIC syndrome, the presence of which exacerbates microcirculation disorders. At the same time, microthrombs form in the vessels, a sludge phenomenon develops (a kind of gluing of erythrocytes), which leads to a violation of the rheological properties of blood and even greater deposition of it. In the phase of hypocoagulation with DIC syndrome, there is a tendency to bleeding (see the pathological anatomy in the general question about SHOCK (IT IS THE SAME))