54. Shock: definition of concept, types, stages. Macro- and microscopic changes in organs during shock.

Shock is an acutely developing pathological process caused by the action of an extremely strong stimulus and characterized by a violation of the central nervous system, metabolism and, most importantly, the autoregulation of the microcirculatory system, which leads to the destruction of organs and tissues.

Types of shock:

• hypovolemic shock, which is based on an acute decrease in the volume of circulating blood (or fluid);

• traumatic shock, the trigger of which is excessive afferent (mainly painful) impulses;

• cardiogenic shock resulting from a rapid decrease in the contractile function of the myocardium and an increase in the flow of afferent (mainly hypoxic) impulses;

• anaphylactic (allergic) shock;

• septic (toxic-infectious) shock caused by endotoxins of pathogenic microflora.

The morphological picture of shock is determined by a violation of hemocoagulation in the form of DIC syndrome, hemorrhagic diathesis, liquid blood in the vessels, which is the basis for the diagnosis of shock at autopsy. Violations of hemodynamics and rheological properties of blood are manifested by widespread vascular spasm, microthrombs in the microcirculation system, signs of increased capillary permeability, hemorrhages. A number of common changes develop in the internal organs — fatty degeneration

necrosis caused by hemodynamic disorders, hypoxia, the damaging effect of biogenic amines, endotoxins of pathogenic microflora. Morphological changes in shock have a number of features due to both the structural and functional specialization of the organ and the predominance of one of its links in the pathogenesis of shock - neuroreflective, hypoxic or toxic. Guided by this provision, the term "shock organ" is used to characterize shock.

In the shock liver, hepatocytes lose glycogen, undergo hydropic dystrophy, develop centrolobular necrosis of the liver; signs of structural and functional insufficiency of stellate reticuloendotheliocytes appear. Shock lung is characterized by hemostasis and blood clots in the microcirculatory bed, foci of atelectasis, serous hemorrhagic edema with loss of fibrin into the lumen of the alveoli, which causes the development of acute respiratory failure.

Changes in the myocardium during shock consist in the development of dystrophy and necrobiosis of cardiomycetes: the disappearance of glycogen, the appearance of lipids, contractures and fragmentation of myofibrils. Small foci of necrosis may appear.

55. DIC-syndrome: definition of the concept, mechanisms of development, stages, microscopic signs in organs.

DIC syndrome (disseminated intravascular coagulation syndrome, thrombohemorrhagic syndrome, consumption coagulopathy) is an acquired nonspecific process of hemostasis disorder that develops as a result of excessive activation of prothrombin and thrombin formation due to the entry of blood coagulation activators and erythrocyte aggregation into the bloodstream.

Stages of DIC syndrome:

1. 1st stage - hypercoagulation and aggregation of shaped blood elements

2. 2nd stage - transitional with increasing consumption coagulopathy and thrombocytopenia

3. 3rd stage – hypocoagulation

4. 4th stage - recovery or stage of outcomes and complications Depending on the duration of the course: a) acute (hypercoagulation phase up to several minutes it is replaced by hypocoagulation) b) acute (within 24 hours) c) subacute (for several days with recurrence)

Etiology:

infections, especially generalized ones (sepsis - 30-50% of all cases of DIC syndrome)

all kinds of shock

acute intravascular hemolysis and cytolysis in incompatible transfusions

obstetric pathology (premature placental abruption, etc.)

tumors, especially leukemias

thermal and chemical burns

immune and immune complex diseases (rheumatic, GH)

Pathogenesis: activation of the hemostasis exo polysystem- and endogenous factors → scattered intravascular coagulation of blood and aggregation of shaped elements mainly in the MCR → activation of plasmin, kallikrein-kinin and complementary systems → secondary endogenous intoxication with products of proteolysis and tissue destruction → hemorrhagic syndrome due to microcirculatory disorders, consumption of blood clotting factors, thrombocytopenia and thrombocytopathy, accumulation of proteolysis products → alterative (dystrophy, necrosis) changes in various organs and tissues due to hemodynamic disorders and blockage of the vascular bed by aggregates of shaped blood elements, microthrombs

The central place in the pathogenesis of DIC syndrome is

1. thrombin, which cleaves fibrinogen

2. plasmin, which dissolves fibrin.

Clinic

In the clinical picture of DIC syndrome, there are:

1. in stage 1, symptoms of the underlying disease and signs of thrombohemorrhagic syndrome (with predominance of generalized thrombosis), hypovolemia, metabolic disorders.

2. in the 2nd stage, signs of multiple organ damage and blockade of the microcirculation system of parenchymal organs, hemorrhagic syndrome (petechial purple type of bleeding) appear.

3. in stage 3, these disorders are joined by signs of multiple organ failure (acute respiratory, cardiovascular, hepatic, renal, intestinal paresis) and metabolic disorders (hypokalemia, hypoproteinemia, metabolic syndrome of a mixed type (petechiae, hematomas, bleeding from mucous membranes, massive gastrointestinal, pulmonary, intracranial and others bleeding, hemorrhages in vital organs).

4. in stage 4 (with a favorable outcome), the main vital functions and hemostasis indicators gradually return to normal.

In DIC, polymerization of fibrin monomers is disrupted and "blocked" fibrinogen is formed (due to activation of proteolysis) → connection of fibrin monomers with fibrinogen, fibronectin and other molecules → soluble fibrin monomer complexes (products of paracoagulation), poorly coagulating and rapidly eliminated by leukocytes and endothelium → hypocoagulation