9. Myocardial fatty degeneration: terminology, causes, mechanisms of development, macro- and microscopic changes, clinical manifestations, outcomes, complications.

Fatty myocardial dystrophy can occur most often as a result of hypoxia or intoxication (diphtheria, alcohol, phosphorus poisoning, arsenic, etc.). In both cases, damage to the mitochondria develops and a decrease in the intensity of fatty acid oxidation. Micro-: Tiny fat droplets appear in muscle cells (pulverized obesity), which, with increasing changes (small-drop obesity), replace the cytoplasm. The process is focal in nature and is observed in groups of muscle cells along the venous knee of capillaries as well as small veins, which explains the peculiar appearance of the heart: yellow transverse stripes (“tiger” heart) are visible from the endocardium. Macro-: The myocardium is flabby, the size of the heart can be increased, and the cavities are expanded. Outcome and complications: The outcome of parenchymal fatty myocardial dystrophy depends on the degree of its severity. The initial changes are reversible, deep ones lead to a pronounced impairment of function.

10. Mesenchymal dystrophies: definition, classification, causes, mechanisms of development. Disease examples.

Stromal vascular (mesenchymal) dystrophy is the result of metabolic disorders in the connective tissue of the stroma of organs and vascular walls. They develop on the territory of the histione, which is formed by a segment of the microcirculatory bed with surrounding elements of connective tissue (basic substance, fibrous structures, cells) and nerve fibers. Among the mechanisms of development of stromal vascular dystrophy, violations of trophic transport systems, common morphogenesis, the possibility of not only combining different types of dystrophy, but also the transition of one species to another prevail. Mesenchymal dystrophy is detected in the stroma of organs and the walls of blood vessels, and depending on the type of metabolic disorder, they are divided into protein, fat and carbohydrate.

11. Mesenchymal protein dystrophies: stages of connective tissue disorganization, causes, mechanisms. Macro- and microscopic changes in the connective tissue. Disease examples.

Stromal vascular dysproteinosis includes mucoid swelling, fibrinoid swelling (fibrinoid) and hyalinosis. Previously, they included amyloidosis.

• Mucoid swelling is a superficial and reversible disorganization of connective tissue. Causes: hypoxia, infections, especially streptococcal, immunopathological reactions (hypersensitivity reactions) play an important role in the development of mucoid swelling. At the same time, the accumulation and redistribution of glycosaminoglycans occur in the main substance due to an increase in the content, primarily hyaluronic acid. Glycosaminoglycans have hydrophilic properties, their accumulation causes an increase in tissue and vascular permeability. As a result, plasma proteins (mainly globulins) and glycoproteins are mixed with glycosaminoglycans. Hydration and swelling of the main interstitial substance develop. Mucoid swelling occurs in the stroma of various organs and tissues, but more often in the walls of arteries, heart valves, endocardium and epicardium, i.e. where chromotropic substances are found normally, while the number of chromotropic substances increases sharply. It is most often observed in infectious and allergic diseases, rheumatic diseases, atherosclerosis, endocrinopathies. Micro-: the phenomenon of metachromasia is a change in color, which is based on a violation of the state of the main interstitial substance with the accumulation of chromotrap (coloring) substances. Collagen fibers usually retain their bundle structure, but swell and undergo fibrillar fibrillation. Changes in the basic substance and collagen fibers during mucoid swelling are accompanied by cellular reactions - the appearance of lymphocytic, plasma cell and histiocytic infiltrates. Macro-: the appearance of a tissue or organ with mucoid swelling is preserved, characteristic changes are established by histochemical reactions during microscopic examination. The outcome is twofold: complete tissue restoration or transition to fibrinoid swelling. The function of the organ suffers at the same time (for example, cardiac dysfunction due to the development of rheumatic endocarditis, valvulitis).

• Fibrinoid swelling is a deep and irreversible disorganization of connective tissue, which is based on the destruction of its basic substance and fibers, accompanied by a sharp increase in vascular permeability and the formation of fibrinoid. The impregnation of tissues with plasma proteins continues, which accumulate in the main substance and collagen fibers, destroying them and turning them into a homogeneous mass containing fibrinoid - a complex substance consisting of fibrin, polysaccharides, immune complexes (in rheumatism), nucleoproteins (in systemic lupus erythematosus).Micro-bundles of collagen fibers impregnated with plasma proteins become homogeneous, forming strong insoluble compounds with fibrin; they are eosinophilic, pyrofuxin stained yellow, sharply Chic-positive and pyroninophilic in the Brachet reaction, argyrophilic in impregnation with silver salts. Metachromasia of connective tissue is not pronounced. As a result of fibrinoid swelling, fibrinoid necrosis usually develops - complete destruction and homogenization of connective tissue.