5. Reversible cell damage: definition, classification, causes, mechanisms of development.

Dystrophy (degeneration) is a complex pathological process based on a violation of the tissue (cellular)metabolism, leading to structural disorders, as a result, unusual substances accumulate in the tissues-products of impaired metabolism. The causes may be violations of both cellular and extracellular mechanisms that provide trophism:

1. Disorders of autoregulation (may be caused by hyperfunction, toxic substances, radiation, hereditary insufficiency or lack of enzyme)-> energy deficiency, violation of enzymatic processes->fermentopathy (the main link in the pathogenesis of dystrophy).

2. A violation. functions of transport systems→hypoxia→dyscirculatory dystrophy.

3. A violation. endocrine regulation of trophism (thyrotoxicosis, diabetes)-endocrine dystrophies,disorders of nervous regulation of trophism (impaired innervation, tumor)-nervous dystrophy

4. intrauterine (related to the mother's disease)→malformations.

Classification:

1. Depending on the predominance of morphological changes in specialized elements of the parenchyma or stroma and vessels:

1. parenchymal;

2. stromal vascular;

3. mixed.

2. According to the predominance of disorders of one or another type of metabolism: protein; fat; carbohydrate; mineral.

3. Depending on the influence of genetic factors: acquired and hereditary.

4. According to the prevalence of the process: general and local.

Mechanisms:

1) Infiltration (excessive penetration of metabolic products from blood and lymph into cells or intercellular.Secondly, their accumulation is due to the insufficiency of the enzyme systems that metabolize these products. Example:inf. coarse protein of the epithelium of the proximal tubules of the kidneys in nephrotic syndrome, intimal cholesterol in a/c).

2) Decomposition (phanerosis) is the breakdown of ultrastructures, leading to metabolic disorders and accumulation of products in the tissue (cell).Example: fatty acid CMC in diphtheria intoxication).

3) Perverted synthesis-synthesis of non-normalized b-B. Example:amyloid, alcoholic hyaline).

4) Transformation (formation of products of the same type of metabolism from common starting products used for protein synthesis, fats and carbohydrates.(transfer of carbon and fat components into proteins).

6. Parenchymal proteinaceous dystrophy: definition, causes, mechanisms of development, macro- and microscopic signs. Disease examples.

The essence of parenchymal dysproteinosis consists in changing the physico-chemical and morphological properties of cell proteins. They undergo denaturation and coagulation or, conversely, colliquation, which leads to hydration of the cytoplasm. When the connection of proteins with lipids is disrupted, the destruction of cell membrane structures occurs. As a result of these disorders, coagulation (dry) or colliquation (wet) necrosis may develop. Causes: damage due to hypoxia. Hypoxia is caused by impaired blood supply to cells (temperature, changes in atmospheric pressure), functional overstrain of cells, exposure to toxic substances that disrupt ATP production, etc.

Parenchymal dysproteinosis includes granular, hyaline drip, hydropic and horny dystrophy.

1. Granular dystrophy, in which protein grains are detected in the cells of parenchymal organs during light-optical examination. At the same time, the organs themselves are enlarged, flabby and dull in the incision, which was the reason to call granular dystrophy a dull (cloudy) swelling. A morphological pattern similar to granular dystrophy can occur with hypertrophy and hyperplasia of the ultrastructures of parenchymal organ cells as an expression of their functional tension and adaptation to excessive stress in response to various influences. With granular dystrophy, a pattern of cloudy swelling of the organ develops, which excludes adaptation processes. Granular dystrophy appears in cells at the beginning of decompensation of organ function. The outcome of granular dystrophy is its elimination, this dystrophy is reversible. If the cause of cell damage is not eliminated, then granular dystrophy is transformed into hyaline drop dystrophy.

2. With hyaline droplet dystrophy, large hyaline-like protein lumps and droplets appear in the cytoplasm, merging with each other and filling the cell body. The cause of this dystrophy lies in the coagulation of cytoplasmic proteins with pronounced destruction of the ultrastructural elements of the cell – focal coagulation necrosis; it occurs in the kidneys, less often in the liver, and very rarely in the myocardium; the appearance of organs with this dystrophy does not have any characteristic features. Micro-: in the kidneys - accumulation of large grains of bright pink protein – hyaline droplets – found in nephrocytes; at the same time, destruction of mitochondria, endoplasmic reticulum, and brush border is observed; hyaline droplet dystrophy of nephrocytes is based on insufficiency of the vacuolar-lysosomal apparatus of the epithelium of the proximal and distal convoluted tubules, normally reabsorbing proteins; often occurs in nephrotic syndrome. In the liver, lumps and droplets of a protein nature are found in hepatocytes – this is alcoholic hyaline, which is at the ultrastructural level irregular aggregates of microfibrils and hyaline irregularly shaped inclusions (Mallory corpuscles) – found in alcoholic hepatitis.Outcome: unfavorable - it ends in an irreversible process leading to total coagulation necrosis of the cell. The functional significance of this dystrophy is very great – there is a sharp decrease in organ function. An example of the disease: Wilson-Konovalov disease.

3. Hydropic, or vacuolic, dystrophy is characterized by the appearance of vacuoles in the cell filled with cytoplasmic fluid in the cisterns of the endoplasmic reticulum and in mitochondria, less often in the cell nucleus. The mechanism of development reflects violations of water-electrolyte and protein metabolism, leading to a change in colloidal osmotic pressure in cells, an important role is played by a violation of the permeability of cell membranes, accompanied by their decay. Causes: in the kidneys – this is damage to the glomerular filter (glomerulonephritis, amyloidosis, diabetes mellitus); in the liver - with viral and toxic hepatitis; There are infections and allergies in the epidermis. Macro-: the appearance of organs and tissues changes little with hydropic dystrophy. Micro: parenchymal cells are enlarged in volume, their cytoplasm is filled with vacuoles containing a transparent liquid; the nucleus shifts to the periphery, sometimes vacuolates or shrinks; an increase in hydropy leads to balloon dystrophy. Outcome: unfavorable - results in total colliquation necrosis of the cell. Examples of diseases:viral hepatitis, encephalopathy (Kreutzfeld-Jakob disease), HIV infection.

4. Corneal dystrophy, or pathological keratinization, is characterized by excessive formation of corneal matter in the keratinizing epithelium (hyperkeratosis, ichthyosis) or formation of corneal matter where it normally does not occur – pathological keratinization on mucous membranes, for example, in the oral cavity (leukoplakia), esophagus, cervix. Corneal dystrophy can be local or general, congenital or acquired. Causes: chronic inflammation associated with infectious agents, the action of physical and chemical factors, vitamin deficiency, congenital skin development disorder, etc. The outcome can be twofold: eliminating the causative cause at the beginning of the process can lead to tissue repair, but in far-reaching cases, cell death occurs. Examples of diseases: ichthyosis, hyperkeratosis,

A number of dystrophies adjoin the group of parenchymal dysproteinoses, which are based on violations of the intracellular metabolism of a number of amino acids as a result of hereditary insufficiency of the enzymes that metabolize them, i.e. as a result of hereditary fermentopathy. These dystrophies are classified as accumulation diseases.

Hereditary parenchymal dysproteinoses, which are caused by a violation of intracellular metabolism of amino acids, include: cystinosis, tyrosinosis and phenylpyruvic oligophrenia (phenylketonuria). In these diseases, the liver, kidneys, bone marrow, spleen and nervous system are most often affected.