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Theoretical part. Dystrophy is a pathological process based on metabolic disorders and caused by impairement of cellular and extracellular mechanisms of trophic regulation. This process reflects inhibition and disorder of cellular function, that’s characterized by impaired fermental function (fermentopathy) with future accumulation of waste products (which are changed in quantity and quality) in cytoplasm and intercellular surroundings.

Morphological evidens of impaired metabolism are observed in cells and intercellular surroundings. That’s why there are: cellular (parenchimatous), extracellular (stromal) and mixed degenerations. Infiltration, transformation, perversional synthesis and decomposition are based on accumulation of the products in cytoplasm and in intermediate tissue.

“Granular” degeneration, hyalinic-drop degeneration, hydropic change, horny degeneration belong to parenchimatous proteinosis. In case of “granular” degenerations organs increase in their sizes, rose-colored protein granules appear in cytoplasm (stained with hematoxylin and eosin). V.V.Serov, A.I.Strukov (1993) thank that this kind of degenerations couldn’t exist independently. They said that “granular” degenerations based on ultrastructural hyperplasia of parenchimatous cells caused by organ overload, but not by accumulation of protein granules in cytoplasm. In such case ultrastructural hyperplasia looks like the protein granules under the light microscope.

In fact in some cases ultrastructural morphology of parenchimatous cells (especially myocardium and liver) does not indicate dystrophic changes. It is a result of cell overload, that is why it has no attitude to degenerations. This kind of degenerations is a manifestation of compensatory processes that are based on intracellular regeneration and ultrastructural hyperplasia. So the “granular” degeneration of the renal proximal convoluted tubules indicates the level of protein resorption in case of epithelial cells overload and it isn’t really pathological process. But in most cases an influence of pathogenic agents is accompanied by cellular functional damage which is characterized by decreasing of its fermental activity (enzymopathy). That’s why “granular” degenerations is a pathological process that must have an independent meaning.

In case of parenchimatous degenerations disturbance of metabolism appear in highly specialized cells in such organs as the heart, the liver and the kidneys. It is caused by development of aquired or hereditary enzymopathies. Parenchimatous proteinosis ischaracterized by appearance of protein inclusions in cytoplasm. As a rule this process is accompanied by K+-Na+-pump work disturbance. It indicates accumulation of ions Na+ in the cell and its hydration. Hydropic change and hyalinic-drop degeneration in the kidneys have the infiltration mechanism of onset with further decomposition because vacuoles and lysosomes of nephrocytes are damaged, that is the main apparatus which provides proteins reabsorbtion. Besides hydropic change can be connected by these mechanisms with the other system of reabsorbtion. We speak about basal labyrinth which works on Na+-K+-dependent ÀÒP synthase providing sodium and water reabsorbtion.



“Granular” degenerations, hyaline degenerations, hydropic changes may be considered as different steps of protein metabolism disturbance of the cell. Breach of the chemical connections between proteins with cytoplasmic lipoids and colloids, protein denaturation, increasing membrane penetration and accumulation water in the cell (as a result of Na+-K+-pump disturbance) reduce the level of oxygen-related processes in the cell (“acidification of cytoplasm”) increase enzymes activity in lysosomes, which break intramolecular connections (as a result of joining water to them) and lead to their destruction. Under the circumstances increasing protein denaturation processes is accompaned with “granular” or hyaline degenerations. Increasing hydration of the cell causes hydropic change. Prolongation of these processes cause irreversible changes such as coagulational or coliquational focal ones (sequestration) or total necrosis. Horny degenerations is characterized by excessive hornation at horny layer of epithelium or in others structures where this process isn’t usually observed.

In case of parenchimatous lipidosis disturbance of lipids metabolism in the heart, in the liver, and in the kidneys are usually observed. Lipids are piling in the cells, in such places where they are usually absent or their chemical structure formation is abnormal (in case of parenchimatous lipidosis). Typically the neutral lipids gather in cytoplasm and there are esters of glycerine and fatty acids. Lipid metabolism disturbance also concerns fatty-like substances such as lipoids (phosphatides, sterols, sphingolipids and wax) which also comprise cytoplasmic lipids. Here these lipids connect with proteins and form compound complexes of lipids and proteins – so called lipoproteides that together with proteins compose the base of membranous structures of the cell.

The mechanism of lipidosis development depends on not only the main causes (hypoxia, infections, vitamin deficiency) but the structural and functional characteristics of the organ or tissue where it usually occurs. So, decomposition (the cell membrane desintegration with lipids release) is observed in hypoxia or intoxication in the liver or in the heart. Infiltration is usually observed in the cytoplasm of the liver cells in general obesity and in the proximal convoluted tubular epithelial cells of the kidney in nephrotic syndrome. Disturbance of lipids syntesis is the main cause of accumulation diseases (inherited enzymopathia). For example, cerebrosides are accumulated because of lysosomal glucocerebroside absence (Gaucher's disease) or accumulation of sphingomyelin because of lysosomal sphingomyelinase absence (Niemann-Pick's disease) and others.

Parenchimatous carbohydrate degenerations result from glycogen, glycosaminoglycans and glycoproteids (mucins and mucoids) metabolism disturbances. Glycogen metabolic disorders are characterized by glycogen increase or decrease in cytoplasm and also its synthesis in those places where it is not usually observed. Such disturbances are usually observed in diabetes mellitus and in inherited carbohydrates degenerations, so called glycogenosis.

Glycogen usually accumulates in the epithelial cells of narrow segment of Henle’s loop and in the distal convoluted tubules when diabetes mellitus occurs. Eventually diabetes microangiopathia (intercapillary glomerulonecrosis) develops. Inherited carbohydrate degenerations is caused by absence or insufficient activity of enzymes in lysosomes which take part in glycogen metabolism. Consequently cell doesn’t assimilate this glycogen and it accumulates in cytoplasm. Glycogen structure remains normal in some diseases (Girke’s disease, Pompe’s disease, Mac-Ardl’s disease, Gerse’s disease) and deeply changed in others (Fobs-Kori’s disease, Andersen’s disease).

Glycoproteids (mucin, mucoid) metabolism disorder cause mucous degenerations. Gland epithelial cells produce excessive mucin or pseudomucin in parencyimatous mucous degenerations. This process is usually observed in epithelial tumors. Mucin and mucous substances can condence and become colloid (colloid degenerations). It is usually observed in the thyroid in case of goitre.

Practical part.

Dim swelling of the kidneys.Gross specimen.

The kidneys increase in size. They are of flaccid consistence, anaemic and dim. Parenchyma has the signs of swelling on the sectional view and boil over the capsule. Sectional surface loses its gloss, becomes dim, gray and looks like the boiled meat. Analogous picture is characteristic for postmortal changes. The main macroscopic feature of this process is the most considerable swelling of the organ. And the main microscopic feature is increased size of the cells.

Fatty change in the liver. Gross specimen. The liver increases in size, its edge is disc-shaped. It has flaccid consistence. Parenchyma is yellow on sectional view. There is a lipid reminder on the sectional surface.

Granular degeneration of the kidneys epithelium. Microscopic specimen.

Epithelial cells of the proximal convoluted tubules are increased in size at the big magnification. These cells project into the tubules lumens. As a result the tubules constrict and become crevix-like. Cytoplasm of the cell is cloudy and comprises pink-colored protein granules of different size. One of the characteristic features is dim contours of the endoplasts and their basal localisation. There are homogeneous or small-granular protein masses (protein cylinders) in the tubule lumens.

Hydropic change of the kidneys epithelium. Microscopic specimen.

Epithelial cells of the proximal convoluted tubules are increased in size. Cytoplasm of the cell is light and comprises optically empty vacuoles. The apical parts of the cells are usually destroyed. Endoplasts are usually absent in the most cells and have bad contours with lyse features in other ones.

Fatty ingrowth in the liver (stained with sudan III).Microscopic specimen.

Structure of the liver lobule remains. There are numerous different lipid granules in cytoplasm of the hepatocyte. These granules usually mask endoplasts. Endoplasts are situated peripherally because of lipid accumulation or are absent at all (“fatty cysts”). There are different sizes of optical vacuoles (place of lipid localisation at staining with alcohol).

Thyroid colloid degenerations.Microscopic specimen. The follicules lumens are broadened. Cubical epithelium is situated on basilar membrane. There are homogenous pink-colored, dense accumulation of colloid in the follicules.

Mucous degenerations (cancer of the stomach).Microscopic specimen.

Mucous hypersecretion is usually observed in the tumor the that look like pale – pink-colored swelling. There is mucus producing cancer cells with hyperchromic peripheral endoplasts (the ring cells).

Vacuolar degeneration in cardiomyocyte.Electron micrograph. Endoplasmic reticulum is enlarged. The big vacuoles form is a result of the fragmentation of endoplasmic reticulum ducts. There are osmiofobe material in vacuoles.

Fatty ingrowth in the heart.Microscopic specimen.

Stained with sudan III (“tiger-stripe” heart). The process is local. Sudanophilous lipid drops appear in sarcoplasm of cardiomyocyte around the venous capillaries and small veins.

Granular degeneration in hepatocyte. Electron micrograph.

There are different kinds of organelles and mitochondrions in the cytoplasm. Most of them have the swelling features with diffuse matrix enlightening, local crysts desorganisation with some membrane dissociation. The ducts of endoplasmic reticulum are partially fragmented and form the vacuoles. There is granular material with the medium electronic density in the vacuoles. Endoplasmic reticulum occurs rarely. The structure of endoplasts is normal.

Granular degeneration in cardiomyocyte. Electron micrograph.

Mitochondrions are abnormal with swelling features. Local or diffuse matrix swelling is also observed, it’s loop-sided enlightening and crysts desorganisation with some membrane dissociation.

Fatty ingrowth in cardiomyocyte.Electron micrograph.

Multiple liposomes accumulate in sarcoplasm in interfibrillar interval and near the mitochondrions.

Cardiomyocyte in glycogenosis (Pompe’s disease, type II). Electron micrograph.

Glycogen is accumulated near sarcolemma. Mitochondrions demonstrate distrophic changes.

The classification of parenchimatous degenerations. Table.

The mechanisms of dystrophies’ development. Table.

Fatty ingrowth in the heart ( “tiger-stripe” heart). Slide.

The heart is enlarged and yellow. Yellow-white streakes are observed on the endocardial side, which are especially noticeable on the papillary muscles and on the trabeculae of the ventricles. Some separate cardiomyocits groups fatness is observed around the venous capillaries and small veins. There are lipid drops in sarcoplasm which are red ( stained with sudan III) or black (stained with osmium).


Date: 2016-03-03; view: 706


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Theme: Degenerations. Parenchimatous degenerations (dystrophies). | Theme: Mesenchymal degenerations
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