FATTY DYSTROPHY (synonym dystrophic obesity) — the disturbance of exchange of cytoplasmatic fat which is followed by damage of cellular structures; it is expressed in increase in amount of fat in the cells supporting him it is normal, in emergence of fat where it usually does not meet also education in cells or in extracellular substance of fat of unusual chemical structure.
Development. by it is usually connected with air hunger (a fabric hypoxia) therefore it quite often meets at diseases of cardiovascular system, hron, diseases of lungs, anemias, hron, alcoholism etc. arises at many infections (diphtheria, tuberculosis, sepsis, etc.) and intoxications (phosphorus, arsenic, chloroform, a dichloroethane, etc.) leading to exchange disturbances, sometimes at avitaminosis and the unilateral low-proteinaceous food which is followed by deficit of enzymes and lipotropic factors. Development. can be connected also with hereditary deficit of the enzymes metabolizing certain types of fats (lipoida) that leads to development of hereditary system lipoidoses (see. Lipidoses ).
Emergence of fat in a cell or intercellular substance at. can be connected with receipt it from blood and a lymph (fatty infiltration), disintegration of zhirobelkovy complexes of an ultrastructural cell of components (fatty decomposition, or faneroz), with the increased formation of fat from carbohydrates and proteins (fatty transformation) perverted by synthesis. In some cases these mechanisms are combined or replace each other. Dominance of this or that mechanism of development. by it is connected not only with an originality of the reason, but also with strukturnofunktsionalny features of body (fabric), develops in Krom. Studying of a morphogenesis. dystrophic obesity allowed to combine with so-called simple obesity (see), the fat of cytoplasm of a «healthy» cell connected with infiltration.
Most often. is observed in parenchymatous bodies — heart, a liver, kidneys in which cells fat comes to light by means of a row histochemical methods of a research (see): Sudan III and sharla paint it in red color, Sudan IV and osmic to - that is in black, sulfate Nile blue paints fat to - you in dark blue color, and neutral fats in red. In heart find the powdered or small-drop obesity of muscle cells developing hl. obr. by a lipofaneroz: the majority of mitochondrions breaks up, cross striation of fibers disappears, the kernel becomes piknotichny or is exposed to a lysis. Process has focal character and is observed in groups of muscle cells on the course of venous circulatory capillaries and venules. Accumulations of such fibers have an appearance of ochroleucous strips (tsvetn. fig. 5) which are well noticeable under an endocardium of ventricles, especially in papillary muscles and trabeculas. The endocardium becomes ischerchenny and spotty («tiger heart»). Heart at. increases in sizes, its cameras are stretched, a myocardium flabby, a clay look.
O Zh. (obesity) of a liver speak when the amount of the fat which is contained in hepatocytes is normal, its qualitative players increase sharply and changed. Obesity can be powdered, small - or krupnokapelny (fig. 1 and 2). The fatty drop pushes aside rather safe organellas on the periphery of a hepatocyte which becomes cricoid. Single hepatocytes (the so-called disseminated obesity), groups of hepatocytes (zone obesity) or all parenchyma of a liver (diffusion obesity) are involved in process. In cases of a hypoxia and intoxication obesity of hepatocytes arises preferential tsentrolobulyarno, in other cases (protein-vitamin insufficiency, obesity, a lipidemia) — hl. obr. periportalno. At sharp fatty infiltration hepatocytes perish, fatty drops merge and form fatty cysts around which there is a cellular reaction, connecting fabric develops. A liver at. by it is increased, flabby, yellow or red-brown coloring.
. of kidneys has resorptive character (resorptive obesity) more often, i.e. is connected with infiltration of an epithelium of proximal and distal departments of nephrons (tsvetn. fig. 6) and stromas fat at the lipidemia so characteristic of a nephrotic syndrome of any etiology. Normal fat meets in an epithelium of a thin segment (Henle's loops), inserted departments of tubules and collective tubes. Usually it is neutral fat, cholesterol, phospholipids. Fatty infiltration leads to increase in the sizes of kidneys, expansion of cortical substance, in Krom the yellow impregnations noticeable on a surface and a section of a renal parenchyma appear
. of walls of vessels (arteries) is the cornerstone atherosclerosis (see). At the same time in an intima of arteries collect not only cholesterol and its ester, but also beta lipoproteids and proteins of plasma. The collecting krupnomolekulyarny substances lead to destruction of an intima, break up and saponified. In a result in to an intima the zhirobelkovy detritis is formed, connecting fabric expands, the fibrous plaque forms.
At hereditary lipoidoses in fabrics cerebrosides can collect (see. to Gosha disease ), sphingomyelins (see. Nimanna-Pika disease ), gangliosides (Teja — the Saxophone a disease and generalized gangliozidoz), cholesterol and its ester (a family giperkholesterinemichesky xanthomatosis)
. leads to disturbance or loss of function of bodies in whom dystrophy develops. of a myocardium, e.g., very often is morfol, expression heart failure (see), and. of kidneys — morfol. expression nephrotic syndrome (see). In a liver against the background of. develops cirrhosis. Fatty infiltration of an internal cover of arteries can be one of causes of infringement of passability of vessels.
Outcome. depends on its expressiveness. If it is not followed by deep damage of cellular structures, then it is, as a rule, reversible. Deep disturbance of exchange of cellular fat leads to death of a cell.
Bibliography: Davydovsky I. V. General pathology of the person, page 89, M., 1969; Ivanovskaya T. E. and L. V Tsinzerling. Pathological anatomy, page 26, M., 1976; Serov V. V. and V. S Spiders. Ultrastructural pathology, page 142, M., 1975; Handbuch der allgemeinen Pathologie, hrsg. v. F. Biich-ner u. a., B. u. a., 1968; Molekulare Biolo-gie der Zelle, hrsg. v. H. Bielka, Jena, 1973.
B. B. Serov.