FIBRINOID TRANSFORMATION

From Big Medical Encyclopedia

FIBRINOID TRANSFORMATION

(fibrin + Greek eidos look; synonym: fibrinoid change, fibrinoid swelling) — a type of mesenchymal proteinaceous dystrophy (an extracellular disproteinoz), at Krom happens deep and irreversible disorganization of connecting fabric. At F. the item is formed unstructured homogeneous substance — fibrinoid, proteins and polysaccharides of the breaking-up collagenic fibers, the main substance of connecting

fabric and a blood plasma, and also cellular nucleoproteids are a part to-rogo; its obligatory component is fibrin. The terms «fibrinoid swelling», «fibrinoid» are also connected with the last.

T. the item is found at many diseases of connecting

fabric and vessels, in particular, it

is morfol. manifestation of the attack of rheumatism (see), hypertensive crisis (see Crises), aggravations of a peptic ulcer (see) etc. Fibrinoid transformation leads to dysfunction of the struck body, napr, at a rheumatic carditis, or to the termination of its function, napr, as a result of acute renal nedo

statochnost at a malignant form of an idiopathic hypertensia (see).

T. the item for the first time described in 1896 Neymannom (E. Neumann) as the fibrinoid degeneration caused as he considered, damage and disintegration of collagenic fibers, to-rye gained ability in gistol. drugs to be painted as fibrin (see). Further began to attach great value to a condition of the main substance of connecting fabric and first of all accumulation in it of the acid glikozoaminogli-kan (see Mucopolysaccharides) which are released at damage of fibrous and cellular structures of connecting fabric (see). Nek-ry researchers connected formation of fibrinoid only with acid glikozoaminoglika-us, first of all with hondroitinsul-phages. However most of researchers consider that formation of fibrinoid is impossible without proteins of a blood plasma and, first of all, fibrinogen (see) with its subsequent transformation into fibrin. Apparently, contradictory ideas of composition of fibrinoid are to some extent connected with the fact that he is various at different diseases.

Among etiol. the factors causing widespread (system) F. items, the greatest value have infectious and allergic (e.g., causing formation of fibrinoid of vessels at the tuberculosis proceeding with giperergichesky reactions), allergic and autoimmune (e.g., causing F. of connecting fabric at collagenic diseases, vessels at primary vasculites, capillaries of renal balls at a glomerulonephritis), angioneurotic (e.g., causing formation of fibrinoid in arterioles at an idiopathic hypertensia and gipertenzionny states). In other cases F. the item arises locally as manifestation of an inflammation, especially chronic, in a certain body, napr, in a worm-shaped shoot at appendicitis, day hron. ulcers at a peptic ulcer of a stomach, in trophic ulcers of skin, etc.

Among the pathogenetic factors leading to development F. to the item and formation of fibrinoid, the main consider destruction of collagenic fibers and the main substance of connecting fabric in combination with increase in the vascular and fabric permeability (see) providing transport of krupnomolekulyarny proteins and polysaccharides of a blood plasma through biol. membranes. At the same time in one cases destruction of connecting fabric, in others — increase in permeability can prevail. The prevailing value of one of these factors depends on features of an etiology and pathogeny of diseases. So, at collagenic diseases (see), system vasculites (see Vasku of litas), etc. formation of fibrinoid is connected by hl. obr. with immu-nokompleksny destruction of connecting fabric and the subsequent sorption of fibrin. As a result of it so-called fibrinoid of destruction, or fibrinoid of cell-bound immune complexes is formed. At a phenomenon of Ar-tyusa (see Artyus a phenomenon) fibrinoid, in addition to cell-bound immune complexes, contains the fragmented and split collagenic fibrilla and fibrin. Presence at fibrinoid at this disease of the nuclear material which is painted at Feylgen's reaction is connected with an antinuclear orientation of cell-bound immune complexes at a system lupus erythematosus (see. Deoxyribonucleic acid). At diseases of angioneurotic and plaz-morragichesky genesis, as well as at coagulopathies, in creation of fibrinoid the leading role belongs to increase in permeability of proteins of a blood plasma. In these cases it is possible to speak about so-called fibrin-fib-rinoide since the factor of destruction is pushed the background and fibrinoid it is identical to fibrin. Fibrinoid of a placenta — Nitabukh's layer is also identical to fibrin (see the Placenta).

Bodies and fabrics, in to-rykh F develops. items, are macroscopically poorly changed. Characteristic for F. items of change are found usually only at microscopic examination: the bunches of collagenic fibers impregnated with proteins of plasma become homogeneous, form the insoluble strong compounds which are greedy perceiving acid dyes, napr, eosine with fibrin, are painted in yellow color by pikro-fuchsin by Van-Gizona's method (see Van-Gizona a method), I is sharp 111 And { - also pironinofilna at reaction across Vra-tpa are positive (see CHIC reaction) (see RNA), and also argirofilna at impregnation by silver (see Impregnation, Silverings methods). Metachrome, Asia (see) connecting fabric at the same time is not expressed or expressed poorly that is explained by a depolymerization of glikozoaminglikan of the main substance. During the progressing F. the item sometimes develops the fibrinoid necrosis which is characterized by full destruction of connecting fabric. T. the item quite often comes to the end with a hyalinosis (see).

ShM. also Proteinaceous dystrophy.

Bibliogrobshchy pathology of the person, under the editorship of A. I. Strukov, etc., M., 1982; Serov V. V. and Shekhter A. B. Connecting fabric, M., 1981; With tr at-to about in A. I. and B e of l and r I am A. G N. Pathological anatomy and pathogeny of collagenic diseases, M., 1963; F a s s b e n-d e of H. G. Pathology of rheumatic diseases, V. and. lake, 1975; Neumann E. Zur Kenntniss des fibrinoiden Degeneration des Bindegewebes bei Entzundungen, Virchows Arch. path. Anat., Bd 114, S. 201, 1896; Robbins S. L., Angel 1 M. a. Kumar V. Basic pathology, Philadelphia a. o., 1981. V. V. Serov.

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