STROMAL VASCULAR PROTEIN CHANGES
Stromal vascular protein changes develop in the connective tissue as a result of metabolic disturbances in it. Pathological process develops in a structural unit of connective tissue, i.e. histion. Histion is formed by a segment of microcirculatory channel with the surrounding elements of connective tissue and nerve fibers. Connective tissue elements are collagen, reticular and elastic fibers, cells: fibroblasts, which producing collagen, macrophages, fibrocytes as well as the main substance. It should be mentioned that in addition to collagen, fibroblasts produce glycosami-noglycanes of the main substance.
Albuminous (protein) changesmanifest as mucoid swellings, fibrinoid changes, hyalinosis and amyloidosis.
The first three types are the stages of connective tissue disorganization. Their development is based on
blood plasma protein accumulation in the main substance due to increased vascular permeability (plasmorrhagia). Besides, connective tissue elements destruction accompanied by formation of protein-polysaccharide complexes is present. In amyloidosis the protein-polysaccharide complex includes abnormal fibril protein.
Mucoid swellingis superficial reversible disorganization of the connective tissue. The amount of hyaluronic acid and its derivatives (HAH), possess which hydrophilic properties increases. Increased vascular permeability (due to HAH action) and plasmorrhagia develop resulting in HAH, globulin, and blood glycoproteides accumulation in the main substance and hydration and swelling of the main substance. Microscopic examination shows meta-chromasia. Under normal conditions the main substance is basophilic. In this case staining with toluidine blue demonstrates reddish coloring. Collagen fibers are swollen though band structure is preserved. Macroscopic study does not reveal any changes. The outcome may be reversible. In other cases development of fibrinoid swelling is possible.
The causes of mucoid swelling, fibrinous changes and hyalinosis are the same as they are the stages of one process. They are immunopathological and autoimmune states, hypoxia, infections. These types of connective tissue disorganization are frequently observed in hypertension, rheumatism and other
diseases of the connective tissue accompanied by immune disturbances as well as in allergic diseases, etc.
In the majority of cases the arterial walls, heart valves, endocardium, epicardium, articular connective tissue are involved.
Fibrinoid changes.There are two stages in the fibrinoid changes.
Stage 1 is fibrinoid swelling which is deep and irreversible connective tissue disorganization. Stage 2 is fibrinoid necrosis. As a result of the main substance destruction and sharp increase in vascular permeability, fibrinoid is formed. It is a complex substance consisting of decomposed collagen fibers, proteins, blood plasma, main substance, cellular nucleoproteids, fibrin. In different diseases histochemical composition of fibrinoid is different and very often is a diagnostic criterion (e.g. in lupus erythematosus). The appearance of the organs is changed a little. The main signs are revealed microscopically: the bands of collagen fibers are homogenous, impregnated with plasma proteins. Metachromasia is not marked due to HAH depo-lymerization of the main substance. Fibrinoid swelling may be generalized (in systemic diseases of the connective tissue) and localized (in chronic inflammations, e.g. in the bed of chronic ulcer). The outcome is fibrinoid swelling followed by fibrinoid necrosis, sclerosis or hyalinosis.
Hyalinosis(greek «hyalos»—transparent, glass-like) is formation of semitransparent dense masses
(hyalin) resemble hyaline cartilage in the connective tissue. Hyalinosis develops as a result of plasma impregnation, fibrinoid swelling, inflammation, necrosis, sclerosis. Hyalinosis are classified according to their localization (vascular hyalinosis, connective tissue hyalinosis) and propagation (generalized and localized). Each of the above forms may be generalised and localized.
Vascular hyalinosis involves the arterioles and small arteries. In their walls, endothelium, basal membranes, and smooth muscle cells are damaged. Impregnation of the wall with plasma is observed. Microscopic study of the arteries demonstrates thickened walls with a sharply narrowed or obliterated lumina. At first, hyalin is accumulated in subendo-thelial areas of the vascular wall, then it destroys elastic plate and middle membrane. Vascular hyalinosis is generally a systemic process. It characterizes hypertension and diabetic cardiomyopathy. The vessels of the brain, kidneys, retina are the most frequently involved. Three types of vascular hyalin are distinguished depending on the pathogenetic character of its formation: 1) simple, 2) lipohyalin, 3) compound-hyalin.
Connective tissue hyalinosis is usually a localized condition, it develops in scars, adhesions, in the areas of chronic inflammation (e.g. «glazed spleen»).
The outcome of hyalinosis is irreversible as a rule, but in the scars called keloids hyalin can loosen and resolve (e.g. in the breast).
Functional significance of hyalin is different. Thus, vascular hyalinosis is fatally dangerous, rupture or occlusion of the vessel may result in infarct, insult, nephrosclerosis. Local hyalinosis in the cardiac valves results in heart defects.
Amyloidosis(originates from amylum—starch) is pathology in which amyloid, an abnormal metabolic product, appears in the interstitial tissue and vascular walls.
In 1844 K.Rokitansky described so-called «sebaceous disease», when the organs were enlarged, dense, sebum-like. Later R.Virchow discovered that it is associated with accumulation of the substance which stained blue with iodine and sulfuric acid. The disease was called amyloidosis. It was proved that amyloid has nothing to do with starch as it is of protein origin.
Chemical composition of amyloid is complicated. Its main components are F-component and P-compo-nent. F-component is fibrillar proteins, forming fibrils. At present 4 types of protein fibrils are described. Fibril proteins are produced by amyloido-blasts. They are macrophages, plasma cells, myelogenetic cells and possibly fibroblasts, endo-theliocytes, cardiomyocytes, beta-cells of pancreas, P-component is blood plasma glycoproteides.
Laboratory tests for amyloid. When a physician suspects that a patient has amyloidosis, the biopsy is performed, which may be of the rectum, tongue or lip,
or abdominal fat pad. Histochemically amyloid is stained with Congo-red in orange. Immunohisto-chemical method of investigation is modern one. Monoclonal antibodies to each of the preceding amyloid proteins allow diagnosis of the specific type of amyloidosis.
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