Pathologic anatomy rheumatism

When Mokoena swelling (I phase rheumatic disorganization of connective tissue) in interstitial substance of the connective tissue or in the walls of blood vessels is an accumulation and redistribution of mucopolysaccharides and glucoproteins. First accumulate hyaluronic acid, then appear sulfatirovannah mucopolysaccharides and glucoproteins. In the hearth muhidnova swelling accumulate plasma proteins, especially gamma-globulins, whose content in the blood plasma rheumatism increases.
The question about changes in the early phase of rheumatism fibrous connective tissue structures remains controversial. Some authors believe that when Mokoena swelling fibrous structures (collagen, elastin, reticular) change not; for others, fiber, especially collagen, swell and some change their structure.
Fibrinogene changes, or fibrinoid (II phase). Fibrinoid is a chemically heterogeneous substance (, Century Orel in forming the participation of all components of the connective tissue and blood plasma proteins, primarily fibrinogen. The conditions of fibrinoid are: to improve the tissue-vascular permeability; changes interstitial substance-related depolymerization and redistribution of polysaccharides and accumulation of plasma proteins; the collapse of the complex of collagen fibers, which, depending on the depth of damage to acquire different tinctorial properties (eosinophilia, pyroninophilia, perrineville, positive reaction to fibrin, argyrophile and so on). There are fibrinoid fibrin, fibrinoid with fibrin and fibrinoid necrosis (see Fibrinogene transformation).
Phase muhidnova swelling and fibrinoid changes characterize first alterative-exudative phase pathology connective tissue rheumatism, Klinge (F. Klinge) and C. T. Talalaeva. When Mokoena swelling the question is not only about the very early and reversible changes; fibrinoid is a more profound and irreversible disruption of connective tissue (A. I. Strukov).
Wegener (III phase) reaction of connective tissue cells in the foci of its disruption. Histiocytes form rheumatic nodules, or granulomas (Fig. 2), first described by Asifa (L. Aschoff) and studied in detail V.T. Talalaeva (ashoff-talalaevsky granuloma). Part of granulomas, in addition histiocytes are lymphoid cells, leukocytes and cardiomotility myocytes Anichkov). Cell granuloma have a different shape, large nucleus, basophilic cytoplasm and are often perivascular in a rosette around the hearth disorganization of the connective tissue. Cell granuloma rich glycogen, ribonucleic acid, proteins; the activity of a number of redox enzymes are considerably higher than in other mesenchymal cells. These data suggest that the cells rheumatic granuloma, rich plastic material and energy substances belong to a large role in the processes of absorption and metabolism products disorganization of the connective tissue (phagocytosis, scarring). On the other hand, granuloma reflects tissue immune response, as evidenced by the complement fixation in rheumatic nodules [Giler and Calm (G. Geiler, P. Stiel)].
The most frequent localization of rheumatic granuloma - perivascular connective tissue diseases. In addition infarction, classic ashoff-talalaevsky knots occur frequently in the valve and parietal the endocardium, tendon chords. Granulomas and find out the heart: in the synovial membrane and articular bags, periarticular and peritonsillar fabrics, leather, intermuscular connective tissue and so on Granuloma extracardiac localization differ in their degree of destructive-exudative changes and morphology of cells, which usually are small, elongated shape and a weak basophilia cytoplasm. In the connective tissue of the liver, kidneys, salivary glands and other organs rheumatic granulomas are not met.
Rheumatic nodules undergo fibroplastic transformation. The cycle is 3-4 months. (Such As Talalaev). Therefore, in different periods of the disease morphology rheumatic granuloma different. There are fresh, blooming, or "restless", granuloma, which along with cell proliferation pronounced alterative-exudative component; "calm" granuloma, which are characterized by complete resorption products disorganization of connective tissue; cicatrizing granuloma, which among elongated cells appear collagen fibers. The correspondence between the presence or absence of granulomas and clinical manifestations of rheumatism no (M. A. Skvortsov). For judgments about the dynamics of rheumatism greater degree of disorganization of the connective tissue than the presence of granulomas.
Sclerosis and hyalinosis (IV phase disruption of connective tissue) are, as a rule, system character, but is most pronounced in the heart, blood vessels and serous membranes. There are two types of rheumatic sclerosis: a primary cell-free), developing in Exodus fibrinogen changes, rarely muhidnova swelling, and secondary (cellular)arising out of maturation and fibroplastic transformation of cell infiltrates, in particular rheumatic granulomas. In areas of sclerosis occurs random deposition of procollagen modified, lost the right structure kulastamine, the formation of new, abnormal combinations of proteins and polysaccharides, which is reflected in the appearance of atypical fibrous bundles and pathological structures. There is no strong ties procollagen and kulastamine, there are lots drop prokollagena. Thus, rheumatic sclerosis is formed defective scar.
Under the new rheumatic fever in the zone of the old scars still arise tissue destruction in the form muhidnova swelling, fibrinoid, cellular responses with the same outcome sclerosis. Sclerotherapy in such cases takes a progressive (progressive multiple sclerosis).
In each of the four phases of rheumatic disorganization of the connective tissue can occur nonspecific cell response (M. A. Skvortsov). They have expressed exudative character, most often develop in the pericardium, joints, rarely in the pleura, peritoneum, myocardium, endocardium, etc. among non-specific manifestations include and vasculitis (capillarity, arteritis, phlebitis, aortic), that are of systematic character and are of great clinical value. In each case can meet the loss of one or another phase, such as second-and third-or only a third (such as Talalaev). Naturally there and simultaneous combination of all four phases of the rheumatic process, allowing to speak about its continuity (A. I. Strukov).
Depending on the predominant lesion of a particular system are the following clinical-morphological forms of rheumatism: cardiovascular (visceral), polyarthritises, knotted (nadasny) and nervous.
When cardiovascular form of morphological manifestations of rheumatism represented most clearly. It is considered that rheumatism always accompanied endocarditis (see), which is usually related valves, most of the mitral and aortic valve endocarditis), less parietal of the endocardium (the parietal endocarditis). Morphologically there are diffuse (initial) endocarditis (valvola talalaeva), warty endocarditis (thromboangiitis), return warty endocarditis and fibrous (fibroelastosis) endocarditis. The outcome of all kinds of rheumatic endocarditis are heart diseases (see). Myocarditis rheumatism as is often the case, as endocarditis. It can be granulomatous productive or diffuse exudative (Fig. 3); the latter occurs mainly in children, coupled with the defeat of vessels (M. A. Skvortsov). In Exodus rheumatic myocarditis develops focal cardiosclerosis (see) or diffuse myofibres. In the pericardium usually develops serous, sero-fibrinous and fibrinous inflammation (pericarditis), but can be formed and granulomas. The consequence of pericarditis are synechia and obliteration of the cavity of the heart bags.
The most often for rheumatism observe combination of endo -, and myocarditis (rheumatic heart disease), in some cases, the process involved all lining of the heart (rheumatism pancarditis).


In the aorta observed lesions type Mesaoria or periaortic. In large and small arteries molignee swelling or fibrinogene changes intima combined with Wegener and gistiotitarnaya infiltration. This nature rheumatic arteritis are most pronounced in the blood vessels of the heart (coronaria - Fig. 4). In the veins observed inflammation, thrombosis (thrombophlebitis), the formation warty growths in the field of valves (verrucose indefinite). Changes of the capillaries in the form of plasturgie, proliferation of endothelial tissue (rheumatoid endotelia) and parazitov are systemic in nature and can be observed in all organs and tissues (Fig. 5). In the lungs capillarity can be combined with diffuse or uzelkove cell infiltrates in millionarmy partitions, with protein membranes and accumulation of mononuclear elements in the alveoli (N. A. Kraevsky). Kidney often develops glomerulonephritis, which often has alopecia is a common, less diffuse character. In Exodus rheumatoid vasculitis occurs sclerosis of vessels (aortic sclerosis, atherosclerosis, arteriolosclerosis, fleboscleros).
When polyarthritises form during the attack of rheumatism the joint cavity is found serous or sero-fibrinous exudate. In synovial membrane find pockets myxomatosis edema, hyperemia vessels, the proliferation of their endothelium and perivascular lymphocytic clutch. In fibrous tissue of joints, tendons, periarticular connective tissue arise pockets muhidnova swelling, rarely fibrinogen changes with the development around them cell responses; rheumatic granulomas are formed rare. In Exodus rheumatic affection of joints sclerotic deformations of them do not usually have.
When nodular forms e (nodosanas) in the connective tissue adjacent to the aponeurosis in the joints of the extremities, in the aponeurosis of the occipital and parietal areas, in subcutaneous adipose tissue may experience large lesions of the connective tissue in the form of nodes of various sizes. Education sites begins with a sero-fibrinous exudation, muhidnova swelling and fibrinoid change, which joins both proliferation. Later comes the fibrous transformation of these lesions with the deposition sometimes in the center of their lime.
The greatest clinical significance when nervous form of rheumatism are changes in the Central nervous system, especially in children; they appear in the form of so-called Horai (see). Expressed dystrophic changes and atrophic character marked in the ganglion cells of the striatum, the granular layer of the bark, molecular layer of the cerebellum, the cells of the subthalamic nucleus and the black substance; these changes are complemented by vascular-glial reaction. Adult great importance proliferative vasculitis and thrombovascular, on soil of which can lead to local changes of the brain. The same vascular changes occur in the meninges.
Morphological expression busy immunogenesis rheumatism is plasmafysica lymphoid tissue tonsils, lymph nodes and spleen [Furlender (K. O. Vorlaender)].

Fig. 2. Rheumatic granuloma.
Fig. 3. Diffuse pleural myocarditis.
Fig. 4. Coronary rheumatism.
Fig. 5. The nodular lesions and capillarity in the attack of rheumatism.