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Tema:

BOLILE REUMATICE. VALVULOPATIILE CARDIACE


I. PIESE MICROSCOPICE

59. Endo-miocardit reumatic productiv granulomatoas (coloraie H-E) Indicaii: 1) granuloame reumatice Aschoff n endocardul parietal 2) necroz fibrinoid n centrul granulomului 3) macrofage la periferia granulomului 4) miocardul adiacent cu modificri distrofice 127. Tromboendocardit parietal (coloraie H-E) Indicaii: 1) mase trombotice pe suprafaa endocardului parietal 2) endocardul parietal cu infiltraie inflamatorie cronic 3) miocardul adiacent cu modificri distrofice 125. Periarterit nodoas (coloraie H-E) Indicaii: 1) peretele arterial ngroat 2) infiltraia limfo-macrofagal difuz localizat preponderent n adventiie 3) lumenul stenozat al arterei

II.

MACROPREPARATE

16. Endocardit valvular verucoas recurent 6. Valvulopatie mitral reumatic 11. Pericardit fibrinoas 12. Cardioscleroz difuz 18. Tromboendocardit parietal 8. Tromb sferic n atriul stng 7. Viciu cardiac congenital (defect al septului interventricular) III. ELECTRONOGRAME

18. Intumescena mucoid i fibrinoid a esutului conjunctiv 19. Glomerulonefrit lupic

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DEGENERATIVE SYSTEMIC CONNECTIVE TISSUE PATHOLOGY Microspecimens 59. Rheumatic granulomatous endocarditis (H.E.). Microscopic appearance of Aschoff body. It has a circumscribed collection of mononuclear inflammatory cells, including some large histiocytes with prominent nucleoli and a prominent binuclear histiocyte, and central necrosis. 127. Thromboendocarditis (H.E.). valvulitis; inflammatory infiltration and edema in the stroma of the valves with superimposed presence of rheumatic vegetations, and thrombotic masses. 125. Periarteritis nodosa (H.E.). Nodular thickenings with reduction of the lumen. Thrombosis. Fragmentation of the internal elastic lamina. Granulomatous inflammation of the inner half of the media centered on the internal elastic membrane. Macrospecimens Rheumatic mitral malformation. Left atrium round thrombus. Fibrinous pericarditis. Diffuse cardiosclerosis. Nonbacterial verrucous endocarditis Thromboendocarditis. Electronomicrography 18. Fibrinoid intumescence of the connective tissue. - Accumulation of glycosaminoglycans among collagen fibres with their subsequent swelling, interfibrilare spaces are considerably wider. Collagen fibers retain their normal structure and transverse strip (mucoid edema, mixomatosis). - Irreversible disarrangement of connective tissue characterized by destruction of the fundamental substance and collagen fibers and fibrinoid formation. This process can lead to fibrinoid necrosis.

19. Glomerulonephritis in SLE. Electron dense deposits are demonstrated with a distribution similar to the one of the immune deposits. With this technique some small subendothelial deposits, in classes II and V, are more evident; some subepithelial deposits are evidenced in many cases, but they are extensive and predominant only in class V lesions. Some deposits can have an organization in fingerprint, there are seen like parallel, regularly curved and spaced deposits, with waved aspect and intersections; these structures are similar to the described ones in cryoglobulinemia and seem to correspond to cryoglobulins. In the cytoplasm of glomerular endothelial cells tubuloreticular inclusions can be seen, they are not specific of lupus nephritis, and they can also be seen in HIV and renal allograft rejection; it is believed that they are an effect of the interferon. In podocytes we can see effacement of podocyte foot processes, similar to the changes seen in other glomerulopathies with nephrotic syndrome.