Productive inflammation

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Productive inflammation


<ul><li> 1. CHRONICINFLAMMATION</li></ul> <p> 2. InflammationAccording to prevailing one ofphases of inflammation- exudative,- proliferative. 3. The proliferation isconcluding phase ofinflammation,which leads to restorationof tissue. 4. Cellular proliferation in different typesof inflammations. There is no significant cellular proliferation in acutebacterial infections except in typhoid fever in which there isintestinal lymphoid hyperplasia. Viral infections have the ability to stimulate cellularproliferation, e.g. epidermal cell proliferation in herpessimplex, chickenpox arid smallpox. In glomerulonephritis, there is proliferation of glomerularcapsular epithelial cells resulting in formation of'crescents'. In chronic inflammation, cellular proliferation ofmacrophages, fibroblasts and endothelial cells occurs. 5. Reproduction of cells in chronicinflammation Hematogenic origin T-lymphocytes, B-lymphocytes,plasma cells, monocytes,macrophages, histiocytes, epithelioud cellsgiant cells of Langhans and foreign bodies Histiogenic origin endothelium, reticular cells,fibroblasts etc. 6. Types of proliferative inflammation: interstitial inflammation, granulomatousinflammation, inflammation withformation of polyps andpointed condyloma. 7. Interstitial inflammation is characterizedby cellular infiltration formation instroma of organs (myocardium, liver,kidney, lung).The inflammatory cell infiltration consistsof lymphocytes, monocytes,plasmocytes, eosinophils and othercells.Prolonged interstitial inflammation canresult in sclerosis of organ. 8. Granulomatous inflammation ischaracterized by formation of granulomas.Granuloma is a local accumulation of cells, which have abilityof phagocytosis.Granuloma is circumscribed tiny lesion, about 1 mm indiameter, composed predominantly of macrophages,epithelioid cells, and lymphoid cells at the periphery. Insome cases granulomas contein giant cells.The giant cells are formed by fusion of adjacent epithelioidcells and can have 50-100 nuclei. These nuclei can bearranged at the periphery like horseshoe or ring (Langhans'giant cells), or can be present centrally (foreign body giantcells). 9. Infl048.htm 10. Granulomas(according to etiology) infectious (endemic typhus andepidemic typhus, tuberculosis,leprosy, siphylis, tularemia), noninfectious (asbestosis, silicosis,medicamentous hepatitis,lipogranuloma, oilgranuloma,granuloma around foreign body), granulomas with unknown etiology(sarcoidosis, Crohns disease). 11. Specific granuloma ischaracterized by definitemorphological changes, whichallow to make diagnosis.Infections, which accompanied bydevelopment of specific granulomas,are tuberculosis, leprosy, siphylis,scleroma. 12. Morphologyof tubercular granuloma: caseous necrosis centrally, domination of epithelioid cellsand presens of Langhans'giant cells, vessels are absent (or verysmall amount of capillaries), miliary and multiple, outcome is soft sclerosis. 13. Infl048.htm 14. Morphologyof syphilitic granuloma: colliquative necrosiscentrally, domination of lymphocytesand plasmocytes, large amount of capillaries, solitary, outcome is gross sclerosis. 15. Inflammation with formation ofpolyps and pointed condylomaoccurs on the mucousmembranes and in the borderlinewith squamous epithelium. 16. Polyps are the end-result ofprolonged chronic irritation. Macroscopically they aregelatinous masses with smoothand shining surface. Microscopically they are composedof loose edematous connectivetissue containing some mucousglands and varying number ofinflammatory cells (lymphocytes,plasmocytes, eosinophils). 17. Condyloma is commonlylocated on the coronalsulcus on the penis orthe perineal area. 18. Chronic inflammationis defined as prolongedprocess in which tissue,destruction and inflammationoccur at the same time. 19. Chronic inflammationcan be caused by:1. Chronic inflammation following acute inflammation - whenthe tissue destruction is extensive, or the bacteria surviveand persist in small numbers at the site of acuteinflammation, e.g. in osteomyelitis, pneumonia terminatingin lung abscess.2. Recurrent attacks of acute inflammation - when repeatedbouts of acute inflammation culminate in chronicity of theprocess, e.g. in recurrent urinary tract infection leading tochronic pyelonephritis, repeated acute infection of gallbladder leading to chronic cholecystitis.3. Chronic inflammation starting de novo. 20. Though there may be differencesin chronic inflammatory responsedepending upon the tissueinvolved and causative organisms,there are some basic similaritiesamongst various types of chronicinflammation. 21. General features that characterizeany chronic inflammation:1. Mononuclear infiltration. Chronic inflammatory lesions areinfiltrated by mononuclear inflammatory cells likephagocytes and lymphoid cells. Phagocytes arerepresented by circulating monocytes, tissuemacrophages, epithelioid cells and sometimes,multinucleated giant cells. The macrophages comprise themost important cells in chronic inflammation.2. Tissue destruction and necrosis. Tissue destruction andnecrosis are common in many chronic inflammatorylesions and are brought about by activated macrophagesby release of a variety of biologically active substances.3. Proliferative changes. As a result of necrosis, proliferationof small blood vessels and fibroblasts is stimulatedresulting in formation of inflammatory granulation tissue.Eventually, healing by fibrosis takes place. 22. The outcomes depend on thetype of inflammation,morphofunctionalcharacteristics of the definiteorgan or tissue.Sclerosis develops in themajority of cases. 23. Thank you for yourattention! </p>