5.chronic inflammation dr ashutosh kumar

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5.chronic inflammation dr ashutosh kumar

  1. 1. CHRONIC INFLAMMATION
  2. 2. CHRONIC INFLAMMATION-DEFENSE ATA PRICE PROLONGED DURATION WKS TO MONTHS  ACTIVE INFLAMMATION,  TISSUE DESTRUCTION AND  REPAIRALL occurs SIMULTANEOUSLY
  3. 3. CAUSES PERSISTENT INFECTION  Eg:TB,SYPHILIS  LOW TOXICITY  EVOKE DELAYED HYPERSENSITIVITY REACTION PROLONGED EXPOSURE TO TOXIC AGENTS  ENDO-TOXIC LIPIDS IN ATHEROMA  EXO-SILICOSIS, AUTOIMMUNE:caused by excessive and inappropriate activation of the immune system  Eg. RA,MS,IBD, Br. Asthma
  4. 4. FEATURES MONONUCLEAR INFILTRATIION- MACROPHAGES,LYMPHOS,PLASMA CELLS TISSUE DESTRUCTION ATTEMPTS AT HEALING: angiogenesis+ fibrosis
  5. 5. Chronic infl. Acute infl.collection of chronic inflammatory cells (*) alveolar spaces filled with neutrophilsdestruction of parenchyma Congested blood vesselsfibrosis, (arrows)
  6. 6. CELLS-MACROPHAGES KEY ROLE PART OF MONOCYTE PHAGOCYTE SYSTEM ORIGIN IN BM BLOOD MONOCYTES TISSUE MACROPHAGES TISSUE MACROPHAGES-MICROGLIA,KUPFFER CELLS,ALVEOLAR MACROPHAGES,OSTEOCLASTS
  7. 7. CELLS-MACROPHAGES AFTER 48 HRS EMIGRATE INTO SITE OF INFLAMMATION ACTIVATION  BY CYTOKINES(IFN GAMMA), ENDOTOXINS  INCREASE IN SIZE, MORE LYSOSOMAL ENZYMES, INCREASED METABOLIC ACTIVITY  WIDE VARIETY OF BIOLOGICALLY ACTIVE SUB
  8. 8. CELLS-MACROPHAGES IF IRRITANT PERSISTS MACROS ACCUMULATE RECRUITMENT LOCAL PROLIF IMMOBILIZATION
  9. 9. CELLS-MACROPHAGES PRODUCTS OF MACROPHAGES  ELIMINATION OF MICROBES  TISSUE INJURY-PROTEASES,NO,AA METABOLITES  FIBROSIS
  10. 10. CELLS-OTHERS LYMPHOCYTES  BOTH IN IMMUNE AND NON IMMUNE  TWO WAY INTERACTION WITH MACRO PLASMA CELLS  FROM ACTIVATED B-LYMPHOS  tertiary lymphoid organs: long standing R.A. EOSINOPHILS  IMMUNE,PARASITIC d/t MBP  EOTAXIN
  11. 11. GRANULOMATOUS INFLAMMATION It is a cellular attempt to contain an offending agent that is difficult to eradicate. A granuloma is a focus of chronic inflammation consisting of a microscopic aggregation of macrophages that are transformed into epithelium-like cells, surrounded by a collar of mononuclear leukocytes, principally lymphocytes and occasionally plasma cells.
  12. 12. GRANULOMATOUS INFLAMMATION-EXAMPLES TB SARCOID SYPHILIS(GUMMA) CAT SCRATCH DISEASE LEPROSY BERYLLIOSIS HISTOPLASMA FOREIGN BODY
  13. 13. GRANULOMA EPITHELIOID CELLS  ACTIVATED/MODIFIED MACROPHAGES  INDISTINCT CELL BORDERS  PALE PINK CYTOPLASM  VESICULAR NUCLEUS-SLIPPER SOLE SHAPED LYMPHOCYTES  USUALLY FORM A CUFF AROUND EP CELLS  MAY BE ADMIXED WITH PLASMA CELLS
  14. 14. GRANULOMA GIANT CELLS  FUSION OF EPITHELIOID CELLS  LANGHANS G.C-NUCLEUS IN PERIPHERY-HORSE SHOE MANNER  FOREIGN BODY-HAPHAZARD ARRANGEMENT  NO SP SIGNIFICANCE ABOUT UNDERLYING CAUSE FIBROSIS  SURROUNDING LYMPHOS  BURNT OUT-SCARRING
  15. 15. GRANULOMA TWO MAIN TYPES BASED ON PATHOGENESIS- FB (SUTURE,TALC) AND IMMUNE (TB) IMMUNE  POORLY DEGRADABLE AGENT  CELL MEDIATED IMMUNITY
  16. 16. GRANULOMA CENTRAL NECROSIS IS SEEN IN SOME GRANULOMAS PROTOTYPE-TB  CASEOUS NECROSIS  GROSSLY-CHEESE LIKE  MICRO-EOSINOPHILIC,AMORPHOUS GRANULAR DEBRIS
  17. 17. Granuloma
  18. 18. A granuloma: a collection ofepithelioid histiocytes
  19. 19. SYSTEMIC EFFECTS OF INFLAMMATION ACUTE PHASE RESPONSE OR SYSTEMIC INFLAMMATORY RESPONSE(SIRS) DUE TO CYTOKINES-TNF,IL-1
  20. 20. SYSTEMIC EFFECTS OF INFLAMMATION FEVER IL-1 AND TNF ACT ON HYPOTHALAMUS PRODUCE PGs RESET TEMP AT HIGHER LEVEL HOW USEFUL??????
  21. 21. OSLER“HUMANITY HAS BUT 3 GREATENEMIES-FEVER ,FAMINE ANDWAR,OF THESE BY FAR THEGREATEST ,THE MOST TERRIBLE ISFEVER”
  22. 22. SYSTEMIC EFFECTS OF INFLAMMATION ACUTE PHASE PROTEINS SYN IN LIVER,CIRCULATE IN PLASMA MANY FOLD INCREASE IN INFLAMMATION CRP,FIBRINOGEN,SAA POSSIBLE ROLE AS OPSONINS INCREASED ESR-DUE TO FIBRINOGEN
  23. 23. SYSTEMIC EFFECTS OF INFLAMMATION LEUCOCYTOSIS INCREASED RELEASE FROM BM INCREASED PROLIFERATION FROM PRECUSORS NEUTROPHILIA-MOST BACTERIA LYMPHOCYTOSIS-VIRAL EOS-PARASITIC,ALLERGIC
  24. 24. SYSTEMIC EFFECTS OF INFLAMMATION ANOREXIA,SOMNOLENCE,DECREASED APPETITE SEV BACTERIAL INFECTION-SEPTIC SHOCK
  25. 25. IMPT TOPICS ESSAY  CHEMICAL MEDIATORS OF INFLAMMATION  CELLULAR EVENTS OF INFLAMMATION SHORT TOPICS  ADHESION MOLECULES  PHAGOCYTOSIS  GRANULOMAS  SYSTEMIC EFFECTS OF INFLAMMATION  CELLULAR EVENTS OF INFLAMMATION  VASCULAR EVENTS OF INFLAMMATION  KILLING AND DEGRADATION

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