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FATE OF ACUTE INFLAMMATION

FATE OF ACUTE INFLAMMATION. 1.RESOLUTION 2.HEALING BY SCARRING 3.PROGRESSION TO SUPPURATION 4.PROGRESSION TO CHRONIC INFLAMMATION. RESOLUSION. MEANS COMPLETE RETURN TO NORMAL TISSUE FOLLOWING ACUTE INFLAMMATION. RESOLUSION. TISSUE CHANGES ARE REVERSIBLE

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FATE OF ACUTE INFLAMMATION

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  1. FATE OF ACUTE INFLAMMATION 1.RESOLUTION 2.HEALING BY SCARRING 3.PROGRESSION TO SUPPURATION 4.PROGRESSION TO CHRONIC INFLAMMATION

  2. RESOLUSION MEANS COMPLETE RETURN TO NORMAL TISSUE FOLLOWING ACUTE INFLAMMATION

  3. RESOLUSION TISSUE CHANGES ARE REVERSIBLE EXAMPLE –RESOLUTION IN LOBAR PNEUMONIA

  4. 2.HEALING BY SCARRING OCCUR WHEN TISSUE DESTRUCTION IS EXTENSIVE THERE IS NO TISSUE REGENERATION- THERE IS HEALING BY FIBROSIS

  5. 3.PROGRESSION TO SUPPURATION PYOGENIC BACTERIA CAUSING ACUTE INFLAMATION RESULT IN SEVERE NECROSIS. THIS PROGRESSES TO SUPPURATION INTENSE NEUTROPHILIC INFILTRATION

  6. SUPPURATION PUS IS MADE UP OF MIXTURE OF NEUTROPHILS, BACTERIA,FRAGMENTS OF NECROTIC TISSUE,CELL DEBRIS & FIBRIN & CONTAINED IN A CAVITY TO FORM AN ABSCESS

  7. SUPPURATION THE ABSCESS IF NOT DRAINED ,MAY GET ORGANISED BY DENSE FIBROUS TISSUE & UNDERGO DYSTROPHIC CALCIFICATION

  8. 4. PROGRESSION TO CHRONIC INFLAMMATION

  9. NATURE AND TYPES OF EXUDATION 1. SEROUS- EXUDATE RESEMBLE SERUM OR IS WATERY EXAMPLE – PLEURAL EFFUSION IN TUBERCULOSIS BLISTER IN BURNS

  10. TYPES OF EXUDATION 2.FIBRINOUS - FIBRIN CONTENT IS HIGH - PNEUMOCOCCAL & RHEUMATIC PERICARDITID.

  11. TYPES OF EXUDATION 3. PURULENT & SUPPURATIVE EXUDATE - PYOGENIC ORGANISMS – ABSCESS ,ACUTE APPENDICITIS

  12. TYPES OF EXUDATION 4. HAEMORRHAGIC - HAEMORRHAGIC PNEUMONIA IN INFLUENZA

  13. TYPES OF EXUDATION 5.CATARRHAL - INCREASED SECRETION OF MUCOUS - COMMON COLD

  14. CHRONIC INFLAMMATION DEFINITION- PROLONGED PROCESS INWHICHTISSUE DESTRUCTION AND INFLAMMATION OCCUR AT THE SAME TIME CAN BE CAUSED BY ONE OF 3 WAYS 1. CHRONIC INFLAMMATION FOLLOWING ACUTE INFLAMMATION 2. RECURRENT ATTACKS OF ACUTE INFLAMMATION 3. CHRONIC INFLAMMATION STARTING de novo –eg -TUBERCULOSIS

  15. CHRONIC INFLAMMATION GENERAL FEATURES OF CHRONIC INFLAMMATION 1. MONONUCLEAR CELL INFILTRATION PHAGOCYTES ,LYMPHOCYTES,EPITHELOID CELLS,SOMETIMES MULTINUCLEATED GIANT CELLS,PLASMA CELLS,EOSINOPHILS AND MAST CELLS.

  16. CHRONIC INFLAMMATION LYMPHOCYTES AND MACROPHAGES INFLUENCE EACH OTHER AND RELEASE MEDIATORS OF INFLAMMATION

  17. CHRONIC INFLAMMATION 3. TISSUE DESTRUCTION AND NECROSIS BROUGHT ABOUT BY ACTIVATED MACROPHAGES WHICH RELEASE VARIETY OF BIOLOGICALLY ACTIVESUBSTANCES-PROTEIASE,ELASTASE,COLLAGENASE,LIPASE,REACTIVE OXYGEN RADICALS,CYTOKINES(IL1,IL8,TNF α)

  18. CHRONIC INFLAMMATION 3. PROLIFERATIVE CHANGES –BLOOD VESSELS,FIBROBLASTS WITH FORMATION OF GRANULATION TISSUE EVENTUALLY CAUSE FIBROSIS

  19. SYSTEMIC EFFECTS OF CHRONIC INFLAMMATION 1. FEVER OFTEN WITH LOSS OF WEIGHT AND WEAKNESS 2. ANAEMIA 3. LEUKOCYTOSIS –LYMPHOCYTOSIS 4. INCREASED ESR 5. AMYLOIDOSIS

  20. TYPES OF CHRONIC INFLAMMATION 2 TYPES 1.NON-SPECIFIC=IRRITANT SUBSTANCE PRODUCES A NONSPECIFIC INFLAMMATORY REACTION WITH FORMATION OF GRANULATION TISSUE AND HEALING BY FIBROSIS- CHRONIC OSTEOMYELITIS,CHRONIC ULCER

  21. TYPES OF CHRONIC INFLAMMATION 2. SPECIFIC –WHEN INJURIOS AGENT CAUSES A CHARACTERISTIC HISTOLOGIC TISSUE RESPONSE-TUBERCULOSIS, LEPROSY,SYPHILIS SO CHRONIC INFLAMMATION IS CLASSIFIED INTO 1. CHRONIC NONSPECIFIC INFLAMMATION 2. CHRONIC GRANULOMATOUS INFLAMMATION

  22. CHRONIC GRANULOMATOUS INFLAMMATION GRANULOMA DEFINITION GRANULOMA IS DEFINED AS A CIRCUMSCRIBED TINY LESION,ABOUT 1 mm IN DIAMETER,COMPOSSED OF COLLECTION OF MODIFIED MACROPHAGES CALLED EPITHELOID CELLS,AND RIMMED AT THE PERIPHERY BY LYMPHOCYTES

  23. CHRONIC GRANULOMATOUS INFLAMMATION WORD GRANULOMA IS DERIVED FROM GRANULE MEANING CIRCUMSRIBED GRANULE LIKE LESION. OMA MEANS MASS

  24. CHRONIC GRANULOMATOUS INFLAMMATION PATHOGENESIS OF GRANULOMA TYPE 4 GRANULOMATOUS HYPERSENSITIVITY REACTION-A PROTECTIVE DEFENSE REACTION BY THE HOST BUT EVENTUALLY CAUSE TISSUE DESTRUCTION BECAUSE OF PERSISTANCE OF POORLY DIGESTIVE ANTIGEN

  25. PATHOGENESIS OF GRANULOMA 1.ENGULFMENT BY MACROPHAGES- TRY TO DIGEST IT AND DESTROY.SINCE ANTIGEN IS POORLY DEGRADABLE,MACROPHAGES FAIL TO DIGEST AND DEGRADE THE ANTIGEN,BUT UNDERGO MORPHOLOGIC CHANGES TO EPITHELOID CELLS

  26. PATHOGENESIS OF GRANULOMA 2. CD4 + T LYMPHOCYTES -MACROPHAGES PRESENT THE ANTIGEN TO CD4 + T CELLS.T LYMPHOCYTES GET ACTIVATED AND ELABORATE LYMPHOKINES(IL-1,IL2,INTERFERON γ, TNFα).

  27. PATHOGENESIS OF GRANULOMA 3. CYTOKINES – VARIOUS CYTOKINES FORMED BY ACTIVATED MACROPHAGES PERFORM THE FOLLOWING ROLES a. IL1 AND IL2 –STIMULATE PROLIFERATION OF MORE T CELLS b .INTERFERON ץACTIVATES MACROPHAGES

  28. PATHOGENESIS OF GRANULOMA c. TNFα - PROMOTES FIBROBLAST PROLIFERATION AND ACTIVATES ENDOTHELIUM TO SECRETE PROSTAGLANDINS d. GROWTH FACTORS(TRANSFORMING GROWTH FACTOR β,PLATELET DERIVED GROWTH FACTOR) STIMULATE FIBROBLAST GROWTH

  29. COMPOSITION OF GRANULOMA 1. EPITHELOID CELLS –HAS EPITHELIAL LIKE APPEARANCE- THEY ARE MODIFIED MACROPHAGES. EPITHELOID CELLS ARE SOMEWHAT ELONGATED WITH VESICULAR AND LIGHTLY STAINING SLIPPER SHAPPED NUCLEUS,PALE STAINING ABUNDANT CYTOPLASM WITH HAZY OUTLINES.EPITHELOID CELLS ARE WEAKLY PHAGOCYTIC

  30. GRANULOMA –EPITHELOID CELL COLLECTION WITH A MULTINUCLEATED GIANT CELL

  31. COMPOSITION OF GRANULOMA 2. MULTINUCLEATED GIANT CELLS- FORMED BY FUSION OF ADJACENT EPITHELOID CELLS AND MAY HAVE 20 OR MORE NUCLEI

  32. COMPOSITION OF GRANULOMA THE NUCLEI MAY BE ARRANGED AT THE PERIPHERY LIKE HORSESHOE OR RING OR ARE CLUSTERED AT THE TWO POLES(LANGHANS’ GIANT CELLS), OR MAY BE PRESENT CENTRALLY(FOREIGN BODY GIANT CELLS) –WEAKLY PHAGOCYTIC

  33. CASEATING GRANULOMA OF TUBERCULOSIS

  34. COMPOSITION OF GRANULOMA 3. LYMPHOID CELLS- AS A CELL MEDIATED REACTION TO ANTIGENS 4. NECROSIS –A FEATURE OF SOME GRANULOMAs – TUBERCULOSIS -CASEOUS NECROSIS , CASEOUS MEANING CHEESE LIKE APPEARANCE.

  35. GRANULOMA –EPITHELOID CELL COLLECTION WITH A MULTINUCLEATED GIANT CELL

  36. CASEATING GRANULOMA OF TUBERCULOSIS

  37. COMPOSITION OF GRANULOMA 5.FIBROSIS WHEN HEALED

  38. MECHANISM OF GRANULOMA FORMATION CELL INJURY (eg M.TUBERCULOSIS ,TALC) FAILURE TO DIGEST AGENT WEAK ACUTE INFLAMMATORY RESPONSE - ENGULFMENT BY MACROPHAGES

  39. MECHANISM OF GRANULOMA FORMATION - PERSISTANCE OF INJURIOUS AGENT T CELL MEDIATED POORLY DIGESTIBLE MATERIAL IMMUNE RESPONSE ACTIVATION OF CD+ T CELLS- RELEASE OF LYMPHOKINES-IL1,IL2,GROWTH FACTORSIFNץ AND TNF α, MONOCYTE CHEMOTACTIC FACTOR- ACUMULATION OF TISSUE MACROPHAGES BY LOCAL PROLIFERATION AND FROM CIRCULATION,PROLIFERATION OF T CELLS -

  40. MECHANISM OF GRANULOMA FORMATION - MACROPHAGES ACTIVATED BY IFN ץ - CAUSE TRANSFORMATION TO EPITHELOID CELLS AND GIANT CELLS AND SECRETION OF FIBROBLASTIC PROLIFERATING CYTOKINES(TGF β,PDGF) GRANULOMA AND FIBROSIS

  41. GRANULOMA –EPITHELOID CELL COLLECTION WITH A MULTINUCLEATED GIANT CELL

  42. CASEATING GRANULOMA OF TUBERCULOSIS

  43. EXAMPLES OF DISEASES WITH GRAULOMATOUS INFLAMMATION 1.TUBERCULOSIS – MYCOBACTERIUM TUBERCULOSIS 2. LEPROSY - MYCOBACTERIUM LEPRAE 3. SYPHILIS - TREPONEMA PALLIDUM 4. SARCOIDOSIS - UNKNOWN ETIOLOGY

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