Inflammation 7


Published on

Designed for UG Pathology teaching.

Published in: Technology, Health & Medicine
  • Be the first to comment

No Downloads
Total views
On SlideShare
From Embeds
Number of Embeds
Embeds 0
No embeds

No notes for slide

Inflammation 7

  1. 1. Inflammationand Repair - 7 Dr.CSBR.Prasad, M.D. v3-CSBRP-May-2012
  2. 2. Out comes of Acute Inflammation May have one of three outcomes: 1. Complete resolution 2. Healing by fibrosis 3. Chronic inflammation v3-CSBRP-May-2012
  3. 3. Out comes of Acute InflammationMay have one of three outcomes:1. Complete resolution2. Healing by fibrosis3. Chronic inflammationThis occurs when:• There is persistence of injurious agent• There is interference with normal healing processEg: Peptic ulcer, Complicated pneumonia v3-CSBRP-May-2012
  4. 4. v3-CSBRP-May-2012
  5. 5. Chronic Inflammation• It’s inflammation of prolonged duration (weeks or months)• Here tissue injury, and attempts at repair coexist v3-CSBRP-May-2012
  6. 6. Chronic Inflammation• May follow an acute inflammation or• May begin insidiously v3-CSBRP-May-2012
  7. 7. v3-CSBRP-May-2012
  8. 8. Chronic InflammationCAUSES:1. Persistent infections  Mycobacteria, viruses, fungi, & parasites2. Immune-mediated inflammatory diseases  Autoimmune diseases  Allergic diseases3. Prolonged exposure to toxic agents  Silicosis (Silica)  Atherosclerosis (Lipid) v3-CSBRP-May-2012
  9. 9. Chronic InflammationMORPHOLOGIC FEATURES: 1. Mononuclear infiltrates 2. Tissue destruction 3. Angiogenesis & 4. Fibrosis Vvvvvvvv In acute inflammation: 1.Vascular changes 2.Edema 3.Neutrophilic infiltration v3-CSBRP-May-2012
  10. 10. v3-CSBRP-May-2012
  11. 11. Chronic Inflammation ROLE OF MACROPHAGESThe macrophage is the dominant cellular player in chronic inflammationMacrophages are one component of the mononuclear phagocyte systemThe half-life of blood monocytes is about 1 day, whereas the life span of tissue macrophages is several months or yearsEmigrate into extravascular tissues quite early in acute inflammation, and within 48 hoursExtravasation is governed by: Adhesion molecules & chemical mediators v3-CSBRP-May-2012
  12. 12. Maturation of mononuclear phagocytes v3-CSBRP-May-2012
  13. 13. Chronic Inflammation ROLE OF MACROPHAGESMacrophages may be activated by a variety of stimuli:Microbial products binding with TLRsCytokines (e.g., IFN-γ) andother chemical mediators v3-CSBRP-May-2012
  14. 14. Chronic Inflammation ROLE OF MACROPHAGESThe products of activated macrophages1. serve to ELIMINATE injurious agents &2. to initiate the process of REPAIR3. responsible for much of the TISSUE INJURY v3-CSBRP-May-2012
  15. 15. Chronic Inflammation ROLE OF MACROPHAGESActivation of macrophages results in:1. increased levels of lysosomal enzymes2. reactive oxygen and nitrogen species3. production of cytokines, growth factors4. other mediators of inflammation5. Some of these products are toxic to microbes and host cells6. Cytokines, chemotactic factors7. Growth factors – PDGF, Angiogenesis v3-CSBRP-May-2012
  16. 16. v3-CSBRP-May-2012
  17. 17. IFN-ɣ IL-4v3-CSBRP-May-2012
  18. 18. Chronic InflammationOTHER CELLS IN CHRONIC INFLAMMATION Lymphocytes Plasma cells Eosinophils & Mast cells v3-CSBRP-May-2012
  19. 19. Chronic Inflammation OTHER CELLS IN CHRONIC INFLAMMATIONLymphocytes & macrophages interact biderectionally:Lymphocytes: IFNɣ arms MØMacrophages: IL12 acts on T-cells v3-CSBRP-May-2012
  20. 20. v3-CSBRP-May-2012
  21. 21. Chronic Inflammation OTHER CELLS IN CHRONIC INFLAMMATIONPlasma cells:• Develop from activated B lymphocytes• Produce antibodies• Abs may act against persistent foreign or self antigens v3-CSBRP-May-2012
  22. 22. Chronic Inflammation OTHER CELLS IN CHRONIC INFLAMMATIONEosinophils:• Immune reactions mediated by IgE• Parasitic infections• Chemokine that recruits EØ is eotaxin• Eosinophilic granules that contain major basic protein• MBP is toxic to parasites• EØs are of beneficial in controlling parasitic infections, but they contribute to tissue damage v3-CSBRP-May-2012
  23. 23. Chronic Inflammation OTHER CELLS IN CHRONIC INFLAMMATIONMast cells:Widely distributed in connective tissuesParticipate in acute and chronic inflammationsMast cell receptor (FcεRI) binds Fc portion of IgEDegranulation – releases histamine and prostaglandinsAllergic reactions – sometimes fatal - anaphylactic shockSecrete a plethora of cytokinesHave the ability to both promote and limit inflammatory reactions in different situations v3-CSBRP-May-2012
  24. 24. v3-CSBRP-May-2012
  25. 25. GRANULOMATOUS INFLAMMATION• It’s a distinctive pattern of chronic inflammation• Seen in some infectious and noninfectious conditions• It’s an attempt to contain an offending agent that is difficult to eradicate v3-CSBRP-May-2012
  26. 26. GRANULOMATOUS INFLAMMATIONInfective causes: Non-Infective causes:• Tuberculosis • Sarcoidosis• Leprosy • Berylliosis• Cat-scratch disease • Reactions to irritant• LGV lipids• Brucellosis • Autoimmune diseases• Syphilis • Crohn’s disease• Mycotic infections v3-CSBRP-May-2012
  27. 27. GranulomaDef: 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. v3-CSBRP-May-2012
  28. 28. GranulomaComponents:Epithelioid cells: have a pale pink granular cytoplasm with indistinct cell boundaries, often appearing to merge into one another. The nucleus is oval or elongate, and may show folding of the nuclear membrane (boomarang)Giant cells: Epithelioid cells fuse to form giant cells in the periphery or sometimes in the center of granulomas. - Langhans-type giant cell / foreign body–type giant cellOlder granulomas develop an enclosing rim of fibroblasts and connective tissue v3-CSBRP-May-2012
  29. 29. GranulomaTypes:There are two types of granulomas, which differ in their pathogenesis:1. Foreign body granulomas Eg: Silica2. Immune granulomas Eg: TB v3-CSBRP-May-2012
  30. 30. Granuloma v3-CSBRP-May-2012
  31. 31. v3-CSBRP-May-2012Caseating granuloma of TB
  32. 32. Non-caseating granulomas of sarcoidosis v3-CSBRP-May-2012
  33. 33. Silica granulomas – under polarized light v3-CSBRP-May-2012
  34. 34. v3-CSBRP-May-2012Lipid granulomas
  35. 35. ENDv3-CSBRP-May-2012
  36. 36. v3-CSBRP-May-2012