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Chronic inflammation

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pathophysiology of chronic inflammation

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Chronic inflammation

  1. 1. INFLAMMATIO N AND HEALING Mohammad Muztaba Khan Assistant professor(Jr.) Department of Pharmacology Bhavdiya institute sibar Sohawal Ayodhya
  2. 2. Chronic inflammation • It is the inflammation of prolong duration (weeks or months). • It is occurred as: • Following acute inflammation. • Occurs, incidentally as active inflammation. • With tissue destruction. With repair process.
  3. 3. Chronic Inflammation (Chronic Bronchitis)
  4. 4. Chronic Inflammation (Tissue destruction-Pancreas)
  5. 5. Chronic Inflammation (Fibrosis-pancreas)
  6. 6. Causes of Chronic inflammation I - Persistent infection. II - Prolonged exposure to potentially toxic agents. III - Autoimmunity.
  7. 7. Chronic Bronchitis
  8. 8. Chronic Bronchitis
  9. 9. Chronic Inflammation (Lung)
  10. 10. Causes of Chronic inflammation I - Persistent infection: • Bacteria. • Viruses. • Fungi. • Parasites
  11. 11. Chronic Gastritis
  12. 12. Chronic Inflammation
  13. 13. Causes of Chronic inflammation II - Prolonged exposure to potentially toxic agents: • Endogenous, (atherosclerosis). • Exogenous, ( particulate silica-Silicosis).
  14. 14. Fatty Streaks
  15. 15. Lesions of Atherosclerosis in Aorta
  16. 16. Atheromatous Plaque
  17. 17. Silicosis
  18. 18. Causes of Chronic inflammation III - Autoimmunity: Occurs in: • Rheumatoid arthritis. • Lupus erythmatosus.
  19. 19. Chronic Inflammation (Rheumatoid arthritis)
  20. 20. Chronic Inflammation (Rheumatoid arthritis)
  21. 21. Chronic inflammation • Lymphocyte, macrophage, plasma cell (mononuclear cell) infiltration • Tissue destruction by inflammatory cells • Attempts at repair with fibrosis and angiogenesis (new vessel formation) • When acute phase cannot be resolved – Persistent injury or infection (ulcer, TB) – Prolonged toxic agent exposure (silica) – Autoimmune disease states (RA, SLE)
  22. 22. Morphological Features of Chronic Inflammation These are characterized by: I - Infiltration by mononuclear cells. II - Tissue destruction. III - Removal of damaged tissue, (healing).
  23. 23. Morphological Features of Chronic Inflammation I - Infiltration by mononuclear cells: The mononuclear cells are become predominant after 48 hours. These include: • Macrophages. • Lymphocytes. • Plasma cells. • Eosinophils. • Mast cells.
  24. 24. Morphological Features of Chronic Inflammation • Macrophages – Scattered all over (microglia, Kupffer cells, sinus histiocytes, alveolar macrophages, etc. – Circulate as monocytes and reach site of injury within 24 – 48 hrs and transform – Become activated by T cell-derived cytokines, endotoxins, and other products of inflammation
  25. 25. Morphological Features of Chronic Inflammation • T and B lymphocytes – Antigen-activated (via macrophages and dendritic cells) – Release macrophage-activating cytokines (in turn, macrophages release lymphocyte-activating cytokines until inflammatory stimulus is removed) • Plasma cells – Terminally differentiated B cells (of lymphocytes). – Produce antibodies.
  26. 26. Morphological Features of Chronic Inflammation Eosinophils – Found especially at sites of parasitic infection, or at allergic (IgE-mediated) sites. – Eosinophils have highly cationic proteins, which are toxic to parasites.
  27. 27. Morphological Features of Chronic Inflammation II - Tissue destruction Occur due to: • Inflammatory cells. • Persistent infecting material.
  28. 28. Morphological Features of Chronic Inflammation III - Removal of damaged tissue, (healing): • Occur by proliferation of small blood vessels, (angiogenesis). • Proliferation of fibroblast, (fibrosis-repair).
  29. 29. Granulomatous Inflammation • Clusters of T cell-activated macrophages, which engulf and surround indigestible foreign bodies (mycobacteria, H. capsulatum, silica, suture material) • Resemble squamous cells, therefore called “epithelioid” granulomas with peripheral lymphocytes, fibrosis & multinucleated giant cells.
  30. 30. Chronic Granulomatous Inflammation
  31. 31. Chronic Granulomatous Inflammation
  32. 32. Chronic Granulomatous Inflammation
  33. 33. Lymph Nodes and Lymphatics • Lymphatics drain tissues – Flow increased in inflammation – Antigen to the lymph node – Toxins, infectious agents also to the node • Lymphadenitis, lymphangitis • Usually contained there, otherwise bacteremia ensues • Tissue-resident macrophages must then prevent overwhelming infection
  34. 34. Systemic effects • Fever – One of the easily recognized cytokine- mediated (esp. IL-1, IL-6, TNF) acute-phase reactions including • Anorexia • Skeletal muscle protein degradation • Hypotension • Leukocytosis – Elevated white blood cell count
  35. 35. Systemic effects (cont’d) – Bacterial infection (neutrophilia) – Parasitic infection (eosinophilia) – Viral infection (lymphocytosis)
  36. 36. Thank You

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