Inflammation Lab Slides

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Inflammation Lab Slides

  1. 1. INFLAMMATION
  2. 2. POLYMORPHONUCLEAR NEUTROPHIL
  3. 3. MONOCYTE
  4. 4. EOSINOPHIL
  5. 5. BASOPHIL
  6. 6. SMALL LYMPHOCYTE
  7. 7. LARGE LYMPHOCYTE
  8. 8. PLASMA CELL
  9. 9. Foreign body giant cell. The giant cell contains suture material.
  10. 10. Langhans’ giant cell. Mycobacteria, which are acid-fast organisms, are present within the giant cell and stain red with a Kinyoun stain.
  11. 11. A low power phomicrograph of granulomatous inflammation
  12. 12. A granuloma is characterized by a collection of epithelioid macrophages with abundant pale eosinophilic cytoplasm and indistinct cell borders surrounded by a rim of lymphocytes.
  13. 13. Langhan’s Giant Cell Picture Robbins Textbook of Pathology 1971 Langhans’ giant cell
  14. 14. ACUTE APPENDICITIS Histologic hallmark are the presence of neutrophils at the muscularis layer (arrow).
  15. 15. LEFT : THERE IS A DENSE DERMAL INFILTRATE RIGHT : THE INFILTRATE IS COMPOSED OF FOAMY EPITHELIOID HISTIOCYTES KNOWN AS LEPRA CELLS L E P R O S Y S K I N
  16. 16. RED STAINING TUBERCULOID ORGANISMS IN THE LEPRA CELLS ARE SEEN WITH FITE-FORACO STAIN.
  17. 17. REPAIR
  18. 18. Granulation tissue is the hallmark of repair. Young granulation tissue is composed of a proliferation of blood vessels and fibroblasts in an edematous stroma. RBC exravasation is prominent because of leaky blood vessels.
  19. 19. Older granulation tissue is composed of well-developed blood vessels with an inflammatory infiltrate in the interstitial tissue.
  20. 20. SCAR. A scar is composed of parallel bundles of collagen with few fibroblasts and few blood vessels.
  21. 21. KELOID. A keloid is composed of thick collagen bundles of whorled arrangement.
  22. 23. Whole mount view of chronic peptic ulcer. The external muscle layer has been totally destroyed. Note the overhanging mucosa on one edge and the sloping mucosa on the other.
  23. 25. GASTRIC ULCER (PEPTIC ULCER). Chronic active ulcers are characterized by four distinct zones.
  24. 26. The first two zones can be seen. The ulcer base is covered by fibrinopurulent debris (zone 1), beneath which is an active suppurative inflammatory infiltrate (zone 2). Zone 1 Zone 2
  25. 27. GASTRIC ULCER (PEPTIC ULCER). The third zone of a chronic active ulcer is composed of granulation tissue.
  26. 28. GASTRIC ULCER (PEPTIC ULCER). The fourth zone is composed of dense fibrous tissue.
  27. 29. Liver cirrhosis, gross
  28. 30. Cirrhosis resulting from chronic viral hepatitis. Note the broad scar and coarse nodular surface.
  29. 31. CIRRHOSIS. It is the common end point of many disease processes. Fibrous bands diffusely divide the liver into regenerative nodules. A trichrome stain accentuates the nodularity and proves that the bands are made of collagen.
  30. 32. ALCOHOLIC CIRRHOSIS (LAENNEC’S CIRRHOSIS). In early alcoholic cirrhosis, bridging fibrosis with entrapped portal tracts is noted. Hepatocytes degenerate, and central veins and portal tracts become trapped in the fibrous scar. Bile plugs and fatty change is noted in the remaining hepatocytic parenchyma.
  31. 33. Cirrhosis <ul><li>Most common cause is alcoholic liver disease </li></ul><ul><li>Key features: </li></ul><ul><ul><li>The parenchymal injury & consequent fibrosis are diffuse . </li></ul></ul><ul><ul><li>The nodularity is part of the diagnosis  reflects balance between regeneration and scarring. </li></ul></ul><ul><ul><li>Vascular architecture is re-organized by the parenchymal damage and scarring  formation of abnormal interconnections </li></ul></ul><ul><ul><li>Fibrosis is the key feature of progressive liver damage. </li></ul></ul>
  32. 34. CAUSES OF CIRRHOSIS
  33. 35. Cirrhosis <ul><li>Pathogenesis: </li></ul><ul><li>Progressive fibrosis & re-organization of vascular micro-architecture of liver </li></ul>Collagen deposition (types I & III) in the lobule Loss of fenestration of sinusoidal endothelial cells New vascular channels in the septae Create delicate or broad septal tracts Impaired hepatocellular protein secretion (albumin, clotting factors, lipoproteins) Shunting of blood around the parenchyma
  34. 36. Cirrhosis <ul><li>Main characteristics </li></ul><ul><ul><li>Bridging fibrous septae </li></ul></ul><ul><ul><ul><li>link portal tracts with one another & portal tracts with terminal hepatic vein </li></ul></ul></ul><ul><ul><li>Parenchymal nodules </li></ul></ul><ul><ul><ul><li>contain proliferating hepatocytes encircled by fibrosis </li></ul></ul></ul><ul><ul><ul><li>micronodules - < 3 mm diameter </li></ul></ul></ul><ul><ul><ul><li>macronodules - > 3 mm to several cm </li></ul></ul></ul><ul><ul><li>Disruption of architecture of entire liver </li></ul></ul>

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