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Cell injuryadaptation 3

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Cell injuryadaptation 3

  1. 1. SDUMC-Path-CSBRP Cell Injury & Adaptation-3Cell Injury & Adaptation-3 Dr.CSBR.Prasad, M.D.Dr.CSBR.Prasad, M.D.
  2. 2. SDUMC-Path-CSBRP Cell injuryCell injury • Reversible injuryReversible injury 1-Cell swelling 2-Fatty change 3-Mitochondrial swelling 4-ER disruption 5-Membrane blebs 6-Cytoskeleton disruption • Irreversible injuryIrreversible injury 1-Apoptosis 2-Necrosis
  3. 3. Morphologic changes in reversible cell injury and necrosis SDUMC-Path-CSBRP
  4. 4. SDUMC-Path-CSBRP Figure 1-16 Timing of biochemical and morphologic changes in cell injury.
  5. 5. SDUMC-Path-CSBRP NECROSISNECROSIS
  6. 6. TermsTerms • Necrosis • Infarction • Gangrene • Tissue fixed in formaline SDUMC-Path-CSBRP
  7. 7. SDUMC-Path-CSBRP DefinitionDefinition Morphological alterations that are brought about by the progressive degradative action of enzymes on a lethally injured cell in living tissue. NECROSISNECROSIS
  8. 8. SDUMC-Path-CSBRP • Is a manifestation of irreversible cell injury • Loss of membrane integrity Leakage of contents • Leaked contents may elicit inflammation Source of enzymes:Source of enzymes: 1. Lysosomes from the necrotic cell itself (autolysis) 2. Enzymes from the immigrant leucocytes NECROSISNECROSIS
  9. 9. SDUMC-Path-CSBRP Morphology:Morphology: Cytoplasmic changes Nuclear changes NECROSISNECROSIS
  10. 10. SDUMC-Path-CSBRP Morphology:Morphology: Cytoplasmic changes  Increased eosinophilia (loss of RNA)  Glassy look (Loss of glycogen)  Moth eaten apperance of cytoplasm  Calcification  Myelin figures (phospholipid precipitates) EM:EM:  Overt discontinuity in membranes  Dilated mitochondria with amorphous densities  Myelin figures  Aggregation of fluffy material NECROSISNECROSIS
  11. 11. SDUMC-Path-CSBRP Proximal tubular cell showing irreversible ischemic injury. Note the markedly swollen mitochondria containing amorphous densities, disrupted cell membranes, and dense pyknotic nucleus.
  12. 12. SDUMC-Path-CSBRP Morphology:Morphology: Nuclear changes May take any one of three patterns Karyolysis Karyorrhexis Pyknosis NECROSISNECROSIS
  13. 13. SDUMC-Path-CSBRP Morphologic patterns:Morphologic patterns: 1. Coagulative necrosis 2. Liquefactive necrosis 3. Caseous necrosis 4. Fat necrosis 5. Fibrinoid necrosis NECROSISNECROSIS
  14. 14. SDUMC-Path-CSBRP NECROSISNECROSIS Coagulative necrosis:Coagulative necrosis: • Basic outline of the cell is preserved • The affected tissues has firm consistency • Increasing intracellular acidosis denatures all proteins including enzymes Coagulative necrosis, is characteristic of hypoxicCoagulative necrosis, is characteristic of hypoxic death of cells in all tissues except the braindeath of cells in all tissues except the brain Eg: The myocardial infarct is an excellent example in which acidophilic, coagulated, anucleate cells may persist for weeks.
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  19. 19. SDUMC-Path-CSBRP Splenic infarct
  20. 20. SDUMC-Path-CSBRP Figure 1-18 Ischemic necrosis of the myocardium. A, Normal myocardium. B, Myocardium with coagulation necrosis (upper two thirds of figure), showing strongly eosinophilic anucleate myocardial fibers. Leukocytes in the interstitium are an early reaction to necrotic muscle. Compare with A and with normal fibers in the lower part of the figure.
  21. 21. SDUMC-Path-CSBRP Here is myocardium in which the cells are dying. The nuclei of the myocardial fibers are being lost. The cytoplasm is losing its structure, because no well-defined cross- striations are seen.
  22. 22. SDUMC-Path-CSBRP Can you guess this tissue?
  23. 23. SDUMC-Path-CSBRP NECROSISNECROSIS Liquefactive necrosis:Liquefactive necrosis: • Characteristic of focal bacterial or fungal infections • There is complete digestion of dead cells • Tissue will be transformed into a liquid viscous mass Hypoxic death of cells within the centralHypoxic death of cells within the central nervous system often evokes liquefactivenervous system often evokes liquefactive necrosisnecrosis
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  27. 27. SDUMC-Path-CSBRP Figure 1-19 Coagulative and liquefactive necrosis. A, Kidney infarct exhibiting coagulative necrosis, with loss of nuclei and clumping of cytoplasm but with preservation of basic outlines of glomerular and tubular architecture. B, A focus of liquefactive necrosis in the kidney caused by fungal infection. The focus is filled with white cells and cellular debris, creating a renal abscess that obliterates the normal architecture.
  28. 28. SDUMC-Path-CSBRP NECROSISNECROSIS Caseous necrosis:Caseous necrosis: • a distinctive form of coagulative necrosis • Seen most often in foci of tuberculous infection Caseous = cheesy whiteCaseous = cheesy white (gross appearance) Microscopy: amorphous granular debris, composed of fragmented, coagulated cells with a distinctive inflammatory border known as a granulomatous reaction Unlike coagulative necrosis, the tissue architectureUnlike coagulative necrosis, the tissue architecture is completely obliterated.is completely obliterated.
  29. 29. SDUMC-Path-CSBRP This is the gross appearance of caseous necrosis in a hilar lymphnode infected with tuberculosis. The node has a cheesy tan to white appearance. Caseous necrosis is really justCaseous necrosis is really just a combination of coagulativea combination of coagulative and liquefactive necrosis thatand liquefactive necrosis that is most characteristic ofis most characteristic of granulomatous inflammation.granulomatous inflammation.
  30. 30. SDUMC-Path-CSBRP Caseous necrosis == Coagulative necrosis ++ Liquefactive necrosis
  31. 31. SDUMC-Path-CSBRP Multiple granulomas with areas of caseous necrosis.
  32. 32. Caseous necrosis -Tuberculosis of the lung SDUMC-Path-CSBRP
  33. 33. SDUMC-Path-CSBRP TB lymphadenitis
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  35. 35. SDUMC-Path-CSBRP Well-defined granulomas are seen here. They have rounded outlines. The one toward the center of the photograph contains several Langhan's giant cells.
  36. 36. SDUMC-Path-CSBRP The edge of a pulmonary granuloma is shown here at medium power magnification. Amorphous pink caseous material composed of the necrotic elements of the granuloma. A Langhan’s giant cell is seen as well.
  37. 37. SDUMC-Path-CSBRP At high magnification, the granuloma demonstrates that the epithelioid macrophages are elongated with long, pale nuclei and pink cytoplasm. The typical giant cell for infectious granulomas is called a Langhans giant cell and has the nuclei lined up along one edge of the cell.
  38. 38. SDUMC-Path-CSBRP ZN-stain for acid fast bacilli (AFB stain). The mycobacteria stain as red rods. (1000x)
  39. 39. SDUMC-Path-CSBRP NECROSISNECROSIS Fat necrosisFat necrosis • It’s not a specific pattern of necrosis • It’s descriptive of focal areas of fat destruction • Occurs in acute pancreatitis
  40. 40. SDUMC-Path-CSBRP NECROSIS –NECROSIS – fatfat necrosisnecrosis
  41. 41. SDUMC-Path-CSBRP Foci of fat necrosis with saponification in the mesentery.
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  43. 43. SDUMC-Path-CSBRP NECROSISNECROSIS Fat necrosis:Fat necrosis: On histologic examination:On histologic examination: • shadowy outlines of necrotic fat cells • basophilic calcium deposits • inflammatory reaction around the focus
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  45. 45. SDUMC-Path-CSBRP NECROSISNECROSIS Fibrinoid necrosis:Fibrinoid necrosis: • It’s a special form of necrosis • Typically occurs with immunecomplex deposition in the walls of arteries • Fibrin leaks out of vessels • Immunologically mediated vasculitis syndromes histologically show this feature
  46. 46. SDUMC-Path-CSBRP NECROSISNECROSIS Fibrinoid necrosis:Fibrinoid necrosis: On histologic examination:On histologic examination: Immunecomplexes and fibrin deposition gives a bright pink and amorphous appearance in H&E “FIBRINOID” (fibrin-like)
  47. 47. SDUMC-Path-CSBRP Fibrinoid necrosis in an artery
  48. 48. SDUMC-Path-CSBRP GangreneGangrene
  49. 49. SDUMC-Path-CSBRP GangreneGangrene Def: Necrosis with superadded putrefaction
  50. 50. SDUMC-Path-CSBRP GangreneGangrene Gangrenous necrosis:Gangrenous necrosis: It’s not a distinctive pattern of cell death the term is still commonly used in surgical practice
  51. 51. SDUMC-Path-CSBRP GangreneGangrene Gangrenous necrosis:Gangrenous necrosis: Involved structure appear: Black Boggy Foul smelling Crepitus / crackling And are Function less
  52. 52. SDUMC-Path-CSBRP GangreneGangrene Gangrenous necrosis:Gangrenous necrosis: Foul smellFoul smell Many bacteria may participate (Polymicrobial)
  53. 53. SDUMC-Path-CSBRP GangreneGangrene Gangrenous necrosis:Gangrenous necrosis: Boggy / emphysematous Because the gases are produced within the tissue, clinically --- it may appear boggy / emphysematous --- crackling / crepitus can be appreciated
  54. 54. SDUMC-Path-CSBRP GangreneGangrene Gangrenous necrosis:Gangrenous necrosis: Dark brown or Black in colour Due to changes in hemoglobin present in the tissue More blood in the tissue, more dark the colour will be
  55. 55. SDUMC-Path-CSBRP GangreneGangrene Types :Types : Based on the cause for tissue necrosis 1- Primary1- Primary 2- Secondary2- Secondary
  56. 56. SDUMC-Path-CSBRP GangreneGangrene Types :Types : Based on the cause for tissue necrosis 1.1. PrimaryPrimary 2.2. SecondarySecondary Criteria Primary. GPrimary. G Secondary. GSecondary. G Necrosis Both caused by same agent i.e. bacteria Both caused by different agents Putrefaction
  57. 57. SDUMC-Path-CSBRP GangreneGangrene Primary gangrene :Primary gangrene : • Due to infection with specific bacteria • Later, putrefaction is brought about by other saprophytic bacteria • Agent: Cl.perfringens, Cl.edematiens & Cl.septicum • Source: intestines, soil • Mode of entry: thru wounds • Requirement: anerobic environment
  58. 58. SDUMC-Path-CSBRP GangreneGangrene Primary gangrene :Primary gangrene : • Agent: Cl.perfringens, Cl.edematiens & Cl.septicum • Toxins: Lecithinase (lysis of cell membranes) Hyaluronidase (digestion of intercellular cement) Collagenases (digestion of connective tissue) • Production of H2 & CO2 by fermentation of sugars • Secondary invasion by saprophytes -- putrefaction
  59. 59. SDUMC-Path-CSBRP GangreneGangrene Primary gangrene :Primary gangrene : Sites & events that predispose to Primary.G: 1. Complication of appendicitis 2. Strangulated hernia 3. Puerperal infection of the uterus
  60. 60. SDUMC-Path-CSBRP GangreneGangrene Primary gangrene :Primary gangrene : Clinical course: 1. Rapidly spreading along tissue planes 2. Hemolysins may cause hemolysis 3. Severe toxaemia 4. Circulatory collapse 5. Distant spread is a terminal event
  61. 61. SDUMC-Path-CSBRP GangreneGangrene Primary gangrene :Primary gangrene : • Wounds must be treated with early excision of devitalized tissue • Treated with antibiotics to prevent infection • With the clinical suspicion institution of antigasgangrene serum • Clostridia may also cause cellulitis without affecting the underlying muscle
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  67. 67. SDUMC-Path-CSBRP GangreneGangrene Primary gangrene :Primary gangrene : other examples • Meleney’s postoperative synergistic gangrene • Noma (cancrum oris) • Forneyer’s gangrene
  68. 68. SDUMC-Path-CSBRP FOURNIER´S GANGRENE
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  71. 71. SDUMC-Path-CSBRP Meleney’s postoperative synergistic gangrene
  72. 72. SDUMC-Path-CSBRP Secondary GangreneSecondary Gangrene Dry gangrene :Dry gangrene : When coagulative necrosis predominates Wet gangrene :Wet gangrene : When liquifactive necrosis predominates
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  80. 80. SDUMC-Path-CSBRP E N DE N D

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