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Lect.no.4
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  • 44
  • 32
  • In light microscopy inability to recognize nuclei because they broke up (karyorhexis, karyolysis) is a common criterion of cell death.
  • Fibrinoid necrosis looks like fibrin microscopically. In fact, often, it IS fibrin.
  • Dry gangrene is deader, i.e., longer standing, than the death of wet gangrene.

Transcript

  • 1. Irreversible Cell injury (Cell Death)
  • 2. CELLS REACT TO INJURIOUS STIMULI• ADAPTING• SUSTAINING REVERSIBLE INJURY• SUFFERING IRREVERSIBLE INJURY AND DYING
  • 3. TYPES OF CELL DEATH• APOPTOSIS (“normal” death or physiologic death)• NECROSIS (“premature” or “untimely” death due to “causes”(Pathologic death)
  • 4. NECROSIS• It refers to a series of morphologic changes that follow cell death in living tissues• OR is the gross and light-microscopic appearances that indicate cell death.
  • 5. • The surrounding living tissue almost always show inflammatory reaction • The necrotic cell undergo lysis • Autolysis is the dead cell being self-digested by its lysosomal enzymes, while heterolysis is the cell being digested by the bodys living white cells.
  • 6. Morphology of Necrotic Cells• Increased Eosinophilia of cytoplasm - loss of RNA (basophilia) - denatured cytoplasmic protein bind tightly to eosin• Nuclear Changes - Pyknosis ( shrinkage & ↑ basophilia) - Karyorrhexis (Fragmentation of pyknotic nuclei) - Karyolysis (fading of chromatine – DNAase effect• Myelin figure (EM) – large, whorled phospholipid mass (phospholipid precipitate)
  • 7. HISTOLOGIC FEATURES OF COAGULATIVE NECROSISNormal Reversiblecell cell injury Karyorrhexi with s cytoplasmic Irreversible & organelle cell injury with swelling, rupture of Karyolysis blebbing & membrane & ribosome organelles, & detachment nuclear pyknosis
  • 8. Myocardial infarction (coagulative necrosis)Cytoplasmic eosinophilia & nuclear karyolysis
  • 9. Pathogenesis of necrosis1.Denaturation of intracellular proteins ( structural & enzymatic)2. Enzymetic digestion of the cell (Auto & Heterolysis)
  • 10. Morphologic Pattern of Necrotic Cell mass TYPES OF NECROSIS • COAGULATIVE NECROSIS • LIQUEFACTIVE NECROSIS • CASEOUS NECROSIS • FAT NECROSIS • FIBRINOID NECROSIS • GANGRENE
  • 11. COAGULATIVE NECROSIS• Death of groups of cells with preservation of general tissue architecture-tombstone appearance for at least a few days.• Affected tissue is firm due to denaturation of structural & enzymatic proteins(intracellular acidosis)• – Example . Ischemic injury of heart, kidney, ,spleen.
  • 12. Coagulative necrosis  Preservation of structure  Firm  Protein denaturation  Hypoxic tissue death (except brain)
  • 13. Spleen; Coagulative necrosis
  • 14. • The microscopy is distinctive. After loss of their nuclei, the cytoplasm of the cells remains intact for days. The "tombstones" reveal the structure of the living tissue. If the patient lives, the edges of the necrotic area become inflamed, and eventually the dead cells will be removed by white blood cells• RULE: Unless otherwise specified in this section, the death of a group of cells will result in coagulation necrosis• (Ischemic necrosis=Infarction)
  • 15. Kidney infarct exhibiting coagulative necrosis, with loss of nucleiand clumping of cytoplasm but with preservation of basic outlines of glomerular and tubular architecture
  • 16. DEATH:LIGHT MICROSCOPY
  • 17. Morphologic pattern of Necrotic Cell mass• Liquefactive Necrosis - focal bacterial (or fungal) infections – accumulation of inflammatory cells - hypoxic death of cells within CNS
  • 18. LIQUEFACTIVE NECROSIS• (* "colliquative necrosis" in Europe): When the cells die, they are rapidly destroyed by lysosomal enzymes, either their own or those from neutrophilic leukocytes• The tissue becomes liquid viscous mass• Material is creamy yellow in color• Seen in ischemia of brain, abscess
  • 19. Normal brain Liquefactive necrosis
  • 20. CASEOUS NECROSIS*Type of coagulative necrosis*Tissue is cheesy white in appearance*All the cells in the area die & surrounded by inflammatory cells (granulomatous inflammation).*The tissue architecture is completely distructed & turn into friable tissue.*Seen in tuberculous infections &certain fungal infections (as Histoplasmosis)
  • 21. A tuberculous lung with a large area of caseousnecrosis
  • 22. Caseous necrosis of lymph nodes
  • 23. Caseous necrosis with Giant cells
  • 24. Fat necrosis Not a specific pattern Focal areas of fat digestion Usually via release of lipases from pancreas Lipase releases free fatty acid (saponification) from the local lipids (membranes, depot triglyceride). FFA combine with Ca to produce salt “soaps”
  • 25. Foci of Fat necrosis with saponification in the mesentry . Theareas of white chalky deposits represent calcium soapformation at sites of lipid breakdown.
  • 26. Microscopic appearance of fat necrosis
  • 27. FIBRINOID NECROSIS• is a term for damage to the walls of arteries which allows plasma proteins to leak out, and precipitate in, the media
  • 28. FIBRINOID NECROSIS
  • 29. GANGRENE• ("gangrenous necrosis") is not a separate kind of necrosis at all, but a term for necrosis that is advanced and visible grossly. The word gangrene comes from the Latin word gangraena, an eating sore. Gangrene is death and decay of a body part mostly ischemic necrosis of limbs
  • 30. • Gangrene is defined as the gradual destruction of living tissue, due to an obstruction in the supply of blood and oxygen to an area of the body (Ischemia)• Gangrene = ischemic necrosis
  • 31. TYPES OF GANGRENE • .DRY GANGRENE • .WET GANGRENE
  • 32. • Dry gangrene This is mostly coagulative necrosis without infection (free of infection). It is usually brought on by frostbite, or poor circulation that cause the tissues to become dry & black.
  • 33. “DRY” GANGRENE
  • 34. dry gangrene (coagulative necrosis)
  • 35. WET GANGRENE• theres mostly liquefactive necrosis (i.e., the typical foul-smelling, oozing foot infected with several different kinds of bacteria).
  • 36. "wet gangrene in patient with Diabetes millitus”
  • 37. Ischemic necrosis of the bowel (bowel infarction)