Irreversible cell injury

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Irreversible cell injury

  1. 1. IRREVERSIBLECELL INJURY<br />
  2. 2. The molecular mechanisms connecting most forms of cell injury to ultimate cell death have proved elusive, for several reasons.<br />
  3. 3. First, there are clearly many ways to injure a cell, not all of them invariably fatal.<br />
  4. 4. Second, the numerous macromolecules, enzymes, and organelles within the cell are so closely interdependent that it is difficult to distinguish a primary injury from secondary (and not necessarily relevant) ripple effects.<br />
  5. 5. Third, the "point of no return," at which irreversible damage has occurred, is still largely undetermined; thus, we have no precise cut-off point to establish cause and effect.<br />
  6. 6. Finally, there is probably no single common final pathway by which cells die. It is, therefore, difficult to define the stage beyond which the cell is irretrievably doomed to destruction.<br />
  7. 7. Classes of Cell Injury<br />Reversible<br />If stressor removed, and<br />If cell damage mild: cells survive<br />Irreversible --> cell death. Types:<br />Apoptosis: normal<br />(leaves falling) as in menses, aging<br />PROGRAMMED<br />Necrosis: patho-logical...<br /> Autolysis: after death of entire organism<br />(dissolution of dead cells by its own digestive enzymes)<br />
  8. 8. PROBABLE CAUSES<br />The first is the inability to reverse mitochondrial dysfunction (lack of oxidative phosphorylation and ATPgeneration) even after resolution of the original injury.<br />The second is the development of profound disturbances in membrane function.<br />
  9. 9. NECROSIS<br />
  10. 10. NECROSIS<br />DEFINITION:<br />Death of a group of contiguous cells within a living tissue or organ<br />Affect both nucleus and cytoplasm<br />Unregulated cell death with inflammation<br />
  11. 11. Morphological changesDURING NECROSIS<br /><ul><li>Cytoplasmic
  12. 12. Nuclear</li></ul>Cytoplasmic changes :<br />Cytoplasmiceosinophilia due to loss of normal basophilia& increased binding of eosin to denaturated proteins<br />(Granular or homogenous glassy) <br />Nuclear changes:<br />Pyknosis: shrinkage-increased staining with haematoxylin<br />Karyorrhexis: fragmentation<br />Karyolysis: total disappearance<br />
  13. 13. TYPES: NECROSIS<br />Coagulative<br />Liquefactive<br />Caseation<br />Fat<br />
  14. 14. COAGULATIVE NECROSIS<br />In: infarcts of kidney, heart, spleen<br />Gross: pale , yellow, opaque, firm<br />Mic.: All cellular details are lost but general architecture of the tissue is preserved<br />Surrounding tissue----acute inflammation<br />Ex: Infarction - heart <br /> Infarction - kidney        <br />
  15. 15. LIQUEFACTIVE NECROSIS<br />In: centers of pyogenic abscess<br />amoebiasis<br />infarcts of C.N.S.<br />Necrotic tissue---completely liquified---turbid fluid----absorbed----space<br /> Ex: Brain - infarction <br />Amoebiasis ---liver <br />
  16. 16. CASEATION NECROSIS<br />In: Tuberculosis<br />Necrotic tissue is partially liquefied---cheesy material (caseation)<br />Mic: Both cellular details & general architecture of dead tissue are lost---structurelesseosinophilic material<br />
  17. 17. FAT NECROSIS<br />Traumatic: in female breast<br />Enzymatic: in acute hemorrhagic pancreatitis<br />Gross: opaque & white<br />fat cells appear cloudy, surrounded by chronic inflammatory cells, histiocytes, foreign body giant cells      <br />
  18. 18. APOPTOSIS<br />
  19. 19. APOPTOSIS  <br />(programmed cell death) <br />Definition:death of individual cells surrounded by viable cells<br />when a cell dies through activation of an internally suicide program<br />It is an active process—energy dependent<br />Does not elicit inflammatory response<br />May be physiologic or pathologic<br />
  20. 20. APOPTOSIS CAUSES<br />PHYSIOLOGIC<br />During embryogenesis e.g. removal of interdigital webs during embryonic development of toes and fingers<br />Hormone-dependent e.g. endometrial cellloss in menstruation<br />PATHOLOGIC<br />Irradiated tissues<br />Cell death induced by cytotoxic T-lymphocytes<br />Viral infections e.g. viral hepatitis<br />Cell death in tumours<br />
  21. 21. Differences between necrosis and apoptosis<br />Necrosis<br />Death of groups of cells<br />A passive process—not energy-dependent<br />Elicits inflammatory response<br />Always pathologic<br />Apoptosis<br />Death of individual cells<br />Active process—energy-dependent<br />Does not elicit inflammatory response<br />May be pathologic or physiologic<br />
  22. 22. FATNECROSIS<br />
  23. 23. FATTY CHANGE <br />Definition:<br />-abnormal accumulation of triglycerides within parenchymal cells<br />Sites:<br />Liver (the most common)<br />Others, heart, kidney,--<br />Pathogenesis: <br />Excessive accumulation of triglycerides within the liver may result from defects in any one of the events in the sequence from fatty acid entry to lipoprotein exit<br />
  24. 24. FATTY CHANGE CAUSES<br />Congestive heart failure<br />Diabetes mellitus<br />Severe anaemia<br />Ischaemia<br />Septicaemia<br />Poisons<br />malnutrition<br />
  25. 25. FATTY CHANGE EFFECTS<br />In all organs, fatty change appears as clear vacuoles within parenchymal cells<br />Due to fat solvents used in paraffin embedding<br />To identify fat, frozen tissue sections are stained with Sudan IV or Oil Red-O---orange-red colour<br />When mild - - - no effects on cell function<br />Severe - - - - - -impair cell function<br />
  26. 26. THANK YOU!<br />

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