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Irreversible cell injury
The molecular mechanisms connecting cell injury to cell death are complex and not fully understood. There are many potential causes of cell injury that may or may not be fatal, and the "point of no return" where damage becomes irreversible is still unclear. Additionally, cells can die through different pathways, making the definition of irreversible injury difficult. Cell injury can result in either reversible or irreversible cell death through mechanisms like apoptosis, the body's normal programmed cell death process, or necrosis, pathological cell death resulting in inflammation.
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Irreversible cell injury
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- 2. The molecular mechanismsconnecting most forms of cell injury to ultimate cell death have proved elusive, for several reasons.
- 3. First, there areclearly many ways to injure a cell, not all of them invariably fatal.
- 4. Second, the numerousmacromolecules, 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.
- 5. Third, the "pointof 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.
- 6. Finally, there isprobably 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.
- 7. Classes of CellInjuryReversibleIf stressor removed, andIf cell damage mild: cells surviveIrreversible --> cell death. Types:Apoptosis: normal(leaves falling) as in menses, agingPROGRAMMEDNecrosis: patho-logical... Autolysis: after death of entire organism(dissolution of dead cells by its own digestive enzymes)
- 8. PROBABLE CAUSESThe firstis the inability to reverse mitochondrial dysfunction (lack of oxidative phosphorylation and ATPgeneration) even after resolution of the original injury.The second is the development of profound disturbances in membrane function.
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- 10. NECROSISDEFINITION:Death of a group of contiguouscells within a living tissue or organAffect both nucleus and cytoplasmUnregulated cell death with inflammation
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- 12. NuclearCytoplasmic changes :Cytoplasmiceosinophilia dueto loss of normal basophilia& increased binding of eosin to denaturated proteins(Granular or homogenous glassy) Nuclear changes:Pyknosis: shrinkage-increased staining with haematoxylinKaryorrhexis: fragmentationKaryolysis: total disappearance
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- 14. COAGULATIVE NECROSISIn: infarctsof kidney, heart, spleenGross: pale , yellow, opaque, firmMic.: All cellular details are lost but general architecture of the tissue is preservedSurrounding tissue----acute inflammationEx: Infarction - heart Infarction - kidney
- 15. LIQUEFACTIVE NECROSISIn: centersof pyogenic abscessamoebiasisinfarcts of C.N.S.Necrotic tissue---completely liquified---turbid fluid----absorbed----space Ex: Brain - infarction Amoebiasis ---liver
- 16. CASEATION NECROSISIn: TuberculosisNecrotictissue is partially liquefied---cheesy material (caseation)Mic: Both cellular details & general architecture of dead tissue are lost---structurelesseosinophilic material
- 17. FAT NECROSISTraumatic: infemale breastEnzymatic: in acute hemorrhagic pancreatitisGross: opaque & whitefat cells appear cloudy, surrounded by chronic inflammatory cells, histiocytes, foreign body giant cells
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- 19. APOPTOSIS (programmed cell death) Definition:death of individualcells surrounded by viable cellswhen a cell dies through activation of an internally suicide programIt is an active process—energy dependentDoes not elicit inflammatory responseMay be physiologic or pathologic
- 20. APOPTOSIS CAUSESPHYSIOLOGICDuring embryogenesise.g. removal of interdigital webs during embryonic development of toes and fingersHormone-dependent e.g. endometrial cellloss in menstruationPATHOLOGICIrradiated tissuesCell death induced by cytotoxic T-lymphocytesViral infections e.g. viral hepatitisCell death in tumours
- 21. Differences between necrosisand apoptosisNecrosisDeath of groups of cellsA passive process—not energy-dependentElicits inflammatory responseAlways pathologicApoptosisDeath of individual cellsActive process—energy-dependentDoes not elicit inflammatory responseMay be pathologic or physiologic
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- 23. FATTY CHANGE Definition:-abnormal accumulationof triglycerides within parenchymal cellsSites:Liver (the most common)Others, heart, kidney,--Pathogenesis: 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
- 24. FATTY CHANGE CAUSESCongestiveheart failureDiabetes mellitusSevere anaemiaIschaemiaSepticaemiaPoisonsmalnutrition
- 25. FATTY CHANGE EFFECTSInall organs, fatty change appears as clear vacuoles within parenchymal cellsDue to fat solvents used in paraffin embeddingTo identify fat, frozen tissue sections are stained with Sudan IV or Oil Red-O---orange-red colourWhen mild - - - no effects on cell functionSevere - - - - - -impair cell function
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