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Cell injury

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pathology

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Cell injury

  1. 1. Dr. Manisha Tambekar
  2. 2. Introduction General considerations…… • Adapt or die! • Reaction patterns in a given cell/tissue is often limited • Degree of injury is a function of type, duration and severity of insult
  3. 3. Definition Cell injury: The effect of a variety of stresses due to etiological agents a cell encounters resulting in changes in its internal & external environment. Cellular response to stress vary & depends upon 1. Host factors: type of cell & tissue involved 2. Factors pertaining to injurious agent : extent & type of cell injury.
  4. 4. Introduction • Pathology: the study (logos) of suffering (pathos) • Four aspects of a disease process that form the core of pathology 1. its cause (etiology) 2. Mechanisms of its development ( pathogenesis) 3. Structural alterations induced in cells & organs ( morphological changes) 4. Functional consequences of the morphologic changes ( Clinical significance)
  5. 5. Causes of cell injury Genetic causes Acquired causes -Hypoxia and ischemia -Physical agents -Chemical agents and drugs -Microbial agents -Immunological agents -Nutritional derangements -Psychological factors
  6. 6. Causes of cell injury Acquired causes 1. Oxygen Deprivation  Ischemia ( loss of blood supply from impeded arterial flow or reduce venous drainage) Local e.g. embolus Systemic e.g. cardiac failure  Hypoxia ( deficiency of oxygen causing cell injury by reducing aerobic oxidative respiration) Oxygen problems e.g. altitude Haemoglobin problems e.g. anaemia  Oxidative phosphorylation E.g. cyanide poisoning
  7. 7. Causes of cell injury 2. Physical agents Direct Physical Effects - Exposure of tissue to extreme heat or cold results in direct injury that is often irreversible, resulting in a pattern of coagulative necrosis. - Sudden changes in pressure can cause cellular disruption (e.g. a hammer blow to the thumb). - Electrical currents can cause direct breakdown of cellular membranes that may be irreversible.
  8. 8. Causes of cell injury 3. Chemical agents & drugs: Common poisons (arsenic, cyanide, mercury) interfere with cellular metabolism. If ATP levels drop below critical levels, affected cells will die.  The list of pharmaceuticals that may have toxic effects on cells is enormous. Some act directly, but most have their effect through breakdown metabolites. Metabolism of alcohol (a type of drug) to acetaldehyde is one example.
  9. 9. Causes of cell injury 4. Microbial agent Injuries by microbes include infections caused by Fungi, Rickettsiae, Bacteria, parasites and Viruses 5. Immunologic agents: Double –edged sword’- protects the host against various injurious agents but it may also cause cell injury.  Hypersensitivity reactions Anaphylactic reactions to a foreign body Autoimmune diseases
  10. 10. Causes of cell injury 6. Nutritional Imbalances:  Dietary insufficiency of protein, vitamins and/or minerals can lead to injury at the cellular level due to interference in normal metabolic pathways.  Dietary excess  can likewise lead to cellular and tissue alterations that are detrimental e.g. fat is the biggest offender, or excess ingestion of "health supplements"
  11. 11. Causes of cell injury 7. Psychogenic diseases: No specific biochemical or morphologic changes in acquired mental diseases. problems of drug addiction, alcoholism & smoking results in various organic diseases such as liver damage, chronic bronchitis, lung cancer, peptic ulcer, HT, IHD etc, 8. Genetic derangements: result in a defect as severe as the congenital malformations associated with down syndrome, caused by chromosomal abnormalities. Inborn error of metabolism arising from enzymatic abnormalities.
  12. 12. Causes of cell injury 9. Iatrogenic causes 10. Idiopathic diseases: ‘Unknown cause’. Exact cause is undetermined. Most common form of HT ( 90%) is idiopathic ( or essential ) HT. 11. Ageing: it is result of a progressive decline in the proliferative capacity & life span of cells and the effects of continous exposure to exogenous influences that result in progressive accumulation of cellular and molecular damage.
  13. 13. Cellular responses 1. Cellular adaptations 2. Reversible & irreversible cell injury 3. Subcellular changes 4. Intracellular accumulations.
  14. 14. Cellular responses Adaptive Responses Atrophy Hypertrophy Hyperplasia Metaplasia Cell Injury Reversible Irreversible  Cell death Necrosis Apoptosis
  15. 15. Adaptation In case of severe stress, the narrow range of alteration in structure & function is not sufficient, the cell undergoes an altered but steady state e.g. atrophy, hypertrophy.
  16. 16. Cellular responses 1. Cellular adaptations: Increased functional demand ↓ cell adapt to the changes ↓ expressed morphologically ↓ revert back to normal after the stressed is removed.
  17. 17. Adaptive response: Hypertrophy: An increase in the size of cells and ,with such change ,an increase in the size of the organ ( without any change in the number of cells) Hypertrophied organ has no new cells ,just large cells. Atrophy : shrinkage in the size of the cell substance is known as atrophy. Hypoplasia : Term used for developmentally small size. Aplasia: Extreme failure of development so that only rudimentary tissue is present.
  18. 18. Adaptive response Hyperplasia: An increase in number of cells in an organ or tissue resulting in enlargement of the organ or tissue. Metaplasia: Reversible change in which one adult cell type ( epithelial or mesenchymal) is replaced by another adult cell type.  A regressive change in the adult cells manifested by variation in their size, shape & orientation. Commonly associated with chronic inflammation and irritation or is seen adjacent to cancerous change. There is tendency to develop into cancer in some cases.
  19. 19. Adaptive response Intracellular accumulations : one of the manifestations of metabolic derangements in cells is the intracellular accumulations of abnormal amounts of various substance. 1. A normal cellular constituent- water, lipid, proteins & carbhohydrates. 2. An abnormal substance Exogenous : minerals or products of infectious agents Endogenous : products of abnormal synthesis or metabolism 3. Pigments
  20. 20. HEART( lipid accumulation) lipid accumulation in two forms: 1.Tigroid effect: bands of yellowed myocardium alternating with bands of darker, red brown myocardium uninvolved in patients with profound anemia 2.Diffuse ,uniform appearance of myocardium e.g: Diphtheritic myocarditis & severe anemia.
  21. 21. Cellular responses : Subcellular changes Residual effects of reversible cell injury persist in cell as evidence of cell injury at Subcellular level (Subcellular changes) or metabolites may accumulate within the cell (Intracellular accumulations).
  22. 22. Cellular responses: Reversible & Irreversible cell injury Cell injury : If the cell’s adaptive capability is exceeded or if adaptive response is not possible, cell injury develops.  Two types 1. Reversible cell injury ( Degeneration ):stress is mild to moderate ; injured cell may recover. 2. Irreversible cell injury ( Necrosis ) : Persistent & severe form of cell injury leads to cell death.
  23. 23. Reversible change Fatty change ( Steatosis) Abnormal accumulation of triglycerides within parenchymal cells. Organs: 1. Liver ( common , organ involved in fat metabolism) 2.Heart 3. Muscle 4.Kidney
  24. 24. Fatty change ( Steatosis) Causes : 1. Toxins ( Alcohol abuse) 2.DM 3. Protein malnutrition 4.Obesity 5.Anoxia 6.kwashiorkor in children
  25. 25. Fatty liver
  26. 26. Foam cells Accumulation of triglycerides, cholesterol & cholesterol esters in phagocytic cells. Scavenger macrophages, whenever in contact with the lipid debris of necrotic cells or abnormal forms of plasma lipids become stuffed with lipid becoz of phagocytic activities. Cytoplasm becomes vacuolated & are called as ‘ FOAM CELLS’. E.g: Atheroslcerosis of aorta
  27. 27. ATHEROSLCEROSIS Fatty dots F.Atheroma Plaques Complicated
  28. 28. Fatty Liver: Microscopy  Appears as clear vacuoles within parenchymal cells  D/D: Intracellular accumulations of water & polysaccharides ( glycogen) produce clear vacuoles. 1. Lipids:  Avoidance of fat solvents used in paraffin embbeding.  Frozen section : to identify fat.  Special stains: Sudan IV, Oil Red- O (orange red ), Osmic acid, Sudan black( color: black )
  29. 29. Fatty Liver: Microscopy 2. Glycogen: PAS ( Periodic Acid Schiff ) Reaction 3. Water/ Fluid with a low protein content : Neither fat nor glycogen can be demonstrated.
  30. 30. Cellular swelling/ cloudy swelling Organs: kidney ,liver Causes: ischemia, hypoxia, effect of poison. Mech : cells are incapable to maintain ionic and fluid homeostasis. Gross: organ is swollen, c/s bulges outwards, pale, hazy & has a grey parboiled appearance. Soft in consistency. Microscopy: cells are swollen, indistinct cell margins and cytoplasm filled with eosinophilic(proteinaceous ) granules and cell borders might be grayed releasing granules.
  31. 31. Reversible cell injury Hydropic degeneration : vacuoles appear in the cytoplasm. In extreme forms ,cells get distended with fluid & rupture, resulting in death of cells. e.g. blisters, Microvasculature of organ is compressed by swollen cells ( hepatic sinusoids, capillaries of renal cortex) resulting in pallor of the organ
  32. 32. Irreversible cell injury Necrosis: Death of a cell or group of cells in the midst of living tissue. 1. Coagulative necrosis 2.Liquefactive necrosis 3. Caseous necrosis 4.Fat necrosis 5.Fibrinoid necrosis 6.Gangrenous necrosis Apoptosis: Programmed cell death.
  33. 33. Classification of morphologic forms of cell injury 1. Reversible cell injury 2. Irreversible cell injury 3. Programmed cell death 4. Deranged cell metabolism 5. After-effects of necrosis Retrogressive changes Cell death –necrosis Apoptosis Intracellular accumulation of lipid, protein, carbhohydrate Gangrene, pathologic calcification.

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