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REVERSIBLE CELL INJURY

 By
 Libason Hosea
MD2 student Muhimbili university
e mail: hlibason@gmail.com
REVERSIBLE CELL INJURY
        (non lethal cell injury)
 ADAPTIVE RESPONSE TO NOXIOUS STIMULI OR STRESS TO A
                   CELL INCLUDES;

-HYPERTROPHY
-HYPERPLASIA
-METAPLASIA
-ATROPHY



 IF THE STIMULUS PERSISTS OR IF IT IS SEVERE FROM THE
                     BEGINNING,




          THEN WHAT FOLLOWS IS CELL INJURY
Reversible cell injury

 injury follows after adaptive capability of the cell is
 exceeded and there is severe membrane damage and
 nuclear alteration.
               1. Reversible cell injury
              2. Irreversible cell injury
Causes of cell injury

1.  Hypoxia
2.  Ischemia
3.  Chemical agents eg reactive oxygen species
4.  Infectious agents
5.  Immunologic reaction eg.autoimmune disease
6.  Nutritional imbalances
7.  Genetic defects eg. Hbs causing premature death of RBCs
8.  Physical agents eg. Radiations, extrem temperatures, etc.
9.  Aging
10. Nutritional imbalances ie.
    undernutrition eg kwarshiorkor and marasmus
   Overnutrition eg. Artherosclerosis
Morphologic alterations of cell injury

 Cellular swelling
 Fatty change
 Other changes
Cellular swelling

 Is the result of failure of energy dependent ion
  pumps in plasma membrane leading to inability to
  maintain ionic and fluid homeostasis
 Cellular swellings are difficult to see in light
  microscope
 Microscopic examination may reveal small clear
  vacuole within the cytoplasm
 These represents pinched off segment of ER
2.Fatty change

 Occurs in hypoxic injury and various forms of toxic
  or metaplastic injury
 Manifested by appearance of large or small lipid
  vacuole in the cytoplasm
 Occur in cells involved and dependant on fat
  metabolism such as hepatocytes and myocardial cells
 Injured cells may show increased esinophilic staining
  which becomes much more pronounced with
  progression to necrosis
3.Other changes;

 Plasma cell membrane alterations
 Distortion of microvilli
 Mitochondrial changes such as mitochondrial
  swelling
 Dilatation of ER
 Nuclear alteratins
 Eosinophilia alterations
if the the stimuli persists

 Irreversible cell injury
 Necrosis
Thank you

REFERENCE:CHAPTER 1, ROBBINS BASIC
            PATHOLOGY
              8 TH E D
           KUMAR ET AL

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Reversible cell injury

  • 1. REVERSIBLE CELL INJURY  By Libason Hosea MD2 student Muhimbili university e mail: hlibason@gmail.com
  • 2. REVERSIBLE CELL INJURY (non lethal cell injury) ADAPTIVE RESPONSE TO NOXIOUS STIMULI OR STRESS TO A CELL INCLUDES; -HYPERTROPHY -HYPERPLASIA -METAPLASIA -ATROPHY IF THE STIMULUS PERSISTS OR IF IT IS SEVERE FROM THE BEGINNING, THEN WHAT FOLLOWS IS CELL INJURY
  • 3. Reversible cell injury  injury follows after adaptive capability of the cell is exceeded and there is severe membrane damage and nuclear alteration. 1. Reversible cell injury 2. Irreversible cell injury
  • 4. Causes of cell injury 1. Hypoxia 2. Ischemia 3. Chemical agents eg reactive oxygen species 4. Infectious agents 5. Immunologic reaction eg.autoimmune disease 6. Nutritional imbalances 7. Genetic defects eg. Hbs causing premature death of RBCs 8. Physical agents eg. Radiations, extrem temperatures, etc. 9. Aging 10. Nutritional imbalances ie.  undernutrition eg kwarshiorkor and marasmus  Overnutrition eg. Artherosclerosis
  • 5. Morphologic alterations of cell injury  Cellular swelling  Fatty change  Other changes
  • 6. Cellular swelling  Is the result of failure of energy dependent ion pumps in plasma membrane leading to inability to maintain ionic and fluid homeostasis  Cellular swellings are difficult to see in light microscope  Microscopic examination may reveal small clear vacuole within the cytoplasm  These represents pinched off segment of ER
  • 7. 2.Fatty change  Occurs in hypoxic injury and various forms of toxic or metaplastic injury  Manifested by appearance of large or small lipid vacuole in the cytoplasm  Occur in cells involved and dependant on fat metabolism such as hepatocytes and myocardial cells  Injured cells may show increased esinophilic staining which becomes much more pronounced with progression to necrosis
  • 8. 3.Other changes;  Plasma cell membrane alterations  Distortion of microvilli  Mitochondrial changes such as mitochondrial swelling  Dilatation of ER  Nuclear alteratins  Eosinophilia alterations
  • 9. if the the stimuli persists  Irreversible cell injury  Necrosis
  • 10. Thank you REFERENCE:CHAPTER 1, ROBBINS BASIC PATHOLOGY 8 TH E D KUMAR ET AL