3 Rs of success: Respect for self, Respect for others and Responsibility for all your actions

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3 Rs of successRespect for self, Respect
for others and Responsibility for all your actions
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Cellular Injury

• Dr. Venkatesh M. Shashidhar
• Senior Lecturer in Pathology
• Fiji School of Medicine

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Cellular Injury Adaptation

• Normal cell is in a steady state Homeostasis
• External stimuli bringing changes in cell
  physiology and or anatomy - Injury
• Reversible / Irreversible
• Adaptation / Injury / cell death / autolysis

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Terminology

• Necrosis Morphologic changes seen in dead cells
  within living tissue.
• Autolysis Dissolution of dead cells by the cells
  own digestive enzymes. (not seen)
• Apoptosis Programmed cell death. Physiological,
  cell regulation.

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Causes of cell Injury

• Reduced oxygen - Ishemia, infarction
• Physical agents
• Chemical
• Toxins
• Biological agents - Viruses, Bacteria etc.
• Immune reaction - Hypersensitivity
• Nutritional deficiencies.
• Genetic abnormalitiy - Sickle, Hemophilia

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Targets of cell Injury

• Respiration,
• Integrity of cell membrane,
• synthesis of proteins,
• integrity of genetic apparatus.
• Injury at one locus results in wide ranging
  secondary effects.
• Morphology becomes apparent late.

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General Considerations

• Morphology becomes apparent late in cell injury.
• Reaction of cell to injury depends on type of
  injury, duration and severity.
• Reaction of cell to injury also depends on the
  type, state adaptability of the cell.

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Response to Injury

• Adaptations (reversible)
• Hydropic degeneration
• Hypertrophy
• Hyperplasia
• Atrophy
• Accumulations - hyaline, fat, etc.
• Necrosis (irreversible)..

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Types of Necrosis

• Coagulative - Infarction
• Liquifactive - Brain, abscess
• Caseous - Bacterial / Tuberculosis
• Fat Necrosis
• Gangrene - With infection
• Fibrinoid -

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Sequels of Necrosis

• Autolysis - Apoptosis
• Phagocytosis
• Organization fibrous repair
• Dystrophic calcification

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Normal Ischemic - kidney tubule
Microvilli
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Stages of cell death in blood lymphocyte
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Infarct Adrenal gland
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Cerebral atrophy - Alzheimers
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Left ventricle hypertrophy - HPTN
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Caseous necrosisTuberculosishilar lymphnode
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Extensive Caseous necrosisTuberculosis
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Caseous necrosis - Tuberculosis
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Muscle ischemic atrophy
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Cirrhosis - Healing by fibrosis
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Cervix dysplasia-Cervicitis - HPV infection
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Dystrophic calcification - Stomach.
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Fat Necrosis - Peritoneum.
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Fatty Liver - Alcoholism
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Gangrene - Diabetic foot
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Gangrene - Amputated Diabetic foot
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BPH - Benign Prostatic Hyperplasia.
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Gangrene Intestine - Thrombosis.
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Lipofuscin - Wear Tear pigment - Age
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Stroke- Liquifactive necrosis
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Lung abscess Liquifactive necrosis
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Liver abscess Liquifactive necrosis
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Liver - Mallory hyaline - Alcoholism
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Lung- Metaplasia in smoker
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Oesophagitis - Gastric metaplasia.
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Myocardial Infarction- Necrosis
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Renal Infarction - Coagulative
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Renal Infarction - Coagulative necrosis
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Splenic Infarction - Coagulative necrosis
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Conclusions

• Cellular Injury - Various causes
• Reversible Injury - Adaptations
• Hypertrophy, Hyperplasia, Atrophy
• Accumulations - Hydropic, hyaline, fat..
• Irreversible Injury - Necrosis
• Coagulative, Liquifactive, Caseous, fat
• Ageing - Lipofuscin
• Apoptosis - Programmed cell death.

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Thank you...

• Dr. Venkatesh M. Shashidhar
• Senior Lecturer in Pathology
• Fiji School of Medicine