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Cellular Injury

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'Progressive time related loss of structural and functional capacity of cells leading to death' ... Clock genes. Metabolic: Reduced Mitochondrial oxidative reactions ... – PowerPoint PPT presentation

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Title: Cellular Injury


1
Cellular Injury Ageing
  • Dr. Venkatesh M. Shashidhar
  • Senior Lecturer in Pathology
  • Fiji School of Medicine

2
Objectives
  • Disease
  • terminology, classification, etiology
  • Cellular Injury
  • Etiology, types, features.
  • Ageing
  • Etiology, Features, theories.

3
Cellular Injury Adaptation
  • Normal cell is in a steady state Homeostasis
  • Homeostasis Sum of all chemical reactions
  • Injury is any stimulus bringing changes in cell
    physiology and or anatomy Internal/External
  • Injury can be Reversible / Irreversible
  • Adaptation is the changes in a cell due to
    reversible Injury
  • cell death / autolysis

4
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

5
Terminology
  • Hydropic swelling water collection within cell
  • Fatty change accumulation of fat
  • 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.

6
Targets of cell Injury
  • Respiration Poisoning, ischemia
  • Integrity of cell membrane Toxins, bacteria
  • synthesis of proteins Alcohol
  • integrity of genetic apparatus. - Radiation
  • Injury at one locus results in wide ranging
    secondary effects.

7
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.

8
Response to Injury
  • Adaptations (reversible)
  • Hydropic degeneration
  • Hypertrophy, Hyperplasia, Atrophy
  • Accumulations - hyaline, fat, etc.
  • Cell death / Necrosis (irreversible)
  • Coagulative Infarction - Heart
  • Liquifactive - Brain, abscess
  • Caseous - Tuberculosis
  • Gangrene - With infection limbs.

9
LVH - Heart in Hypertension
Left Ventricular Hypertrophy
10
Goitre Iodine Deficiency
11
Renal Artery stenosis - Atrophy
Nephrosclerosis Atrophic Kidney
12
Cerebral Infarction (Stroke)
Haemorrhagic Necrosis
13
Normal Ischemic - kidney tubule
Microvilli
14
Renal Infarction - Coagulative
15
Infarct Adrenal gland
16
Caseous necrosisTuberculosishilar lymphnode
17
Extensive Caseous necrosisTuberculosis
18
Muscle - ischemic atrophy
19
Splenic Infarction - Coagulative necrosis
20
Stroke- Liquifactive necrosis
21
Liver abscess Liquifactive necrosis
22
Gangrene Intestine - Thrombosis.
23
Gangrene - Diabetic foot
24
Gangrene - Amputated Diabetic foot
25
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26
Ageing
27
Ageing
  • Progressive time related loss of structural and
    functional capacity of cells leading to death
  • Senescence, Senility, Senile changes.
  • Ageing of a person is intimately related to
    cellular ageing.
  • Countdown starts with birth!

28
Factors affecting Ageing
  • Genetic Clock genes, (fibroblasts)
  • Diet malnutrition, obesity etc.
  • Social conditions -
  • Diseases Atherosclerosis, diabetes etc.
  • Genetic disease - Werners syndrome.

29
Cellular mechanisms of ageing
30
Telomerase in ageing
Germ Cells Somatic Cells
31
Cellular ageing mechanisms
  • Nuclear
  • Reduced synthesis of nucleic acids
  • Telomere shortening
  • Clock genes
  • Metabolic
  • Reduced Mitochondrial oxidative reactions
  • Reduced protein synthesis, Protein cross
    linking.
  • Decreased cell receptors, transcription factors.
  • Oxidative peroxidation of organelles.

32
Ageing Morphologic changes
  • Loss of skin elasticity
  • Easy bruising fragile capillaries.
  • Glycosylation of lens proteins
  • Accumulation of Lipofuscin pigment Brown
    atrophy.

33
Normal Brain surface
34
Cerebral atrophy - Alzheimers
35
Elastosis of skin
36
Pathology of Ageing
37
Conclusions
  • Cellular Injury - Various causes
  • Reversible Injury - Adaptations
  • Hypertrophy, Hyperplasia, Atrophy
  • Accumulations - Hydropic, hyaline, fat..
  • Irreversible Injury - Necrosis
  • Coagulative, Liquifactive, Caseous, fat
  • Ageing Physiological pathological.
  • Time related, several theories.

38
Thank You
  • Dr. Venkatesh M. Shashidhar
  • Senior Lecturer in Pathology
  • Fiji School of Medicine
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