DR. ROOPAM JAIN PROFESSOR & HOD, PATHOLOGY & BLOOD BANK

1. Cell Injury, Cellular Adaptations &
Cellular Ageing
1
DR. ROOPAM JAIN
PROFESSOR & HEAD, PATHOLOGY

2. CELL INJURY

3. • effect of a variety of stresses due to etiologic agents a cell
encounters resulting in changes in its internal and external
environment
• The cellular response to stress may vary and depends upon
following two variables:
• i) Host factors i.e. the type of cell and tissue involved.
• ii) Factors pertaining to injurious agent i.e. extent and type of
cell injury.

4. Cellular responses to cell injury

5. ETIOLOGY OF CELL INJURY
• The cells may be broadly injured by two major ways:
• A. Genetic causes
• B. Acquired causes

6. Acquired causes
• 1. Hypoxia and ischaemia
• 2. Physical agents
• 3. Chemical agents and drugs
• 4. Microbial agents
• 5. Immunologic agents
• 6. Nutritional derangements
• 7. Ageing
• 8. Psychogenic diseases
• 9. Iatrogenic factors
• 10. Idiopathic diseases.

7. HYPOXIA AND ISCHAEMIA
• Th e most common mechanism - by reduced supply
of blood to cells due to interruption i.e. ischaemia.
• impaired blood supply from causes other than
interruption e.g. disorders of oxygencarrying RBCs
(e.g. anaemia, carbon monoxide poisoning), heart
diseases, lung diseases and increased demand of
tissues

8. PHYSICAL AGENTS
• i) mechanical trauma (e.g. road accidents);
• ii) thermal trauma (e.g. by heat and cold);
• iii) electricity;
• iv) radiation (e.g. ultraviolet and ionising); and
• v) rapid changes in atmospheric pressure.

9. CHEMICALS AND DRUGS
• i) chemical poisons such as cyanide, arsenic, mercury;
• ii) strong acids and alkalis;
• iii) environmental pollutants;
• iv) insecticides and pesticides;
• v) oxygen at high concentrations;
• vi) hypertonic glucose and salt;
• vii) social agents such as alcohol and narcotic drugs; and
• viii) therapeutic administration of drugs.

10. MICROBIAL AGENTS
• Injuries by microbes include infections caused
by bacteria, rickettsiae, viru ses, fungi,
protozoa, metazoa, and other parasites

11. IMMUNOLOGIC AGENTS
• i) hypersensitivity reactions;
• ii) anaphylactic reactions; and
• iii) autoimmune diseases

12. NUTRITIONAL DERANGEMENTS
• Nutritional deficiency diseases may be due to overall
deficiency of nutrients (e.g. starvation), of protein
calorie (e.g. marasmus, kwashiorkor), of minerals (e.g.
anaemia), or of trace elements.
• Nutritional excess is a problem of affluent societies
resulting in obesity, atherosclerosis, heart disease and
hypertension.

13. AGEING
• Cellular ageing or senescence leads to impaired ability
of the cells to undergo replication and repair, and
ultimately lead to cell death culminating in death of the
individual.

14. PATHOGENESIS OF
CELL INJURY

15. common scheme applies to most forms of cell injury by
various agents:
• 1. Factors pertaining to etiologic agent and host
• 2. Common underlying mechanisms
• 3. Usual morphologic changes
• 4. Functional implications and disease outcome

16. PATHOGENESIS OF ISCHAEMIC &
HYPOXIC INJURY

18. REVERSIBLE CELL INJURY
• 1. Decreased generation of cellular ATP: Damage by
ischaemia from interruption versus hypoxia from other
causes
• 2. Intracellular lactic acidosis: Nuclear clumping
• 3. Damage to plasma membrane pumps: Hydropic
swelling and other membrane changes
• 4. Reduced protein synthesis: Dispersed ribosomes

19. IRREVERSIBLE CELL INJURY
• Two essential phenomena always distinguish irreversible
from rever sible cell injury
• Inability of the cell to reverse mitochondrial
dysfunction on reperfusion or reoxygenation.
• Disturbance in cell membrane function in general, and
in plasma membrane in particular

20. IRREVERSIBLE CELL INJURY
• 1. Calcium influx: Mitochondrial damage
• 2. Activated phospholipases: Membrane damage
• 3. Intracellular proteases: Cytoskeletal damage
• 4. Activated endonucleases: Nuclear damage
• 5. Lysosomal hydrolytic enzymes: Lysosomal damage,
cell death and phagocytosis

21. Ultrastructural changes during cell injury
due to hypoxia-ischaemia.

22. Ultrastructural changes during cell injury
due to hypoxia-ischaemia.

23. Ultrastructural changes during cell injury
due to hypoxia-ischaemia.