L51: Cell Injury and Cell Death

Question 1

Causes of cell injury/death

Answer 1

1. Hypoxia
2. Physical agents (trauma, temperature)
3. Chemical agents (drugs, poisons)
4. Biological agents (bacterial toxins)
5. Immunological agents (hypersensitivity)

Question 2

4 Intracellular systems vulnerable to injurious agents

Answer 2

1. Aerobic respiration
2. Cell membranes (also nuclear/ER membranes)
3. Enzymatic and structural protein synthesis
4. Genetic apparatus

Question 3

4 types of reversible cell injury

Answer 3

1. Intracellular oedema/hydropic degeneration
2. Fatty change
3. Hyaline degeneration (glassy, pink appearance in H&E stain)
4. Intracellular accumulation (e.g. pigments, haemosiderin)

Question 4

Causes of fatty change in cells

Answer 4

1. Hypoxia
2. Starvation
3. Chemicals e.g. Alcohol
4. Metabolic e.g. DM

Question 5

2 morphological patterns in cell death / irreversible cell injury

Answer 5

Apoptosis

Necrosis

Question 6

Apoptosis vs Necrosis

Answer 6

Apoptosis:
Affect single cell
Cell actively take part (suicide)
DNA fragmentation and chromatin condensation
Shrinkage and condensation of nucleus and cytoplasm
Break up into apoptotic bodies (eosinophilic cytoplasms)
phagocytosed and degraded in phagolysosome
Mitochondrial pathways (intrinsic)
Death receptor pathways (extrinsic)

Necrosis:
Death of groups of cells while still living
Unprogrammed
Autolysis: self-digestion by own lysosomal hydrolase
Heterolysis: digested by phagocytosis and proteolytic enzyme
Nuclear changes:
Pyknosis: dense haematoxylinophilic chromatin
Karyorrhexis: chromatin break into fragments
Karyolysis: complete dissolution of nuclear matter (uniform eosinophilic staining)

Question 7

Morphological types of necrosis

Answer 7

1. Coagulative necrosis (firm, dull and yellowish, e.g. myocardial infarction)
2. Liquefaction necrosis (soft and liquid, e.g. ischaemic necrosis of brain)
3. Caseous necrosis (crumbling, whitish, high in lipid e.g. TB infection)
4. Fat necrosis:
   - Enzymatic fat (TG in cells hydrolysed —> FA react with Ca to form soap e.g. chalky white patches in pancreatitis)
   - Traumatic fat (lipid released trigger chronic inflammation e.g. indurated mass in breast)
5. Fibrinoid necrosis (eosinophilic degeneration of collagen and fibrin deposition in joints and arteries)

Question 8

Effects of necrosis

Answer 8

1. Loss of function
2. Release of cell contents
3. Acute inflammation
4. Repair / regeneration
5. Dystrophic calcification
6. Infection

Question 9

Autophagy

Answer 9

Lysosomal digestion of own organelle
Autophagosome
Adaptive response during nutrient deprivation or infection
Can be dysregulated in cancer/neurogenerative diseases