Cell Injury And Death

Question 1

Cell injury

Answer 1

• injurious stimuli- reversible cell injury- necrosis
• injurious stimuli- reversible stage?- apoptosis

Question 2

Pathogenesis

Answer 2

• damage to: mitochondria, disrupted aerobic respiration/ATP synthesis
• cell membrane, disrupted ion concentration
  -cytoplasm and ribosomes, disrupted enzyme and structural protein synthesis and architecture
• nucleus: disrupted DNA maintenance and DNA damage

Question 3

Oxidative stress

Answer 3

• caused by reactive oxygen species
• normally formed in small amounts as a byproduct of respiration
• formed pathologically by absorption of radiation, toxic chemicals, hypoxia
• lack of antioxidants makes damage more likely

Question 4

Reversible cell injury

Answer 4

• nature of changes are same whether reversible/ irreversible
• reversible are less severe and include
• cloudy swelling: osmotic disturbance loss of energy-dependent Na pump leads to Na influx and build up of intracellular metabolites
  Cytoplasmic blebs, disrupted microvilli, swollen mitochondria
  “Fatty change”: accumulation of lipid vacuoles in cytoplasm caused by disruption of fatty acid metabolism, especially in liver.

Question 5

cell death by necrosis or apoptosis

Answer 5

Cell death by necrosis;
-injury due to external stimuli
-uncontrolled cell death
-always pathological
-cell contents leak from breakdown of cell membrane
-often elicits inflammatory response
- Cell death by apoptosis;
-can be physiological e.g. during embryogenesis and development
-can be pathological e.g. in viral infection
-active controlled or “programmed” cell death
-cell contents do not leak due to intact cell membrane
-does not elicit an inflammatory response

Question 6

necrosis:histological changes

Answer 6

-Cell swelling, vacuolation and disruption of membranes of cell and its organelles including mitochondria, lysosomes and ER.
-Release of cell contents (cell lysis) including enzymes causes adjacent damage and elicits acute inflammation

Question 7

necrosis:morphological subtypes

Answer 7

Coagulative:
-firm, tissue outline retained
*Haemorrhagic: due to blockage of venous drainage
*Gangrenous: larger area especially lower leg
-Colliquitive:
*tissue becomes liquid and its structure is lost e.g. infective abscess, cerebral infarct
-Caseous:
*combination of coagulative and colliquitive, appearing “cheese-like” (caseous): classical for granulomatous inflammation, especially TB
Fat:
due to action of lipases on fatty tissue

Question 8

effects on necrosis

Answer 8

• functional: depends on the tissue/organs
  -inflammation: release of cell contents activates inflammation and causes damage.
• either acute with removal of stimulus and then healing and repair
• or chronic with persistence of stimulus and chronic inflammation

Question 9

apoptosis

Answer 9

-genetically programmed/activated cell death
-required energy and distinct pathways involved
- important physiological role, but can occur in pathological situations
- does not cause inflammation but may be caused by immunological mechanisms
- different morphology from necrosis

Question 10

apoptosis: physiological

Answer 10

• embryogenesis: deletion of cell populations
• hormone dependent involution: uterus, breast, ovary
  -cell deletion in proliferating cell populations to maintain constant number of cells, epithelium - deletion of inflammatory cells after an inflammatory response
  -deletion of self-reactive lymphocytes in thymus

Question 11

apoptosis: pathological

Answer 11

• viral infection: cytotoxic t-lymphocytes
  -dna damage
  -hypoxia/ischaemia
• autoimmune disease
  -graft vs host disease