Cell Injury Flashcards

1
Q

How is a steady cell state maintained?

A
  • Preservation of genetic integrity
  • Normal enzyme content
  • Intact membranes and transmembrane proteins
  • Adequate supply of substrates and oxygen
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2
Q

Define hyperplasia/hypertrophy, metaplasia and atrophy, give examples of these

A

Hyperplasia/hypertrophy- increased cellular activity- heart
Atrophy- decreased cellular activity- adrenal glands
Metaplasia- Changed cell morphology- uterus/vagina, Barrett’s oesophagus

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3
Q

What are types of physical trauma?

A

Mechanical- Disruption of cell structures, thrombosis leading to ischaemia
Extreme temperatures- Fever, ice crystals and heat denature

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4
Q

Name some chemical agents that cause damage to the body

A
Alcohol
Tobacco
Drugs
Poison
Environmental
Occupational
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5
Q

Describe infectious organisms

A
  • Produce bacterial endotoxin or exotoxin (C.Diff)
  • Collateral damage by inflammation
  • Hijacking of cell machinery by viruses (cell lysis)
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6
Q

Describe Irradiation and its mechanism

A
  • Ionising (x-rays, UV light)
  • Generates free radicals and direct damage to macromolecules
  • Different organs have different sensitivity- high=bone marrow, gonads and intestines low=uterus, pancreas and adrenal
  • Induce inflammatory response several hours after exposure
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7
Q

What might be affected by cell injury?

A
  • Mitochondrial function
  • Membrane integrity and function
  • Protein synthesis
  • Cytoskeleton
  • Genetic apparatus
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8
Q

Describe the mechanism of action for reversible ischaemic injury

A
  • Cellular swelling/oedema caused by hypoxia/toxins/fever
  • Decreased oxidative phosphorylation so reduced ATP levels
  • Activity of ATP plasma membrane Sodium pump reduced so influx of Na and Ca= isosmotic gain of water and cellular swelling
  • Anaerobic glycolysis inc to generate ATP from glycogen, dec glycogen stores = accumulation of lactic acid = dec intracellular pH
  • Dec pH and ATP= ribosomes detach from rough ER and reduction in protein synthesis
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9
Q

What is Sublethal cell injury?

A

Cell swelling (cloudy) and fatty change - usually alcohol & liver

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10
Q

How does free radical toxicity cause injury?

A
  • Chain reaction with molecules in membrane to produce more radicals
  • Damages proteins & nucleic acids leading to apoptosis
  • Detoxification by Superoxide dismutase & antioxidants (Vit A,C,E)
  • Bacterial killing by neutrophils& macrophages depends on formation of superoxide
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11
Q

How can membrane defects occur by cell injury?

A

-Compromised by bacterial toxins, viral proteins, cytolytic lymphocytes
-Loss of membrane barriers lead to breakdown in metabolite gradients
-Inc Ca2+ leads to activation of enzymes:
ATPase, Phospholipase(causes membrane damage), Protease(breakdown membrane & cytoskeletal proteins), Endonuclease(DNA fragmentation)

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12
Q

What is necrosis? What types of necrosis are there?

A
  • Passive multiple cell death due to injury causing an inflammatory reaction
  • plasma membrane disrupted and enlarged cell size
  • Coagulative, Caseous, Gangrene, Fibrinoid(fat), Colliquative
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13
Q

Describe Coagulative necrosis

A
  • Denaturation of intracytoplasmic proteins
  • Dead tissue = firm and slightly swollen
  • Retention of microscopic architecture
  • Most common & typical of ischaemic injury (NOT brain)
  • Cellular proteins may leak into blood
  • Protein levels can be checked in a blood test of a suspected MI
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14
Q

Describe Colliquative necrosis

A
  • Brain due to no collagen structure

- Liquefaction and then cyst formation

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15
Q

Describe Caseous necrosis

A
  • Characteristic of Tuberculosis
  • Cheese like
  • Cellular detail destroyed surrounded by granulomatous inflammation
  • Dead tissues lack structure
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16
Q

Describe gangrenous necrosis

A
  • Dry gangrene=limbs-diabetes

- Wet gangrene=ischaemic bowel

17
Q

What is apoptosis?

A
  • Programmed single cell death
  • Active (requires energy)
  • Plasma membrane intact and reduced cell size
  • Physiological = embryogenesis, involution, elimination of self-reacting lymphocytes
  • Pathological= viral infection, protein/DNA damage, cell killing by cytotoxic T cells, chemo/radiotherapy
18
Q

Describe the mechanism of apoptosis

A

-Apoptosis initiating factor & cytochrome C in mitochondria
-Released into cytosol activating caspases (effector molecules) leading to apoptosis
-P53 activated by DNA damage
-Bcl-2 binds to cytochrome C inhibiting it and blocking apoptosis
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