Cellular injury, adaptation and death Flashcards

1
Q

What does cell injury lead to? (4)

A
  • ATP depletion
  • Cell membranes of increased permeability
  • Disruption of biochemical pathways
  • DNA damage
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2
Q

How can the injured cell react to damage?

A
  • adaptation
  • degeneration
  • death
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3
Q

Describe the mechanisms of oxygen deficiency (often ultimate cause of injury)

A
  • inadequate oxygenation of blood e.g. cardiac or respiratory failure
  • reduced vascular perfusion (ischaemia)
  • reduced oxygen transport e.g. anaemia
  • inhibition of respiratory enzymes in the cell e.g. cynaide
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4
Q

What are the physical agents leading to cell injury?

A
  • trauma
  • temp extremes
  • ionising radiation
  • electric shock
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5
Q

What are the infectious agents leading to cell injury?

A
  • prions
  • viruses
  • bacteria
  • fungi
  • parasites
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6
Q

What are the nutritional imbalances leading to cell injury?

A
  • dietary deficiencies
  • long term starvation
  • caloric excess
  • dietary toxicities
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7
Q

What are the genetic derangements leading to cell injury?

A
  • Inherited diseases
  • metabolic disease
  • neoplasia
  • autoimmune diseases
  • susceptibility to infection
  • congenital defects
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8
Q

How can workload imbalances lead to cell injury?

A
  1. Increased workloads
    - respond by hypertrophy or hyperplasia (cell dependent)
    - if excessive- leads to cell degeneration and death
  2. Reduced workload
    - loss of innervation, hormones or growth factors
    - lead to atrophy
    - excessive cells can be removed by apoptosis
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9
Q

How do chemicals, drugs and toxins lead to cell injury?

A
  • alter homeostasis
  • toxicity depends on cell tolerance
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10
Q

What does cell susceptibility to chemical, drugs and toxins depend on?

A
  • mitotic rate
  • ability to:
  • take-up
  • bind
  • concentrate
  • metabolise
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11
Q

How does immunological dysfunction lead to cell injury?

A
  • failure to respond
  • overreaction
  • reaction to self
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12
Q

How does ageing lead to cell injury?

A

-accumulated damage to cells (proteins, lipids, nucleic acids) (depends on the ability to replicate/ repair)

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13
Q

Pneumonic to remember causes of disease?

A

V - vascular

I - iatrogenic, idiopathic

T - trauma, toxicity

A - autoimmune, allergy, ageing

M - metabolic

I - infectious, inflammatory

N - nutritional, neoplasia

D -degenerative, developmental

E- endocrine

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14
Q

When is cell injury reversible?

A
  • if the cell can regain homeostasis
  • and can then return to normal structure and function
  • injury isn’t too severe or prolonged
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15
Q

What happens when the injury is reversible?

A

(MITOCHONDRIAL DAMAGE)

  • reduced oxidative phosphorylation
  • reduced ATP
  • increased glycolysis
  • dysfunction of membrane ion pumps
  • reduced protein synthesis
  • dysfunction of chromatin based processes
  • cell swelling
  • ER swelling
  • loss of microvilli
  • membrane blebs
  • clumped chromatin
  • lipid accumulation
  • myelin figures
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16
Q

What happens in irreversible cell injury?

A

(UNREPAIRABLE DAMAGE TO INFRASTRUCTURE)

  • mitochondrial dysfunction
  • cell membrane damage
  • production of ROS
  • release of lysosomal enzymes
17
Q

What happens in cell death?

A

(CELL WIDE SYSTEMS BREAK DOWN)

  • cytocavitary system
  • cytoskeleton
  • chromatin
  • oncotic necrosis
  • apoptosis
  • pyknosis
  • karyorrhexis
  • karyolysis
  • absence of nucleus
  • cytoplasmic eosinophilia
18
Q

What is acute cell swelling?

A
  • initial response to loss of homeostasis
  • caused by influx of water
19
Q

What are the other names for acute cell swelling?

A
  • hydropic degeneration - hepatocytes
  • ballooning degeneration-keratinocytes
  • cytotoxic oedema - CNS
20
Q

Describe the molecular mechanism of acute cell swelling

A
  • in homeostasis: N-K-ATP pump maintains electrochemical gradient (NaOUT, Kin) -water follows Na
  • when you lose homeostasis: Na floods in, water follows
  • so disruption results in the disruption of electrochemical gradient and the influx of water leads to swelling
21
Q

What are the gross morphological changes when acute cell swelling occurs?

A
  • increase vol and weight of parenchymal organs
  • may impart pallor
22
Q

What does this show?

A
  • white dots are uniform (all around a central vein)
  • show acute cell swelling in liver
23
Q

What microscopic morphological changes would you see in acute cell swelling?

A
  • dilutes the cytosol
  • separates organelles
  • distends the cell
  • swollen, pale, finely vacuolated appearance
24
Q
A
25
Q

If the injury is sublethal and chronic what can the cell do?

A
  • adapt
  • accumulate normal or abnormal substances
26
Q

what is autophagy?

A
  • self eating
  • protection mechanism
  • eats its own proteins and carbs for nutrients until more can be sourced
  • consumes organelles
  • limits inflam if the cell does die - factors to promote heterophagy and stops bits of cells lying around
  • heterophagy - when a cell phagocytoses another cell or a part of a cell
27
Q

What is atrophy?

A
  • decrease in tissue mass due to decreased number/size of cells after reaching normal size
28
Q

What are the causes of atrophy?

A
  • nutrient deprivation
  • compression
  • decreased workload
  • decreased hormore stimulation
  • reduced innervation
29
Q

What does this show?

A
  • mammary atrophy in a spayed dog
30
Q

What is hypertrophy?

A
  • increase in tissue mass due to increase size of cells (parenchymal cells)
  • increase in number of organelles in cells
31
Q

What are the causes of what is seen?

A
  • hypertrophy
  • increased workload
  • increased hormonal stimulation
32
Q

What is hyperplasia?

A
  • increase in tissue mass due to increased number of cells
33
Q

What are the causes of hyperplasia?

A
  • increased workloadd
  • increased hormonal stimulation
  • inflammation
  • physical trauma
  • precursor to neoplasia
34
Q
A