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PATH2220 > 22 - Cell injury, death & adaptations > Flashcards

22 - Cell injury, death & adaptations Flashcards

1
Q

Causes of cell injury

A
  • Hypoxia and ischaemia
  • Toxins
  • Infectious agents
  • Immunologic reactions
  • Genetic abnormalities
  • Nutritional imbalances
  • Physical agents
  • Aging
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2
Q

Reversible cell injury

A

Stage of cell injury where the function and morphology of the injured cells can return to normal if damaging stimulus is removed

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3
Q

Characteristics of reversible cell injury

A
  • Cellular swelling (increased permeability of cell membrane)
  • Fatty change
  • Eosinophilic cytoplasm (red)
  • Plasma membrane alterations
  • Nuclear alterations
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4
Q

Irreversible cell injury

A

With persistent or excessive exposure, cells pass a “point of no return” and undergo cell death

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5
Q

Three phenomena in irreversible cell injury

A
  • Inability to restore mitochondrial function
  • Loss of structure & function of the plasma membrane and intracellular membranes
  • Loss of DNA and chromatin structural integrity
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6
Q

Necrosis

A
  • ‘Accidental’ cell death due to severe disturbance
  • Cell membranes fall apart, cell enzymes leak and digest cell
  • Elicits inflammation
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7
Q

Apoptosis

A
  • ‘programmed’ cell death due to less severe injury
  • Elimination of cells during normal processes
  • Occurs in healthy tissues during development
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8
Q

Cytoplasmic changes of necrosis

A
  • ↑ eosinophilia due to increased binding of eosin (red) to denatured proteins and loss of basophilic (blue) RNA
  • Vacuolated (“moth-eaten”) due to enzymes digesting cytoplasmic organelles
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9
Q

Nuclear changes of necrosis

A
  • DNA and chromatin degradation result in one of three patterns (Pyknosis, Karyorrhexis, Kayolysis)
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10
Q

Pyknosis

A

Basophilia of nucleus due to condensation of DNA

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11
Q

Karyorrhexis

A

Fragmentation of pyknotic nucleus

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12
Q

Karyolysis

A

Basophilia fades due to digestion of DNA by DNAase

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13
Q

Purpose of apoptosis

A

To eliminate:
- Potentially harmful cells
- Cells that have outlived their usefulness
- Irreparably damaged cells

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14
Q

Process of apoptosis

A
  • Activation of cellular enzymes (caspases) leads to
    degradation of nuclear DNA and cytoplasmic proteins
  • Fragments (apoptotic bodies) of the cells break off
  • Plasma membrane remains intact but is altered and apoptotic bodies are consumed by phagocytes
  • Little leakage of cell contents & thus no inflammation
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15
Q

Cell size in Necrosis vs Apoptosis

A

Enlarged (swelling) vs reduced (Shrinkage)

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16
Q

Nucleus in necrosis vs apoptosis

A

Pyknosis, karyorrhexis and karyolysis vs fragmentation into neucleosome sized fragments

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17
Q

Plasma membrane in necrosis vs apoptosis

A

Disrupted vs intact

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18
Q

Cellular contents in necrosis vs apoptosis

A

Enzymatic digestion (may leak out of cell) vs intact (may be released in apoptotic bodiesA

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19
Q

Adjacent inflammation in necrosis vs apoptosis

A

Frequent vs no inflammation

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20
Q

Physiologic or pathologic role in necrosis vs apoptosis

A

Invariably pathologic (culmination of irreversible cell injury) vs physiologic means of eliminating unwanted cells (can be pathologic after cell injury)

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21
Q

Necroptosis

A

includes features of both necrosis and apoptosis and is regulated by particular signalling pathways, not well understood

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22
Q

Pryoptosis

A

Associated with activation of the inflammasome, can lead to the release of proinflammatory cytokines that can initiate apoptosis

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23
Q

Autophagy

A
  • An adaptation to nutrient deprivation in which cells digest their own organelles and recycle them to provide energy and substrates
  • If the stress is too severe for autophagy to cope with, cell death by apoptosis will occur
24
Q

What causes a reversible cell injury

A

Low doses of toxins or a brief period of ischaemia

25
Q

What causes irreversible injury and cell death

A

Larger toxin doses or longer ischemic times

26
Q

What do consequences of an injurious stimuli depend on

A

The type, status, adaptability, and genetic makeup of the injured cell. (e.g. skeletal muscle in leg can tolerate ischemia for 2 - 3 hours but cardiac muscle dies after 20 mins)

27
Q

What triggers necrosis

A

Deprivation of oxygen and nutrients primarily impairs energy-dependent cellular
functions

28
Q

What triggers apoptosis

A

damage to proteins and DNA

29
Q

Hypoxia

A

Tissues deprived of oxygen

30
Q

Ischaemia

A

Reduced blood supply leading to oxygen deprivation and deficiency of essential nutrients

31
Q

Causes of hypoxia

A
  • Ischemia resulting from an arterial obstruction (most common)
  • Inadequate oxygenation of the blood (less common)
32
Q

Examples of Inadequate oxygenation of the blood causing hypoxia

A
  • Variety of diseases affecting the lung
  • Reduction in the oxygen-carrying capacity of the blood (anemia)
  • Carbon monoxide (CO) poisoning.
33
Q

What is one of the most frequent causes of cell injury and necrosis in clinical medicine

A

Oxygen deprivation as it leads to failure of many energy dependent metabolic pathways (no oxygen = no ATP)

34
Q

What is ATP needed for

A

membrane transport, protein synthesis, lipogenesis, and the deacylation-reacylation reactions necessary for phospholipid turnover

35
Q

What produces ATP

A

ATP is produced from ADP by oxidative phosphorylation during reduction of oxygen in the electron transport system of mitochondria

36
Q

Ischaemia reperfusion injury

A

Restoration of blood flow to ischaemic but viable tissues can paradoxically result in further cell injury

37
Q

Mechanisms of ischaemia reperfusion injury

A
  • Increased generation of reactive oxygen species (ROS)
  • Inflammation may increase with reperfusion due to influx of leukocytes and plasma proteins
38
Q

Reactive oxygen species (ROS)

A
  • Free radicals (chemical species with unpaired electron in outer orbit –> unstable)
  • Produced in all cells during reduction oxidation reactions
  • Produced in phagocytes for inflammation and host defence
39
Q

Accumulation of ROS

A

Leads to cell injury by:
- Damage to cell membrane by peroxidation
- protein cross-linking
- DNA damage

40
Q

Two general mechanisms of cell injury caused by toxins

A
  • Direct-acting toxins act by combining with a critical
    molecular component or cellular organelle
  • Latent toxins must first be converted to reactive metabolites, which then act on target cells
41
Q

Endoplasmic reticulum stress

A
  • The accumulation of misfolded proteins in a cell can stress compensatory pathways in the ER and lead to apoptosis
  • Caused by ↑ production of misfolded proteins and ↓ ability to eliminate them
42
Q

What causes ↑ production of misfolded proteins and ↓ ability to eliminate them

A
  • Gene mutations (increased proteins that cannot fold properly)
  • Aging, (decreased capacity to correct misfolding)
  • Infections (when large amounts of microbial
    proteins are synthesized within cells)
  • Increased demand for secretory proteins such as insulin in insulin-resistant
    states
43
Q

How can protein misfolding cause disease

A

By creating a deficiency of an essential protein or by inducing apoptosis

44
Q

What induces DNA damage

A
  • Exposure of cells to radiation, chemotherapeutic agents
  • Intracellular generation of ROS
  • Acquisition of mutations
45
Q

DNA damage

A
  • Sensed by intracellular sentinel proteins, which transmit signals that lead to the accumulation of p53
    protein
  • p53 first arrests the cell cycle (at the G1 phase) to allow the DNA to be repaired before it is replicated
  • If the damage is too great to be repaired, apoptosis is triggered
46
Q

What elicits an inflammatory reaction

A
  • Pathogens
  • Necrotic cells
  • Dysregulated immune responses (Autoimmune diseases and Allergy)
47
Q

Cellular adaptations to stress

A

Reversible changes in the number, size, phenotype, metabolic activity, or functions of cells in response to changes in their environment

48
Q

Physiological adaptations to stress

A

responses of cells to normal stimulation by hormones or endogenous chemical mediators or the demands of mechanical stress (e.g. enlargement of uterus during pregnancy and muscle growth with weightlifting)

49
Q

Pathologic adaptations to stress

A

Responses to stress that allow cells to modulate their structure and function and thus escape injury, but at the expense of normal function

50
Q

Example of pathologic adaptions to stress

A

Squamous metaplasia of bronchial epithelium in smokers

51
Q

Examples of cellular adaptations to stress

A
  • Hypertrophy
  • Hyperplasia
  • Atrophy
  • Metaplasia
52
Q

Hypertrophy

A
  • Increased cell and organ size, in response to increased workload
  • Induced by growth factors produced in response to mechanical stress or other stimuli
  • Occurs in tissues incapable of cell division
53
Q

Hyperplasia

A
  • Increased cell numbers in response to hormones and other growth factors
  • Occurs in tissues whose cells are able to divide or contain abundant tissue stem cells
  • Can be physiologic or pathologic
54
Q

Atrophy

A
  • Decreased cell and organ size, as a result of decreased
    nutrient supply or disuse
  • Decreased synthesis of cellular building blocks
  • Increased breakdown of cellular organelles and autophagy
55
Q

Metaplasia

A
  • Change in phenotype of differentiated cells, due to chronic irritation that makes cells better able to withstand the stress
  • May result in reduced functions or increased propensity for malignant transformation

PATH2220 (33 decks)

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