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[OS 201] 4th Exam > Trans - Cellular Responses to Stress: Adaptation and Injury > Flashcards

Trans - Cellular Responses to Stress: Adaptation and Injury Flashcards

1
Q

stages in the cellular response

A
  1. normal cell
  2. cellular adaptation
  3. cellular injury
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2
Q

homeostasis - define

A

process by which cells control the composition of their immediate environment and internal milieu within a narrow range of physiological parameters

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3
Q

adaptation - define

A

process by which cells reach a new steady state compatible with their new environment

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4
Q

cells adapt by:

A

altering their pattern of growth

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5
Q

cellular damage occurs when:

A

adaptive mechanisms can no longer compensate for changing environment

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6
Q

2 outcomes of cellular injury

A
  1. reversible

2. irreversible

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7
Q

reversible injury

A

return to normal when stress is removed

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8
Q

irreversible injury

A

severe injury leading to cell death (apoptosis and necrosis)

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9
Q

cellular response to injurious stimuli depends on these four factors

A
  1. type of injury
  2. duration of injury
  3. severity / intensity of injury
  4. vulnerability of cell
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10
Q

[T/F] relatively nonspecialized cells are more vulnerable to injury because they are more exposed to the environment

A

F, more specialized cells have high vulnerability (ex. brain)

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11
Q

which is lost first - symptoms of injury, or cell function?

A

cell function

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12
Q

generally, cell injury is caused by:

A

abnormalities on the biochemical and molecular level caused by stress

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13
Q

consequence of interdependence of biochemical systems in the context of injury

A

injury at one site typically causes secondary or tertiary injuries to other cellular processes

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14
Q

4 major molecular targets of cellular injury

A
  1. cell membrane
  2. mitochondrial function
  3. functional and structural proteins
  4. genetic integrity
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15
Q

5 general mechanisms of cellular injury

A
  1. ATP depletion
  2. loss of plasma membrane integrity
  3. loss of Ca2+ homeostasis
  4. mitochondrial damage
  5. oxygen deficiency
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16
Q

ATP depletion and decreased ATP synthesis are frequently associated with:

A

hypoxic and chemical injury

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17
Q

[T/F] cells with greater glycolytic capability are first injured in prolonged ischemia

A

F, cells with greater glycolytic capacity have greater capacity for anaerobic respiration

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18
Q

possible consequence of acidosis within the cell

A

damage to DNA

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19
Q

consequence of damage to plasma membranes

A

lysis due to disrupted ion balance

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20
Q

consequences of potassium leaking from plasma membrane

A

decreased ability to maintain resting membrane potential

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21
Q

consequences of injury to mitochondrial membrane

A
  1. impairment of energy metabolism

2. initiation of apoptosis due to release of cytochrome c

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22
Q

consequences of injury to lysosomal membrane

A

autophagy due to release of hydrolytic enzymes

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23
Q

consequences of injury to golgi-ER complex

A

impaired protein synthesis and protein transport

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24
Q

effect of ischemia in concentration of Ca and O2 within the cell

A

increase Ca

decrease O2

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25
Q

4 effects of increased cytosolic Ca

A
  1. phospholipid degradation due to activation of phospholipases by Ca
  2. degradation of the membrane due to activation of proteases by Ca
  3. activation of ATPase by Ca –> less ATP
  4. activation of endonucleases by Ca –> DNA damage
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26
Q

cytosolic Ca activates which two types of enzymes

A
  1. phospholipases

2. proteases

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27
Q

how does a decrease in ATP affect the membrane stability of a cell

A

a decrease in ATP causes a decrease in reacylation/synthesis of new phospholipids, which in turn allows the degradation of the membrane

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28
Q

high conductance channel in mitochondria that appears when the mitochondria are damaged

A

mitochondrial permeability transition

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29
Q

where in the mitochondria is the mitochondrial permeability transition located

A

inner mitochondrial membrane

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30
Q

2 main effects of mitochondrial membrane damage

A
  1. decrease in ATP

2. release of cytochrome C into the cytosol

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31
Q

effect of cytochrome C

A

facilitates apoptosis pathway

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32
Q

how does a cell maintain Ca homeostasis

A

through energy dependent pumps that keep cytosolic Ca low

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33
Q

free radical - define

A

highly reactive, unstable species with one unpaired electron, may facilitate damaging chain reactions that create other free radicals

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34
Q

how are free radicals generated

A
  1. from cellular metabolism (redox)
    2, from enzymatic metabolism of exogenous enzymes
  2. through ionizing radiation
  3. divalent metals
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35
Q

how are free radicals physiologically utilized in the body?

A

used by leukocytes in antimicrobial processes

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36
Q

how are free radicals neutralized

A
  1. spontaneous decay
  2. superoxide dismutase (for superoxide)
  3. glutathione (for OH)
  4. catalase (for H2O2)
  5. vitamin E, A, C, beta carotene, other antioxidants
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37
Q

examples of O2 determined free radicals

A
  1. superoxide O2-
  2. H2O2
  3. OH-
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38
Q

how do free radicals damage membranes

A

through lipid peroxidation –> attack on double bonds of unsaturated phospholipids

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39
Q

how do free radicals damage proteins

A

chain reactions

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40
Q

how do free radicals damage DNA

A

react with thymine in mitochondrial DNA, creating single strand breaks and abnormal cross linking

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41
Q

reaction wherein O2- is converted to H2O2 and then to OH

A

Fenton reaction

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42
Q

Fenton reaction is catalyzed by:

A

Cu 2+, Fe 2+

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43
Q

superoxide dismutase is used against

A

superoxide

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44
Q

catalase is used against

A

H2O2

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45
Q

glutathione is used against

A

OH

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46
Q

in general, damage to enzymes results to

A

very slow reactions and impaired transport mechanisms

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47
Q

hypoxia - define

A

oxygen deprivation

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48
Q

ischemia - define

A

blood deprivation

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49
Q

differentiate hypoxia and ischemia

A

hypoxia - only oxygen is gone

ischemia - oxygen and other metabolic substances gone

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50
Q

which is more serious? hypoxia or ischemia?

51
Q

causes of hypoxia

A
  1. cardiopulmonary failure
  2. hypoperfusion
  3. decrease in O2 carrying capacity of blood
  4. toxins
  5. low inspired O2
52
Q

how does anemia and CO2 poisoning cause hypoxia

A

both interfere with the O2 carrying capacity of blood

53
Q

effects of hypoxia

A

decrease in ATP, accumulation of cytosolic Ca

54
Q

phenomena wherein restoration of blood flow to an ischemic area causes acceleration of injury

A

reperfusion damage

55
Q

mechanism of reperfusion damage

A
  1. exposure of damaged cells to Ca

2. increase in free radicals due to damaged cell structures attempting to execute functional biochemical reactions

56
Q

mechanical trauma - 2 types

A

acute and chronic

57
Q

mechanisms of heat damage

A
  1. increased metabolic activity leading to inadequate O2

2. direct heat damage

58
Q

mechanisms of cold damage

A
  1. crystal formation leading to puncture

2. slowing down and stopping of metabolism

59
Q

3 types of radiation that may damage

A
  1. ionizing
  2. nonionizing
  3. ultraviolet
60
Q

radiation above ultraviolet wavelength

A

ionizing radiation

61
Q

mechanism of ionizing radiation damage

A

contact causes electron imbalance –> free radical formation

62
Q

radiation below ultraviolet wavelength

A

nonionizing

63
Q

mechanism of nonionizing radiation damage

A

prolonged contact causing misalignment of atoms

64
Q

mechanism of UV damage

A

DNA damage –> formation of thymine dimers

65
Q

which type of radiation is least dangerous?

A

nonionizing radiation

66
Q

which type of radiation has the greatest chance of causing direct damage?

A

ionizing radiation

67
Q

which type of radiation has the greatest chance of causing cancer?

68
Q

mechanism of electric damage

A

direct electrical damage, may be converted to direct heat damage and necrosis

69
Q

2 types of chemical agent that may cause damage

A
  1. direct

2. indirect

70
Q

differentiate direct and indirect chemical damage

A

direct –> chemical itself causes the damage

indirect –> metabolism of the chemical is toxic

71
Q

cyanide - type of chemical damage and mechanism

A

direct damage through inhibition of cytochrome oxidase in aerobic respiration

72
Q

mercury - type of chemical damage and mechanism

A

direct damage through inhibition of Na-K pump

73
Q

example of indirect chemical damage

A

drug overdoses

74
Q

damage through biological activity - mechanisms

A
  1. direct cytopathic activity
  2. toxins
  3. trigger harmful immune/inflammatory response
75
Q

examples of direct cytopathic damage by biological agents

76
Q

examples of toxin damage by biological agents

A

diptheria and clostridium bacteria

77
Q

damage from immunologic reactions - mechanisms

A
  1. hypersensitivity
  2. autoimmunity
  3. abnormal suppression of response
78
Q

cellular changes in adaptation

A

change in

  1. size
  2. number
  3. type
  4. organelles
79
Q

atrophy - definition

A

acquired decrease in cell size leading to decrease in organ/tissue size

80
Q

physiological atrophy - examples

A
  1. involution of thymus in adult

2. cease of ova maturation in menopause

81
Q

causes of pathological atrophy

A
  1. decreased workload
  2. no innervation
  3. decreased blood supply
  4. inadequate nutrition
82
Q

causes of physiological atrophy

A
  1. loss of endocrine stimulation

2. aging

83
Q

cell/tissue changes in atrophy

A
  1. smaller cell size
  2. organ stroma more prominent than parenchyma (support framework more prominent than functional component)
  3. lipofucsin present
84
Q

lipofucsin - origin

A

remnants of autophagy from lysosomes

85
Q

hypertrophy - define

A

increase in cell size causing increase in tissue/organ size

86
Q

hypertrophy - found in which cells

A

cells that cannot divide (muscle, neuron)

87
Q

mechanism of hypertrophy

A

accelerated protein synthesis

88
Q

physiological hypertrophy - example

A

cardiac muscle hypertrophy during stenosis of aorta

89
Q

hypertrophy - causes

A
  1. increased functional demand

2. hormonal stimulation

90
Q

aplasia - define

A

no growth at all, resulting in rudimentary or absent organ

91
Q

hypoplasia - define

A

incomplete growth

92
Q

hyperplasia - define

A

increase in cell number, resulting in increase of tissue/organ size

93
Q

hyperplasia is often accompanied by

A

hypertrophy

94
Q

hyperplasia - found in which cells

A

cells that are capable of mitosis

95
Q

2 types of physiological hyperplasia

A
  1. hormonal

2. compensatory

96
Q

2 types of pathological hyperplasia

A
  1. hormonal (overstimulation)

2. due to noxious stimuli

97
Q

example of hyperplasia due to noxious stimuli

A

formation of callus

98
Q

metaplasia - define

A

adaptive conversion between cell types in adults

99
Q

metaplasia is a response to:

A

chronic irritation/inflammation

100
Q

example of metaplasia

A

replacement of PCCE to SSE in respiratory tract of smokers

101
Q

dysplasia - define

A

abnormal cell growth of disproportionate cell types

102
Q

displasia - cause

A

always pathologic

103
Q

differentiate displasia and cancer

A

displasia is reversible, and displacia cells are nonautonomous / not mutated

104
Q

[T/F] when dealing with cell injury, it is possible to identify the point of no return (from reversible to irreversible damage)

105
Q

result of reversible damage

A

degradation

106
Q

result of irreversible damage

107
Q

what cells are more vulnerable to degradation, parenchymal or stromal?

A

parenchymal

108
Q

what is the cause of degradation?

A

minor, reversible damage caused by low-intensity injury

109
Q

cloudy swelling - cause

A

inability to maintain fluid homeostasis (failure of pumps)

110
Q

term for accumulation of water in cells affected by cloudy swelling

A

hydropic change

111
Q

fat accumulation - where can this occur

112
Q

fat accumulation - appearance under microscope

A

“signet ring” cells

113
Q

2 types of pathologic calcification

A
  1. dystrophic

2. metastatic

114
Q

deposition of Ca in injured tissue

A

dystrophic pathologic calcification

115
Q

deposition of Ca in tissues when in hypercalcemic states

A

metastatic pathologic calcification

116
Q

necrosis - define

A

antemortem pathologic cell death

117
Q

apoptosis - define

A

antemortem physiologic cell death

118
Q

autolysis - define

A

postmotem cell death

119
Q

autolysis - cause

A

cease of function

120
Q

pyknosis - characteristics

A

dark shrunken nuclei

121
Q

karyolysis - characteristics

A

faint, indistinct nuclei

122
Q

karyorrhexis - characteristics

A

fragmented nuclei

123
Q

characteristics of apoptotic cell death

A
  1. cell shrinkage
  2. chromatin condensation
  3. formation of cytoplasmic blebs and apoptotic bodies

[OS 201] 4th Exam (5 decks)

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