Trans - Cellular Responses to Stress: Adaptation and Injury Flashcards

(123 cards)

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
4 effects of increased cytosolic Ca
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
26
cytosolic Ca activates which two types of enzymes
1. phospholipases | 2. proteases
27
how does a decrease in ATP affect the membrane stability of a cell
a decrease in ATP causes a decrease in reacylation/synthesis of new phospholipids, which in turn allows the degradation of the membrane
28
high conductance channel in mitochondria that appears when the mitochondria are damaged
mitochondrial permeability transition
29
where in the mitochondria is the mitochondrial permeability transition located
inner mitochondrial membrane
30
2 main effects of mitochondrial membrane damage
1. decrease in ATP | 2. release of cytochrome C into the cytosol
31
effect of cytochrome C
facilitates apoptosis pathway
32
how does a cell maintain Ca homeostasis
through energy dependent pumps that keep cytosolic Ca low
33
free radical - define
highly reactive, unstable species with one unpaired electron, may facilitate damaging chain reactions that create other free radicals
34
how are free radicals generated
1. from cellular metabolism (redox) 2, from enzymatic metabolism of exogenous enzymes 3. through ionizing radiation 4. divalent metals
35
how are free radicals physiologically utilized in the body?
used by leukocytes in antimicrobial processes
36
how are free radicals neutralized
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
37
examples of O2 determined free radicals
1. superoxide O2- 2. H2O2 3. OH-
38
how do free radicals damage membranes
through lipid peroxidation --> attack on double bonds of unsaturated phospholipids
39
how do free radicals damage proteins
chain reactions
40
how do free radicals damage DNA
react with thymine in mitochondrial DNA, creating single strand breaks and abnormal cross linking
41
reaction wherein O2- is converted to H2O2 and then to OH
Fenton reaction
42
Fenton reaction is catalyzed by:
Cu 2+, Fe 2+
43
superoxide dismutase is used against
superoxide
44
catalase is used against
H2O2
45
glutathione is used against
OH
46
in general, damage to enzymes results to
very slow reactions and impaired transport mechanisms
47
hypoxia - define
oxygen deprivation
48
ischemia - define
blood deprivation
49
differentiate hypoxia and ischemia
hypoxia - only oxygen is gone | ischemia - oxygen and other metabolic substances gone
50
which is more serious? hypoxia or ischemia?
ischemia
51
causes of hypoxia
1. cardiopulmonary failure 2. hypoperfusion 3. decrease in O2 carrying capacity of blood 4. toxins 5. low inspired O2
52
how does anemia and CO2 poisoning cause hypoxia
both interfere with the O2 carrying capacity of blood
53
effects of hypoxia
decrease in ATP, accumulation of cytosolic Ca
54
phenomena wherein restoration of blood flow to an ischemic area causes acceleration of injury
reperfusion damage
55
mechanism of reperfusion damage
1. exposure of damaged cells to Ca | 2. increase in free radicals due to damaged cell structures attempting to execute functional biochemical reactions
56
mechanical trauma - 2 types
acute and chronic
57
mechanisms of heat damage
1. increased metabolic activity leading to inadequate O2 | 2. direct heat damage
58
mechanisms of cold damage
1. crystal formation leading to puncture | 2. slowing down and stopping of metabolism
59
3 types of radiation that may damage
1. ionizing 2. nonionizing 3. ultraviolet
60
radiation above ultraviolet wavelength
ionizing radiation
61
mechanism of ionizing radiation damage
contact causes electron imbalance --> free radical formation
62
radiation below ultraviolet wavelength
nonionizing
63
mechanism of nonionizing radiation damage
prolonged contact causing misalignment of atoms
64
mechanism of UV damage
DNA damage --> formation of thymine dimers
65
which type of radiation is least dangerous?
nonionizing radiation
66
which type of radiation has the greatest chance of causing direct damage?
ionizing radiation
67
which type of radiation has the greatest chance of causing cancer?
UV
68
mechanism of electric damage
direct electrical damage, may be converted to direct heat damage and necrosis
69
2 types of chemical agent that may cause damage
1. direct | 2. indirect
70
differentiate direct and indirect chemical damage
direct --> chemical itself causes the damage | indirect --> metabolism of the chemical is toxic
71
cyanide - type of chemical damage and mechanism
direct damage through inhibition of cytochrome oxidase in aerobic respiration
72
mercury - type of chemical damage and mechanism
direct damage through inhibition of Na-K pump
73
example of indirect chemical damage
drug overdoses
74
damage through biological activity - mechanisms
1. direct cytopathic activity 2. toxins 3. trigger harmful immune/inflammatory response
75
examples of direct cytopathic damage by biological agents
virus
76
examples of toxin damage by biological agents
diptheria and clostridium bacteria
77
damage from immunologic reactions - mechanisms
1. hypersensitivity 2. autoimmunity 3. abnormal suppression of response
78
cellular changes in adaptation
change in 1. size 2. number 3. type 4. organelles
79
atrophy - definition
acquired decrease in cell size leading to decrease in organ/tissue size
80
physiological atrophy - examples
1. involution of thymus in adult | 2. cease of ova maturation in menopause
81
causes of pathological atrophy
1. decreased workload 2. no innervation 3. decreased blood supply 4. inadequate nutrition
82
causes of physiological atrophy
1. loss of endocrine stimulation | 2. aging
83
cell/tissue changes in atrophy
1. smaller cell size 2. organ stroma more prominent than parenchyma (support framework more prominent than functional component) 3. lipofucsin present
84
lipofucsin - origin
remnants of autophagy from lysosomes
85
hypertrophy - define
increase in cell size causing increase in tissue/organ size
86
hypertrophy - found in which cells
cells that cannot divide (muscle, neuron)
87
mechanism of hypertrophy
accelerated protein synthesis
88
physiological hypertrophy - example
cardiac muscle hypertrophy during stenosis of aorta
89
hypertrophy - causes
1. increased functional demand | 2. hormonal stimulation
90
aplasia - define
no growth at all, resulting in rudimentary or absent organ
91
hypoplasia - define
incomplete growth
92
hyperplasia - define
increase in cell number, resulting in increase of tissue/organ size
93
hyperplasia is often accompanied by
hypertrophy
94
hyperplasia - found in which cells
cells that are capable of mitosis
95
2 types of physiological hyperplasia
1. hormonal | 2. compensatory
96
2 types of pathological hyperplasia
1. hormonal (overstimulation) | 2. due to noxious stimuli
97
example of hyperplasia due to noxious stimuli
formation of callus
98
metaplasia - define
adaptive conversion between cell types in adults
99
metaplasia is a response to:
chronic irritation/inflammation
100
example of metaplasia
replacement of PCCE to SSE in respiratory tract of smokers
101
dysplasia - define
abnormal cell growth of disproportionate cell types
102
displasia - cause
always pathologic
103
differentiate displasia and cancer
displasia is reversible, and displacia cells are nonautonomous / not mutated
104
[T/F] when dealing with cell injury, it is possible to identify the point of no return (from reversible to irreversible damage)
F
105
result of reversible damage
degradation
106
result of irreversible damage
necrosis
107
what cells are more vulnerable to degradation, parenchymal or stromal?
parenchymal
108
what is the cause of degradation?
minor, reversible damage caused by low-intensity injury
109
cloudy swelling - cause
inability to maintain fluid homeostasis (failure of pumps)
110
term for accumulation of water in cells affected by cloudy swelling
hydropic change
111
fat accumulation - where can this occur
liver
112
fat accumulation - appearance under microscope
"signet ring" cells
113
2 types of pathologic calcification
1. dystrophic | 2. metastatic
114
deposition of Ca in injured tissue
dystrophic pathologic calcification
115
deposition of Ca in tissues when in hypercalcemic states
metastatic pathologic calcification
116
necrosis - define
antemortem pathologic cell death
117
apoptosis - define
antemortem physiologic cell death
118
autolysis - define
postmotem cell death
119
autolysis - cause
cease of function
120
pyknosis - characteristics
dark shrunken nuclei
121
karyolysis - characteristics
faint, indistinct nuclei
122
karyorrhexis - characteristics
fragmented nuclei
123
characteristics of apoptotic cell death
1. cell shrinkage 2. chromatin condensation 3. formation of cytoplasmic blebs and apoptotic bodies