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Principles of Medicine (POM) > POM 03 - Cell injury and inflammation > Flashcards

POM 03 - Cell injury and inflammation Flashcards

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1
Q

what are the 6 possible causes of cell stress and injury

A

physical injury

chemical injury

biological causes (eg viral infection)

immunological causes

genetic derangements

nutritional imbalances

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2
Q

what are the 3 outcomes that cell injury can lead to

A

no effect

adaptation

cell injury

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3
Q

what does it mean when the injurious agent or stress has no effect on the cell

A

the cell can cope with it, can function and survive in hostile environment

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4
Q

what does it mean when the injurious agent or stress causes adaptation in the cell

A

the cell can change itself in order to resist or adapt to the injury

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5
Q

what does it mean when the injurious agent or stress results in cell injury

A

there is a physical and biochemical change in the cell beyond amount of injury that can be fixed by turning on signal pathways and generating adaptation

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6
Q

cell injury can either be __ or __

A

irreversible leading to death or reversible

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7
Q

what is an example of cells that are no affected by injurious agents or stress

A

neutrophils

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8
Q

what is adaptation in cells a response to (2 things)

A

mild injurious agents

mild stress

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9
Q

what is an example of mild injurious agents

A

chronic irritant

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10
Q

what is an example of mild stress

A

altered environmental conditions

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11
Q

what does adaptations allow the cell to do

A

allows cell to continue to function without being injured despite the stress or change in environment

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12
Q

what are the 4 types of adaptation a cell can undergo

A

hypertrophy

hyperplasia

atrophy

metaplasia

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13
Q

what is hyperplasia

A

number of cells increases by stem cell dividing due to increased demand on cell

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14
Q

is adaptations in cell (the 4 types) active/passive processes and what drives them

A

active process

driven by signalling pathways

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15
Q

what is hypertrophy

A

individual cells gaining size - NOT increasing number of cells

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16
Q

what is atrophy

A

cells shrink smaller in size

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17
Q

what is metaplasia

A

stem cells reprogram themselves in order for cells to be better adapted in hostile environment

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18
Q

what are two broad types of signalling pathways that are activated by cell stress/injury

A

heat shock factors

stress enzymes

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19
Q

what are heat shock factors

A

transcription factors which induce expression of heat shock proteins which act in a circular loop that further activates heat shock factors

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20
Q

which two stress enzymes initiate the phosphorylation cascades

A

p38 MAP kinase

Jun N-terminal kinase

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21
Q

what does the p38 MAP kinase and Jun N-terminal kinase enzymes initiate

A

phosphorylation cascades

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22
Q

what is p53 activated by

A

DNA damagew

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23
Q

hat does p53 do to cell division and why

A

halts it to allow repair so they dont perpetuate damage while repairing or induces cell suicide

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24
Q

what does p53 sense

A

senses DNA damage

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25
what is BMF a sensor for
actin cytosckeleton damage
26
what is Bim a sensor for
microtubule damage
27
what is Bad a sensor for
cell stress due to inadequate stimulation by growth factors
28
what are 3 stress enzymes starting with B
BMF Bim Bad
29
what is BMF, Bim and Bad examples of
stress enzymes
30
what are the 4 main cellular components that are due to the effect of stress/injury on cells
decreased ATP/energy membrane damage increased intracellular Calcium reactive oxygen species
31
why does depletion of ATP occur in cell - 3 reasons
less ATP produced due to: lack of oxygen (blood supply interrupted = less removal of CO2 = prevents oxidative phosphorylation) damage to enzymes involved in ATP production damage to mitochondria (decreases aerobic respiration)
32
why is decreased ATP in cell injury bad for the cell - 3 things
enzymes that repair damaged DNA needs ATP ATP driven membrane pumps need ATP protein synthesis needs ATP
33
what happens to when ATP driven membrane ion pumps dont have enough ATP - Na+ pumps
Na+ pump doesn't work as well without ATP so sodium and water accumulate = cell swelling = can burst, lose function and alter tissue architecture
34
what happens to when ATP driven membrane ion pumps dont have enough ATP - Ca2+ pumps
Ca2+ pump doesnt work as well without ATP so Ca2+ influx into cytosol = activates destructive Ca2+ dependent enzymes (can lead to autolysis)
35
why is protein synthesis decreasing due to ATP dropping from cell injury bad
need protein synthesized for repairing damaged cell
36
what are 6 examples of membranes that are damaged in the membrane damage due to cell injury
plasma membranes lysosomal membranes mitochondrial membranes nuclear membranes endoplasmic reticular membranes motile membranes
37
what does plasma membrane damage result in - 4 things
loss of cellular contents loss of osmotic balance influx of fluids and ions loss of proteins, enzymes, coenzymes and ribonucleic acids
38
what does lysosomal membrane damage result in
leakage of enzymes into cytoplasm = digestion of cellular components (autolysis)
39
what does mitochondrial membrane damage result in and what are the two flow on effects of this
formation of nonselective high-conductance channels in the inner mitochondrial membrane of 1. removes transmembrane potential and allows leakage of cytochrome c in wrong position for oxidative phosphorylation 2. allows leakage of cytochrome c into cytosol = primes cells for apoptosis
40
what is cytochrome c and why is it important in mitochondrial membrane damage induced by cell stress/injury
its part of energy producing apparatus so decreases energy if damaged also is signalling molecule that turns on apoptosis
41
what does increased cytosolic Ca2+ as a result of cell stress/injury do
activates enzymes that cause autolysis
42
what are 5 ways that free radicals can be caused by
irradiation metabolism of chemicals or drugs oxygen toxicity inflammation reperfusion (O2 reintroduced after period of blocked blood flow)
43
what are the 3 core changes due to free radical damage in a cell
free radicals attack the double bonds in unsat. fatty acids oxidises amino acid side chains react with thymine
44
what results when free radicals react with thymine
DNA damage
45
what results when free radicals oxidises amino acid side chains
causes enzyme damage and enzymes may stop functioning
46
what results when free radicals attack the double bonds in unsat. fatty acids
lipid peroxidation and further damages membranes
47
free radicals propagate a chain of damage via ____ reactions
autocatalytic reactions
48
all together when multiple cellular components are targeted simultaneously what does it lead to for proteins and DNAs - what does it increase and decrease
increase proteins breakdown and DNA damage decrease protein and DNA repair
49
when cell injury is irreversible what are the 2 options
necrotic death and apoptotic death
50
how do cells die via the necrotic death pathway
cells passively murdered injury/damage is overwhelming and cells cant do anything about it so they just die
51
how do cells die via the apoptotic death pathway
programmed process where cells recycle themselves by wrapping up components in membrane bound coffins which are taken up by adjacent cells/macrophages components of cell can be reused
52
what are the 4 main differences between necrosis and apoptosis
necrosis is passive (dont need energy) while apoptosis uses energy necrosis is unorganised and messy, apoptosis is organised in membrane bound vesicles components of cell can be reused in apoptosis but not in necrosis necrosis destructive enzymes already active while apoptosis is programmed and turned on carefully
53
why is necrosis described as a messy process
cant see alot of structure once it happens because destructive enzymes like lysosomes chew up components = autolysis
54
why is apoptosis described as an organised process
cleans up dead cells and makes it easier to recover initial structure and function of tissue
55
how can necrosis cause inflammatory response and why
cytosolic contents can leak out causing inflammatory response
56
what does the cell look like after necrosis
featureless cytoplasm and faded/fragmented chromatin
57
on what scale does necrosis act on cells
affects large numbers of cells in a tissue
58
what is the characteristic appearance of a cell undergone apoptosis - 3 things
membrane blebs (vesicles), shrinkage, pyknosis
59
how are the membrane bound vesicles disposed of in apoptosis
phagocytosed by passing macrophages or neighbouring cells
60
what are the 2 pathways for apoptosis initiation
mitochondria = cells with internal derangement or insufficient energy or growth factors turn on apoptosis pathway death receptors = cell surface receives death signals
61
what do the 2 pathways for apoptosis initiation cause activation of
activation of a cascade of upstream caspases
62
the 2 pathways for apoptosis initiation both feed down into what
feeds down into cascade of caspase enzymes (executioner enzymes)
63
the cascade of caspase enzymes (executioner enzymes) has what two parts
organisers = organised dismantalling of cell executioners
64
what is the most potent activator of inflammation
necrosis
65
what is inflammation
bodys immediate response to tissue injury
66
what does inflammation involve in terms of cells migrating
leukocytes leaving blood vessels into tissues
67
what does it mean when we say inflammation is stereotyped
almost every cell does inflammation the same way irrespective of the tissue involved but there can be a few modifications in different organs/tissues
68
what are 6 trigger of inflammation
infections trauma physical and chemical agents tissue necrosis foreign bodies immune reactions
69
what are the 6 stages of acute inflammation
1. triggering 2. blood flow and permeability changes 3. endothelial cell signalling and gene expression changes (incl adhesion molecule regulation) 4. neutrophil signalling and gene expression changes (neutrophil adhesion to endothelial cells and migration into tissues through tight junctions betw endothelial cells) 5. neutrophil activation, survival, function and death 6. inflammation subsides or continues with other leukocytes entering tissue (chronic inflamm)
70
what are the gatekeepers of acute inflammation
endothelial cells
71
what does TNF alpha do in acute inflammation
binds to TNF receptor = NFkB transcription factor = other genes = neutrophil adhesion and passage into tissues
72
what does inflammation associated gene expression and signaling change in endothelial cells regarding the cell adhesion molecules
increase cell adhesion molecules
73
what does inflammation associated gene expression and signaling change in endothelial cells regarding anti-apoptosis molecules
increase anti-apoptosis molecules
74
what does inflammation associated gene expression and signaling change in endothelial cells regarding the cytoskeleton stabilizers
decreases cytoskeleton stabilizers
75
what does inflammation associated gene expression and signaling change in endothelial cells regarding the coagulation factors
increases coagulation factors
76
what does inflammation associated gene expression and signaling change in endothelial cells regarding the pro-angiogenesis factors
increases pro-angiogenesis factors
77
what happens to blood flow during inflammation how does this relate to the physical changes
increased blood flow hyperaemia = tissues become red and warm
78
what happens to fluid and protein during inflammation why what happens
lost through exudation tight junctions leak out fibrinogen and tissue odema occurs
79
what is the main leukocyte involved in acute inflammation
neutrophils
80
what is the first leukocyte type to enter inflammed tissues
neutrophils
81
what do selectin molecules do
slow down neutrophils
82
what does integrin do
help neutrophil firmly adhere to endothelial cells
83
what does diapedesis mean
process of neutrophil passing between endothelial cells
84
neutrophils move into tissue and become activated by what 4 things
endothelial cell surface molecules (activate neutrophils when they touch) interlukin 1 and tumour necrosis factor alpha bacterial products that bind to neutrophil toll-like receptors chemotactic factors (eg C5a and IL-8)
85
how does neutrophils attack the cause of inflammation
generate small self contained versions of oxidative stress
86
the killing potential of neutrophils via oxidative stress reactions is dependent on what
dependent on oxygen
87

Principles of Medicine (POM) (11 decks)

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