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

POM 03 - Cell injury and inflammation Flashcards

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
Q

what is BMF a sensor for

A

actin cytosckeleton damage

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26
Q

what is Bim a sensor for

A

microtubule damage

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27
Q

what is Bad a sensor for

A

cell stress due to inadequate stimulation by growth factors

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28
Q

what are 3 stress enzymes starting with B

A

BMF
Bim
Bad

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29
Q

what is BMF, Bim and Bad examples of

A

stress enzymes

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30
Q

what are the 4 main cellular components that are due to the effect of stress/injury on cells

A

decreased ATP/energy

membrane damage

increased intracellular Calcium

reactive oxygen species

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31
Q

why does depletion of ATP occur in cell - 3 reasons

A

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)

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32
Q

why is decreased ATP in cell injury bad for the cell - 3 things

A

enzymes that repair damaged DNA needs ATP

ATP driven membrane pumps need ATP

protein synthesis needs ATP

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33
Q

what happens to when ATP driven membrane ion pumps dont have enough ATP - Na+ pumps

A

Na+ pump doesn’t work as well without ATP so sodium and water accumulate = cell swelling = can burst, lose function and alter tissue architecture

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34
Q

what happens to when ATP driven membrane ion pumps dont have enough ATP - Ca2+ pumps

A

Ca2+ pump doesnt work as well without ATP so Ca2+ influx into cytosol = activates destructive Ca2+ dependent enzymes (can lead to autolysis)

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35
Q

why is protein synthesis decreasing due to ATP dropping from cell injury bad

A

need protein synthesized for repairing damaged cell

36
Q

what are 6 examples of membranes that are damaged in the membrane damage due to cell injury

A

plasma membranes

lysosomal membranes

mitochondrial membranes

nuclear membranes

endoplasmic reticular membranes

motile membranes

37
Q

what does plasma membrane damage result in - 4 things

A

loss of cellular contents

loss of osmotic balance

influx of fluids and ions

loss of proteins, enzymes, coenzymes and ribonucleic acids

38
Q

what does lysosomal membrane damage result in

A

leakage of enzymes into cytoplasm = digestion of cellular components (autolysis)

39
Q

what does mitochondrial membrane damage result in and what are the two flow on effects of this

A

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
Q

what is cytochrome c and why is it important in mitochondrial membrane damage induced by cell stress/injury

A

its part of energy producing apparatus so decreases energy if damaged

also is signalling molecule that turns on apoptosis

41
Q

what does increased cytosolic Ca2+ as a result of cell stress/injury do

A

activates enzymes that cause autolysis

42
Q

what are 5 ways that free radicals can be caused by

A

irradiation

metabolism of chemicals or drugs

oxygen toxicity

inflammation

reperfusion (O2 reintroduced after period of blocked blood flow)

43
Q

what are the 3 core changes due to free radical damage in a cell

A

free radicals attack the double bonds in unsat. fatty acids

oxidises amino acid side chains

react with thymine

44
Q

what results when free radicals react with thymine

A

DNA damage

45
Q

what results when free radicals oxidises amino acid side chains

A

causes enzyme damage and enzymes may stop functioning

46
Q

what results when free radicals attack the double bonds in unsat. fatty acids

A

lipid peroxidation and further damages membranes

47
Q

free radicals propagate a chain of damage via ____ reactions

A

autocatalytic reactions

48
Q

all together when multiple cellular components are targeted simultaneously what does it lead to for proteins and DNAs - what does it increase and decrease

A

increase proteins breakdown and DNA damage

decrease protein and DNA repair

49
Q

when cell injury is irreversible what are the 2 options

A

necrotic death and apoptotic death

50
Q

how do cells die via the necrotic death pathway

A

cells passively murdered

injury/damage is overwhelming and cells cant do anything about it so they just die

51
Q

how do cells die via the apoptotic death pathway

A

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
Q

what are the 4 main differences between necrosis and apoptosis

A

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
Q

why is necrosis described as a messy process

A

cant see alot of structure once it happens because destructive enzymes like lysosomes chew up components = autolysis

54
Q

why is apoptosis described as an organised process

A

cleans up dead cells and makes it easier to recover initial structure and function of tissue

55
Q

how can necrosis cause inflammatory response and why

A

cytosolic contents can leak out causing inflammatory response

56
Q

what does the cell look like after necrosis

A

featureless cytoplasm and faded/fragmented chromatin

57
Q

on what scale does necrosis act on cells

A

affects large numbers of cells in a tissue

58
Q

what is the characteristic appearance of a cell undergone apoptosis - 3 things

A

membrane blebs (vesicles), shrinkage, pyknosis

59
Q

how are the membrane bound vesicles disposed of in apoptosis

A

phagocytosed by passing macrophages or neighbouring cells

60
Q

what are the 2 pathways for apoptosis initiation

A

mitochondria = cells with internal derangement or insufficient energy or growth factors turn on apoptosis pathway

death receptors = cell surface receives death signals

61
Q

what do the 2 pathways for apoptosis initiation cause activation of

A

activation of a cascade of upstream caspases

62
Q

the 2 pathways for apoptosis initiation both feed down into what

A

feeds down into cascade of caspase enzymes (executioner enzymes)

63
Q

the cascade of caspase enzymes (executioner enzymes) has what two parts

A

organisers = organised dismantalling of cell

executioners

64
Q

what is the most potent activator of inflammation

A

necrosis

65
Q

what is inflammation

A

bodys immediate response to tissue injury

66
Q

what does inflammation involve in terms of cells migrating

A

leukocytes leaving blood vessels into tissues

67
Q

what does it mean when we say inflammation is stereotyped

A

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
Q

what are 6 trigger of inflammation

A

infections

trauma

physical and chemical agents

tissue necrosis

foreign bodies

immune reactions

69
Q

what are the 6 stages of acute inflammation

A
  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
Q

what are the gatekeepers of acute inflammation

A

endothelial cells

71
Q

what does TNF alpha do in acute inflammation

A

binds to TNF receptor = NFkB transcription factor = other genes = neutrophil adhesion and passage into tissues

72
Q

what does inflammation associated gene expression and signaling change in endothelial cells regarding the cell adhesion molecules

A

increase cell adhesion molecules

73
Q

what does inflammation associated gene expression and signaling change in endothelial cells regarding anti-apoptosis molecules

A

increase anti-apoptosis molecules

74
Q

what does inflammation associated gene expression and signaling change in endothelial cells regarding the cytoskeleton stabilizers

A

decreases cytoskeleton stabilizers

75
Q

what does inflammation associated gene expression and signaling change in endothelial cells regarding the coagulation factors

A

increases coagulation factors

76
Q

what does inflammation associated gene expression and signaling change in endothelial cells regarding the pro-angiogenesis factors

A

increases pro-angiogenesis factors

77
Q

what happens to blood flow during inflammation

how does this relate to the physical changes

A

increased blood flow

hyperaemia = tissues become red and warm

78
Q

what happens to fluid and protein during inflammation

why what happens

A

lost through exudation

tight junctions leak out fibrinogen and tissue odema occurs

79
Q

what is the main leukocyte involved in acute inflammation

A

neutrophils

80
Q

what is the first leukocyte type to enter inflammed tissues

A

neutrophils

81
Q

what do selectin molecules do

A

slow down neutrophils

82
Q

what does integrin do

A

help neutrophil firmly adhere to endothelial cells

83
Q

what does diapedesis mean

A

process of neutrophil passing between endothelial cells

84
Q

neutrophils move into tissue and become activated by what 4 things

A

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
Q

how does neutrophils attack the cause of inflammation

A

generate small self contained versions of oxidative stress

86
Q

the killing potential of neutrophils via oxidative stress reactions is dependent on what

A

dependent on oxygen

87
Q
A

Principles of Medicine (POM) (11 decks)

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