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Pathology > Cellular response to stress > Flashcards

Cellular response to stress Flashcards

1
Q

define pathology

A

the structural, biochemical and functional changes in cells, tissues and organs that underlie diseases

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2
Q

what is the meaning of aetiology

A

the cause of the injury or disease

eg isit, genetic, infection or physical harm etc

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3
Q

list some points in the checklist of potential aetiologies of injury or disease

A
  • genetic (chromosomal anomaly)
  • congenital (e.g. down’s syndrome)
  • neoplastic (tumour)
  • infective (eg virus)
  • immune (eg arthritis)
  • toxic (eg toxic reaction to medicine)
  • vascular (eg hypertensive or diabetes)
  • iatrogenic (clinician caused it, e.g. surgery gone bad)
  • idiopathic (don’t know the aetiology)
  • traumatic (e.g. blunt trauma)
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4
Q

what is the etiologic agent

A

the causative agent

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5
Q

how do you determine the pathogenesis

A

what is the sequence of events in the cells and tissues in response to the etiologic agent (causative agent) from the initial event to the final manifestation of the disease

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6
Q

what can stress to normal cell homeostasis lead to

A

adaptation

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7
Q

what can injurious stimulus to normal cell homeostasis lead to

A

cell injury

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8
Q

what can also lead to cell injury

A

inability of adapted cell to adapt

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9
Q

what can a mild transient of cell injury lead to

A

reversible injury

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10
Q

give an example to mild transient to cell injury

A

minor burn which can heal

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11
Q

what can severe, progressive cell injury lead to

A

irreversible injury

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12
Q

give an example of a irreversible injury

A

broken bone to heal to the same extent

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13
Q

what can irreversible injury lead to

A

cell death e.g.
- necrosis
or
- apoptosis

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14
Q

give an example to adaptation

A

hyperplasia

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15
Q

what is hyperplasia

A

increase number of cells due to adaptation to change

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16
Q

name and give examples of hyperplasia

A
  • physiological (eg puberty) vs pathological (eg virus-wart)

- hormonal hyperplasia at puberty

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17
Q

give an example of a what hyperplasia can respond to

A

viral infections ie papillomavirus

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18
Q

what is hypertrophy

A

increase in size of the cells, not the amount, in response to stress

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19
Q

give an example of what hypertrophy will respond to

A

hypertension, causes heart cells to increase to pump more blood but can cause a heart attack/myocardial infarction

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20
Q

what can happen when cells become too large to handle a large blood supply

A

tissue damage

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21
Q

what is atrophy

A

decrease in cell size and number

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22
Q

what types of atrophy are there

A
  • physiological vs pathological
    &
  • embryogenesis = physiological
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23
Q

list things that can cause atrophy

A
  • decreased workload
  • deinervation
  • diminished blood supply
  • inadequate nutrition
  • loss of endocrine stimulation (lose hormones)
  • pressure (tumour may obstruct blood supply to organ or tissue)
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24
Q

what can an atrophy cause to the brain

A
  • big sulci and giri become larger
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25
Q

what is metaplasia

A

stem cells differentiate to a different lineage i.e. columnar epithelium to squamous epithelium (which can handle more stress)
e.g. smoking changes lung cells

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26
Q

when is hypertrophy no longer useful

A

cell injury & cell death

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27
Q

quote what happens due to cell injury & cell death

A

injury occurs when cells are stressed so severely that they are no longer able to adapt or when cells are exposed to an intrinsically damaging agent (e.g. virus) or suffer from intrinsic (genetic change in cell or from smoking) abnormalities

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28
Q

list the causes of cell injury

A
  • oxygen deprivation: (hypoxia) decreased blood low ischemia
  • physical agents: hot/cold, trauma
  • chemical agents/drugs: medication side effects
  • infectious agents: bacteria, fungi, virus
  • immunologic reactions: (autoimmune disease) SLE, RA
  • genetic abnormalities: chromosome defect or an external agent e.g. smoking or UV
  • nutritional imbalances: not enough calcium effects bones etc
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29
Q

describe the necrosis pathway

A
  • normal cell
  • damage
  • irreversible injury
    (e.g. sodium and potassium pump breaks down) causes swelling to the cell
    myelin figure (breakdown of cell wall & nuclear membrane & lipid rafts formed)
    swelling of endoplasmic reticulum and mitochondria (no water balance)
    membrane blebs
    & can lead to
  • progressive injury to cell which can cause
    breakdown of plasma membrane, organelles and nucleus
    which results in leakage of contents of cell, organelles spill out and become degraded
  • cell inflammation causes the presence of neutrophils associated with necrosis
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30
Q

what is always a result from pathologic insult

A

necrosis

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31
Q

list the steps that lead to necrosis

A
  • cell swelling (can’t maintain cell volume)
  • plasma membrane blebs initially
  • myelin figures - derived from damaged cell membrane and damaged cells nearby e.g. from lysosomes which attracts neutrophils and macrophages to clean up the area of necrosis
  • nucelus damage DNA fragmentation
  • breakdown of cell membrane
  • leakage of cellular constituents - lysozymes, proteins, enzymes
  • attract neutrophils/macrophages
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32
Q

list the patterns of tissue necrosis

A
  • coagulative
  • liquefactive
  • gangrenous
  • caseous
  • fat
  • fibrinoid
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33
Q

describe an example of coagulative necrosis

A

ischemia of kidney results in coagulative necrosis where this injury results in denaturing of proteins and enzymes, the tissue remains firm and structurally intact for several days

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34
Q

what does the area of necrotic change look like in coagulative necrosis

A

hard and firm

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35
Q

which types of organs does coagulative necrosis happen to

A

firm organs such as

liver, spleen and heart

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36
Q

describe how liquefactive necrosis occurs

A

in contrast to coagulative necrosis, the cellular enzymes liquify the tissue resulting in a liquid/viscous mass also know as pus

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37
Q

what tissue does liquefactive necrosis occur on and on which type of tissue

A

central nervous system

breakdown of the soft tissue in the CNS from infarcts

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38
Q

what does gangrenous necrosis usually describe the necrosis of

A

peripheral limbs following ischemia

39
Q

which type of people is gangrenous necrosis seen in

A

diabetics (if not controlled, which leads to peripheral vascular nervous system)

40
Q

what does gangrenous necrosis have a similar pattern to

A

coagulative necrosis

41
Q

what is gangrene feet a mixture of

A

apoptosis and necrosis

42
Q

describe caseous necrosis

A

necrosis surrounded by an inflammatory cell border, giving rise to a granuloma

43
Q

which patients typically have caseous necrosis

A

TB patients

44
Q

what resemblance does caseous necrosis have

A

cheese like

45
Q

describe where caseous necrosis occurs, which causes TB

A

an infection at the apex of the lungs which is furthest away from oxygen
a sharp border of granular tissue (scarring) forms which protects the rest of the lungs from infection

46
Q

what is fat necrosis associated with and how does it happen

A

associated with the pancreas

with pancreatic lipases that then liquefy cells in the abdomen

47
Q

what is fatty necrosis the accumulation of

A

calcium deposits with lipids

48
Q

what are fibrinoid necrosis associated with and how does it occur

A

associated with blood vessels (blood constriction o vessels)

where immune complexes (antibodies & antigens) attach to fibrin that has leaked from arterial walls

49
Q

what is fibrinoid necrosis seen in

A

nephritis with SLE

50
Q

give an example of fibrinoid necrosis

A

lupus, is a systemic disease
it gets autoimmune complexes, binding to the endothelial cells in the blood vessels, initiating a wound healing reaction which creates fibrosis of collagen fibres which results in restriction of the vessels aka fibrinoid

51
Q

what occurs from the mechanism of cell injury

A

depletion of ATP (from decrease of oxygen supply) by 5-10% is trouble

52
Q

what is the mechanism of depletion of ATP associated with

A

chemical or hypoxia stress (depletion of oxygen)

eg in diabetes, hypertension, glaucoma and ARMD

53
Q

list the mechanism of cell injury

A
  1. decrease activity of NaKaTPase pump (sodium potassium)
  2. glycolysis - anaerobic - lactic acid (increase = more acid)
  3. CaATPase pump falls (calcium pump which pumps calcium out of the cell)
  4. structural proteins not synthesised/loss of ribosomes
  5. protein misfolding (can’t undergo cell replication/protein synthesis)
  6. mitochondrial and lysosomal membranes damaged and cell passes to necrosis (cell becomes injured and theres a risk of death, so proteins are misfolding, mitochondria is dislodged & lysosomes breakdown)
54
Q

list the effect that damage to the mitochondrion by ischemia has

A
  • decreased oxidative phosphorylation which leads to
  • decreased ATP which leads to
  • decreased sodium pump (so pumps the sodium out), increased anaerobic glycolysis (increase in glycogen reduced from decreased ATP and oxygen) and a detachment of ribosomes
  • the decrease in the sodium pump leads to, an influx of calcium (as calcium pump breaks), water and intracellular sodium, which leads to
  • swelling of endoplasmic reticulum, cellular swelling and loss of microvilli blebs (breakdown of cell membrane)
  • an increase of anaerobic glycolysis lead to, decreased glycogen, increased lactic acid and decreased pH
  • the decrease of pH leads to clumping of nuclear chromatin so the DNA becomes denatured
  • the detachment of ribosomes leads to decreased protein synthesis as ATP prevents the attachment to the endoplasmic reticulum
  • the decrease in protein synthesis leads to, increased lipid deposition so the lipids become clumped and broken down as there is no structural cytoskeleton
55
Q

what happens when the calcium ATPase pump breaks down

A

there is an influx of calcium

56
Q

what are high levels of intracellular calcium to the cell

A

toxic

57
Q

what do high levels of calcium activate

A

a lot of enzymes and increased mitochondrial transition

58
Q

what is calcium normally stored in

A

the endoplasmic reticulum and mitochondria

59
Q

what happens when theres a excess of intracellular calcium

A

further cell damage occurs

60
Q

what do the activation of cellular enzymes lead to

A
  • phospholipase
  • protease
  • endo-nuclease
  • ATPase
61
Q

what does phospholipase do

A

breaks down the cell

62
Q

what does protease do

A

breaks down protons

63
Q

what does end-nuclease do

A

breaks down DNA

64
Q

what happens to the ATPase with the activation of cellular enzymes

A

will be deactivated

65
Q

what does phospholipase lead to

A

a decrease of phospholipids

66
Q

what does a decrease od phospholipids lead to

A

membrane damage

67
Q

what does protease lead to

A

disruption of membrane and cytoskeletal proteins

68
Q

what does disruption of membrane and cytoskeletal proteins lead to

A

membrane damage

69
Q

what does end-nuclease lead to

A

nuclear damage

70
Q

what does the deactivated ATPase lead to

A

increased mitochondrial permeability transition

71
Q

describe reactive oxygen species ROC

A

free radicals ROC are oxygen species with a single unpaired electron in a outer orbit

72
Q

what do free radicals ROC damage

A

phospholipids
proteins
carbohydrates
nucleic acids

73
Q

what do free radical ROC electrons do

A

find other electrons in cells to pair up with e.g. can go into the nucleus of a lipid cell to grab an electron which destroys everything in the process

74
Q

cells usually have a low level of ROS, but what is the reason for its increase

A

owing to stress, the imbalance is high then so called ‘oxidative stress’ occurs and cell damage/necrosis ensues

75
Q

what can blue light reaching the macula cause

A

damage to the retina & free radicals causing ARMD

76
Q

what is the formation of ARMD the accumulation of

A

reactive oxygen species

77
Q

what does incomplete reduction of oxygen and inflammation, radiation, chemicals, reperfusion, injury lead to in a mitochondria cell which generates reactive oxygen species

A

Superoxide -an anion which has a lone electron, is an enzyme called superoxdimutase which converts the superoxide anion into hydrogen peroxide (which is toxic) which undresses the fenton reaction with the iron catalyst which produced hydroxyl free radical electron which can pair up with an amino acid, lipid, anything

78
Q

list the pathological effects in steps of ROS cell injury and death when ROS reacts with fatty acids

A
  • oxidation leads to
  • generation of lipid peroxidases leads to
  • disruption of plasma membrane organelles
79
Q

list the pathological effects in steps of ROS cell injury and death when ROS reacts with proteins

A
  • oxidation leads to

- loss of enzymatic activity, abnormal folding

80
Q

list the pathological effects in steps of ROS cell injury and death when ROS reacts with DNA

A
  • oxidation leads to

- mutations, breaks

81
Q

how does removal of free radicals via the antioxidant methods work

A

the SOD (super oxide) in the mitochondria converts oxygen into hydrogen peroxide (h202)

  • glutathione peroxidase (in mitochondria) converts the hydroxyl anion into hydrogen peroxide into water and oxygen
  • catalase (in peroxisomes) converts hydrogen peroxide into water and oxygen
82
Q

what is apoptosis

A

programmed cell death

83
Q

how does apoptosis occur

A
  • specific enzymes degrade their own nuclear DNA which initiates cell death
84
Q

what is the condition of the cell membrane of an apoptotic cell

A

it remains intact

even though it breaks down into small apoptitic bodies, we don’t get spewing out of the entire cell content

85
Q

what are apoptitic cells phagocytosed by

A

macrophages
eg osteoclasts within bones
microglial within retina

86
Q

how does apoptosis in pathologic conditions occur with DNA damage

A

radiation triggers cell death e.g. high exposure to radiation

87
Q

how does apoptosis in pathologic conditions occur with accumulation of misfolded proteins owing to genetic mutation trigger

A

triggers cell death

can be inherited or from trauma e.g. UV or radiation

88
Q

how does apoptosis in pathologic conditions occur with viral infections

A

trigger cell death to prevent further spread of virus (altruism)
so the tissue remains healthy but the viral cell becomes apoptitic to prevent spread

89
Q

what are the two methods of apoptosis

A

intrinsic

& extrinsic

90
Q

how does the intrinsic method of apoptosis occur

A

mitochondria damage
release of cytochrome-c
initiates caspases (enzyme which breaks down nucleic acids into fragments)
cell death by endonucleases cleaving DNA

91
Q

what are caspases

A

enzyme which breaks down nucleic acids into fragments

92
Q

how does the extrinsic method of apoptosis occur

A

expression of Fas and TNF receptors recognised by T-cells

that then induce apoptosis via caspases and endonucleases

93
Q

which method of apoptosis is less common

A

extrinsic

Pathology (20 decks)

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