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X Understanding Disease > Cell Injury and Death > Flashcards

Cell Injury and Death Flashcards

1
Q

What are the 4 aspects of disease?

A
  • Aetiology
  • Pathogenesis
  • Molecular and morphological changes
  • Functional derangements and clinical manifestations
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2
Q

What are the 2 main causes of disease?

A
  • Genetic

- Acquired

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3
Q

What 3 different genetic causes are there of disease?

A
  • Inherited mutations
  • Polymorphisms
  • Disease associated gene variants
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4
Q

What is pathogenesis?

A

The sequence of events of disease - cell response to aetiology

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5
Q

What is the basic pathogenesis of cystic fibrosis?

A

Defective gene -> biochemical/morphological events -> formation of cysts etc.

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6
Q

What are molecular and morphological changes?

A

Structural alterations

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7
Q

What are functional derangements and clinical manifestations?

A

Signs
Symptoms
Progress

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8
Q

Lethal and sub-lethal injury are another term for what?

A

Irreversible and reversible injury

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9
Q

What causes of injury are there? Example of each

A
  • Hypoxia e.g. myocardial ischaemia from coronary atherosclerosis
  • Autoimmune e.g. thyroid gland damage from self-directed antibodies
  • Infection e.g. bacterial/viral
  • Genetic e.g. Duchenne muscular dystrophy
  • Physical e.g. uv damage from sunburn
  • Chemical e.g. acid damage
  • Thermal e.g. excess heat or cold
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10
Q

Mechanisms of injury for cell membrane damage

A
  • cell mediated lysis
  • bacterial toxins
  • free radicals
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11
Q

Mechanisms of injury for mitochondrial damage -> inadequate aerobic respiration

A
  • hypoxia

- cyanide poisoning

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12
Q

Mechanisms of injury for ribosome damage -> altered protein synthesis

A
  • alcohol in liver cells - alcoholics

- antibiotics in bacteria - antibiotics interfere with ribosomes in bacteria

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13
Q

Mechanisms of injury for nuclear damage

A
  • viruses - damage nucleus
  • radiation - DNA (single/double strand break) (point mutation
  • free radicals
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14
Q

What are free radicals?

A

Highly reactive unpaired electrons in outer orbit

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15
Q

Where are free radicals produced and in response to what?

A

produced in cells in response to:

  • radiation
  • normal metabolic oxidative reactions
  • drug metabolism
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16
Q

What do the consequences of cell injury depend on?

A
  • the cell
  • injurious agent
  • both
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17
Q

what 3 cell features affect outcome of disease?

A
  • specialisation of the cell
  • cell state
  • regenerative ability
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18
Q

what aspects of the specialisation of the cell affect the outcome of disease?

A
  • what enzymes the cell has
  • specialised organelles
  • the more specialised, the more vulnerable
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19
Q

what aspects of cell state affect the outcome of disease?

A
  • if it has adequate O2, hormones, nutrients, growth factors

- if not enough, more vulnerable

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20
Q

what aspects of the regenerative ability of the cell affect the outcome of disease?

A
  • damage to populations of permanent cells don’t regenerate
  • e.g. head (neurones) can’t regenerate
  • e.g. skin can replace
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21
Q

what are liable cells?

A

constantly active self-renewal

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22
Q

what are examples of liable cells?

A

gastrointestinal mucosa, skin, haematopoietic cells

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23
Q

what are stable cells?

A

low level of renewal

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24
Q

what are examples of stable cells?

A

liver, renal tubule cells, glial cells of CNS

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25
Q

what are permanent cells?

A

no capacity to replace cells

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26
Q

what are examples of permanent cells?

A

adult neurones, renal glomeruli, retinal epithelial cells

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27
Q

what 3 aspects of injury affect outcome of disease?

A
  • type
  • exposure type
  • severity
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28
Q

how does the type of injury affect disease?

A

different types of injury e.g. ischaemic/toxic/chemical - different cells more susceptible to different types

i.e. heart muscle and ischaemia

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29
Q

how does injury exposure time affect disease?

A

toxin/lack of oxygen

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30
Q

how does injury severity affect disease?

A

hypoxia or anoxia = low or no O2

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31
Q

what 4 sites are important in cell injury/death?

A

mitochondria
plasma membrane
ion channels in cell membranes
cytoskeleton

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32
Q

reversible or irreversible? cell swelling

A

reversible

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33
Q

reversible or irreversible? mitochondrial swelling

A

reversible

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34
Q

reversible or irreversible? EPR swelling

A

reversible

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35
Q

reversible or irreversible? ribosomal detachment

A

reversible

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36
Q

reversible or irreversible? myelin figures

A

reversible

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37
Q

reversible or irreversible? loss of microvilli

A

reversible

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38
Q

reversible or irreversible? surface blebs

A

reversible

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39
Q

reversible or irreversible? chromatin clumping

A

reversible

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40
Q

reversible or irreversible? lipid deposition

A

reversible

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41
Q

reversible or irreversible? lysosomal enzyme release

A

irreversible

42
Q

reversible or irreversible? protein digestion

A

irreversible

43
Q

reversible or irreversible? loss of basophilia

A

irreversible

44
Q

reversible or irreversible? membrane disruption

A

irreversible

45
Q

reversible or irreversible? leakage of enzymes

A

irreversible

46
Q

reversible or irreversible? pyknosis

A

irreversible

47
Q

reversible or irreversible? karyorrhexis

A

irreversible

48
Q

reversible or irreversible? karyolysis

A

irreversible

49
Q

what is pyknosis?

A

nuclear shrinkage

50
Q

what is karyolysis?

A

nuclear dissolution

51
Q

what is karyorrhexis?

A

nuclear break up

52
Q

what happens during lysozyme rupture?

A

break down what cell is made of (autodigest)

53
Q

what is protein digestion?

A

enzyme and structural

54
Q

what happens when the basophilia is lost?

A

cell less likely to stain with blue basic stain - more likely to stain with red acidic stain

55
Q

how can you tell when someones had a heart attack?

A

measure cardiac cell enzymes in blood which will be released when cell is damaged

56
Q

what 5 cellular adaptations to stress are there?

A 
atrophy
hypertrophy
hyperplasia
metaplasia
dysplasia
57
Q

what is atrophy?

A

cells get smaller

58
Q

what is hypertrophy?

A

cells get bigger

59
Q

what is hyperplasia?

A

increase in number of cells

60
Q

what is metaplasia?

A

cells change appearance - thin and broad.

early cancerous changes

61
Q

what is dysplasia?

A

cells disorganise

62
Q

what is the mechanism of cell response to reversible injury?

A
  1. transient ischaemia
  2. less O2 to cells
  3. less aerobic, more anaerobic
  4. anaerobic increases cytoplasmic activity
  5. ATP generation stops
  6. plasma membrane pump swells
  7. water is allowed in
  8. chromatin clumps
  9. pH change
63
Q

what are the microscopic changes when cells are injured?

A

colour - red staining - more acidic
vacuolation - holes
clumping of chromatin
cells bigger/swollen

64
Q

what is the mechanism of cell response to irreversible injury?

A
  1. continued ischaemia
  2. reversible changes
  3. irreversible changes
  4. cell membrane damage/rupture
  5. calcium influx

calcium influx leads to:

  • cessation of mitochonrial function (ATP production)
  • digestive enzymes triggered (that are Ca2+ dependent), cell skeleton destroyed

= loss of vital cytoplasm/nuclear material
and lysosomal autodigestion triggered (due to membrane damage)

65
Q

what happens if the mitochondria stops phosphorylation?

A

less ATP -> less Na pump ability

when Na/K pump stops working as well, water follows Na into cell = swelling

66
Q

what causes an increase in phosphofructokinase?

A

decline in mitochondrial phosphorylation and decrease in ATP

67
Q

what happens when phosphofructokinase increases?

A
  1. increase in anaerobic glycolysis
  2. increase in lactate
  3. reduction in pH
  4. clumping of nuclear chromatin
68
Q

what happens when theres a decline in protein production?

A

polysomes detach from EPR

69
Q

what happens during early ischaemic injury of kidney tubules?

A

surface blebs
eosinophilia
swollen cells

70
Q

what happens during necrosis of kidney tubules?

A

fragmentation of cells
loss of nuclei
leakage of contents

71
Q

what is autolysis?

A

processing of cell/tissue after you die by digestive enzymes (lysozymes)

72
Q

what is apoptosis?

A

programmed cell death

73
Q

how does apoptosis work?

A

Apoptotic cells remain viable and membrane pumps function until a terminal stage in the process
Cell shrinks
Nuclear chromatin condenses
Cell breaks up into apoptotic bodies
Macrophages or neighbouring cells phagocytose apoptotic bodies
Phagocytes recognise apoptotic cells by newly expressed membrane proteins

74
Q

how is apoptosis initiated?

A

activation of genes for new proteins involved in apoptotic process e.g. endonuclease - causes DNA fragmentation

75
Q

4 examples of physiological apoptosis

A

embryogenesis
menstrual cycle
breast feeding
immune cell development

76
Q

3 examples of pathological apoptosis

A

tumours
atrophy
viral illness - e.g. hepatocytes during hepatitis

77
Q

how does fas initiate apoptosis?

A

Binding of FAS ligand to FAS receptor

78
Q

which cells express FAS ligand?

A

activated T cells

79
Q

why do T cells express FAS?

A

to get rid of T cells over time to prevent accumulation of responsive immune cells/autoimmunity

80
Q

what do cytotoxic T cells use FAS for?

A

use FAS with perforin to kill target cells

81
Q

which cells with immune privilege express FAS ligand?

A

cornea, testis

82
Q

why do the cornea and testis express FAS?

A

immune system doesnt recognise - so if immune system comes into contact then apoptose infiltrating lymphocytes

83
Q

when is FAS turned off?

A

during pregnancy

84
Q

what is tumour counter-attack?

A

over expression of FAS ligand by tumours to kill the cells that would kill the tumour

85
Q

what is neoplasia?

A

formation of new, abnormal tissue

86
Q

which oncogenes turn off apoptosis?

A

bcl-2

87
Q

what are the microscopic changes of necrosis from irreversible injury?

A 
Nuclear
pyknosis
karyorrhexis
karyolysis
Increased eosinophilia of cytoplasm
88
Q

what are the ultrastructural changes of necrosis from irreversible injury?

A

high amplitude mitochondrial swelling
membrane defects
lysosomal membrane rupture
nuclear condensation, fragmentation, dissolution

89
Q

what 5 types of necrosis are there?

A
  1. coagulative
  2. liquifactive
  3. caseous
  4. fat
  5. gangrene
90
Q

what is coagulative necrosis?

A
  • firm tissue
  • becomes denser
  • looks paler/dry under microscope
  • seen in infarction and ischaemia
  • denied O2
  • not so much trauma/toxins
91
Q

what is liquifactive necrosis?

A
  • liquid viscous mass from bacterial/fungal infections
  • cell completely digested by hydrolytic enzymes
  • soft area with pus/fluid
  • dead leukocytes = creamy yellow pus
  • associated with abscesses
  • seen in the nervous system
92
Q

what is caseous necrosis?

A
  • cheese-like
  • soft, white mass
  • TB, syphillis, some fungi
93
Q

what is fat necrosis?

A
  • action upon fat by digestive enzymes
  • lipase releases fatty acids from triglycerides and calcium = soaps
  • white chalky deposits from calcium
  • e.g. trauma of pancreas/acute pancreatitis
94
Q

what is gangrene necrosis?

A
  • ischaemia/infection
  • thrombosis or clostridium perfringens
  • risk with diabetes/smoking
  • dry, wet or gas forms
95
Q

what type of necrosis is a splenic infarction likely to be?

A

coagulative necrosis

96
Q

what type of necrosis is a stroke likely to be?

A

liquifactive necrosis

97
Q

what type of necrosis is a liver abscess likely to be?

A

liquifactive necrosis

98
Q

what type of necrosis is TB likely to be?

A

caseous necrosis

99
Q

what type of necrosis is intestine-thrombosis likely to be?

A

gangrene

100
Q

what is the mechanism of calcium influx?

A
  1. injurious agent
  2. Ca2+ released from ER/other vacuoles
  3. cytosolic Ca2+ levels increase
  4. phospholipase, protease, ATPase and endonuclease released

phospholipase -> phospholipid
protease -> membrane cytoskeleton
ATPase -> reduce ATP
endonuclease -> chop chromosomes

101
Q

what are the results of necrosis?

A

end of function
cellular enzyme release e.g. cardiac enzymes after MI
inflammatory response

102
Q

how can you tell the difference between apoptosis/necrosis?

A

run DNA

X Understanding Disease (10 decks)

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