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Immunology > Cell Injury, Death & Adaptation > Flashcards

Cell Injury, Death & Adaptation Flashcards

1
Q

4 mechanisms of adaptation to reversible injury / stress

A

Hypertrophy, Hyperplasia, Atrophy, Metaplasia

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2
Q

Cellular injury resulting from decreased oxygen

A

Ischemia

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3
Q

5 mechanisms of cell damage

A

Oxidative stress
Membrane damage
Mitochondrial damage
DNA damage
Disturbance of calcium homeostasis

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4
Q

Molecule with unpaired electron in outer orbit
Highly reactive

A

Free radical

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5
Q

Highly reactive molecules which contain oxygen atoms

A

Reactive oxygen species

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6
Q

ROS are produced normally during these 2 processes

A

Cellular respiration
Leukocytes during inflammation (respiratory burst)

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7
Q

During the red-ox reactions of mitochondrial respiration, sequential reduction of O2 to H2O2 can result in the occasional “lost” electron, which can form this

A

Superoxide
Lost e- is added to oxygen to form O2-

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8
Q

Enzyme that forms superoxide radical from oxygen atom

A

Phagocyte/NADPH oxidase

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9
Q

Enzyme that forms hydrogen peroxide from superoxide radical

A

Superoxide dismutase

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10
Q

Enzyme that forms hypochlorite from hydrogen peroxide

A

Myeloperoxidase

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11
Q

What is the Fenton reaction?

A

Hydrogen peroxide is converted to OH- (hydroxyl) in the presence of Fe2+

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12
Q

Hydrogen peroxide is converted to hydroxyl OH- in the presence of this

A

Transition metals (Cu and Fe)

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13
Q

ROS damage cells in these 3 ways

A

Membrane lipid oxidation
Protein oxidation
DNA damage

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14
Q

4 mechanisms of membrane damage

A

Oxidative stress
Decreased phospholipid synthesis
Increased phospholipid degradation
Cytoskeletal abnormalities

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15
Q

2 ions whose cytosolic levels increase during membrane damage

A

Ca2+ and Na+

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16
Q

Increased phospholipid degradation may occur when phosphatases are activated by increase cytosolic levels of this

A

Calcium

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17
Q

Mitochondrial membrane damage can result in these 4 things

A

Loss of compartmentalization (mitochondrial dysfunction)
Decreased ATP generation
Pro-apoptotic state
Generation of free radicals

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18
Q

Lysosome membrane damage can result in these 2 things

A

Autolysis and/or necrosis

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19
Q

Glycolytic and citric acid cycle enzymes are found in this part of the mitochondria

A

Core

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20
Q

Respiratory chain enzymes are found in this part of the mitochondria

A

Inner membrane

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21
Q

ATP generation occurs in this part of the mitochondria

A

Intermembrane space

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22
Q

Porin proteins selectively permit small molecules to pass and are found in this part of the mitochondria

A

Outer membrane

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23
Q

Increased cytosolic calcium leads to this

A

Enzyme activation
Phospholipidases cause membrane damage
Proteases degrade structural proteins and others

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24
Q

2 mechanisms of mitochondrial damage

A

Increased cytosolic calcium leads to enzyme activation (phospholipidases, proteases)
Lack of oxygen results in ROS

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25
Q

ATP depletion as a result of mitochondrial damage leads to apoptosis or necrosis?

A

Necrosis

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26
Q

ATP depletion as a result of mitochondrial damage has these 3 effects

A

Inability to run Na/K ATPase (increased cytosolic Na, increased H2O)
Decreased oxidative phosphorylation (increased glycolysis, increased lactic acid, protein dysfunction)
Ribosome detachment from rER

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27
Q

Decreased oxidative phosphorylation as a result of mitochondrial damage leads to this

A

Increased glycolysis, increased lactic acid, protein dysfunction

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28
Q

Leakage of mitochondrial proteins like cytochrome C during mitochondria damage leads to this

A

Apoptosis

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29
Q

Leakage of cytochrome C into cytosol signals cell damage, and activates this

A

Caspase enzyme pathway
(DNase activation, protease activation, programmed cell death)

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30
Q

This activates the caspase enzyme pathway during mitochondrial damage

A

Leakage of cytochrome C into cytosol

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31
Q

Incomplete oxidative phosphorylation during mitochondrial damage produces these

A

Free radicals

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32
Q

DNA damage is often repaired with this pathway

A

p53 pathway

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33
Q

During the p53 pathway of DNA damage repair, the cell cycle is arrested in this phase

A

G1

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34
Q

What happens if the p53 pathway of DNA damage repair is unsuccesful?

A

Apoptosis occurs; mediated through bcl-2/Bax/Bak pathway

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35
Q

Are normal cytosolic levels of calcium high or low?

A

Very low due to pumps and membranes

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36
Q

Disturbance of calcium homeostasis has these 2 effects

A

Influx into mitochondria (swelling, decreased ATP generation)
Inappropriate enzyme activation (endonucleases, proteases, phospholipases, ATPase)

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37
Q

3 intracellular accumulations that are signs of damage/degeneration

A

Water, Fat, Lipofuscin

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38
Q

2 extracellular accumulations that are signs of damage/degeneration

A

Hyaline material, Calcium deposition

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39
Q

Accumulation of intracellular lipid
Sign of reversible injury
Occurs mostly in cells involved in lipid metabolism (liver)

A

Steatosis

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40
Q

Lipid is _______ so it does not dissolve in cytoplasm

A

Hydrophobic

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41
Q

Excess lipid is morphologically seen as these

A

Droplets

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42
Q

What produces vacuolization of cytoplasm?

A

Excess lipid, which is hydrophobic and does not dissolve in cytoplasm, so instead is seen as droplets

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43
Q

Golden-brown intracellular indigestible material made of lipid and protein
“Wear and tear” pigment
Gradually accumulates as cells age
Mostly seen in post-mitotic cells (liver, heart, neurons)

A

Lipofuscin

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44
Q

What is lipofuscin?

A

Golden-brown intracellular indigestible material made of lipid and protein

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45
Q

Lipofuscin is mostly seen in this type of cell

A

Post-mitotic cells (liver, heart, neurons)

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46
Q

Any material that appears dense, amorphous, and intensely eosinophilic
Also intracellular amorphous pink deposits

A

Hyaline

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47
Q

Vascular hyaline may be due to long-term ______

A

Hypertension

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48
Q

What is hyaline?

A

Any material that appears dense, amorphous, and intensely eosinophilic

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49
Q

Damaged proteins deposited in the kidney glomerulus in diabetes

A

Hyaline

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50
Q

Calcium deposits may form in these two pathological categories

A

Dystrophic calcification
Metastatic calcification

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51
Q

Category of pathological calcium deposition:
Calcium deposits in abnormal tissue, usually necrotic

A

Dystrophic calcification

52
Q

Category of pathological calcium deposition:
Calcium precipitates in tissues due to abnormally high serum concentrations

A

Metastatic calcification

53
Q

Occurs when cell swells due to increased cytoplasmic water content
H2O mostly in ER cisternae
Number of organelles does not increase, just water content
Morphology shows lighter staining
Occurs due to decreased ability to maintain ion concentrations, especially Na+

A

Hydropic swelling

54
Q

Morphology of hydropic swelling will appear this color of staining

A

Lighter staining / pale

55
Q

When Na/K ATPase is dysfunctional, it fails to pump Na ____ of cell

A

Out

56
Q

What causes hydropic swelling?

A

Decreased ability to maintain ion concentrations (leakiness, pump failure)

57
Q

Is hydropic swelling a sign of reversible or irreversible injury?

A

Reversible
If injury ceases (O supply restored, toxin removed, nutrients given), ATPase function is restored and water balance is restored

58
Q

4 morphological features of hydropic swelling

A

Cytoplasm volume increases and is pale
Organelles are dispersed, not increased in number
Nucleus remains in normal location
Water is not in vacuoles, just dispersed

59
Q

Cellular adaptation involving increased cell size
E.g. muscle cell increases number of contractile elements

A

Hypertrophy

60
Q

Define hypertrophy

A

Cellular adaptation involving Increased cell size

61
Q

Cellular adaptation involving increased cell number
E.g. high altitude living leads to increased number of RBCs

A

Hyperplasia

62
Q

Define hyperplasia

A

Cellular adaptation involving increased cell number

63
Q

Chronic skin disorder characterized by the presence of hard, extremely itchy bumps known as nodules
Example of hyperplasia

A

Prurigo Nodularis (Picker’s nodule)

64
Q

Cellular adaptation involving decreased cell size and/or function
E.g. uterine muscle shrinks after pregnancy

A

Atrophy

65
Q

Define atrophy

A

Cellular adaptation involving decreased cell size and/or function

66
Q

Uterine muscle shrinking after pregnancy is this kind of cellular adaptation

A

Atrophy

67
Q

Cellular adaptation involving a change in cell type; change of one phenotype of another as a response to irritation/stress
New cell type is more able to handle stress

A

Metaplasia

68
Q

Metaplasia example:
Squamous epithelium changes to this if increased acid is present in esophagus

A

Glandular epithelium

69
Q

Metaplasia example:
Glandular epithelium changes to this in bronchus after prolonged exposure to smoke

A

Squamous epithelium
This change can lead to squamous cancer in the lungs

70
Q

Type of cell death that induces cell fragmentation which elicits inflammatory response (WBCs)

A

Necrosis

71
Q

6 types of necrosis

A

Coagulative
Liquefactive
Gangrenous
Caseous
Fat necrosis
Fibrinoid

72
Q

Necrosis is cell death which induces cell _______ which elicits inflammatory response (WBCs)

A

Cell fragmentation

73
Q

Class form of necrosis due to ischemia (aka infarction)
All tissues except CNS undergo this type when infarcted
Lack of blood supply and delayed ability to dissolve cell

A

Coagulative necrosis

74
Q

All tissues except ____ will undergo coagulative necrosis when infarcted

A

CNS

75
Q

Type of necrosis where morphological cell outlines remain intact for a period
Nucleus is absent or faint/eosinophilic

A

Coagulative necrosis

76
Q

Morphology of nucleus in coagulative necrosis

A

Nucleus is absent or faint/eosinophilic

77
Q

Type of necrosis that occurs when rate of dissolution greatly exceeds rate of repair
Dead tissue becomes digested by proteolytic enzymes
Typical necrosis in bacterial infections (e.g. abscess), results in viscous yellow fluid (pus)
Also seen in CNS infarction

A

Liquefactive necrosis

78
Q

When does coagulative necrosis occur?

A

All tissues except CNS will undergo coagulative necrosis when infarcted

79
Q

When does liquefactive necrosis occur?

A

Occurs when rate of dissolution greatly exceeds rate of repair

80
Q

Viscous yellow fluid (pus) is distinctive of this type of necrosis

A

Liquefactive necrosis

81
Q

Typical necrosis in bacterial infections (e.g. abscess)

A

Liquefactive necrosis

82
Q

Liquefactive necrosis is typical in this type of infection

A

Bacterial infections (e.g. abscess)

83
Q

Type of necrosis involving ischemic necrosis of several tissue planes

A

Gangrenous necrosis

84
Q

Common sites of gangrenous necrosis

A

Limb/digit, Penile, Bowel

85
Q

When does gangrenous necrosis occur?

A

Ischemic necrosis of several tissue planes

86
Q

Type of gangrenous necrosis involving loss of blood supply resulting in dried tissue planes

A

Dry gangrene

87
Q

Type of gangrenous necrosis involving superimposed bacterial infection resulting in liquefaction

A

Wet gangrene

88
Q

Type of necrosis where cells are fragmented resulting in particulate, crumbly appearance
Tuberculosis is typical example

A

Caseous necrosis

89
Q

Tuberculosis involves this type of necrosis

A

Caseous necrosis

90
Q

In tuberculosis, the center of the granuloma is filled with this

A

Caseous necrosis

91
Q

In tuberculosis, caseous necrosis is surrounded by this

A

Granulomatous inflammation (macrophages, giant cells, fibrotic wall)

92
Q

What is characteristic of caseous necrosis?

A

Necrotic cells are fragmented resulting in particulate, crumbly appearance

93
Q

Type of necrosis involving enzymatic digestion of lipid resulting in saponification
Typical example is pancreatitis

A

Fat necrosis

94
Q

What is fat necrosis?

A

enzymatic digestion of lipid resulting in saponification

95
Q

Condition which releases pancreatic lipase and is an example of fat necrosis

A

Pancreatitis

96
Q

Pancreatitis is an example of this type of necrosis

A

Fat necrosis

97
Q

Pancreatic lipase is normally in this intracellular location

A

Membrane bound vesicles
Cellular damage releases lipase, which digests peripancreatic fat. Triglycerides are digested to release fatty acids, which combine with calcium and form insoluble calcium salts.

98
Q

In fat necrosis in pancreatitis, cellular damage releases lipase from membrane bound vesicles. It then digests peripancreatic fat, and triglycerides are digested to release fatty acids.
These fatty acids then combine with an ion to form these

A

Combine with calcium to form insoluble calcium salts

99
Q

Morphology of fat necrosis

A

Fat lobules become white and firm
Saponified fat does not dissolve in processing (remains on histology slide)

100
Q

Type of necrosis of vascular wall resulting in leakage of plasma proteins
These deposit in wall and is seen in certain types of vasculitis

A

Fibrinoid necrosis

101
Q

What is fibrinoid necrosis?

A

Necrosis of vascular wall resulting in leakage of plasma proteins

102
Q

Type of necrosis seen in certain types of vasculitis

A

Fibrinoid necrosis

103
Q

Morphology of apoptotic cells

A

Cell shrinks (dense eosinophilic cytoplasm)
Chromatin condenses at periphery
Nucleus fragments and form apoptotic bodies (phagocytes apoptotic bodies but no inflammation)

104
Q

2 pathways of apoptosis

A

Mitochondrial and extrinsic

105
Q

Cytochrome C is released into the cytoplasm during mitochondrial damage, and then binds to and activates this

A

Caspase 9
pathway to apoptotic death

106
Q

Caspase 9 is activated by this

A

Cytochrome c (which is released into the cytoplasm during mitochondrial damage)

107
Q

Mitochondrial pathway of apoptosis is inhibited by this

A

Bcl2 protein

108
Q

Bcl2 protein inhibits this

A

Mitochondrial pathway of apoptosis

109
Q

Apoptosis pathway involving the release of cytochrome C into cytoplasm, which binds and activates caspase 9

A

Mitochondrial

110
Q

Apoptosis pathway where molecules bind death receptors on cell surface, leading to caspase 8 activation

A

Extrinsic

111
Q

During the extrinsic pathway of apoptosis, molecules bind death receptors on cell surface and activate this

A

Caspase 8

112
Q

Fas binds Fas ligand, leading to apoptotic death of auto-reactive T cells, is an example of this apoptosis pathway

A

Extrinsic

113
Q

Apoptosis enzyme activated in the extrinsic pathway

A

Caspase 8

114
Q

Apoptosis enzyme activated in the mitochondrial pathway

A

Caspase 9

115
Q

Caspase 8 is activated in this apoptosis pathway

A

Extrinsic

116
Q

Caspase 9 is activated in this apoptosis pathway

A

Mitochondrial

117
Q

Both apoptosis pathways (mitochondrial and extrinsic) converge as a common execution phase pathway with these 3 effects

A

Nucleus dissolved via DNAases
Cytoplasmic blebs –> apoptotic bodies
Apoptotic bodies removed by phagocytes

118
Q

Pro-apoptotic forces in healthy cells that are inhibited by growth factor signaling (bcl) mediators

A

BAX and BAK

119
Q

Levels of BAX, BAK, and bcl-2 in healthy cells

A

Pro-apoptotic forces (BAX and BAK) inhibited by growth factor signaling (bcl) mediators

120
Q

Levels of BAX, BAK, and bcl-2 in cells with lack of pro-growth signaling

A

Balance shifted to BAX/BAK; increased release of BAX/BAK
Decreased bcl-2

121
Q

Increased release of BAX/BAK during intrinsic apoptosis form this

A

Form membrane channels in mitochondria, leading to release of cytochrome C

122
Q

BAX/BAK form membrane channels in mitochondrion, releasing this

A

cytochrome C

123
Q

Process by which a cell digests parts of itself
Used in states of deprivation
Cell constituents delivered to lysosomes –> autophagosome
Recycles nutrients, organelles, etc.
Defective/dysregulation in various disease states (neoplasia, neurodegenerative diseases)

A

Autophagy

124
Q

In autophagy, cell constituents are delivered to these

A

Lysosomes –> autophagosome

125
Q

This process is defective/dysregulation in various disease states such as neoplasia and neurodegenerative diseases

A

Autophagy

Immunology (14 decks)

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