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MF2 Final study > Cell injury, death & adaptation > Flashcards

Cell injury, death & adaptation Flashcards

1
Q

Cellular injury resulting from decreased oxygen

A

Ischemia

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2
Q

ROS are produced normally during these 2 processes

A

Cellular respiration
Leukocytes during inflammation (respiratory burst)

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3
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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4
Q

Enzyme that forms superoxide radical from oxygen atom

A

Phagocyte/NADPH oxidase

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5
Q

Enzyme that forms hydrogen peroxide from superoxide radical

A

Superoxide dismutase

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6
Q

Enzyme that forms hypochlorite from hydrogen peroxide

A

Myeloperoxidase

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7
Q

What is the Fenton reaction?

A

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

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8
Q

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

A

Transition metals (Cu and Fe)

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9
Q

2 ions whose cytosolic levels increase during membrane damage

A

Ca2+ and Na+

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10
Q

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

A

Calcium

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11
Q

Lysosome membrane damage can result in these 2 things

A

Autolysis and/or necrosis

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12
Q

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

A

Core

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13
Q

Respiratory chain enzymes are found in this part of the mitochondria

A

Inner membrane

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14
Q

ATP generation occurs in this part of the mitochondria

A

Intermembrane space

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15
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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16
Q

Increased cytosolic calcium leads to this

A

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

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17
Q

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

A

Necrosis

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18
Q

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

A

Apoptosis

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19
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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20
Q

This activates the caspase enzyme pathway during mitochondrial damage

A

Leakage of cytochrome C into cytosol

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21
Q

Incomplete oxidative phosphorylation during mitochondrial damage produces these

A

Free radicals

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22
Q

DNA damage is often repaired with this pathway

A

p53 pathway

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23
Q

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

A

G1

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24
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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25
Q

Are normal cytosolic levels of calcium high or low?

A

Very low due to pumps and membranes

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26
Q

3 intracellular accumulations that are signs of damage/degeneration

A

Water, Fat, Lipofuscin

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27
Q

2 extracellular accumulations that are signs of damage/degeneration

A

Hyaline material, Calcium deposition

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28
Q

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

A

Steatosis

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29
Q

Lipid is _______ so it does not dissolve in cytoplasm

A

Hydrophobic

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30
Q

Excess lipid is morphologically seen as these

A

Droplets

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31
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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32
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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33
Q

What is lipofuscin?

A

Golden-brown intracellular indigestible material made of lipid and protein

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34
Q

Lipofuscin is mostly seen in this type of cell

A

Post-mitotic cells (liver, heart, neurons)

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35
Q

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

A

Hyaline

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36
Q

Vascular hyaline may be due to long-term ______

A

Hypertension

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37
Q

What is hyaline?

A

Any material that appears dense, amorphous, and intensely eosinophilic

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38
Q

Damaged proteins deposited in the kidney glomerulus in diabetes

A

Hyaline

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39
Q

Calcium deposits may form in these two pathological categories

A

Dystrophic calcification
Metastatic calcification

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40
Q

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

A

Dystrophic calcification

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41
Q

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

A

Metastatic calcification

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42
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

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43
Q

Morphology of hydropic swelling will appear this color of staining

A

Lighter staining / pale

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44
Q

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

A

Out

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45
Q

What causes hydropic swelling?

A

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

46
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

47
Q

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

A

Hypertrophy

48
Q

Define hypertrophy

A

Cellular adaptation involving Increased cell size

49
Q

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

A

Hyperplasia

50
Q

Define hyperplasia

A

Cellular adaptation involving increased cell number

51
Q

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

A

Atrophy

52
Q

Define atrophy

A

Cellular adaptation involving decreased cell size and/or function

53
Q

Uterine muscle shrinking after pregnancy is this kind of cellular adaptation

A

Atrophy

54
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

55
Q

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

A

Glandular epithelium

56
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

57
Q

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

A

Necrosis

58
Q

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

A

Cell fragmentation

59
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

60
Q

All tissues except ____ will undergo coagulative necrosis when infarcted

A

CNS

61
Q

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

A

Coagulative necrosis

62
Q

Morphology of nucleus in coagulative necrosis

A

Nucleus is absent or faint/eosinophilic

63
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

64
Q

When does coagulative necrosis occur?

A

All tissues except CNS will undergo coagulative necrosis when infarcted

65
Q

When does liquefactive necrosis occur?

A

Occurs when rate of dissolution greatly exceeds rate of repair

66
Q

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

A

Liquefactive necrosis

67
Q

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

A

Liquefactive necrosis

68
Q

Liquefactive necrosis is typical in this type of infection

A

Bacterial infections (e.g. abscess)

69
Q

Type of necrosis involving ischemic necrosis of several tissue planes

A

Gangrenous necrosis

70
Q

Common sites of gangrenous necrosis

A

Limb/digit, Penile, Bowel

71
Q

When does gangrenous necrosis occur?

A

Ischemic necrosis of several tissue planes

72
Q

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

A

Dry gangrene

73
Q

Type of gangrenous necrosis involving superimposed bacterial infection resulting in liquefaction

A

Wet gangrene

74
Q

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

A

Caseous necrosis

75
Q

Tuberculosis involves this type of necrosis

A

Caseous necrosis

76
Q

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

A

Caseous necrosis

77
Q

In tuberculosis, caseous necrosis is surrounded by this

A

Granulomatous inflammation (macrophages, giant cells, fibrotic wall)

78
Q

What is characteristic of caseous necrosis?

A

Necrotic cells are fragmented resulting in particulate, crumbly appearance

79
Q

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

A

Fat necrosis

80
Q

What is fat necrosis?

A

enzymatic digestion of lipid resulting in saponification

81
Q

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

A

Pancreatitis

82
Q

Pancreatitis is an example of this type of necrosis

A

Fat necrosis

83
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.

84
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

85
Q

Morphology of fat necrosis

A

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

86
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

87
Q

What is fibrinoid necrosis?

A

Necrosis of vascular wall resulting in leakage of plasma proteins

88
Q

Type of necrosis seen in certain types of vasculitis

A

Fibrinoid necrosis

89
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)

90
Q

2 pathways of apoptosis

A

Mitochondrial and extrinsic

91
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

92
Q

Caspase 9 is activated by this

A

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

93
Q

Mitochondrial pathway of apoptosis is inhibited by this

A

Bcl2 protein

94
Q

Bcl2 protein inhibits this

A

Mitochondrial pathway of apoptosis

95
Q

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

A

Mitochondrial

96
Q

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

A

Extrinsic

97
Q

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

A

Caspase 8

98
Q

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

A

Extrinsic

99
Q

Apoptosis enzyme activated in the extrinsic pathway

A

Caspase 8

100
Q

Apoptosis enzyme activated in the mitochondrial pathway

A

Caspase 9

101
Q

Caspase 8 is activated in this apoptosis pathway

A

Extrinsic

102
Q

Caspase 9 is activated in this apoptosis pathway

A

Mitochondrial

103
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

104
Q

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

A

BAX and BAK

105
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

106
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

107
Q

Increased release of BAX/BAK during intrinsic apoptosis form this

A

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

108
Q

BAX/BAK form membrane channels in mitochondrion, releasing this

A

cytochrome C

109
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

110
Q

In autophagy, cell constituents are delivered to these

A

Lysosomes –> autophagosome

111
Q

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

A

Autophagy

MF2 Final study (28 decks)

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