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Pathoma > Chapter 1: Growth Adaptations, Cellular Injury, and Cell Death > Flashcards

Chapter 1: Growth Adaptations, Cellular Injury, and Cell Death Flashcards

1
Q

What are the steps involved in hypertrophy?

A

gene activation
protein synthesis
production of organelles

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2
Q

hypertrophy vs. hyperplasia

A

hyerptrophy: larger cells
hyperplasia: more cells

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3
Q

what cells can undergo hypertrophy only?

A

permanent tissues, like cardiac muscle, skeletal muscle, and nerve

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4
Q

pathologic hyperplasia can progress to

A

dysplasia and cancer

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5
Q

what tissue has no increased risk of cancer with hyperplasia?

A

prostate

BPH carries no increased risk for cancer

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6
Q

atrophy

A

a decrease in organ size by both a decrease in size and number of cells

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7
Q

how does a decrease in cell number occur?

A

apoptosis

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8
Q

how does a decrease in cell size occur?

A

ubiquitination and proteosome degradation of cytoskeleton

autophagy of cellular components

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9
Q

upiquitin-proteosome degradation

A

intermediate filaments of the cytoskeleton are tagged with ubiquitin and destroyed by proteosomes

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10
Q

autophagy

A

autophagic vacuoles fuse with lysosomes containing hydrolytic enzymes to breakdown cellular components

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11
Q

an increase in stress leads to _________
a decrease in stress leads to ___________
a change in stress leads to ___________

A

an increase in size
a decrease in size
a change in cell type

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12
Q

metaplasia

A

change in cell type to better hand the new stress- change is adaptive

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13
Q

most common cells to undergo metaplasia?

A

surface epithelium

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14
Q

Barret’s esophagus is an example of

A

metaplasia

esophagus is normally lined by nonkeratinizing squamous epithelium and acid reflux causes it to change to nonciliated mucin-producing columnar cells

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15
Q

metaplasia occurs via_______

A

reprogramming cells

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16
Q

is metaplasia reversible?

A

in theory, yes, with the removal of the stressor

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17
Q

what is one tissue that can become metaplastic with no increased risk of cancer?

A

apocrine metaplasia of the breast (fibrocystic change)

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18
Q

vitamin A deficiency can cause metaplasia in ____

A

thin squamous lining of the conjunctiva- becomes stratified keratinizing squamous epithelium

=keratomalcia

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19
Q

dysplasia

A

disordered cell growth

most often refers to proliferation of precancerous cells

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20
Q

is dysplasia reversible?

A

in theory, it is reversible with alleviation of inciting stress

if it persists, dysplasia becomes carcinoma

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21
Q

aplasia

A

failure of cell production during embryogenesis

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22
Q

hypoplasia

A

decrease in cell production during embryogenesis, resulting in small organ

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23
Q

what occurs when a stress exceeds the cells ability to adapt?

A

cellular injury

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24
Q

slowly vs. acutely developing ischemia

A

slow: atrophy
acute: ischemia

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25
Q

_________ is the final electron acceptor

A

oxygen

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26
Q

how does decreased oxygen lead to a lack of ATP

A

impaired oxidative phosphorylation

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27
Q

3 causes of ischemia

A
  1. decreased arterial perfusion (atherosclerosis)
  2. decreased venous drainage (Budd-Chiari syndrome)
  3. shock- generalized hypotension resulting in poor tissue perfusion
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28
Q

aplasia

A

failure of cell production during embryogenesis

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29
Q

hypoxemia

A

PaO2 < 90%

low partial pressure of oxygen in the blood

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30
Q

hypoplasia

A

decrease in cell production during embryogenesis, resulting in small organ

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31
Q

causes of hypoxemia

A
  1. high altitude
  2. hypoventilation
  3. diffusion defect
  4. V/Q mismatch
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32
Q

what occurs when a stress exceeds the cells ability to adapt?

A

cellular injury

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33
Q

cherry-red appearance of the skin and headache

A

CO poisoning

leads to coma and death

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34
Q

cyanosis with chocolate colored blood

A

methemoglobinemia

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35
Q

labs in methemoglobinemia

A

normal PaO2, SaO2 decreased

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36
Q

treatment of methemoglobinemia

A

methylene blue

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37
Q

why do newborns get methemoglobinemia

A

there is always oxidant stress and we have enzymes to reduce but newborns are immature

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38
Q

broad effects of low ATP on cellular functioning

A

Na-K pump dysfunction: water and sodium buildup in the cell

Ca pump: calcium build up in the cell

aerobic glycolysis impaired- switch to anaerobic causing lactic acidosis, which denatures proteins and precipitates DNA

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39
Q

hallmark of reversible injury

A

cellular swelling

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40
Q

cellular swelling

A

cytosol swells: loss of microvilli and membrane blebbing

swelling of RER, causing the dissociation of ER and ribosomes and decreased protein synthesis

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41
Q

hallmark of irreversible injury

A

membrane damage

plasma membrane, mitochondrial membrane, and lysosome membrane

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42
Q

plasma membrane damage results in

A

cytosolic enzymes leaking into the serum and additional calcium entering the cell

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43
Q

mitochondiral membrane damage results in

A

loss of the electron transport chain (inner membrane) and cytochrome c leaking into cytosol and activating apoptosis

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44
Q

lysosome membrane damage results in

A

hydrolytic enzymes leaking into the cytosol and being activated by calcium

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45
Q

normal calcium concentration in the cell

A

very low- calcium is a messenger and turns on lots of pathways

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46
Q

hallmark of cell death

A

loss of nucleus
condensation (pyknosis)
fragmentation (karyorrhexis)
dissolution (karyolysis)

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47
Q

necrosis is always followed by

A

acute inflammation

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48
Q

necrotic tissue that remains firm with cell and organ structure preserved, but nucleus disappears

A

coagulative necrosis

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49
Q

area of infarcted tissue in coagulative necrosis

A

wedge-shaped and pale

50
Q

red infarction

A

if blood reenters a loosely organized tissue

51
Q

necrotic tissue with no structure or solidity- enzymatic lysis of cells and proteins

A

liquefactive necrosis

52
Q

characteristic of ischemia anywhere except the brain

A

coagulative necrosis

53
Q

name 3 places where liquefactive necrosis characteristically occurs

A

brain infarction: proteolytic enzymes from microglial cells liquefy the brain

abscess: neutrophil proteolytic enzymes liquefy tissue
pancreatitis: proteolytic enzymes from pancreas liquefy parenchyma

54
Q

coagulative necrosis that resembles mummified tissue

A

“dry grangrene”

gangrene necrosis

55
Q

example of gangrene necrosis

A

lower limb ischemia

56
Q

soft and friable necrotic tissue with cottage cheese-like appearance

A

caseous nerosis

comb of coagulative and liquefactive necrosis

57
Q

example of caseous necrosis

A

characteristic of granulomatous inflammation due to tuberculosis or fungal infection

58
Q

necrotic adipose tissue with a chalky-white appearance due to deposition of calcium

A

fat necrosis with saponification

59
Q

dystrophic calcification

A

necrotic tissue acts as a nidus for calcium deposition in the setting of normal serum calcium

60
Q

metastatic calcification

A

high serum calcium or phosphate levels lead to calcium deposition in normal tissue (like getting kidney stones from high serum calcium

61
Q

fat necrosis caused by

A

trauma or pancreatitis-mediated damage of peripancreatic fat

62
Q

necrotic damage to blood vessel walls; leaking of proteins into vessel walls leads to bright pink staining of the wall microscopically

A

fibrinoid necrosis

63
Q

energy-dependent, genetically programmed cell death involving single cells or small groups of cells

A

apoptosis

64
Q

what does a cell undergoing apoptosis look like?

A

dying cell shrinks and cytoplasm becomes eosinophilic

nucleus condenses and fragments

65
Q

apoptotic bodies

A

as the cell dies, apoptotic bodies fall from the cell and are removed by macrophages; apoptosis is not followed by inflammation

66
Q

apoptosis is mediated by

A

caspases

67
Q

caspases activate

A

proteases: break down cytoskeleton
endonucleases: break down DNA

68
Q

what are the ways caspase are activated?

A

intrinsic mitochondrial
extrinsic receptor-ligand pathway
cytotoxic CD8+ T cell-mediated pathway

69
Q

intrinsic mitochondrial pathway of caspase activation

A

cellular injury, DNA damage or loss of hormonal stimulation leads to inactivation of Bcl2

cytochrome c leaks from the inner mitochondrial membrane into the cytoplasm and activates caspases

70
Q

Bcl 2

A

inhibits cyt c from leaking from the inner mitochondrial membrane into the cytoplasm

71
Q

extrinsic receptor-ligand pathway of caspase activation

A

Fas ligand binds FAS death receptor (CD95) to activate caspase

tumor necrosis factor (TNF) binds TNF receptor on the target cell to activate caspases

72
Q

CD95

A

Fas death receptor

73
Q

cytotoxic T cell mediated pathway of caspase activation

A

perforins secreted by CD8+ T cells create pores in membrane of target cell

granzyme from CD8+ T cell enters pores and activates caspases

74
Q

free radicals

A

chemical species with an unpaired electron in their outer orbit

75
Q

physiologic generation of free radicals

A

oxidative phosphorylation

  • cyt c oxidase
  • partial reduction of O2 yields superoxie, hydrogen peroxide, and hydroxyl radicals
76
Q

4 ways that free radicals are generated pathologically

A
  1. ionizing radiation
  2. inflammation- NAPDPH oxidase generates superoxide ions in O2 dependent killing by neutrophils
  3. metals
  4. drugs and chemicals
77
Q

free radicals cause cellular injury by

A

peroxidation of lipids

oxidation of DNA and protein

78
Q

enzymes that eliminate free radicals

A

superoxide dismutase
glutathione peroxidase
catalase

79
Q

carbon tetrachloride

A

organic solvent used in dry cleaning that is converted to a free radical in the liver and causes swelling of RER
ribosomes detach and protein synthesis is impaired and fatty change occurs

80
Q

reperfusion injury

A

return of blood to ischemic area results in O2-derived free radicals, which continue to damage tissue

this is the reason that there is a continued rise in cardiac enzymes after reperfusion of infarcted tissue

81
Q

a misfolded protein that deposits in extracellular space and damages tissues

A

amyloid

82
Q

features of amyloidosis in all proteins

A

beta pleated sheet configuration

congo red staining and apple green birefringence with polarized light

83
Q

primary amyloidosis

A

systemic deposition of AL amyloid

-derived from Ig light chains

84
Q

primary amyloidosis is associated with

A

plasma cell dyscrasia (multiple myeloma)

85
Q

secondary amyloidosis

A

AA amyloid deposition systemically of SAA (serum-associated amyloid protein)

86
Q

SAA

A

acute phase reactant increased in chronic inflammatory states, malignancy and familial mediterranean fever

87
Q

Familial Mediterranean fever

A

dysfunction of neutrophils

presents with: fever, acute serosal inflammation (mimics appendicitis, arthritis, myocardial infarction)

88
Q

clinical findings of sysmteic amyloidosis

A 
nephrotic syndrome (most common)
restrictive cardiomyopathy or arrhythmia
tongue enlargement, malabsorption, hepatosplenomegaly
89
Q

treatment for amyloidosis?

A

damaged organ must be transplanted

90
Q

localized amyloidosis

A

single organ

91
Q

senile cardiac amyloidosis

A

non-mutated serum transthyretindeposits in the heart, usually asymptomatic

92
Q

familial amyloid cardiomyopathy

A

mutated serum transthyretin deposits in the heart and causes a restrictive cardiomyopathy

93
Q

non-insulin-dependent diabetes mellitus amyloidosis

A

amylin deposits in the islets of the pancreas (amylin is derived from insulin)

94
Q

alzheimer’s amyloidosis

A

A-beta amyloid deposits in the brain

gene is on chromosome 21

95
Q

dialysis associated amyloidosis

A

B2 microglobulin (component of MHC-I) deposits in joints

96
Q

medullary carcinoma of the thyroid amyloidosis

A

calcitonin (produced by tumor cells) deposits in the tumor

97
Q

FNA of thyroid shows tumor cells in amyloid background

A

medullary carcinoma of the thyroid

98
Q

Epithelium– 3 broad categories

A

Squamous Cell Epithelium
–> keratinizing/non-keratinizing

Columnar Epithelium
–> ciliated?

Transitional
–> really only the bladder lined with this

99
Q

normal esophageal lining?

A

nonkeratinizing squamous epithelium

100
Q

What can happen after trauma to muscle?

A

Myositis ossificans

metaplasia of muscle to bone during healing after trauma

101
Q

fibromuscular dysplasia

A

Most commonly affects renal artery and carotid artery

102
Q

What symptoms does Vitamin A deficiency present with?

A

Vitamin A necessary for differentiation of specialized epithelial surfaces such as the conjunctiva covering the eye, thus deficiency can lead to

keratomalacia or stratified keratinizing squamous epithelium

103
Q

Most common cause of Budd-Chiari syndrome

A

Polycythemia Vera

104
Q

Describe the path of oxygen to tissue using lab values

A

FiO2 –> PAO2 –> PaO2 –> SaO2

pressure of oxygen in air –> pressure of oxygen in alveoli –> pressure of oxygen in blood –> saturation of hemoglobin

105
Q

Lab values in hypoventilation

A

Increased CO2 causes decreased O2 which means O2 sats go down

106
Q

Chocolate colored blood with cyanosis. lab values? treatment?

A

Methemoglobinemia
PaO2 normal
SaO2 decreased
Iron oxidized to Fe+3 and cannot bind oxygen. Seen with OXIDANT STRESS such as nitryl or sulfa drugs.

TREATMENT: Methylene blue, which catalyzes natural reduction of methemoglobin reductase by offering an electron acceptor

107
Q

Describe pathophys of low ATP

A
  1. ) disruption of ATP pump leads to Na+ influx into cell
  2. ) Ca+2 pump needs ATP so influx of Ca+2 as well
  3. ) Ca+2 activates enzymes
  4. ) Anaerobic glycolysis causes lactic acid buildup which lowers pH and precipitates DNA
108
Q

Hallmark of reversible injury and what it leads to

A

Cellular Swelling

  1. ) loss of microvilli
  2. ) cellular blebbing
  3. ) ribosomes fall off rough ER causing decreased protein synthesis
109
Q

Hallmark of irreversible damage is?

what it leads to…

A

Membrane damage

  1. ) allows enzymes to leak into the serum(cardiac troponin after MI/necrosis)
  2. ) more calcium enters cell
  3. ) mitochondrial membrane damage breaks electron transport
  4. ) that same mitochondrial membrane damage allows cytochrome c to leak out which activates apoptosis
  5. ) lysosomal membrane damage allows hydrolytic enzymes to leak into cell and wreak havoc
110
Q

What are the macrophages of the CNS

A

microglial cells

111
Q

Acute inflammation can be caused by…

A

infection OR necrosis

neutrophil count will increase in both

112
Q

Which organs have white infarcts?

A

Heart, Kidney, Spleen

113
Q

Which organs have red infarcts?

A

lungs, liver, testes, ovaries, gut

114
Q

what is fibrinoid necrosis

A

necrotic damage to blood vessel wall causes leaking of proteins into vessel wall(including fibrin)

115
Q

necrosis associated with hypertension or vasculitis

A

fibrinoid necrosis

common example is fibrinoid necrosis of placenta secondary to high Bp due to pre-eclampsia

116
Q

Malignant hypertension can cause what?

A

fibrinoid necrosis of blood vessels

117
Q

Apoptosis activation – intrinsic mitochondrial pathway

A

cellular or DNA damage or loss of hormonal stimulation can cause inactivation of Bcl2

Inactivation of Bcl2 –> leakage of cytochrome c from inner mitochondrial membrane into cytoplasm –> cytochrome c activates caspases in cytoplasm –> caspases activate proteases that wreak havoc, in an orderly fashion

118
Q

Apoptosis activation – extrinsic receptor-ligand pathway

A

FAS ligand binds FAS death receptor(CD95) on target cell, activating caspases
example: negative T-cell selection in Thymus

OR

TNF binds TNF receptor on target cell activating caspases

119
Q

Chronic Granulomatous Disease

A

deficiency in NADPH oxidase. However if extrinsic hydrogen peroxide provided, MPO can make bleach and be bacterial. Thus catalase positive organisms are particularly dangerous to these people.

120
Q

NBT dye is for what?

A

oxidative burst! or…
O2 –> O2 free radical
catalyzed by NADPH oxidase

121
Q

MPO deficiency

A

These people will respond to NBT dye test. But they cannot make HOCl(bleach) because of defective MPO and thus are susceptible to chronic infection

Pathoma (7 decks)

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