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Pathoma > Pathoma Chapter 1 Flashcards > Flashcards

Pathoma Chapter 1 Flashcards

1
Q

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

what are common causes of injury?

A 
inflammation
nutritional deficiency or excess
hypoxia
trauma
genetic mutations
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25
Q

slowly vs. acutely developing ischemia

A

slow: atrophy
acute: injury

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26
Q

_________ is the final electron acceptor

A

oxygen

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27
Q

how does decreased oxygen lead to a lack of ATP

A

impaired oxidative phosphorylation

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28
Q

causes of hypoxia

A

ischemia
hypoxia
decreased O2 carrying capacity

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29
Q

3 causes of ischemia

A

decreased arterial perfusion (atherosclerosis)
decreased venous drainage (Budd-Chiari syndrome)
shock- generalized hypotension resulting in poor tissue perfusion

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30
Q

aplasia

A

failure of cell production during embryogenesis

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31
Q

hypoxemia

A

PaO2 < 90%

low partial pressure of oxygen in the blood

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32
Q

hypoplasia

A

decrease in cell production during embryogenesis, resulting in small organ

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33
Q

causes of hypoxemia

A

high altitude
hypoventilation
diffusion defect
V/Q mismatch

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34
Q

how are PaO2 and SaO2 effected in anemia

A

only decrease in RBC mass not ability to bind O2 so:

PaO2 and SaO2 normal

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35
Q

cherry-red appearance of the skin

A

CO poisoning
leads to coma and death
caused by tight binding of hemoglobin which reflects the light, but they are actually hypoxic

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36
Q

how are PaO2 and SaO2 effected in CO poisoning

A

PaO2 is normal but SaO2 is decreased b/c CO will bind limiting O2 binding

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37
Q

early sign of CO poisoning?

A

headache

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38
Q

cyanosis with chocolate colored blood

A

methemoglobinemia

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39
Q

What state of iron binds O2?

A

Fe2+

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40
Q

what is methemoglobinemia?

A

when iron in heme is oxidized to Fe3+ and cannot bind O2

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41
Q

labs in methemoglobinemia

A

normal PaO2, SaO2 decreased

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42
Q

treatment of methemoglobinemia

A

methylene blue to reduce the Fe3+

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43
Q

When do you see methemoglobinemia?

A 
oxidant stresses (sulfa, nitrates)
newborns
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44
Q

why do newborns get methemoglobinemia

A

there is always oxidant stress and we have enzymes to reduce but newborn’s are immature

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45
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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46
Q

hallmark of reversible injury

A

cellular swelling

47
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

48
Q

hallmark of irreversible injury

A

membrane damage

plasma membrane, mitochondrial membrane, and lysosome membrane

49
Q

plasma membrane damage results in

A

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

50
Q

mitochondiral membrane damage results in

A

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

51
Q

lysosome membrane damage results in

A

hydrolytic enzymes leaking into the cytosol and being activated by calcium

52
Q

normal calcium concentration in the cell

A

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

53
Q

hallmark of cell death

A

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

54
Q

necrosis is always followed by

A

acute inflammation

55
Q

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

A

coagulative necrosis

56
Q

appearance of area of infarcted tissue in coagulative necrosis

A

wedge-shaped and pale, wedge points to area of occlusion

57
Q

when do you get coagulative necrosis?

A

ischemia of any organ except brain

58
Q

what do you see in histology of coagulative necrosis?

A

recognizable structures but no blue nuclei

59
Q

when do you get red infarction

A

if blood reenters a loosely organized tissue

60
Q

explain the occurrence of red infarction in the testes

A

with testicular torsion, the vein is thin walled and gets block but the artery remains open and allows blood to enter

61
Q

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

A

liquefactive necrosis

62
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

63
Q

coagulative necrosis that resembles mummified tissue

A

gangrene necrosis “dry grangrene”

64
Q

example of gangrene necrosis

A

lower limb ischemia or GI tract

65
Q

how do you get wet gangrene?

A

superimposed infection on gangrenous necrosis leads to liquefactive necrosis

66
Q

soft and friable necrotic tissue with cottage cehese-like appearance

A

caseous nerosis

comb of coagulative and liquefactive necrosis

67
Q

example of caseous necrosis

A

characteristic of granulomatous inflammation due to tuberculosis or fungal infection

68
Q

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

A

fat necrosis with saponification

69
Q

dystrophic calcification

A

necrotic tissue acts as a nidus for calcium deposition in the setting of normal serum calcium
ex: psamomma body

70
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

71
Q

fat necrosis caused by

A

trauma or pancreatitis-mediated damage of peripancreatic fat

72
Q

saponification

A

fatty acids released by trauma or lipase join with calcium. Ex: dystrophic calcification

73
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

74
Q

fibrinoid necrosis is characteristic of ___

A

malignant hypertension (if young woman think preeclampsia and placental fibrinoid necrosis) or vasculitis

75
Q

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

A

apoptosis

76
Q

what does a cell undergoing apoptosis look like?

A

dying cell shrinks and cytoplasm becomes eosinophilic
(pink from condensing)
nucleus condenses and fragments

77
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

78
Q

apoptosis is mediated by

A

caspases

79
Q

caspases activate

A

proteases: break down cytoskeleton
endonucleases: break down DNA

80
Q

what are the ways caspase are activated?

A

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

81
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

82
Q

Bcl 2

A

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

83
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

84
Q

CD95

A

Fas death receptor

85
Q

cytotoxic T cell mediated pathway of caspase activation

A

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

granzyme from CD8+ T cell enters pores and activates caspases

86
Q

free radicals

A

chemical species with an unpaired electron in their outer orbit

87
Q

physiologic generation of free radicals

A

oxidative phosphorylation

  • cyt c oxidase
  • partial reduction of O2 yields superoxide, hydrogen peroxide, and hydroxyl radicals
88
Q

4 ways that free radicals are generated pathologically

A

ionizing radiation
(.OH)
inflammation- NAPDPH oxidase generates superoxide ions in O2 dependent killing by neutrophils
metals
(copper and iron)
drugs and chemicals (acetaminophen)

89
Q

free radicals cause cellular injury by

A

peroxidation of lipids

oxidation of DNA and protein

90
Q

how do you eliminate free radicals?

A

antioxidants (glutathione, vit. A, C, E)
enzymes
metal carrier proteins (transferrin and ceruloplasmin)

91
Q

enzymes that eliminate free radicals

A 
superoxide dismutase 
(mito): O2-. --> H2O2
glutathione peroxidase
 (mito): GSH + free radical --> GSSH + H2O
catalase(peroxisome): H2O2 --> O2 + H2O
92
Q

sequence of free radicals

A

O2 –> O2-. –> H2O2 –> OH. –> H2O

93
Q

carbon tetrachloride

A

organic solvent used in dry cleaning that is converted to a free radical CCl3. in the liver and causes swelling of RER
ribosomes detach and protein synthesis is impaired leading to decreased apolipoproteins –> fatty change occurs

94
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

95
Q

a misfolded protein that deposits in extracellular space –> damages tissues

A

amyloid

96
Q

features of amyloid proteins

A

beta pleated sheet configuration
congo red staining and apple green birefringence with polarized light
often deposits around blood vessels

97
Q

primary amyloidosis

A

systemic deposition of AL amyloid

-derived from Ig light chains

98
Q

primary amyloidosis is associated with

A

plasma cell dyscrasia (multiple myeloma): over production of the light chain –> leaks out and misfolds

99
Q

secondary amyloidosis

A

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

100
Q

SAA

A

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

101
Q

Familial Mediterranean fever

A

AR. dysfunction of neutrophils
presents with: fever, acute serosal inflammation (mimics appendicitis, arthritis, myocardial infarction), high SAA –> AA

102
Q

clinical findings of systemic amyloidosis

A 
nephrotic syndrome (most common)
restrictive cardiomyopathy or arrhythmia
tongue enlargement, malabsorption, hepatosplenomegaly
103
Q

diagnosis of amyloidosis?

A

requires tissue biopsy, abdominal fat pad and rectum are accessible

104
Q

treatment for amyloidosis?

A

damaged organ must be transplanted

105
Q

localized amyloidosis

A

single organ

106
Q

senile cardiac amyloidosis

A

non-mutated serum transthyretin deposits in the heart, usually asymptomatic

107
Q

familial amyloid cardiomyopathy

A

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

108
Q

non-insulin-dependent diabetes mellitus amyloidosis

A

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

109
Q

alzheimer’s amyloidosis

A

A-beta amyloid deposits in the brain

gene is on chromosome 21 (A beta amyloid is derived from beta-amyloid precursor protein)

110
Q

clinical significance of A beta amyloid on chromosome 21?

A

alzheimer’s occurs in patients with Down’s syndrome at around age 40

111
Q

dialysis associated amyloidosis

A

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

112
Q

medullary carcinoma of the thyroid amyloidosis

A

calcitonin (produced by tumor cells) deposits in the tumor

113
Q

FNA of thyroid shows “tumor cells in amyloid background”

A

medullary carcinoma of the thyroid

Pathoma (2 decks)

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