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Pathoma > Chapter 1 > Flashcards

Chapter 1 Flashcards

1
Q

What are the two ways that an organ can increase in size?

A

Hyperplasia and hypertrophy

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2
Q

Steps involved in hypertrophy?

A

Gene activation, protein synthesis, production or organelles

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3
Q

What kind of growth is undergone by permanent tissues?

A

Only hypertrophy in cardiac muscle, skeletal muscles, and nerves

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4
Q

What can pathologic hyperplasia lead to?

A

Dysplasia and possibly cancer

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5
Q

What tissue hyperplasia has no increased risk of cancer?

A

BPH

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6
Q

What are the two forms of atrophy?

A

Decrease in cell number via apoptosis

Decrease in cell size via ubiquitin proteosome degradation of the cytoskeleton or autophagy.

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7
Q

How does ubitquitin proteosome degradation occur?

A

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

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8
Q

Autophagy

A

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

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9
Q

a 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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10
Q

most common cells to undergo metaplasia?

A

surface epithelium

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11
Q

Barret’s esophagus is an example of metaplasia?

A

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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12
Q

metaplasia occurs via_______ ≈

A

reprogramming cells

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13
Q

Is metaplasia reversible?

A

Yes, with removal of stressor

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14
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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15
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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16
Q

Mesenchymal(connective tissue) metaplasia example?

A

Myositis ossifican in which CT in muscle changes to bone during healing after trauma.

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17
Q

dysplasia

A

disordered cell growth, most often refers to proliferation of precancerous cells

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18
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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19
Q

Aplasia vs hypoplasia

A

Aplasia: failure of cell production during embryogenesis
Hypoplasia: decrease in cell production during embryogenesis, resulting in small organ

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20
Q

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

A

cellular injury

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21
Q

slowly vs. acutely developing ischemia

A 
Slow= atrophy: renal atherosclerosis
Acute= ischemia: renal artery embolus
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22
Q

What is the final electron acceptor in the electron transport chain?

A

Oxygen

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23
Q

How does decreased oxygen lead to lack of ATP?

A

Impairment of Oxidative phosphorylation

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24
Q

3 causes of ischemia

A

Decreased arterial perfusion- arteriosclerosis
Decreased venous drainage- budd chiari- PV thrombosis seen with polycythemia vera
Shock- generalized hypotension= poor perfusion

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25
Q

hypoxemia

A

PaO2 <60 mmHg, SaO2 < 90%,low partial pressure of oxygen in the blood

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26
Q

Causes of Hypoemia

A

High altitude, hypoventilation, difusion defect, V/Q mismatch

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27
Q

cherry–red appearance of the skin and headache

A

CO poisoning, leads to coma and death

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28
Q

cyanosis with chocolate colored blood

A

Methemogolinemia

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29
Q

Why can’t heme bind O2 in methemoglobin

A

Fe3+ is present, only Fe2+ binds O2.

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30
Q

Treatment for methemoglobin

A

methylene blue

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31
Q

Labs in Carbon Monoxide posioning

A

Normal PaO2, decreased Sao2

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32
Q

Labs in Methemoglobinemia

A

PaO2 normal, Sao2 decreased

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33
Q

why do newborns get methemoglobinemia

A

there is oxidant stress (sulfa or nitratae drugs) and adults have enzymes to reduce but newborns are immature.

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34
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
anaerobic glycolysis impaired– switch to anaerobic causing lactic acidosis, which denatures proteins and precipitates DNA

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35
Q

What is the hallmark of reversible injury?

A

Swelling

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36
Q

What happens with cellular swelling?

A

cytosol swells: loss o microvilli and membrane blebbing and swelling of RER, causing the dissociation of ER and ribosomes and decreased protein synthesis

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37
Q

hallmark of irreversible injury

A

membrane damage (plasma membrane, mitochondrial membrane, and lysosome membrane)

38
Q

plasma membrane damage results in?

A

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

39
Q

mitochondiral membrane damage results in?

A

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

40
Q

lysosome membrane damage results in

A

hydrolytic enzymes leaking into the cytosol and being activated by calcium

41
Q

normal calcium concentration in the cell

A

Very low– calcium is a messenger and turns on lots of pathways

42
Q

hallmark of cell death

A

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

43
Q

necrosis is always followed by

A

acute inflammation

44
Q

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

A

coagulative necrosis

45
Q

area of infarcted tissue in coagulative necrosis

A

wedge–shaped and pale

46
Q

red infarction

A

if blood reenters a loosely organized tissue

47
Q

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

A

liquefactive necrosis

48
Q

characteristic of ischemia anywhere except the brain

A

coagulative necrosis

49
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

50
Q

coagulative necrosis that resembles mummified tissue

A

“dry grangrene”, gangrene necrosis

51
Q

example of gangrene necrosis

A

lower limb ischemia

52
Q

Caseous necrosis

A

soft and friable necrotic tissue with cottage cheese–like appearance. Combination of coagulative and liquefactive necrosis. Sign of tb or fungal infection

53
Q

characteristic of granulomatous inflammation due to tuberculosis or fungal infection
necrotic adipose tissue with a chalky–white appearance due to deposition of calcium

A

fat necrosis with saponification

54
Q

dystrophic calcification

A

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

55
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

56
Q

fat necrosis caused by

A

trauma or pancreatitis–mediated damage of peripancreatic fat

57
Q

fibrinoid necrosis

A

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

58
Q

apoptosis

A

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

59
Q

what does a cell undergoing apoptosis look like?

A

dying cell shrinks and cytoplasm becomes eosinophilic

nucleus condenses and fragments

60
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

61
Q

apoptosis is mediated by

A

caspases

62
Q

caspases activate

A

proteases: break down cytoskeleton
endonucleases: break down DNA

63
Q

what are the ways caspase are activated?

A

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

64
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
65
Q

Bcl 2

A

inhibits cyt c from leaking from the inner mitochondrial membrane into the cytoplasm
extrinsic receptor–ligand pathway of caspase activation Fas ligand binds FAS death receptor (CD95) to activate caspase
tumor necrosis factor (TNF) binds TNF receptor on the target cell to activate caspases

66
Q

CD95

A

Fas death receptor

67
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

68
Q

free radicals

A

chemical species with an unpaired electron in their outer orbit

69
Q

physiologic generation of free radicals

A

oxidative phosphorylation, cyt c oxidase, partial reduction of O2 yields superoxie, hydrogen peroxide, and hydroxyl radicals

70
Q

4 ways that free radicals are generated pathologically

A

ionizing radiation
inflammation– NAPDPH oxidase generates superoxide ions in O2 dependent killing by neutrophils
metals
drugs and chemicals

71
Q

free radicals cause cellular injury by

A

peroxidation of lipids and oxidation of DNA and protein

72
Q

enzymes that eliminate free radiations

A

superoxide dismutase
glutathione peroxidase
catalase

73
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

74
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

75
Q

a misfolded protein that deposits in extracellular space and damages tissues

A

amyloid

76
Q

Features of amyload

A

beta pleated sheet configuration

congo red staining and apple green birefringence with polarized light

77
Q

primary amyloidosis

A

systemic deposition of AL amyloid- derived from Ig light chains

78
Q

primary amyloidosis is associated with

A

plasma cell dyscrasia (multiple myeloma)

79
Q

secondary amyloidosis

A

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

80
Q

SAA

A

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

81
Q

Familial Mediterranean fever

A

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

82
Q

clinical findings of sysmteic amyloidosis

A

nephrotic syndrome (most common)\nrestrictive cardiomyopathy or arrhythmia\ntongue enlargement, malabsorption, hepatosplenomegaly

83
Q

treatment for amyloidosis?

A

damaged organ must be transplanted

84
Q

localized amyloidosis

A

single organ

85
Q

senile cardiac amyloidosis

A

non–mutated serum transthyretindeposits in the heart, usually asymptomatic

86
Q

familial amyloid cardiomyopathy

A

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

87
Q

non–insulin–dependent diabetes mellitus amyloidosis

A

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

88
Q

alzheimer’s amyloidosis

A

A–beta amyloid deposits in the brain

***gene is on chromosome 21

89
Q

dialysis associated amyloidosis

A

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

90
Q

medullary carcinoma of the thyroid amyloidosis

A

calcitonin (produced by tumor cells) deposits in the tumor

91
Q

FNA of thyroid shows tumor cells in amyloid background

A

medullary carcinoma of the thyroid

Pathoma (2 decks)

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