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

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

1
Q

Hypertrophy involves which three cellular processes

A
  1. gene activation
  2. protein synthesis
  3. production of organelles
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2
Q

permanent tissues

A
  1. cardiac muscle
  2. skeletal muscle
  3. nerve
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3
Q

one situation in which hyperplasia does not progress to dysplasia and cancer

A

BPH

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4
Q

mechanism by which a cell degrades its cytoskeleton

A

ubiquitin proteosome degredation

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5
Q

ubiquitin proteosome degredation tags which part of the cytoskeleton

A

intermediate filaments

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6
Q

vitamin A deficiency causes these 3 things

A
  1. night blindness
  2. production of immature immune cells
  3. keratomalacia (metaplasia of conjunctiva of eye)
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7
Q

AML is caused by

A

15, 17 translocation; disrupts retinoic acid receptor and prevents the vitamin A mediated maturation of immune cells

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8
Q

likelihood of cellular injury depends on

A
  1. type of stress
  2. severity
  3. cell type
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9
Q

low delivery of O2 to tissues

A

hypoxia

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10
Q

three main causes of hypoxia

A
  1. ischemia
  2. hypoxemia
  3. decreased O2 carrying capacity
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11
Q

three ways ischemia can occur

A
  1. block artery
  2. block vein
  3. shock
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12
Q

infarction of liver parenchyma via hepatic v. thrombosis

A

Budd Chiari syndrome

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13
Q

some major causes of Budd Chiari syndrome

A
  1. polycythemia vera

2. lupus (pt is hypercoagulable)

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14
Q

decreased perfusion of vital organs

A

shock

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15
Q

low partial pressure of O2 in blood

A

hypoxemia

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16
Q

threshold for hypoxemia

A

< 60 mm Hg (or < 90% SaO2)

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17
Q

what is SaO2

A

O2 saturation = % hemoglobin saturated with O2)

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18
Q

what effects PAO2

A

increases in CO2 in alveolar air space (hypoventilation, COPD, etc.)

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19
Q

in anemia, PaO2 is _________ and SaO2 is ________

A

both normal

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20
Q

signs of CO exposure

A
  1. cherry red skin

2. early sign = headache

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21
Q

high proportion of Fe3+ in heme

A

methemoglobinemia

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22
Q

causes of methemoglobinemia

A
  1. oxidant stress (sulfa and nitrate drugs)

2. newborns (don’t have the machinery needed to reduce Fe3+)

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23
Q

clinical sign of methemoglobinemia

A
  1. chocolate colored blood

2. cyanosis

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24
Q

tx of methemoglobinemia

A

IV methylene blue (helps reduce Fe)

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25
Q

increased cytosolic Ca2+ can lead to

A

enzyme activation

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26
Q

decreased ATP and, therefore, decreased activity of Na/K pump can lead to

A

cellular swelling

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27
Q

cellular swelling leads to

A
  1. loss of microvilli
  2. membrane blebbing
  3. RER swelling which pops off ribosomes and leads to decreased protein synthesis
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28
Q

hallmark of irreversible injury

A

membrane damage

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29
Q

consequence of mitochondrial membrane damage

A

cytochrome C leaks into cytosol and activates apoptosis

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30
Q

consequence of lysosomal membrane damage

A

leaking of lytic enzymes into cytosol (activation exacerbated by increased Ca2+ that enters via plasma membrane damage)

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31
Q

three things that happen to nucleus during cell death

A
  1. pyknosis (shrink)
  2. karyorrhexis (fragment)
  3. karyolysis (broken down to basic building blocks)
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32
Q

necrosis is always followed by

A

acute inflammation

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33
Q

six types of necrosis

A
  1. coagulative
  2. liquefactive
  3. gangrenous
  4. casseous
  5. fat
  6. fibrinoid
34
Q

two forms of coagulative necrosis

A

white and red

35
Q

organ that undergoes liquefactive necrosis

A

brain (and pancreas)

36
Q

what causes liquefactive necrosis in brain tissue

A

microglia

37
Q

three examples of liquefactive necrosis

A
  1. brain infarction
  2. abscess
  3. pancreatitis
38
Q

what causes liquefactive necrosis in an abscess

A

enzymes from neutrophils

39
Q

gangrenous necrosis is most common in

A

lower limb and GI tract

40
Q

wet gangrene is

A

gangrenous (coagulative) necrosis with superimposed infection

41
Q

casseous necrosis is characteristic of

A

granulomatous inflammation from TB or fungal infections

42
Q

saponification

A

when Ca2+ binds with fatty acids released during fat necrosis

43
Q

in dystrophic calcification, Ca2+ levels are ________ and PO4 levels are _________

A

both normal

44
Q

fat necrosis commonly occurs where

A
  1. peripancreatic fat during pancreatitis

2. breast (trauma)

45
Q

areas of fat necrosis can show these cells on pathology

A

giant cells (part of inflammatory response to fat necrosis)

46
Q

fibrinoid necrosis

A

necrotic damage to BV where proteins leak into vessel wall resulting in bright pink staining

47
Q

fibrinoid necrosis can be caused by

A
  1. malignant hypertension
  2. vasculitis
  3. preeclampsia
48
Q

apoptosis is mediated by

A

caspases

49
Q

caspases can be activated in 3 ways

A
  1. intrinsic mitochondrial
  2. extrinsic receptor ligand
  3. cytotoxic CD8+ pathway
50
Q

stabilizes inner mitochondrial membrane

A

Bcl2

51
Q

downregulation of Bcl2 causes

A

destabilization of mitochondrial membrane and subsequent leakage of cytochrome C

52
Q

results in negative selection of T-cells

A

FAS ligand binds CD95 (FAS death receptor)

53
Q

mechanism of CD8+ T-cell induced apoptosis

A

binds to MHC-I presenting viral protein, releases perforins to poke holes in cell membrane followed by granzyme that activates caspases

54
Q

4 causes of pathologic free radical injury

A
  1. radiation
  2. inflammation
  3. metals (Cu and Fe)
  4. drugs/chemicals
55
Q

most damaging free radical is _________ and it is generated from _________

A

hydroxyl free radical, water

56
Q

mechanism of oxidative burst

A

O2 –> O2- using NADPH oxidase, O2- –> H2O2 using superoxide dismutase, H2O2 –> HOCl using myeloperoxidase

57
Q

Fenton reaction

A

unbound iron generates free radicals

58
Q

disease of excess Fe is called _________; disease of excess Cu is called __________

A

hemochromatosis, Wilson’s disease

59
Q

two basic things that free radicals do

A
  1. lipid peroxidation (damage cell membranes)

2. oxidation of DNA and proteins

60
Q

how do we eliminate free radicals?

A
  1. antioxidants (A, C, E)
  2. metal carrier proteins
  3. enzymes
61
Q

what are the enzymes used to eliminate free radicals

A
  1. SOD
  2. glutatione peroxidase (handles hydroxyl free radical)
  3. catalase (H2O2)
62
Q

describe how CCl4 is damaging

A

converted to CCl3 in liver by p450 system, free radical generation causes cellular swelling, leading to decreased protein synthesis (from ER swelling), which leads to decreased apolipoproteins and resultant fatty liver (fat can’t be transported out)

63
Q

mechanism of reperfusion injury

A

O2 and inflammatory cells rush in and generate free radicals; leads to continued injury

64
Q

IHC for amyloid

A

congo red staining with apple green birifringence under polarized light

65
Q

amyloid commonly deposits around

A

blood vessels

66
Q

two major forms of amyloidosis

A
  1. systemic

2. local

67
Q

two major forms of systemic amyloidosis

A
  1. primary

2. secondary

68
Q

primary amyloidosis is characterized by _______ amyloid, which comes from ________ and is associated with ___________

A

AL, Ig light chain, plasma cell dyscrasias

69
Q

secondary amyloidosis is characterized by _______ amyloid, which comes from _______ and is associated with states of ___________

A

AA, SAA, chronic inflammation

70
Q

describe familial Mediterranean fever

A

AR genetic dysfunction of neutrophils that leads to acute serosal inflammation and can mimic heart attack, appendicitis etc. depending on location

71
Q

most common clinical findings in systemic amyloidosis

A
  1. kidney most common (nephrotic syndrome)
  2. restrictive cardiomyopathy and arrhythmia
  3. tongue enlargement
  4. thickened bowel leading to malabsorption
  5. hepatosplenomegaly
72
Q

diagnosis of systemic amyloidosis

A

biopsy of abdominal fat pad or rectum

73
Q

6 types of localized amyloidosis

A
  1. senile cardiac amyloidosis
  2. familial amyloid cardiomyopathy
  3. type II diabetes
  4. AD
  5. dialysis associated
  6. medullary carcinoma of thyroid
74
Q

senile cardiac amyloidosis involves deposits of ___________ in the _________ and is __________

A

normal seum transthyretin, heart, asymptomatic

75
Q

familial amyloid cardiomyopathy involves deposits of _________ leading to __________

A

mutated serum transthyretin, restrictive cardiomyopathy

76
Q

familial amyloid cardiomyopathy is most common in

A

African Americans (5%)

77
Q

in type II diabetes, amyloid deposits form from ________ and are deposited in the __________

A

amylin, islets of pancreas

78
Q

how is amylin produced

A

as a byproduct of insulin production

79
Q

AD amyloid

A

A-beta amyloid from amyloid precursor protein (APP) on chromosome 21

80
Q

dialysis associated amyloidosis

A

beta2 microglobulin (stabilizes MHC-1) deposits in joints

81
Q

medullary carcinoma of thyroid amyloid

A

tumor of c-cells produces lots of calcintonin which deposits as amyloid in thyroid (tumor cells in amyloid background)

82
Q

how is the thyroid biopsied?

A

fine needle aspiration

Pathoma (1 decks)

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