Chapter 1: Growth Adaptations, Cellular Injury, Cell Death Flashcards
(82 cards)
1
Q
Hypertrophy involves which three cellular processes
A
- gene activation
- protein synthesis
- production of organelles
2
Q
permanent tissues
A
- cardiac muscle
- skeletal muscle
- nerve
3
Q
one situation in which hyperplasia does not progress to dysplasia and cancer
A
BPH
4
Q
mechanism by which a cell degrades its cytoskeleton
A
ubiquitin proteosome degredation
5
Q
ubiquitin proteosome degredation tags which part of the cytoskeleton
A
intermediate filaments
6
Q
vitamin A deficiency causes these 3 things
A
- night blindness
- production of immature immune cells
- keratomalacia (metaplasia of conjunctiva of eye)
7
Q
AML is caused by
A
15, 17 translocation; disrupts retinoic acid receptor and prevents the vitamin A mediated maturation of immune cells
8
Q
likelihood of cellular injury depends on
A
- type of stress
- severity
- cell type
9
Q
low delivery of O2 to tissues
A
hypoxia
10
Q
three main causes of hypoxia
A
- ischemia
- hypoxemia
- decreased O2 carrying capacity
11
Q
three ways ischemia can occur
A
- block artery
- block vein
- shock
12
Q
infarction of liver parenchyma via hepatic v. thrombosis
A
Budd Chiari syndrome
13
Q
some major causes of Budd Chiari syndrome
A
- polycythemia vera
2. lupus (pt is hypercoagulable)
14
Q
decreased perfusion of vital organs
A
shock
15
Q
low partial pressure of O2 in blood
A
hypoxemia
16
Q
threshold for hypoxemia
A
< 60 mm Hg (or < 90% SaO2)
17
Q
what is SaO2
A
O2 saturation = % hemoglobin saturated with O2)
18
Q
what effects PAO2
A
increases in CO2 in alveolar air space (hypoventilation, COPD, etc.)
19
Q
in anemia, PaO2 is _________ and SaO2 is ________
A
both normal
20
Q
signs of CO exposure
A
- cherry red skin
2. early sign = headache
21
Q
high proportion of Fe3+ in heme
A
methemoglobinemia
22
Q
causes of methemoglobinemia
A
- oxidant stress (sulfa and nitrate drugs)
2. newborns (don’t have the machinery needed to reduce Fe3+)
23
Q
clinical sign of methemoglobinemia
A
- chocolate colored blood
2. cyanosis
24
Q
tx of methemoglobinemia
A
IV methylene blue (helps reduce Fe)
25
increased cytosolic Ca2+ can lead to
enzyme activation
26
decreased ATP and, therefore, decreased activity of Na/K pump can lead to
cellular swelling
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cellular swelling leads to
1. loss of microvilli
2. membrane blebbing
3. RER swelling which pops off ribosomes and leads to decreased protein synthesis
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hallmark of irreversible injury
membrane damage
29
consequence of mitochondrial membrane damage
cytochrome C leaks into cytosol and activates apoptosis
30
consequence of lysosomal membrane damage
leaking of lytic enzymes into cytosol (activation exacerbated by increased Ca2+ that enters via plasma membrane damage)
31
three things that happen to nucleus during cell death
1. pyknosis (shrink)
2. karyorrhexis (fragment)
3. karyolysis (broken down to basic building blocks)
32
necrosis is always followed by
acute inflammation
33
six types of necrosis
1. coagulative
2. liquefactive
3. gangrenous
4. casseous
5. fat
6. fibrinoid
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two forms of coagulative necrosis
white and red
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organ that undergoes liquefactive necrosis
brain (and pancreas)
36
what causes liquefactive necrosis in brain tissue
microglia
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three examples of liquefactive necrosis
1. brain infarction
2. abscess
3. pancreatitis
38
what causes liquefactive necrosis in an abscess
enzymes from neutrophils
39
gangrenous necrosis is most common in
lower limb and GI tract
40
wet gangrene is
gangrenous (coagulative) necrosis with superimposed infection
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casseous necrosis is characteristic of
granulomatous inflammation from TB or fungal infections
42
saponification
when Ca2+ binds with fatty acids released during fat necrosis
43
in dystrophic calcification, Ca2+ levels are ________ and PO4 levels are _________
both normal
44
fat necrosis commonly occurs where
1. peripancreatic fat during pancreatitis
| 2. breast (trauma)
45
areas of fat necrosis can show these cells on pathology
giant cells (part of inflammatory response to fat necrosis)
46
fibrinoid necrosis
necrotic damage to BV where proteins leak into vessel wall resulting in bright pink staining
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fibrinoid necrosis can be caused by
1. malignant hypertension
2. vasculitis
3. preeclampsia
48
apoptosis is mediated by
caspases
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caspases can be activated in 3 ways
1. intrinsic mitochondrial
2. extrinsic receptor ligand
3. cytotoxic CD8+ pathway
50
stabilizes inner mitochondrial membrane
Bcl2
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downregulation of Bcl2 causes
destabilization of mitochondrial membrane and subsequent leakage of cytochrome C
52
results in negative selection of T-cells
FAS ligand binds CD95 (FAS death receptor)
53
mechanism of CD8+ T-cell induced apoptosis
binds to MHC-I presenting viral protein, releases perforins to poke holes in cell membrane followed by granzyme that activates caspases
54
4 causes of pathologic free radical injury
1. radiation
2. inflammation
3. metals (Cu and Fe)
4. drugs/chemicals
55
most damaging free radical is _________ and it is generated from _________
hydroxyl free radical, water
56
mechanism of oxidative burst
O2 --> O2- using NADPH oxidase, O2- --> H2O2 using superoxide dismutase, H2O2 --> HOCl using myeloperoxidase
57
Fenton reaction
unbound iron generates free radicals
58
disease of excess Fe is called _________; disease of excess Cu is called __________
hemochromatosis, Wilson's disease
59
two basic things that free radicals do
1. lipid peroxidation (damage cell membranes)
| 2. oxidation of DNA and proteins
60
how do we eliminate free radicals?
1. antioxidants (A, C, E)
2. metal carrier proteins
3. enzymes
61
what are the enzymes used to eliminate free radicals
1. SOD
2. glutatione peroxidase (handles hydroxyl free radical)
3. catalase (H2O2)
62
describe how CCl4 is damaging
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
mechanism of reperfusion injury
O2 and inflammatory cells rush in and generate free radicals; leads to continued injury
64
IHC for amyloid
congo red staining with apple green birifringence under polarized light
65
amyloid commonly deposits around
blood vessels
66
two major forms of amyloidosis
1. systemic
| 2. local
67
two major forms of systemic amyloidosis
1. primary
| 2. secondary
68
primary amyloidosis is characterized by _______ amyloid, which comes from ________ and is associated with ___________
AL, Ig light chain, plasma cell dyscrasias
69
secondary amyloidosis is characterized by _______ amyloid, which comes from _______ and is associated with states of ___________
AA, SAA, chronic inflammation
70
describe familial Mediterranean fever
AR genetic dysfunction of neutrophils that leads to acute serosal inflammation and can mimic heart attack, appendicitis etc. depending on location
71
most common clinical findings in systemic amyloidosis
1. kidney most common (nephrotic syndrome)
2. restrictive cardiomyopathy and arrhythmia
3. tongue enlargement
4. thickened bowel leading to malabsorption
5. hepatosplenomegaly
72
diagnosis of systemic amyloidosis
biopsy of abdominal fat pad or rectum
73
6 types of localized amyloidosis
1. senile cardiac amyloidosis
2. familial amyloid cardiomyopathy
3. type II diabetes
4. AD
5. dialysis associated
6. medullary carcinoma of thyroid
74
senile cardiac amyloidosis involves deposits of ___________ in the _________ and is __________
normal seum transthyretin, heart, asymptomatic
75
familial amyloid cardiomyopathy involves deposits of _________ leading to __________
mutated serum transthyretin, restrictive cardiomyopathy
76
familial amyloid cardiomyopathy is most common in
African Americans (5%)
77
in type II diabetes, amyloid deposits form from ________ and are deposited in the __________
amylin, islets of pancreas
78
how is amylin produced
as a byproduct of insulin production
79
AD amyloid
A-beta amyloid from amyloid precursor protein (APP) on chromosome 21
80
dialysis associated amyloidosis
beta2 microglobulin (stabilizes MHC-1) deposits in joints
81
medullary carcinoma of thyroid amyloid
tumor of c-cells produces lots of calcintonin which deposits as amyloid in thyroid (tumor cells in amyloid background)
82
how is the thyroid biopsied?
fine needle aspiration
