1. Growth Adaptations, Cellular Injury, and Cell Death Flashcards

(56 cards)

1
Q

List the permanent tissues (that can undergo hypertrophy but not hyperplasia).

A

1) Cardiac muscle
2) Skeletal muscle
3) Myocytes

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2
Q

What is the exception to the rule that pathologic hyperplasia can progress to dysplasia and cancer?

A

Benign Prostatic Hyperplasia (BPH) does NOT increase the risk for prostate cancer

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3
Q

How does a decrease in cell size occur?

A

ubiquitin-proteosome degradation of the cytoskeleton and autophagy of cellular components

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4
Q

True or false: metaplasia is irreversible.

A

FALSE (it is reversible with the removal of the driving stressor)

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5
Q

What is the exception to the rule that metaplasia can progress to dysplasia and cancer?

A

Apocrine metaplasia of the breast carries NO increased risk for cancer

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6
Q

What are the 2 major consequences of Vitamin A deficiency?

A
  • Night blindness

- Maturation of immune system gets dysregulated

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7
Q

True or false: dysplasia is reversible.

A

TRUE (with alleviation of the inciting stress)

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8
Q

What cell type is most susceptible to ischemic injury (can survive only 3-5 minutes with no oxygen)?

A

Neurons

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9
Q

How does the response to quickly occurring ischemia differ from the response to slowly occurring ischemia?

A

Quickly occurring ischemia often leads to injury while slowly occurring ischemia often leads to growth adaptations

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10
Q

What are the 2 most common causes of Budd Chiari syndrome?

A
  • Polycythemia vera

- Lupus anticoagulant

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11
Q

What is the characteristic PaO2 and SaO2 with anemia?

A

PaO2 and SaO2 are both normal

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12
Q

What is the characteristic PaO2 and SaO2 of CO poisoning?

A

PaO2 is normal and SaO2 is decreased

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13
Q

What is the characteristic PaO2 and SaO2 with methemoglobinemia?

A

PaO2 is normal and SaO2 is decreased

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14
Q

What is the underlying problem in methemoglobinemia?

A

oxidant stress (drugs) or immature machinery (newborns) leads to oxidation of the heme in iron which decreases oxygen binding capacity

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15
Q

How do you treat methemoglobinemia?

A

IV methylene blue

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16
Q

What is the hallmark of reversible cell injury?

A

cellular swelling (Na+/K+ ATPase can’t work so Na+ and water build up in cell)

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17
Q

What is the hallmark of irreversible cell injury?

A

membrane damage

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18
Q

Where is the ETC located?

A

inner mitochondrial membrane

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19
Q

What is the word for nuclear condensation?

A

pyknosis

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20
Q

What is the word for nuclear fragmentation?

A

karyorrhexis

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21
Q

What is the word for nuclear dissolution?

A

karyolysis

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22
Q

What ALWAYS follows necrosis?

A

inflammation

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23
Q

What is the pattern of necrosis where the tissue remains firm and the cell shape and organ structure are preserved (often pale and wedge-shaped)?

A

coagulative necrosis

24
Q

What leads to coagulative necrosis?

A

ischemic infarction

25
What organ does NOT undergo coagulative necrosis after ischemic infarction?
brain (liquefactive necrosis)
26
What pattern of necrosis is coagulative but resembles mummified tissue?
gangrenous necrosis
27
What pattern of necrosis is due to enzymatic lysis of cells and protein?
Liquefactive necrosis
28
What two types of necrosis are seen in pancreatitis?
liquefactive necrosis of parenchyma | fat necrosis peripancreatic fat
29
What pattern of necrosis is soft and friable with a "cottage-cheese like appearance"?
caseous necrosis
30
Caseous necrosis is characteristic of which types of inflammation?
granulomatous inflammation due to Tb or fungal infection
31
What does fat necrosis look like?
chalky white due to deposition of calcium
32
What is saponification?
example of dystrophic calcification in which calcium deposits on dead tissue (in the setting of NORMAL serum calcium and phosphate)
33
What causes endometrial shedding (cellular level) during menses?
apoptosis
34
What happens to virally infected cells?
recognized by CD8+ T cells and signaled to undergo apoptosis
35
Why is apoptosis NOT followed by inflammaiton?
apoptotic bodies are consumed by macrophages
36
What is the MAJOR mediator of apoptosis? What does it do?
caspases (activate proteases that break down the cytoskeleton and activates endonucleases that break down DNA)
37
List the 3 pathways of apoptosis.
- Intrinsic mitochondrial pathway - Extrinsic receptor-ligand pathway - CD8+ T cell-mediated pathway
38
What is involved in the intrinsic mitochondrial pathway of apoptosis?
Bcl2 inactivated by stress, Cytochrone c is allowed to leak from mitochondria to the cytoplasm to activate caspases
39
What is involved in the extrinsic receptor-ligand pathway of apoptosis?
FAS ligand binds FAS death receptor (CD95) on target cell and activates caspases OR TNF binds to TNFR on target cell and activates caspases
40
What is involved in the CD8+ T cell-mediated pathway of apoptosis?
CD8+ T cells recognize Ag on MHC Class 1, release perforins to create pores in membrane of target cells and granzymes to enter these pores and activate caspases
41
What is the most damaging free radical?
hydroxyl free radical
42
What causes oxygen to become superoxide?
partial reduction
43
What causes superoxide to become hydrogen peroxide?
superoxide dismutase
44
What causes hydrogen peroxide to become hydroxyl free radical?
catalase
45
What causes Hydroxyl free radical to change into H2O and GS-SG?
Glutathione Peroxidase
46
Why does CCl4 lead to fatty change in the liver?
decreased apolipoprotein synthesis occurs (due to cellular injury) and fat is allowed into the liver but cannot get out
47
What are the 2 major features shared by all amyloid?
- Beta-pleated sheet configuration | - Congo red staining and apple green birefringence with polarized light
48
What is deposited in primary amyloidosis?
AL amyloid (from immunoglobulin light chain)
49
What is deposited in secondary amyloidosis?
AA amyloid (from SAA acute phase reactant)
50
In what AR disease do you see an increase in SAA and increaed risk of AA amyloidosis?
Familial Mediterranean Fever (mimics serosal inflammation like appendicitis)
51
What is the most common organ involved in amyloidosis?
Kidney (nephrotic syndrome)
52
What is deposited in Senile cardiac amyloidosis?
non-mutated serum transthyretin
53
What is deposited in familial amyloid cardiomyopathy?
mutated serum transthyretin
54
What is deposited in Alzheimer disease?
A-beta amyloid
55
What is deposited in dialysis-associated amyloid?
beta-2 microglobulin (what supports MHC class 1)
56
How do you biopsy the thyroid?
fine needle aspiration