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Pathoma High Yield > 1. Growth Adaptations, Cellular Injury, and Cell Death > Flashcards

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

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
Q

What organ does NOT undergo coagulative necrosis after ischemic infarction?

A

brain (liquefactive necrosis)

26
Q

What pattern of necrosis is coagulative but resembles mummified tissue?

A

gangrenous necrosis

27
Q

What pattern of necrosis is due to enzymatic lysis of cells and protein?

A

Liquefactive necrosis

28
Q

What two types of necrosis are seen in pancreatitis?

A

liquefactive necrosis of parenchyma

fat necrosis peripancreatic fat

29
Q

What pattern of necrosis is soft and friable with a “cottage-cheese like appearance”?

A

caseous necrosis

30
Q

Caseous necrosis is characteristic of which types of inflammation?

A

granulomatous inflammation due to Tb or fungal infection

31
Q

What does fat necrosis look like?

A

chalky white due to deposition of calcium

32
Q

What is saponification?

A

example of dystrophic calcification in which calcium deposits on dead tissue (in the setting of NORMAL serum calcium and phosphate)

33
Q

What causes endometrial shedding (cellular level) during menses?

A

apoptosis

34
Q

What happens to virally infected cells?

A

recognized by CD8+ T cells and signaled to undergo apoptosis

35
Q

Why is apoptosis NOT followed by inflammaiton?

A

apoptotic bodies are consumed by macrophages

36
Q

What is the MAJOR mediator of apoptosis? What does it do?

A

caspases (activate proteases that break down the cytoskeleton and activates endonucleases that break down DNA)

37
Q

List the 3 pathways of apoptosis.

A
  • Intrinsic mitochondrial pathway
  • Extrinsic receptor-ligand pathway
  • CD8+ T cell-mediated pathway
38
Q

What is involved in the intrinsic mitochondrial pathway of apoptosis?

A

Bcl2 inactivated by stress, Cytochrone c is allowed to leak from mitochondria to the cytoplasm to activate caspases

39
Q

What is involved in the extrinsic receptor-ligand pathway of apoptosis?

A

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
Q

What is involved in the CD8+ T cell-mediated pathway of apoptosis?

A

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
Q

What is the most damaging free radical?

A

hydroxyl free radical

42
Q

What causes oxygen to become superoxide?

A

partial reduction

43
Q

What causes superoxide to become hydrogen peroxide?

A

superoxide dismutase

44
Q

What causes hydrogen peroxide to become hydroxyl free radical?

A

catalase

45
Q

What causes Hydroxyl free radical to change into H2O and GS-SG?

A

Glutathione Peroxidase

46
Q

Why does CCl4 lead to fatty change in the liver?

A

decreased apolipoprotein synthesis occurs (due to cellular injury) and fat is allowed into the liver but cannot get out

47
Q

What are the 2 major features shared by all amyloid?

A
  • Beta-pleated sheet configuration

- Congo red staining and apple green birefringence with polarized light

48
Q

What is deposited in primary amyloidosis?

A

AL amyloid (from immunoglobulin light chain)

49
Q

What is deposited in secondary amyloidosis?

A

AA amyloid (from SAA acute phase reactant)

50
Q

In what AR disease do you see an increase in SAA and increaed risk of AA amyloidosis?

A

Familial Mediterranean Fever (mimics serosal inflammation like appendicitis)

51
Q

What is the most common organ involved in amyloidosis?

A

Kidney (nephrotic syndrome)

52
Q

What is deposited in Senile cardiac amyloidosis?

A

non-mutated serum transthyretin

53
Q

What is deposited in familial amyloid cardiomyopathy?

A

mutated serum transthyretin

54
Q

What is deposited in Alzheimer disease?

A

A-beta amyloid

55
Q

What is deposited in dialysis-associated amyloid?

A

beta-2 microglobulin (what supports MHC class 1)

56
Q

How do you biopsy the thyroid?

A

fine needle aspiration

Pathoma High Yield (3 decks)

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