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

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Flashcards in 1. Growth Adaptations, Cellular Injury, and Cell Death Deck (56):
1

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

1) Cardiac muscle
2) Skeletal muscle
3) Myocytes

2

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

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

3

How does a decrease in cell size occur?

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

4

True or false: metaplasia is irreversible.

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

5

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

Apocrine metaplasia of the breast carries NO increased risk for cancer

6

What are the 2 major consequences of Vitamin A deficiency?

-Night blindness
-Maturation of immune system gets dysregulated

7

True or false: dysplasia is reversible.

TRUE (with alleviation of the inciting stress)

8

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

Neurons

9

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

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

10

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

-Polycythemia vera
-Lupus anticoagulant

11

What is the characteristic PaO2 and SaO2 with anemia?

PaO2 and SaO2 are both normal

12

What is the characteristic PaO2 and SaO2 of CO poisoning?

PaO2 is normal and SaO2 is decreased

13

What is the characteristic PaO2 and SaO2 with methemoglobinemia?

PaO2 is normal and SaO2 is decreased

14

What is the underlying problem in methemoglobinemia?

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

15

How do you treat methemoglobinemia?

IV methylene blue

16

What is the hallmark of reversible cell injury?

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

17

What is the hallmark of irreversible cell injury?

membrane damage

18

Where is the ETC located?

inner mitochondrial membrane

19

What is the word for nuclear condensation?

pyknosis

20

What is the word for nuclear fragmentation?

karyorrhexis

21

What is the word for nuclear dissolution?

karyolysis

22

What ALWAYS follows necrosis?

inflammation

23

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)?

coagulative necrosis

24

What leads to coagulative necrosis?

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