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cell adaptation Flashcards

1
Q

the cell can adapt to changes/stimulation

A

cell adaptation

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2
Q

increase in cell with subsequent increase in organ size

A

hypertrophy

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3
Q

causes of hypertrophy

A

increase functional demand, hormonal stimulation

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4
Q

increase in the number of cells in an organ which may then increase organ size

A

hyperplasia

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5
Q

the female breast at puberty and in pregnancy

A

hormonal hyperplasia

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6
Q

liver regeneration after partial resection

A

compensatory hyperplasia

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7
Q

causes of pathologic hyperplasia

A

excess hormones

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8
Q

increased risk for development of endometrial adenocarcinoma

A

atypical hyperplasia

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9
Q

decrease in the size of cell of organ by loss of cell substance can either be both size and number

A

atrophy

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10
Q

physiologic atrophy

A

normal development, uterus following childbirth

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11
Q

causes of pathologic atrophy

A

decreased workload, loss of innervation, decreased blood supply, inadequate nutrition, loss of endocrine stimulation and pressure

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12
Q

atrophy results from both what?

A

decreased protein synthesis and increase protein degredation

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13
Q

incomplete development of an organ so that it fails to reach adult size or the decrease in cell production

A

hypoplasia

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14
Q

a reversible change in which 1 adult cell type is replaced by another adult cell type.

A

metaplasia

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15
Q

what is associated with vitamin a that is caused by chronic irritation and vitamin a deficiency?

A

metaplasia

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16
Q

hyperplasia and metaplasia are _______ changes but a fertile field of dysplasia which is a ______ change.

A

not premalignant, premalignant

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17
Q

atypical proliferative changes due to chronic irritation or inflammation

A

dysplasia

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18
Q

the principles of cell injury

A

a. the cellular response to injurious stimuli depends on the type of injury, its duration and its severity.
b. the consequences of cell injury depends on the type, state and adaptability of the injured cell.
c. cell injury results from different biochemical mechanisms acting on several essential cellular components.

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19
Q

the reversible changes secondary to injury

A

cellular swelling, cell membrane blebs, detached ribosomes, & chromatin clumping,

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20
Q

the irreversible changes secondary to injury

A

lysosome rupture, dense bodies in mitochondria, cell membrane rupture, & karyolysis, karyorrhexis and pyknosis.

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21
Q

melting/dissolution of nucleus

A

karyolysis

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22
Q

fragmentation of nucleus

A

karyorrhexis

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23
Q

the nucleus is shrunken and dark, or the shrinkage of nucleus

A

pyknosis

24
Q

myocardial infarction markers

A

a. 2 hour post infarction - cardiac specific enzymes and proteins
b. 4-12 hours - morphologic changes

25
Q

cell proliferation:
a. continuously dividing cells
b. quiescent cells
c. non-dividing cells

A

a. labile cells
b. stable cells
c. permanent cells

26
Q

susceptibility to ischemic necrosis

A

high: neurons (3-4 mins)
medium: myocardium, hepatocytes, renal epithelium (30 mins to 2 hours)
low: fibroblast, epidermis, skeletal muscles (many hours)

27
Q

3 major consequences of mitochondrial damage

A
  1. mpt pores open, loss of mitochondrial membrane potential. decreased oxidative phosphorylation and decreased atp.
  2. production of ROS
  3. leakage of pro-apoptic proteins
28
Q

loss of ca++ homeostasis

A

a. extracellular is 15x higher than cystosolic ca++
b. loss of atp increases intracellular
c. increased ca++ also increases mitochondrial permeability triggering apoptosis

29
Q

normal metabolism produces..

A

superoxide anion, hydrogen peroxide and hydroxyl ion

30
Q

superoxide is produced in ___

A

neutrophils

31
Q

excess ROS leads to

A

oxidative stress

32
Q

pathologic effects of ROS

A

a. lipid peroxidation (membrane damage)
b. protein damage
c. dna damage

33
Q

what blocks the formation of ROS or inactivates them

A

antioxidant

34
Q

the antioxidant enzymes

A

superoxide dismutase, catalase, glutathione peroxidase

35
Q

vitamins associated with antioxidant

A

vitamins a, e, c (ascorbic acid), glutathione

36
Q

membrane permeability defects

A

a. plasma membrane
b. mitochondrial membrane
c. lysosomal membrane (release of rnas, dnas, and proteases)

37
Q

cell injury causes

A
  1. oxygen deprivation
  2. physical agents
  3. chemical agents and drugs
  4. infectious agents
  5. immunologic reactions
  6. genetic derangements
  7. nutritional imbalances
38
Q

known as the deficiency of oxygen

A

hypoxia

39
Q

causes of hypoxia

A

cardiorespiratory failure, anemia, co poisoning

40
Q

known as the loss of blood supply (oxygen and nutrients)

A

ischemia

41
Q

death of groups of cells after injury & usually with inflammation

A

necrosis

42
Q

death of individual cells usually no imflammation

A

apoptosis

43
Q

the hypoxic death except brain

A

coagulative

44
Q

bacterial infections, also hypoxic death in brain tissue

A

liquefactive

45
Q

associated with tuberculosis in terms of necrosis

A

caseous

46
Q

enzymatic or traumatic damage to fatty tissue like pancreatitis

A

fat

47
Q

usually involves lower extremities and often is a type of coagulative necrosis

A

gangrenous

48
Q

immune complexes in arteries

A

fibrinoid

49
Q

the failure of an organ to develop during embryonic growth and development due to the absence of primordial tissue

A

agenesis

50
Q

failure of the corpus callosum to develop

A

agenesis of the corpus callosum

51
Q

failure of 1 or both kidneys to develop

A

renal agenesis

52
Q

failure of the arms or legs to develop

A

phocomelia

53
Q

failure of the penis to develop

A

penile agenesis

54
Q

failure of the uterus and part of vagina to develop

A

mullerian agenesis

55
Q

failure of the gallbladder to develop

A

`agenesis of the gallbladder

56
Q

failure of the portion of the eyelid margin to develop

A

eye agenesis

mt (54 decks)

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