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Patholoy > Cell Injury > Flashcards

Cell Injury Flashcards

exam 1

1
Q

structural and functional barrier separating the cell’s internal milieu from the external environment

A

Plasma membrane

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2
Q

compartmentalize the internal environment

A

intracellular membrane

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3
Q

one of the most important factors in the maintenance of homeostasis; 25% energy expenditure used for this

A

volume regulation

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4
Q

stress leads to

A

adaptation

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5
Q

increase in the cell size and functional capacity

A

hypertrophy

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6
Q

hypertrophy can co-exist with

A

hyperplasia

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7
Q

hypertrophy leads to an increase in

A

gene expressions, synthesis of structural components and cell survival and decrease in degradation

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8
Q

tissue with cells in hypertrophy are

A

not capable of replication

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9
Q

increased workload, hypertension, cardiomyocyte, hypertrophy

A

pathologic hypertrophy

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10
Q

increased workload, pumping iron, skeletal muscle cell and hypertrophy

A

physiologic hypertrophy

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11
Q

increase in cell number leading to increase in tissue/organ mass

A

hyperplasia

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12
Q

tisssue with cells in hyperplasia are

A

capable of replication

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13
Q

Hyperplasia leads to a proliferation

A

of differentiated cells and stem cells

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14
Q

rapid growth through cell division in endometrial glands and stroma during the proliferative phase of the mestrual cycle

A

physiologic hyperplasia

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15
Q

benign prostatic hyperplasia

A

pathologic hyperplasia

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16
Q

uterus during pregnancy

A

both hyperplasia and hypertrophy

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17
Q

a reduction in the size of an organ or tissue due to a decrease in cell size

A

atrophy

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18
Q

atrophy leads to decrease and diminished

A

workload, metabolic activity and protein synthesis

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19
Q

atrophy leads to an increase in

A

protein degradation and autophagy

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20
Q

often as an adaptive response in which one adult cell type that is sensitive to a particular stress is replaced by a more resistant adult cell type

A

metaplasia

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21
Q

metaplasia results because of a reprogramming of

A

stem cells and undifferentiated mesenchymal cells in the connective tissue

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22
Q

persistent stressful condition may predispose to

A

malignant transformation

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23
Q

reversible change with the replacement of one differentiated cell type by another

A

metaplasia

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24
Q

Barrett’s esophagus

A

metaplasia

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25
Q

disordered growth and maturation of the cellular component a tissue

A

dysplasia

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26
Q

dysplasia results from a response to due a

A

persistence of injurious influence

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27
Q

dysplasia results from a _________ _________ in a proliferating cell population

A

sequential mutation

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28
Q

morphological expression of the disturbance in growth regulation

A

architectural anarchy

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29
Q

shares many cytological features with cancer but usually regress upon removal of stimulus

A

dysplasia

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30
Q

example of dysplasia

A

cervical dysplasia

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31
Q

normal cell with injurious stimulus leads to

A

cell injury

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32
Q

cell injury that is mild and transient

A

reversible injury

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33
Q

cell injury that is severe and progressive

A

irreversible injury

34
Q

two fates of irreversible injury

A
  1. necrosis

2. apoptosis

35
Q

type, duration, severity of injury

A

responses

36
Q

type, state, adaptability of the injured cell

A

consequence

37
Q

oxidative pathway and glycolytic pathway can lead to

A

ATP production and depletion

38
Q

MPTP and Leakage of cytochrome C

A

irreversible mitochondrial damage

39
Q

cell injury occurs as a continuum without sharply define steps

A

progression of cell injury

40
Q

decrease oxygen level

A

hypoxia

41
Q

decreased oxygen and substrates

A

ischemia

42
Q

Progression of ischemic cell injury:

Onset–> reversible—> irreversible—->

A

reperfusion injury

43
Q

temporary loss of volume and energy regulation

A

reversible cell injury

44
Q 
reversible cell injury:
ATP \_\_\_\_
ADP\_\_\_\_\_
aerobic pathway \_\_\_\_
anaerobic pathway\_\_\_\_\_
Glycogen stores\_\_\_\_
catabolites \_\_\_\_\_
intracellular pH\_\_\_\_
protein synthesis \_\_\_\_\_
A 
ATP decreases 
ADP increases
aerobic pathway decreases 
anaerobic pathway increases
Glycogen stores decreases
catabolites accumulate
intracellular pH decreases
protein synthesis decreases
45
Q

vacuolar degeneration where cells stain lighter due to dilution of contents with the influx of water

A

hydropic change associated with reversible cell injury

46
Q

irreversible cell injury leads to a _______ of selective permeability and leakage of ______ molecules out of the cell

A

irreversible cell injury leads to a permanent loss of selective permeability and leakage of large molecules out of the cell

47
Q

appearance of certain large molecules in the serum is a sure sign that

A

irreversible cell injury has taken place

48
Q

nuclear changes is a clear indication of

A

cell death

49
Q

example of a reversible to irreversible cell injury

A

myocardial infarction

50
Q

what appears to be a critical factor in the point of no return

A

ATP depletion

51
Q

ischemia paradox

A

some cells die after re-establishment of blood flow

52
Q

degradation of a cell’s own contents, self-eating

A

autophagy

53
Q

the process is controlled by a number of autphagy-related genes (ATG) and is a selective process mediated by specific

A

cargo-receptor proteins

54
Q

a primary driver of the accumulation of cell damage and aging

A

failure of autophagy

55
Q

acid phosphatase (AcP)

A

Prostate and bone

56
Q

creatine kinase (CK)

A

cardiac muscle and striated muscle

57
Q

Asparate transaminase (AST)

A

liver and cardiac muscle

58
Q

MM isoform

A

striated muscle

59
Q

lipase

A

pancreas

60
Q

amylase

A

pancreas, ovary, salivary glands

61
Q

alkaline phosphatase (ALP)

A

liver, bone, intestine, kidney and placenta

62
Q

MB isoform

A

cardiac muscle

63
Q

alanine transaminase

A

ALT

64
Q

lactate dehydrogenase

A

LDH

65
Q

CCL4, lipid peroxidation, membrane damage fatty change and necrosis in liver

A

free radical induced cell injury

66
Q

what occurs when there is a change in membrane permeability?

A

leakage of small molecules

67
Q

in protein metabolism, when it is disrupted and the polysomes dissociates into monosomes what happens

A

there is a reduction of protein synthesis

68
Q

is there a time lag behind biochemical changes?

A

yes

69
Q

cellular swelling

A

hydropic

70
Q

temporal relationship

A

morphological only becomes apparent until after the biochemical systems

71
Q

rush of calcium into the mitochondria

A

irreversible cell injury

72
Q

reversible change:

changes in volume regulation

A

influx of sodium leads to swelling of the cell

73
Q

reversible change:

changes in energy

A

increase in glycolysis and decrease in pH

74
Q

reversible change:

effects in protein metabolism

A

reduction in protein synthesis

75
Q

reversible change:

morphology

A

tima lag behind biochemical changes

76
Q

reversible injury:

light microscopy

A

cellular swelling- hydropic

77
Q

reversible injury:

electron microscopy

A

blebbing of the plasma membrane, blunting of microvilli, loosening of intracellular attachment

78
Q

irreversible:

changes in volume regulation

A

permanent membrane damage

79
Q

irreversible:

alteration in energy metabolsim

A

influx of calcium

80
Q

irreversible:

other changes

A
  • unfolded protein response
81
Q

irreversible:

light microscopy

A

loss of differential staining and nuclear changes

82
Q

irreversible:

electron microscopy

A

calcium crystals

Patholoy (7 decks)

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