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Pathobio and host defense > cell injury, cell death, and toxin insult > Flashcards

cell injury, cell death, and toxin insult Flashcards

1
Q

what are the main adaptive cellular responses

A

hypertrophy (increase in cell size), hyperplasia (increase in # of cells), atrophy (decrease in size and metabolic activity), and metaplasia (change in phenotype)

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2
Q

physiological adaptation occurs under

A

responses to normal stimuli

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3
Q

pathological adaptation occurs under

A

responses to stress that allows cells to change structure and function

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4
Q

what occurs in hypertrophy

A

-increase in size of cells leading to increase size of organ
- adaptive response in cells with limited capacity to divide

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5
Q

what are the causes for hypertrophy

A

physiological increase hormone or pathological increase workload

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6
Q

what occurs in hyperplasia

A
  • adaptive response in cell capable of replication
  • increase in number of cells
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7
Q

what occurs in atrophy

A

shrinkage in size of cells

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8
Q

what are the etiological factors associated with atrophy

A

decreased workload, loss of innervation, diminished blood supply

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9
Q

what are the mechanisms of atrophy

A

decreased protein synthesis and increased protein degradation

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10
Q

what occurs in metaplasia

A

reversible changes in cell type in response to stress

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11
Q

what are the two types of cell death

A

necrosis- pathologic process
apoptosis- not necessarily associated with pathology

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12
Q

characteristics of necrosis

A

cell swelling, membrane disrupted, no ATP required

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13
Q

characteristics of apoptosis

A

cell shrinkage, requires ATP

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14
Q

what are the causes of cell injury

A

hypoxia, chemical agents, infectious agent, immunological reaction, genetic factors, nutritional imbalance, physical agents, aging

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15
Q

what two phenomena characterize irreversibility

A

inability to correct mitochondria dysfunction
profound disturbance in membrane function

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16
Q

two main morphological correlate of reversible cell injury are

A

cell swelling and fatty change

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17
Q

why is cell swelling first manufactured

A

failure of energy depended ion pumps in plasma membrane

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18
Q

what is seen in fatty change

A

appearance of lipid vacuoles in cytoplasm
occurs in hypoxic injury

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19
Q

necrosis is characterized by

A

changes in cytoplasm and nuclei of injured cells

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20
Q

cytoplasmic changes in necrosis is characterized by

A

increased eosinophilia due to increased binding of eosin to denatured protein

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21
Q

what are the 3 patterns that occur in nuclear changes in necrosis

A

karyolysis, pyknosis, karyorrhexis

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22
Q

karyolysis is seen by

A

basophils of chromatin may fade

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23
Q

pyknosis is seen by

A

nuclear shrinkage and increased basophilia

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24
Q

karyorrhexis is seen by

A

pyknotic nucleus undergoes fragmentation

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25
Q

dead cells may be replaced by

A

myelin figures that can be degraded to fatty acids

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26
Q

fatty acids can bind to

A

calcium salts that may result in dead cells calcified

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27
Q

what are the patterns of tissue necrosis

A

coagulative necrosis, liquefaction necrosis, fat necrosis, caseous necrosis, fibrinoid necrosis, gangrenous necrosis

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28
Q

what are the causes of coagulative necrosis

A

sudden cut of the blood supply (ischemic necrosis)

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29
Q

hypoxia is what

A

deficiency of oxygen

30
Q

ischemia is

A

reduced blood flow

31
Q

ultrastructure changes of reversible injury

A

-blabbing and loss of microvilli in plasma membrane
- modest mitochondria swelling
-dilation with detachment of polysomes of ER

32
Q

ultrastructure changes of irreversible injury

A
  • disruption of plasma membrane
  • massive mitochondria swelling
  • extensive disruption and fragmentation of ER
33
Q

denaturation of cellular proteins in coagulative necrosis causes tissue to appear

A

hard, opaque white and preserve its architecture

34
Q

in coagulative necrosis, it presents area of

A

infarcts

35
Q

liquefactive necrosis is characterized by

A

digestion of dead cells resulting in transformation of tissue into liquid viscous mass

36
Q

what organs is liquefactive necrosis typically seen

A

brain and spinal cord

37
Q

pyogenic abscess is

A

the necrotic core is liquefied by proteolytic enzymes releasing pus

38
Q

what mechanism is seen in liquefactive necrosis

A

lysosomal enzymes released by necrotic cells/neutrophils

39
Q

the most clinical cause of gangrenous necrosis is

A

ischemia to lower extremities

40
Q

caseous necrosis typical for ____ lesions

A

tuberculous

41
Q

the tissue in caseous necrosis appears

A

yellowish white and cheesy

42
Q

necrosis is followed by _____ in caseous necrosis

A

slow partial liquefaction

43
Q

fat necrosis occurs due to

A

enzyme lipase digesting fat cells to fatty acids

44
Q

combination of fatty acids with calcium leads to

A

calcium soaps/ opaque white patches

45
Q

what is the fundamental cause of necrotic death

A

depletion of ATP

46
Q

major causes of ATP depletion are

A
  • decreased O2 and nutrient supply
  • mitochondrial damage
  • toxins
47
Q

what are consequences of ATP depletion

A
  • plasma membrane pumps decreases
  • increase anaerobic glycolysis
  • failure of ATP Ca2+ pumps
  • disruption of protein synthesis
48
Q

what are stimuli for mitochondria injury

A

ischemia, chemical toxins, and radiation

49
Q

mitochondrial damage may result in

A

-failure to oxidative phosphorylation
-abnormal oxidative phosphorylation
- formation of abnormal mitochondria permeability transition pore

50
Q

influx of calcium is caused by

A

ischemia and some toxins

51
Q

what are the effects of increased cytosolic calcium

A

activates enzymes that can deteriorate cells
ex. phospholipase, protease, endonuclease

52
Q

oxidative stress is the ….

A

abnormal accumulation of oxygen derived free radicals

53
Q

the damage caused by free radicals is determined by

A

rate of production and removal of ROS

54
Q

excess free radicals leads to

A

oxidative stress

55
Q

plasma membrane can be damaged by

A

ischemia, microbial toxins, lytic complement components, physical agents, chemical agents

56
Q

major cellular abnormality in oxygen deprived cells are

A

-decrease ATP generation
- mitochondria damage
- accumulation of ROS

57
Q

loss of ATP leads to

A
  • failure of ion pumps
  • depletion of glycogen stores
  • decreased protein synthesis
58
Q

ischemia-reperfusion injury is caused when

A

restoration of blood flow to ischemic tissues leading to cell death

59
Q

apoptosis is normal phenomena that serves to

A

eliminate cells that are no longer needed

60
Q

apoptosis results from activation of

A

caspases enzymes

61
Q

what are the two distinct pathways for apoptosis

A

mitochondria (intrinsic) pathway
death receptor (extrinsic) pathway

62
Q

intrinsic pathway is triggered by…

A

loss of survival signals, DNA damage, and accumulation of misfolded proteins

63
Q

extrinsic pathway is responsible for

A

elimination of self reactive lymphocytes and damage by cytotoxic T cells

64
Q

autophagy refers to

A

lysosomal digestion of cells own components

65
Q

autophagy is survival mechanism in

A

times of nutrient deprevation

66
Q

intracellular organelles and some cytosol sequester into

A

a autophagic vacuole

67
Q

vacuole fuses with lysosomes to form

A

autophagolysosome

68
Q

what substances can accumulate inside cells

A

water, fat, mucin, glycogen, proteins, pigments

69
Q

what are the 2 main pathways of abnormal intracellular accumulations

A
  • inadequate removal of normal substances (fatty liver)
  • failure to degrade a metabolite (storage disorders)
70
Q

dystrophic calcification occurs when…

A

deposition occurs in dead or dying tissues

71
Q

metastatic calcification occurs when…

A
  • deposition of calcium salts in normal tissue
  • reflects hypercalcemia
72
Q

mechanism responsible for cellular aging

A
  • DNA damage
  • decreased cellular replication
  • defective protein homeostasis

Pathobio and host defense (7 decks)

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