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Pathology > Exam 1: Cellular Adaptations to Injury > Flashcards

Exam 1: Cellular Adaptations to Injury Flashcards

1
Q

how do cells adapt to stress or injury

A

by increasing or decresing their size or number

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2
Q

Hypertrophy

A

increase in cell size

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3
Q

hypertrophy is most common in

A

tissues that do not normally replicate

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4
Q

how does hypertrophy usually occur

A

increase in production of cellular proteins

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5
Q

hypertrophy can be ___ or ____

A

physiologic or pathologic

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6
Q

hyperplasia

A

increase in cell number

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7
Q

hyperplasia most common in

A

tissues that normally replicate

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8
Q

what are examples of physiologic hyperplasia

A

mammary gland; granulation; liver regeneration

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9
Q

what are examples of pathologic hyperplasia

A

excess of hormones; papilloma virus wart

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10
Q

atrophy

A

decrease in size of cell, organ, or tissue after normal growth is reached (can also be derease in cell number)

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11
Q

causes of atrophy include

A

deficient nutrient supply, decreased workload, denervation, pressure, loss of endocrine stimulation, and aging

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12
Q

hypoplasia

A

congenital decrease in size

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13
Q

involution

A

physiologic reduction in the size of a tissue or organ (thymus)

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14
Q

metaplasia

A

an adaptive, potentially reversible change in which one adult cell type is replaced by another adult cell type of the same germ line

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15
Q

metaplasia occurs most commonly with ______ but can also occur with _____

A

epithelium, mesenchymal tissues

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16
Q

metaplasia usually occurs to

A

a cell injury

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17
Q

dysplasia

A

disorderly growth

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18
Q

dysplasia is usually applied to

A

epithelial cells

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19
Q

dysplasia can be a prelude to

A

neoplasia

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20
Q

heterotopia

A

normal tissues arise in an abnormal location (ectopic tissue)

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21
Q

what are the four basic mechanisms of intracellular accumulations

A

abnormal metabolism
alterations in protein folding
enzyme deficiencies
inability to phagocytize

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22
Q

abnormal metabolism occurs when

A

a normal endogenous substance is produced at a normal or increased rate, but the rate of metabolism is inadequate to remove it

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23
Q

example of abnormal metabolism

A

hepatic lipidosis

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24
Q

what causes alterations in protein folding

A

mutations

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25
Q

what is an example of alteration in protein folding

A

alpha 1 antitrypsin (not recognized in animals)

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26
Q

enzyme deficiencies prevent what

A

breakdown of substrates, which then accumulate lysosomes

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27
Q

what is an example of an enzyme deficiency

A

lososomal storage diseases (enlarged, foamy cytoplasm of cells)

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28
Q

what is an example of inability to phagocytize particles

A

anthracosis (inhalation of air pollution)

29
Q

extracellular accumulations include what

A

amyloid

mineral

30
Q

what is amyloid

A

a group of chemically diverse extracellular glycoproteins that appear histologically and ultrastructurally similar

31
Q

histologically, amyloid is

A

esoinophilic, amorphous (no shape), hyalin substance on H&E stain
Stains pink with congo red stain and looks light green under polarized light

32
Q

primary amyloidosis is composed of what

A

AL amyloid (amyloid light chain)

33
Q

AL amyloid is composed of

A

immunoglobulin derived from plasma cells

34
Q

what is the most common form of amyloidosis in people

A

primary

35
Q

what is an example of primary amyloidosis in dogs

A

canine plasmocytoma

36
Q

secondary amyloidosis is composed of

A

AA amyloid

37
Q

what is AA amyloid

A

derived from serum amyloid A, an acute phase protein that function in inflammatory response

38
Q

wha is the most common amyloidosis in animals

A

secondary amyloidosis

39
Q

secondary amyloidosis occurs secondary in some cases of ______

A

chronic inflammation

40
Q

amyloid accumulates in what tissues

A

kidney (especially glomeruli)

liver, spleen, GIT, endocrine organs

41
Q

soetimes amyloid is confined to

A

one organ

42
Q

familial amyloidosis

A

a form of secondary; hereditary in certain cat and dog breeds

43
Q

consequences of amyloid in the kidney

A

protein loss from glomeruli and renal failure

44
Q

consequences of amyloid in other tissues

A

compression of cells causing atrophy or death

45
Q

amyloid can appear ____ in tissue

A

yellow

46
Q

identification of amyloid at necropsy is done with

A

iodine solution: will highlight affected glomeruli

47
Q

mineral extracellular accumulations include

A

calcium salts, usually i the form of phosphates and carbonates (mineralization or calcification)

48
Q

what are the two types of mineralization

A

dystrophic and metastatic

49
Q

dsytrophic mineralization occurs in what tissues

A

necrotic tissues

50
Q

how does dystrophic mineralization occur

A

dead cells are no longer able to regulate the influx of Ca into their cytosol

51
Q

serum calcium levels in dystrophic mineralization

A

normal

52
Q

metastatic mineralization occurs in what tissues

A

normal tissue

53
Q

how does metastatic mineralization occur

A

result of hypercalcemia or calcium-phosphorous imbalance in the blood

54
Q

what are the causes of hypercalcemia or calcium phosphorous imbalance

A

renal failure
vitamin d toxicity
parathyroid hormone related protein

55
Q

renal failure

A

retention of P results in lowering of serum Ca and increased secretion of parathyroid hormone (renal secondary hyperparathyroidism)

56
Q

vitamin D toxicity

A

occurs from ingestion of plants, drugs, or rodenticides containing vitamin D

57
Q

parathyroid hormone related protein

A

Secreted by certain neoplasms (lymphoma and anal sac apocrine gland adenocarcinoma in dogs)

58
Q

what is the gross appearance of mineralized tissue

A

usually white (not to be confused with necrotic muscle) and firm; gritty on palpation

59
Q

histologic appearance of mineralized tissue

A

deeply basophilic on H&E

Von Rossa: brown/black

60
Q

how can post mortem changes be ketp to a minimum

A

rapid cooling of the carcass and decreasing the time interval between death and necropsy

61
Q

autolysis

A

decomposition that occurs after death

62
Q

rigor mortis

A

contraction of muscles occurring after death that starts 1-6 hours after death and persists 1-2 days

63
Q

hypostatic congestion

A

(liver mortis) the gravitatinal pooling of blood on the down side of the body

64
Q

where is hypostatic congestion most evident

A

in the lung and skin

65
Q

bile imbibition

A

penetration of bile through the gall bladder wall following death. The bile stains the adjacent liver and GIT yellow to green-black

66
Q

pseudomelanosis

A

dark discoloration of tissue by iron sulfide, which results from the combination of hydrogen sulfide (produced by postmortem bacteria) and hemoglobin (from breakdwon of erythrocytes)

67
Q

bloating

A

result of postmortem bacterial gas formation in the lumen of the GIT.

68
Q

bloating is most severe in what animals

A

in herbivores and in hot weather

Pathology (17 decks)

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