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
what is an example of alteration in protein folding
alpha 1 antitrypsin (not recognized in animals)
26
enzyme deficiencies prevent what
breakdown of substrates, which then accumulate lysosomes
27
what is an example of an enzyme deficiency
lososomal storage diseases (enlarged, foamy cytoplasm of cells)
28
what is an example of inability to phagocytize particles
anthracosis (inhalation of air pollution)
29
extracellular accumulations include what
amyloid | mineral
30
what is amyloid
a group of chemically diverse extracellular glycoproteins that appear histologically and ultrastructurally similar
31
histologically, amyloid is
esoinophilic, amorphous (no shape), hyalin substance on H&E stain Stains pink with congo red stain and looks light green under polarized light
32
primary amyloidosis is composed of what
AL amyloid (amyloid light chain)
33
AL amyloid is composed of
immunoglobulin derived from plasma cells
34
what is the most common form of amyloidosis in people
primary
35
what is an example of primary amyloidosis in dogs
canine plasmocytoma
36
secondary amyloidosis is composed of
AA amyloid
37
what is AA amyloid
derived from serum amyloid A, an acute phase protein that function in inflammatory response
38
wha is the most common amyloidosis in animals
secondary amyloidosis
39
secondary amyloidosis occurs secondary in some cases of ______
chronic inflammation
40
amyloid accumulates in what tissues
kidney (especially glomeruli) | liver, spleen, GIT, endocrine organs
41
soetimes amyloid is confined to
one organ
42
familial amyloidosis
a form of secondary; hereditary in certain cat and dog breeds
43
consequences of amyloid in the kidney
protein loss from glomeruli and renal failure
44
consequences of amyloid in other tissues
compression of cells causing atrophy or death
45
amyloid can appear ____ in tissue
yellow
46
identification of amyloid at necropsy is done with
iodine solution: will highlight affected glomeruli
47
mineral extracellular accumulations include
calcium salts, usually i the form of phosphates and carbonates (mineralization or calcification)
48
what are the two types of mineralization
dystrophic and metastatic
49
dsytrophic mineralization occurs in what tissues
necrotic tissues
50
how does dystrophic mineralization occur
dead cells are no longer able to regulate the influx of Ca into their cytosol
51
serum calcium levels in dystrophic mineralization
normal
52
metastatic mineralization occurs in what tissues
normal tissue
53
how does metastatic mineralization occur
result of hypercalcemia or calcium-phosphorous imbalance in the blood
54
what are the causes of hypercalcemia or calcium phosphorous imbalance
renal failure vitamin d toxicity parathyroid hormone related protein
55
renal failure
retention of P results in lowering of serum Ca and increased secretion of parathyroid hormone (renal secondary hyperparathyroidism)
56
vitamin D toxicity
occurs from ingestion of plants, drugs, or rodenticides containing vitamin D
57
parathyroid hormone related protein
Secreted by certain neoplasms (lymphoma and anal sac apocrine gland adenocarcinoma in dogs)
58
what is the gross appearance of mineralized tissue
usually white (not to be confused with necrotic muscle) and firm; gritty on palpation
59
histologic appearance of mineralized tissue
deeply basophilic on H&E | Von Rossa: brown/black
60
how can post mortem changes be ketp to a minimum
rapid cooling of the carcass and decreasing the time interval between death and necropsy
61
autolysis
decomposition that occurs after death
62
rigor mortis
contraction of muscles occurring after death that starts 1-6 hours after death and persists 1-2 days
63
hypostatic congestion
(liver mortis) the gravitatinal pooling of blood on the down side of the body
64
where is hypostatic congestion most evident
in the lung and skin
65
bile imbibition
penetration of bile through the gall bladder wall following death. The bile stains the adjacent liver and GIT yellow to green-black
66
pseudomelanosis
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
bloating
result of postmortem bacterial gas formation in the lumen of the GIT.
68
bloating is most severe in what animals
in herbivores and in hot weather