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Pharmacology 200 > 3 - thyroid > Flashcards

3 - thyroid Flashcards

1
Q

what the role of thyroid hormones

A

growth, development and maintenance of tissues, metabolic and respiratory rate

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2
Q

what is the structure of thyroid hromones

A

conjugated iodinated tyrosines

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3
Q

what are the major forms of thyroid hormones

A

T3 and T4

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4
Q

what is the ratio of T4 to T3 release

A

14:1

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5
Q

is T3 or T4 the active form

where is it converted

A

T3 is active, converted in periphery

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6
Q

where does T3 bind

A

to nuclear receptors to activate certain genes

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7
Q

where are the T3 and T4 receptors located

A

in nearly all human tissue

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8
Q

why cant you measure T3 and T4 for disorders

A

they are regulated by negative feedback, its easier to measure TSH

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9
Q

which disorder is high TSH

A

hypothyroidism (no negative feegback)

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10
Q

which disorder is low TSH

A

hyperthyroidism (strong negative feegback)

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11
Q

what is TSH

A

thyroid stimulating hormone

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12
Q

how does TSH change with a two fold change in free T4 and T3

A

100 fold change

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13
Q

what is hypotheyroidism

A

clinically significant reduction in thyroid hormone production

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14
Q

what is the most common cause of hypotheyroidism

A

auto-immune

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15
Q

is hypotheyroidism or hypertheyroidism more common

A

hypotheyroidism (5-6X)

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16
Q

are women or men more affected by hypotheyroidism

A

women (7 - 10X)

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17
Q

what are some symptoms of hypotheyroidism

A

fatigue, cold dry skin, hair loss, brittle laids, hypotension, bradycardia

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18
Q

what is the treatment of hypotheyroidism

A

supplement T4 via levothyroxine

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19
Q

what was the historical treatment of hypotheyroidism

A

chew cow and pig thyroid glands

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20
Q

why is chewing a thyroid gland not very safe

A

there can be a variability in amounts of T3 and also other harmful substances

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21
Q

what is levothyroxin

A

T4 to treat hypotheyroidism

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22
Q

why give the body T4 and not T4

A

so the body can convert it to T3 as needed

if it was just T3 then peripheral tissues lose the ability to control local metabolic rates

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23
Q

what is the half life of T4

A

7-10 days

smooth

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24
Q

what is the half life of T3

A

24h

peaks bad

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25
Q

what is thyrotoxicosis

A

too much T3 (not necessarily from the gland)

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26
Q

what is hyperthyroidism

A

increased thyroid hormone synthesis and secretion from the thyroid gland

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27
Q

what is the most common cause of hyperthyroidism

A

Graves disease

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28
Q

what is Graves disease

A

autoimmune disease where antibodies bind to the TSH receptor on thyroid gland follicles resulting in unregulated stimulation of thyroid hormone synthesis

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29
Q

what are the symptoms of hyperthyroidism

A

high metabolitic rate, cardiovascular disease, osteoperosis, agitation, insomnia, muscle wasting

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30
Q

what is opthalmopathy

A

when the eyes pop out due to the antibodies from graves disease triggering TSH receptor in eyes

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31
Q

what happens to beta adrenergic receptor expression in hyperthyroidism

A

increased beta adrenergic expression, increased cAMP, reduce Gi

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32
Q

what is a way to treat hyperthyroidism using radioactivity

A

radioactive iodine

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33
Q

how does radioactive iodine work (131I)

A

partially destroy the thyroid gland (very selective, accumulation)

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34
Q

how does the radioation kill the thyroid

A

energy kills follicular less, gamma rays pass through tissue with no damage, beta particles damage surrounding tissue

35
Q

what do beta particles do with radioactive iodine

A

damage surrounding tissue

36
Q

what do gamma rays do with radioactive iodine

A

pass through tissue with no damage

37
Q

how long does radioactive iodine take to work and why

A

6-18 weeks because there is already lots of stored hormone

38
Q

how can radioactive iodine be used for diagnosis

A

detect for abnormalities in the thyroid gland

39
Q

what is toxic adenoma

A

benign tumor

40
Q

what is the most common cause of hyperthyroidism

A

Graves disease

41
Q

what is Graves disease

A

autoimmune disease where antibodies bind to the TSH receptor on thyroid gland follicles resulting in unregulated stimulation of thyroid hormone synthesis

42
Q

what are the symptoms of hyperthyroidism

A

high metabolitic rate, cardiovascular disease, osteoperosis, agitation, insomnia, muscle wasting

43
Q

what is opthalmopathy

A

when the eyes pop out due to the antibodies from graves disease triggering TSH receptor in eyes

44
Q

what happens to beta adrenergic receptor expression in hyperthyroidism

A

increased beta adrenergic expression, increased cAMP, reduce Gi

45
Q

what is a way to treat hyperthyroidism using radioactivity

A

radioactive iodine

46
Q

how does radioactive iodine work (131I)

A

partially destroy the thyroid gland (very selective, accumulation)

47
Q

how does the radioation kill the thyroid

A

energy kills follicular less, gamma rays pass through tissue with no damage, beta particles damage surrounding tissue

48
Q

what do beta particles do with radioactive iodine

A

damage surrounding tissue

49
Q

what do gamma rays do with radioactive iodine

A

pass through tissue with no damage

50
Q

how long does radioactive iodine take to work and why

A

6-18 weeks because there is already lots of stored hormone

51
Q

how can radioactive iodine be used for diagnosis

A

detect for abnormalities in the thyroid gland

52
Q

what happens differently in toxic adenoma and nodeular goiter

A

they produce hormones regardless of TSH signal

53
Q

why are the thyroid abnormaties detectable

A

because they synthesize excess hormones so they use a lot of the radioactive iodine

54
Q

how can iodine be used to track metastasis

A

because iodine if it spreads, they still use it to make the hormones so iodine will show up in a scan

55
Q

what are antithyroid drugs used for

A

reducing thyroid hormone levels

56
Q

what group of drugs are antithyroid drugs

A

thiourelyene

57
Q

what is an important part of antithyroid drugs’ structure

A

thiocarbamide (S-C-N)

58
Q

how do antithyroid drugs work

A

they inhibit the enzyme peroxidase, which results in less hormone synthesis

59
Q

what is the halflife of propylthiouracil

A

1.5hours

60
Q

what is the halflife of methimazole

A

6 hours

61
Q

why is the duration of antithyroid drugs longer than their halflives

A

because the thyroid gland accumulates the drugs

62
Q

why is the onset of antithyroid drugs effect often delayed

A

due to large store of hormone in follicles

63
Q

what are the two antithyroid drugs

A

propylthiouracil and methimazole

64
Q

which antithyroid drugs has to be dosed more than once a day

A

propylthiouracil

65
Q

which antithyroid drugs can be dosed once a day

A

methimazole

66
Q

which antithyroid drug inhibits conversion of T4 to T3

how

A

propylthiouracil

inhibits the activity of T4 deiodinase

67
Q

which antithyroid drug is preferred due to less hepatotoxicity

A

methimazole

68
Q

what do the antithyroid drugs do to the immune system

why may this be helpful

A

overall supression

good if autoimmunity is the caus

69
Q

how does Iodine transport into the follicle

A

Na+/I- symporter proteins

70
Q

what is pendrin

A

a transport protein that pumps accumulated iodine into the follicle

71
Q

what does thyroid peroxidase do (2 things)

A 
oxidize iodide(-1) to form iodine (0)
AND conjugates MIT and DIT within thyroglobulin to form T3 and T4
72
Q

what is iodide organification

A

iodine added to tyrosine (in thyroglobulin)

73
Q

what happens once iodinated thyroglobulin is formed

A

taken up by cells via endocytosis

74
Q

what happens once thyroglobulin is degraded

A

T4 and T3 are released and secreted

75
Q

what is the structure of thyroid peroxidase (TPO)

where is it found

A

heme group with bound iron, a membrane-bound protein

76
Q

how does thyroid peroxidase (TPO) make TPO-O ox

A

uses H2O2

77
Q

how does thyroid peroxidase (TPO) make TPO-I ox

A

add iodide (I-)

78
Q

what happens to TPO-I ox

A

the iodine is donated to tyrosine in the thyroglobulin protein to form either DIT or MIT

79
Q

what is the mechanism of action of antithyroid drugs

A

the sulfylhydryl groups of these drugs is iodinated instead of the thyroglobulin (competitively)

80
Q

what causes methylimidazole to form

A

iodinated drugs can bind to one another with disulfide link

81
Q

what is the most serious side effect of antithyroid drug use

A

agranulocytosis (autoimmune)

82
Q

when do most cases of agranulocytosis occur and which %

A

0,37 and 0,35

within 90 days, but sometimes after a year

83
Q

what are other risks other than agranulocytosis for antithyroid drugs

A

hepatotoxicity, vasculitis, arthritis

Pharmacology 200 (29 decks)

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