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Pharm > Thyroid Drugs > Flashcards

Thyroid Drugs Flashcards

1
Q

What two active hormones does the thyroid gland synthesize?

A

T3 - more potent
T4 - converted in body to T3

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2
Q

What is the difference in structure between T3 and T4

A

T3 has 3 iodine groups, T4 has 4 iodine groups

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3
Q

What cells of the thyroid gland synthesize and secrete thyroid hormones?

A

follicular cells

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4
Q

What are the steps of thyroid hormone synthesis?

A
  1. uptake: and “trapping” of iodiDE
  2. activation: iodiDE is oxidized by peroxidase to iodiNE
  3. iodination of tyrosine: tyrosine is attached to the protein thyroglobulin, as mono- and di-iodotyrosine (MIT, DIT)
  4. coupling: MIT and DIT to form T3 and T4
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5
Q

Are thyroid hormones stored?

A

Yes, several months supply of thyroid hormones are stored in the colloid

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6
Q

What is involved in the release of thyroid hormones?

A

endocytosis and proteolysis of thyroglobulin to release T3 and T4

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7
Q

What happens to iodine from metabolites?

A

it is reutilized

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8
Q

What is the transport of thyroid hormones?

A

bound to plasma proteins

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9
Q

What are the plasma proteins to which thyroid hormones are bound to during transport?

A

thyroxine-binding globulin
transthyretin

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10
Q

What form of thyroid hormone is active?

A

free form

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11
Q

What is the metabolism of thyroid hormone?

A

peripheral deiodination ( reutilization of iodine)
and conjugation

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12
Q

How are thyroid hormone excreted?

A

via the bile

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13
Q

T3 is ….

A

-LESS protein bound
(higher % is in free form)
-more RAPIDLY metabolized (shorter half life)
-more POTENT
-physiology effects are due to T3

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14
Q

T4 is ….

A

-MORE protein bound
-more SLOWLY metabolized (longer half-life; high protein binding of T4 slows its degradation)
-LESS potent
-most of thyroid hormone in blood is T4

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15
Q

Most of the thyroid hormone that is secreted by the thyroid is T_

A

4

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16
Q

T3 and T4 act of the ____ receptor and cause the ____ effects

A

Same, same

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17
Q

What is the T3/T4 receptor?

A

nuclear transcription regulator (regulates specific thyroid hormone response elements in DNA)

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18
Q

The following are activities of _____ hormones:
1. Stimulation of growth and development (physical and mental)
2. Stimulation of metabolism (synthesis and degradation are increased)
3. Increased heat production and O2 consumption due to metabolism
4. Increased sympathetic activity to support metabolism
5. Increased HR, CO, vasodilation, blood flow
6. Diverse targets
7. Long term effects

A

Thryoid

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19
Q

Treatment of hypothyroidism includes ___ ________ and ________ methods

A

non-pharmacologic (diet)
pharmacologic (replacement thyroid hormones)

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20
Q

What are the 2 dietary changes that help treat hypothyroidism?

A
  1. adequate iodine in diet
  2. avoid foods with “goitrogens”
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21
Q

____ therapy for cretinism and adult hypothyroidism

A

oral

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22
Q

__ plus supportive therapy in ER for myxedema coma

A

IV

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23
Q

is replacement therapy life long?

A

yes, but some remissions occur

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24
Q

Oral therapy for hypothyroidism is

A

effect, cheap, easy, painless and safe

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25
Q

Levothyroxine is the same as endogenous __

A

T4

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26
Q

Levothyroxine is

A

oral, full agonist, has slow onset but long duration (once-daily), covered to more active T3 in body

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27
Q

Levothyroxine has ___ onset but ____ duration

A

slow onset with long duration

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28
Q

Levothyroxine (vs. Liothyronine) is more/less potent?

A

LESS potent

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29
Q

Levothyroxine (vs. Liothyronine) is more/less protein bound

A

MORE protein bound

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30
Q

The high protein binding of levothyroxine contributes to its following properties

A

long half life, lower potency (less free drug)

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31
Q

4 Levothyroxine uses include:

A
  1. primary drug used for hypothyroidism (once daily, compliance, safer, more predictable)
  2. given IV in myxedema coma (more predictable, stable effects)
  3. thyroid cancer for feedback suppression of TSH
  4. thyroid hormone replacement after gland removal
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32
Q

Liothyronine is the same as endogenous T_

A

3

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33
Q

Liothyronine is …

A

oral, full agonist, rapid onset, short DOA (4/day), less highly protein-bound, already in active T3 form

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34
Q

what is the typical replacement dose of levothyroxine?

A

100 ug/day

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35
Q

Liothyronine has a ___ onset and ___ duration of action

A

rapid onset
short DOA (take 4/daily)

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36
Q

Liothyronine (vs. levothyroxine) has _____ potency and has ____ degradation

A

higher potency
rapid degradation

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37
Q

What is the typical replacement dose of Liothyronine?

A

25 ug/day
(4x more POTENT that levothyroxine)

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38
Q

Liothyronine is rarely/often used in chronic therapy?

A

RARELY; rapid onset and sudden dramatic physiologic changes can be dangerous, short half life not good for long-term replacement (multiple pills/day)

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39
Q

Liothyronine can be used short-term prior to and following _____ ______

A

radio iodine treatment

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40
Q

Can Liothyronine be used with surgery for thyroid cancer?

A

Yes; can help with short-term TSH suppression (TSH can stimulate tumor growth) and more rapid onset while T4 takes effect after surgery

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41
Q

thyroid hormone treatment has slow onset (days to weeks) because

A

it takes time to fill empty plasma binding sites and effects are mediated by protein synthesis and resetting metabolism

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42
Q

thyroid hormone treatment has long duration of action and slow reversibility because …

A

large plasma stores, slow changes in synthesis and degradation of the proteins they regulate

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43
Q

thyroid hormone treatment for older patients or patients with cardiac disease require the following considerations:

A

need adequate TH for cardiac function BUT TH-mediated increases in metabolism can strain their weakened hearts so SMALL doses initially and SLOWLY increase with careful observation

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44
Q

Can thyroid hormone be used in pregnancy?

A

Yes, and it is important to continue use for health of mother, to maintain pregnancy, to support fetal development (fetus initially needs maternal TH)

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45
Q

TH requirements increase/decrease in pregnancy?

A

INCREASE; monitor

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46
Q

How is Myxedema coma treated?

A
  1. Levothyroxine IV initially (to fill plasma binding sites)
  2. Oral maintenance levothyroxine
  3. supportive therapy PRN
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47
Q

Side effects of TH generally occur due to OD and symptoms are similar to those of

A

hyperthyroidism

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48
Q

Do TH has many drug interactions?

A

Yes, because many drugs, disease states, physiological status may alter thyroid function and effects

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49
Q

Levothyroxine accelerates degradation of vitamin _ dependent clotting factors

A

K

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50
Q

levothyroxine increases/decreases cardiac responsiveness to catecholamines?

A

INCREASES

51
Q

Thyroid hormone preparations for treating hyPO-thyroidism include:

A

Levothyroxine and Liothyronine

52
Q

One way to treat the symptoms hyperthyroidism is to use

A

propranolol or other “sympatholytics”

53
Q

What are the antithyroid drugs that inhibit synthesis or conversion?

A

thioamides, iodides

54
Q

what is therapeutic radio iodine? and what can it be used to treat?

A

it is a non-surgerical thyroid destruction and can be used to treat hyperthyroidism

55
Q

What is a surgical option for treatment of hyperthyroidism?

A

partial thyroidectomy with drugs used before and after surgery

56
Q

What are the two Thioamide drugs available?

A

Methimazole (MMI)
Propylthiouracil (PTU)

57
Q

What is the MOA of thioamide drugs including MMI and PTU?

A

inhibits peroxidase enzyme in both the iodination and coupling steps of TH synthesis

58
Q

what do thioamide drugs including MMI and PTU NOT do?

A

they do NOT inhibit release of preformed TH; therefore there is a latent period for effects (weeks) and it takes time to use up large stored supply

59
Q

Thioamide drugs (MMI and PTU) are well absorbed ____, rapidly cleared from ______, concentrated in the _____, metabolized by ______, and excreted in the _____

A

ORALLY
CIRCULATION
THYROID
(DOA longer than plasma half life)
CONJUGATION
URINE

60
Q

What are the uses of thioamide drugs (MMI and PTU)

A
  1. first-line therapy, non-destructive
  2. useful for rapid control of TH production (but large stored reservoir)
61
Q

What is the average length of therapy of thioamide drugs (MMI and PTU)?

A

1 year

62
Q

Is disease remission high in patients that use thioamide drugs?

A

No, only about 30% of patients BUT some are well-maintained for longer times, most relapse and progress to radioiodine or surgery

63
Q

Can thioamides be used to treat thyroid crisis (thyroid storm)?

A

YES

64
Q

What is potentially fatal side effect of Thioamides?

A

Agranulocytosis
-rare, but can be fatal
-occurs in first few months of tx
-sx: sore throat, fever
-warn patient to watch for signs
-if signs are present – d/c drug, use abx, do NOT use MTT or PTU again

65
Q

What are other side effects of thioamides?

A

skin rash, drug fever, arthralgia, myalgia

66
Q

Can thioamides cause hypothyroidism?

A

YES, goiter if dose too high

67
Q

MMI vs. PTU
which is more potent?

A

MII 10x more potent, not a major advantage

68
Q

MMI vs. PTU
which has a longer plasma half-life and DOA?

A

MMI, MAJOR advantage
can use 1/daily = good compliance

69
Q

MMI inhibits peroxidase enzyme AND

A

TH synthesis

70
Q

PTU inhibits peroxidase enzyme AND

A

inhibits conversion of T4 to T3 – this makes it preferred in thyroid storm

71
Q

MMI vs. PTU
which is preferred for treatment of thyroid storm and why?

A

PTU, inhibits conversion of T4 to T3

72
Q

does PTU have a long or short half life?

A

SHORT, must day 2-4 times daily = less compliance

73
Q

MMI vs. PTU
which can cause severe liver toxicity/failure in 0.1% of patients?

A

PTU

74
Q

MMI vs. PTU
which is preferred for treatment during 1st trimester

A

PTU because MMI has rare fetal side effects

75
Q

MMI is overall the preferred thioamide drug due to long half life and no liver toxicity EXCEPT in these 2 cases?

A

1st trimester (rare fetal side effects) and thyroid storm

76
Q

Thioamides and pregnancy

A

therapy prior to pregnancy is best choice since both MMI and PTU enter placenta BUT PTU in 1st trimester then switch to MMI

77
Q

Should hyperthyroidism be treated in a pregnant patient?

A

Yes, treat to mild hyperthyroidism to maintain pregnancy but do not risk hypothyroidism in mother/fetus

78
Q

MOA of Iodides

A

acute inhibition of synthesis and release of THs

79
Q

do Iodides effect T4-T3 conversion?

A

No

80
Q

do iodines effect size and vascularity of thyroid gland?

A

YES, decreases size and vascularity of thyroid gland. Vasoconstriction “firms up” the gland and allows for easier surgical removal.

81
Q

What are two therapeutic uses of iodides?

A
  1. Thyroid storm treatment
  2. During the last 10 days prior to thyroidectomy
82
Q

Why is iodide used as treatment of thyroid storm?

A

it inhibits synthesis AND release of preformed THs, rapid but short DOA - NOT useful for long-term therapy

83
Q

Why is iodide use during the last 10 days prior to thyroidectomy?

A

vasoconstriction effect – “tighten” gland for cleaner and safer surgery

84
Q

when should iodide NOT be used?

A

should NOT be used prior to radio-iodine therapy as it will decrease uptake of radioactive iodine into thyroid

85
Q

Iodide can also be useful in radiation release emergencies because

A

it intentionally decreases uptake of radioactive iodine into thyroid (prevents thyroid destruction or cancer)

86
Q

Side effects of Iodides are mild/severe?

A

Mild; sore throat, teeth, gums, burning mouth sensation, brassy taste, rash, diarrhea

87
Q

there are a handful of iodide preparations, one being Potassium Iodide (oral) and this provides protection against

A

thyroid damage from relapse of radioactive iodine from a nuclear accident

88
Q

Radioactive iodine has a half life of

A

8 days

89
Q

Radioactive iodine has 85% weak beta radiation and travels 1-2 mm in tissue and is therefore useful for

A

localized destruction

90
Q

Radioactive iodine has 15% gamma radiation for

A

thyroid diagnostic and imaging use

91
Q

Uses of radioiodine depend on small vs. large

A

doses

92
Q

Radioiodine is small doses can be used in

A

tracer studies of iodine uptake
-for hyperthyroidism dx
-for localization of metastatic thyroid cx
-general assessment of anatomy and function

93
Q

radioiodine in large doses can be used for

A

non-surgical destruction of thyroid tissue
-oral, radioiodine is concentrated in thyroid, local beta radiation destroys thyroid tissue (weeks), no damage to other organs

94
Q

Thioamides can be used prior to scheduled radio-iodine. What are the two reasons why this is done?

A
  1. lowers TH, increase TSH, which will increase radio-iodine uptake
  2. decreasing TH levels also decreases risk of treatment-induced thyroid storm
95
Q

subsequent hypothyroidism may occur after radioiodine and can be treated with replacement …

A

levothyroxine

96
Q

radioiodine is often the treatment of choice because it is

A

easy, effective, cheap, safe, painless w/ minimal radiation to other tissues

97
Q

What are contraindications to radioiodine?

A

pregnancy, breast-feeding, children since radiation can damage rapidly growing tissues

98
Q

High doses of radioiodine can cause radiation thyroiditis and salivary adenines. These are examples of

A

inflammation near site of radiation

99
Q

Partial thyroidectomy is an alternative to radioiodine but is rarely used due to

A

greater risks

100
Q

When would surgery be used?

A

Cx, anti-thyroid drugs fail during pregnancy, may best best treatment for Graves disease, if patient refuses radioiodine

101
Q

Treatment of hyperthyroidism:

A
  1. thioamides for 5-6 w to establish euthyroid state.
  2. iodides last 2 weeks to decrease size and vascularity of gland
  3. surgical removal of bulk of thyroid gland
  4. replacement levothyroxine for hypo that may result
102
Q

How does patients age impact treatment for hyperthyroidism?

A

young = MMI, older = radioactive iodine

103
Q

How does pregnancy impact treatment for hyperthyroidism?

A
  1. PTU during 1st trimester, then MMI
  2. Surgery prior to pregnancy preferred
  3. avoid radioiodine
104
Q

How does Graves disease impact treatment for hyperthyroidism?

A

surgery has unique benefits

105
Q

How do you treat thyroid storm?

A
  1. Iodides (to decrease release of preformed TH)
  2. PTU (to decrease synthesis and conversion of T4 to T3)
  3. Glucocorticoids (prevent shock, slow conversion of T4 to T3)
  4. Propranolol and sympatholytics (for symptomatic relief of sympathetic effects, also inhibits T4-T3)
106
Q

MC cause of primary hypothyroidism in US

A

Hashimoto’s thyroiditis
(autoimmune destruction of thyroid by antithyroid antibodies)

107
Q

causes of primary hypothyroidism?

A
  1. Hashimoto’s thyroiditis
  2. dietary deficiency of iodine
  3. dietary excess of goitrogens
  4. prior treatment for hyperthyroidism
  5. congenital defect
108
Q

cause of secondary hypothyroidism?

A

pituitary or hypothalamus failure

109
Q

What is Cretinism?

A

Infant Hypothyroidism

110
Q

Cretinism signs and symptoms:

A

present at birth, dwarfism, mental retardation, thick dry skin, large tongue, cold, lethargic, routine screening in neonates

111
Q

Adult hypothyroidism characteristics:

A

edema, dry puffy skin, baggy eyes
decreased CO/HR/metabolism/appetite
weight gain
constipation
cold skin, cold intolerance
hypercholesterolemia, arteriosclerosis
weakness, fatiue
mental sluggishness, depression
amenorrhea, menorrhagia, reproductive problems

112
Q

What is Myxedema coma?

A

Severe untreated hypothyroidism

113
Q

What often triggers myxedema coma?

A

precipitating stress

114
Q

Signs and symptoms of myxedema coma?

A

all the HYPOs:
hypothermia
hypoventilation
hypoglycemia
hyponatremia
hypotension
coma

115
Q

Hyperthyroidism causes:

A
  1. Graves disease (aka diffuse toxic goiter) is MC and is due to antibody with TSH activity - no feedback regulation
  2. thyroid adenoma (aka toxic nodular goiter)
116
Q

Thyroid storm is …

A

crisis from severe hyperthyroidism

117
Q

thyroid storm is often triggered by …

A

thyroid surgery, stress of independent illness, trauma, infection, therapeutic radioactive iodide admin

118
Q

signs and symptoms of thyroid storm:

A

fever, marked high HR, weakness, apathy, delirium

119
Q

signs and symptoms of hyperthyroidism

A

increased metabolism
warm, moist skin, heat intolerance
weight loss, increased appetite
catecholamine potentation
nervous, anxiety, insomnia
high HR, flushing, sweating,
diarrhea, weakness, amenorrhea, tired but can’t sleep, decreased ability to concentrate

120
Q

what are the eye signs in hyperthyroidism?

A

lid lag, stare

121
Q

what are the eye signs specific to graves disease?

A

exophthalmos

122
Q

What is goiter?

A

enlargement of thyroid and can occur with euthyroidism, hypothyroidism, hyperthyroidism

123
Q

toxic goiter vs. non-toxic goiter

A

toxic goiter = goiter with hyperthyroidism, increased TH produced by autonomous or overactive thyroid

non-toxic goiter= low T4, T3 production leads to increase TSH secretion –> thyroid hyperplasia

Pharm (6 decks)

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