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Pharm II > Thyroid - DONE > Flashcards

Thyroid - DONE Flashcards

1
Q

What stimulates the release of thyroid hormones?

A

Thyroid releasing hormone (TRH) from hypothalamus is secreted into the capillaries of the pituitary portal venous system, and in the anterior pituitary gland, TRH stimulates the synthesis and release of THYROTROPIN (thyroid stimulating hormone) TSH. TSH in turn stimulates an adenylyl cyclase mediated mechanisms in the thyroid cell to increase the synths and release of T4 & T3.

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2
Q

What are the two hormones produced by the thyroid gland derivatives of?

A

iodinated derivatives of tyrosine

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3
Q

What is the ratio or T4 to T3 produced in the thyroid gland?

A

5:1 ratio of T4 to T3

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4
Q

What is most of circulating T3 derived form?

A

deiodination of T4 by 5’deiodinase

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5
Q

What combines in the thyroglobulin molecule to form thyroxine (T4)?

A

two molecules of DIT (diiodotyrosine)

**at the apical cell membrane, iodide is oxidized by thyroidal peroxidase to iodine, in which form it rapidly iodinates tyrosine residues within the thyroglobulin molecule to form MIT & DIT.
Monoiodotyrosine & Diiodotyrosine

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6
Q

What combines in the thyroglobulin molecule to form triiodothyronine (T3)?

A

1 molecule of MIT and 1 molecule of DIT

***at the apical cell membrane, iodide is oxidized by thyroidal peroxidase to iodine, in which form it rapidly iodinates tyrosine residues within the thyroglobulin molecule to form MIT & DIT.
Monoiodotyrosine & Diiodotyrosine

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7
Q

What is the primary pathway for the peripheral metabolism of thyroxine (T4)?

A

deiodination

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8
Q

What does the deiodination of thyroxine (T4) produce?

A

T3, which is more potent than T4, and rT3

*rT3 is metabolically inactive

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9
Q

What two proteins are T3 and T4 bound to in the serum?

A

Thyroxine binding globulin (TBG) - primarily

Also can be found bound to Albumin

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10
Q

What is the potency ratio of active T3 to T4 ?

A

T3 is in the active form = 4:1 potency of T3:T4

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11
Q

What is the oral bioavailability of current preparations of thyroxine (T4)?

A

80%

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12
Q

What is the oral bioavailability of current preparation of T3?

A

95%

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13
Q

Where is Thyroixine absorbed best?

A

duodenum and ileum

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14
Q

What is the effect of hyper and hypothyroidism on the half life of T3/T4?

A

Hyperthyroid - decreases T1/2

Hypothyroid - increases T1/2

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15
Q

How long is the half life of T4 in a euthyroid patient?

A

7 days

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16
Q

How long is the half life of T3 in a euthyroid patient?

A

1 day

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17
Q

What kind of drugs will cause an increase in metabolism of T4 and T3?

A

P450 inducers

-from book below:
rifampin, phenobarbital, carbamezepine, phenytoin, tyrosine kinase inhibitors, HIV protease inhibitors)

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18
Q

How do euthyroid patients maintain plasma concentration when given P450 inducers?

A

by increasing thyroid funciton

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19
Q

What will a hypothyroid patient require when given a P450 inducer?

A

may require more T4

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20
Q

What is increased by pregnancy, estrogens, or oral contraceptives?

A

TBG (thyroxine-binding globulin)

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21
Q

What does increased TBG (thyroxine-binding globulin) cause?

A

a decrease in free hormone

  • a shift from free to bound
  • found in pregnancy, estrogens, or oral contraceptives
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22
Q

What does a nuclear receptor bind?

A

ONLY T3

* effects mediated by alterations in gene expression.

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23
Q

What are the three synthetic preparations used to treat Hypothyroidism?

A

Levothyroxine
Liothyronine
Liotrix

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24
Q

What is the thyroid preparation of animal origin used to treat hypothyroidism?

A

Desiccated Thyroid

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25
Q

What are the 5 antithyroid agents used to treat hyperthyroidism?

A
  1. Thioamides
  2. Iodides
  3. Anion Inhibitors
  4. Radioactive Iodine
  5. Adrenoceptor antagonists
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26
Q

What is the drug of choice for thyroid replacement and suppression therapy?

A

Levothyroxine

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27
Q

Why is Levotyroxine the DOC for thyroid replacement and suppression therapy?

A

T4 is administered when pt is given Levothyroxine

  1. Low Cost
  2. Long T1/2 = 7 days
  3. Given Once Daily

….from book: T4 is converted to T3 intracellularly; thus administration of T4 produces both hormones.
lack of allergenic foreign protein also

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28
Q

Why is Liothyronine not preferred over Levothyroxine for routine replacement therapy?

A

Because of its shorter half life (24 hours), so you would have give multiple daily dosing, and higher costs

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29
Q

Which is more potent, Levothyroxine or Levothyronine?

A

Levothyronine is more potent than Levothyroxine (3-4X)

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30
Q

What specific patients should Levothyronine be avoided in?

A

patients with CARDIAC DISEASE

because of its greater hormone activity, and consequent greater risk in cardiotoxicity

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31
Q

What is Levothyronine best used for?

A
  • Liothyronine is administration of T3

answer: it is best used for short term suppression of TSH

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32
Q

Which drug used for treatment of Hypothyroidism administers T4 and T3? What is the ratio of T4 to T3?

A

Liotrix
*4:1 of T4:T3
?i didn’t know how to ask this??

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33
Q

Which Thyroid preparation for treatment of hypothyroidism is disadvantageous due to its protein antigenicity?

A

Desiccated Thyroid (Animal Origin)

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34
Q

From the Book: What is the shelf life of synthetic thyroid preparations?

A

2 years

– particularly if they are stored in dark bottles to minimize spontaneous deiodination

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35
Q

Which antithyroid therapy blocks hormone production AND DECREASES TISSUE RESPONSE?

A

Thioamides

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36
Q

Which antithyroid therapy destroys the thyroid gland?

A

Radioactive Iodine

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37
Q

Which antithyroid therapy is an adjunctive therapy?

A

adrenoceptor antagonist

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38
Q

Which three antithyroid therapy agents block hormone production?

A

1 Thioamides

  1. Iodides
  2. Anion Inhibitors
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39
Q

What are the 3 effects of antithyroid agents?

A
  1. decrease hormone production
  2. decrease tissue response
  3. Destroy gland
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40
Q

What is the GENERAL strategy for management of Hypothyroidism?

A

Replacement Therapy

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41
Q

What is the DOC for replacement therapy for hypothyroidism?

A

Levothyroxine

brand or generic prep is fine

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42
Q

T/F Combination of Levothyroxine and Liothyronine has no therapeutic benefit than Levothyroxine alone.

A

true

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43
Q

What do hypothyroid infants require more per kilogram of body weight than hypothyroid adults?

A

T4

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44
Q

What is the average dosage of Levothyroxine for infants 1-6 months?

A

10-15 mcg/kg/d

45
Q

What is the average dosage of Levothyroxine for adult?

A

1.7 mcg/kg/d

46
Q

Who many require less thyroxine for replacement?

A

older adults (>65)

47
Q

T/F Levothyroxine dosage is highly patient specific because of the variability in the absorption of thyroxine.

A

true

48
Q

How many times a day should Levothyroxine be administered? how?

A
  1. Once daily (because of its long half life of 7 days)
  2. on an empty stomach
    (30 min before meal or 1 hour after)
49
Q

How long does it take a starting dose Levothyroxine to reach steady-state levels? How does this effect dosing?

A

6-8 weeks
Dosage changes should be made slowly.
*Start low and titrate up to euthyroid or toxicity will occur

50
Q

What should be measured at regular intervals to ensure successful therapy and avoid toxicity when administering Levothyroxine?

A

Serum TSH and Free Thyroxine

51
Q

What is the optimal range of TSH?

A

0.5 - 2.5 mU/L for TSH

52
Q

What is imperative to monitor in patients taking Levothyroxine, especially elderly patients?

A

Cardiac Toxicity
- Book: the heart is very sensitive to level of circulating thyroxine, and if angina pectoris or cardiac arrhythmia develops, it is essential to stop or reduce the dose of thyroxine immediately.

53
Q

A child presents with restlessness, insomnia, and accelerate bone maturation and growth. After reviewing her patient history you see that she is taking Levothyroxine. What is our diagnosis?

A

Thyroxine toxicity

54
Q

An adult presents with increased nervousness, heat intolerance, episodes of palpations, tachycardia, and weight loss. After reviewing his patient history you see that he is taking Levothyroxine. What is your diagnosis?

A

Thyroxine toxicity

55
Q

What should you test to confirm Thyroxine toxicity?

A

TSH - which will determine whether the symptoms are due to excess thyroxine in the blood.

56
Q

What is the most common cause of Hypothyroidism?

A

Hashimoto’s Thyroiditis

57
Q

Does the presence of a goiter diagnose hypo vs. hyperthyroidism?

A

NO!

Hypothyroidism can be with or without a thyroid enlargement (goiter)

58
Q

Elevated TSH but normal T4/T3 levels =

A

Subclinical Hypothyroidism

*thyroid is compensating

59
Q

End state of untreated hypothyroidism?

A

Myxedema coma

- sever hypothyroidism

60
Q

Book: Progressive weakness, stupor, hypothermia, hypoventilation, hypoglycemia, hyponatremia, water intoxication, shock and death are symptoms of what?

A

Myxedema coma

  • give all preparations IV
  • avoid excessive water intake therefore use caution with IV
61
Q

Book: What is the treatment of choice for Myxedema Coma?

A

loading dose of Levothyroxine IV - usually 300-400 mcg initially…… followed by 50-100 mcg daily.

62
Q

What can drug induced hypothyroidism be satisfactorily managed with?

A

levothryoxine therapy if the offending agent cannot be stopped

63
Q

Removal of the offending agent (drug) usually enough to treat drug induced hypothyroidism. What drug causing hypothyroidism would cause a need to use thyroid therapy even after removal the drug?

A

Amiodarone -
Levothyroxine therapy may be necessary even after discontinuation of amiodarone because of amiodarones very long half life.

64
Q

what are the two thioamide drugs? What are these used for?

A

methimazole & propylthiouracil (PTU)

Thyrotoxicosis

65
Q

Which Thioamide drug is more toxic?

A

Methimazole is 10 X more potent than propylthiouracil

66
Q

Due to black box warning, when should propylthiouracil (PTU) be used?

A

first trimester of pregnancy, in thyroid storm, an din those experiencing adverse reactions to methimazole

67
Q

How is methimazole absorbed?

A

completely, but at variable rates

68
Q

What is the half life of Methimazole compared to PTU?

A

Methimazole = T1/2 - 6 hours

Propylthiouracil (PTU) = T1/2 - 1.5 hours

69
Q

How is propylthiouracil absorbed? bioavailability?

A

rapidly absorbed, reaching peak serum levels after 1 hour

bioavailability = 50-80%

70
Q

How do you dose methimazole compared to Propylthiouracil (PTU)?

A

Methimazole = single daily dose @ 30 mg for mild to moderate hyperthyroidism
Propylthiouracil (PTU) = dosing every 6-8 hours

**both are taken up by the thyroid gland

71
Q

Both thioamides cross the placental barrier, which of the two is preferred during the first trimester of pregnancy?

A

Propylthiouracil , because it is more strongly protein bound, and therefore crosses the placenta less readily.

72
Q

What is the major mechanism of action of thioamides?

A

inhibit thyroid peroxidase catalyzed reactions and blocking iodine organification
**DO NOT BLOCK IODIDE UPDATE

73
Q

Which thioamide prevents peripheral conversion of T4 to T3?

A

PTU …..

Methimazole DOES NOT

74
Q

What is the most common adverse effects of thioamides?

A

most common is a maculopapular pruritic rash, less common are headache, nausea, pain/stiffness of joints

75
Q

What is the most serious adverse effect of thioamides?

A

agranulocytosis/leukopenia

most common in older adults and those on METHIMAZOLE

76
Q

Which antithyroid agent inhibits organification and hormone release causing a decrease in size and vascularity of thyroid gland?

A

Iodides

77
Q

What is the primary mechanism of action of Iodides at therapeutic doses?

A

decreased hormone release

78
Q

Iodides are useful in decreasing the size and vascularity of thyroid. What is a good use of Iodides because of this reason?

A

Preoperative use

79
Q

Should Iodide be used alone? Why or Why not?

A

Iodide should NOT be used alone, because the gland will escape from the iodide block in 2-8 weeks.
This “REBOUND” or “ESCAPE” often occurs in 2-8 weeks because of INCREASED TSH.

80
Q

Book: what antithyroid agent block uptake of iodide by thyroid gland through competitive inhibition of the iodide transport mechanism, but this CAN BE OVERCOME by large amounts of iodides?

A

Ionic Inhibitors
Thiocyanate - (SCN-)
Perchlorate - (ClO4-)

81
Q

Slides:

Monovalent anions that are actively accumulated by the thyroid and inhibit Na/I pump?

A

Ionic Inhibitors
Thiocyanate
Perchlorate

82
Q

What two diseases are ionic inhibitors (thiocyanate and perchlorate) used to treat clinically?

A

Treatment of Graves’ disease and amiodarone-induced thyrotoxicosis

83
Q

Why is perchlorate rarely used clinically?

A

because it can cause aplastic anemia

84
Q

What is the only isotope used to TREAT thyrotoxicosis? (hint: all the other ones are used to diagnose) How do you administer this agent?

A

Radioactive Iodine 131I - administered orally

85
Q

Radioactive Iodine 131I is administered orally, irapidly absorbed and concentrates where?

A

THYROID GLAND

Book: also incorporated into storage follicles

86
Q

What is the mechanism of action of 131I?

A

Its therapeutic effect depends on

EMISSION OF BETA RAYS that DESTROY Glandular tissue

87
Q

What is the half life of Radioactive Iodine I131?

A

T1/2 = 5 days

88
Q

What is the penetration range of Radioactive Iodine 131I?

A

400-2000 um

89
Q

Who is radioactive iodine 131I contraindicated in?

A

pregnancy or nursing mothers

book: because it crosses the placenta and destroys fetus thyroid gland and is excreted in breast milk

90
Q

What are the advantages of Radioactive Iodine 131I?

A

cheap, easily administered, effective, painless

91
Q

What are used to treat the SYMPTOMS associated with thyrotoxicosis? ( usually in thyrotoxic crisis)

A
  1. adrenoceptor blocking agents
  2. calcium channel blockers
  3. Glucocorticoids
92
Q

What are the most common adrenoreceptor blocking agents used in treating symptoms associated with thyrotoxicosis?

A

Beta Blockers without intrinsic sympathomimetic activity (metoprolol, PROPANOLOL, atenolol)

93
Q

What three specific symptoms do adrenoceptor blocking agents, Beta Blockers, treat in thyrotoxicosis?

A

control Tachycardia, Hypertension, and atrial fibrillation

94
Q

Which Beta Blocker may prevent conversion of T4 to T3 in the periphery?

A

Propanol

95
Q

what are the three primary methods of treating Graves’ disease?

A
  1. antithyroid drug therapy
  2. thyroidectomy
  3. Radioactive iodine
96
Q

What is the treatment of a single toxic adenoma?

A

surgical excision or radioactive iodine

97
Q

What is the treatment of a toxic multinodular goiter?

A

antithyroid drug therapy followed by subtotal thyroidectomy

Book: best treated with the antithyroid drug methimazole (preferable) or propylthiouracil followed by subtotal thyroidectomy

98
Q

What is termed spontaneously resolving hyperthyroidism?

A

Subacute Thyroiditis

99
Q

Book: During the a viral infection of the thyroid gland, there is destruction of thyroid parenchyma with transient release of stored thyroid hormones. What is the describing?

A

Subacute Thyroiditis

100
Q

What is the treatment for Subacute Thyroiditis?

A

Usually resolves on its own, but supportive therapy for symptoms can be used, Beta Blockers without intrinsic sympathomimetic activity (Propanolol) for tachycardia and aspirin and non steroidal anti-inflammatory drugs to control local pain

101
Q

Treatment of thyroid storm

A

antithyroid drugs therapy and adjunctive therapy

102
Q

treatment of ophthalmopathy?

A

surgical excision or radioactive iodine therapy

103
Q

treatment of thyrotoxicosis during pregnancy?

A

typically administered propylthiouracil (PTU)

–dosage kept at a minimum

104
Q

What is the treatment of Neonatal Graves’ disease?

A

PTU (Propylthiouracil), Lugol’s solution, and Propanolol

Medication is reduced as clinical signs improve (usually discontinued in 6-12 weeks)

105
Q

What is the treatment of Amiodarone -induced thyrotoxicosis?

A
  • remove amiodarone if possible

- 2 types: type 1 (iodine induced) and type 2 (inflammatory)

106
Q

How do you treat type 1 amiodarone - induced thyrotoxicosis?

A

thioamides

107
Q

How do you treat type 2 thyrotoxicosis?

A

glucocorticoids

108
Q

Due to difficulty distinguishing between type 1 and type 2 amiodarone thyrotoxicosis, how is it typically treated?

A

typically treated with both thioamides and glucocorticoids togehter

Pharm II (13 decks)

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