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Endocrine II - Exam 2 > Pharmacotherapy of Thyroid Diseases - SRS > Flashcards

Pharmacotherapy of Thyroid Diseases - SRS Flashcards

1
Q

What are the thryoid agents we need to know? (2 bold, 4 total)

A
  1. Levothyroxine [T4]
  2. Liothyronine [T3]
  3. Liotrix [4:1 ratio of T4:T3]
  4. Desiccated thyroid
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2
Q

What are the antithyroid agents we need to know? (3 bold, four total)

A
  1. Methimazole
  2. Propylthiouracil [PTU]
  3. Potassium iodide
  4. Radioactive iodine (131I) sodium
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3
Q

Peripheral metabolism is responsible for deiodination of T4 and T3. What are some drugs (4) and conditions (2) that can inhibit this process?

A
  1. Amiodarone
  2. iodinated contrast media
  3. Beta blockers
  4. corticosteroids
  5. severe illness
  6. Starvation
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4
Q

What are two hormones that inhibit release of TSH?

A

Somatostatin

Dopamine

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5
Q

Small amounts of iodide are needed for thyroid hormone synthesis, but large amounts of iodide produce?

A

Wolf-Chaikoff effect - reduced Thyroid hormone production and release

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6
Q

What is the mechanism of action for the following?

  • Levothyroxine
  • liothyroinine
  • liotrix
  • desiccated thyroid
A

Serve as synthetic or xenograft (sort of) source of thyroid hormone, directly stimulate thyroid hormone receptors and thyroid hormone response elements.

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7
Q

What is important to know about how our body handles a dose of thyroid agents (levothyroxine or other)?

A

After absorption, we bind these synthetic or foriegn substances to thyroid binding proteins just as we would endogenous thyroid hormone. Then, we procede to decouple the proteins and hormones at the target tissues.

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8
Q

What impact would the following have on thyroid agents?

  • rifampin
  • phenobarbitol
  • carbamazepine
  • pheytoin
  • HIV protease inhibitors
A

All increase hepatic metabolism and enhance degredation of thyroid hormone,

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9
Q

What are some examples of agents that impair T4 absorption? (9)

A
  1. Oral bisphosphonates
  2. bile acid sequestrants (cholestyramine)
  3. ciprofloxacin
  4. PPIs
  5. sucralfate
  6. antacids
  7. bran
  8. soy
  9. coffee
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10
Q

What are four agents known to induce autoimmune thyroid disease with hypo-or hyperthyroidism?

A

Amiodarone

Interferon-alpha

interferon-beta

Lithium

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11
Q

Why is levothyroxine the preparation of choice? (6)

A
  1. Stability
  2. uniform content
  3. low cost
  4. hypoallergenic
  5. easy lab monitoring
  6. long T1/2
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12
Q

Why is the long half life of levothyroxine a boon?

A
  • Less frequent dosing - once per day
  • A missed dose will have minimal impact

(overall better patient compliance and results)

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13
Q

Levothyroxine is a synthetic preparation of what hormone?

A

T4

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14
Q

What is the bioavailability of levothyroxine?

A

70%

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15
Q

What is the T1/2 for levothyroxine?

A

7 days

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16
Q

What is the half life for T3?

A

1 day

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17
Q

Despite generally good availability, oral preparations must be swapped for IV in some patients. What patients are these?

A

Those with severe myxedema and ileus

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18
Q

Though more potent, levothyronine is not recommended for therapy for what reasons?

4

A
  1. Shorter T1/2
  2. Multiple daily doses
  3. Higher cost
  4. difficult lab monitoring
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19
Q

In what patients would you use liotrix or dessicated thyroid rather than levothyroxine?

A

In no cases.

  1. As oral administration of T3 is unnecessary, use of more expensive mixture of T3 and T4 (liotrix) instead of levothyroxine is never required.
  2. Use of desiccated thyroid rather than synthetic preparations is not justified. Disadvantages: protein antigenicity, product stability, variable hormone concentration, and difficulty in lab monitoring far outweigh advantage of lower cost.
20
Q

What are 6 ADR’s associated with levothyroxine? 6

A
  1. Palpitations
  2. tremor
  3. anxiety
  4. weight loss
  5. tachycardia
  6. increased bowel movement frequency
21
Q

What is the MOA for the thioamides?

A

Prevent thyroid hormone synthesis via…

3 - Iodide conversion to iodine

4 - organification reaction

5 - coupling reaction

22
Q

What additional step does PTU inhibit beyond the 3 MOA common to thioamides?

A

Peripheral deiodination of T4 to T3

23
Q

Describe the onset of action for thioamides and explain why it is what it is.

A
  1. Thioamides affect the synthesis of thyroid hormones rather than the release. Onset of action is slow and often requires 3-4 weeks before stores of T4 are depleted.
24
Q

What is the thioamide drug of choice?

Why?

A
  1. Methimazole: drug of choice; 10x more potent than PTU.
25
Q

Apart from the potency, what other advantages does methimazole have over PTU?

What is the half life?

A

Complete absorption

slower excretion

Accumulates in thyroid so once daily in spite of T1/2 = 6 hrs.

26
Q

PTU is generally a second line antithyroid drug, in what patients does this move up to first line? Why?

A

First trimester of pregnancy d/t limited ability to cross the placental barrier.

Thyroid storm d/t peripheral T4 to T3 inhibition.

27
Q

What are the big deal ADR’s associated with the antithyroid meds?

A
  1. maculopapular pruritic rash (4-6%)
  2. Severe hepatitis (black box warning) - may result in death
  3. Agranulocytosis - most dangerous complication
28
Q

If a patient develops agranulocytosis what must be done?

A

Discontinue medication - this usually results in rapid reversal.

May need to tx with broad spectrum antibiotics for complicating infections.

Consider giving Filgrastim - granulocyte colony stimulating factor

29
Q

If a patient develops agranulocytosis with methimizole, can you switch them to PTU after the crisis is over?

A

No, d/t the fact that there is 50% cross reactivity between the two drugs and thus a recurrance of agranulocytosis is a significant possibility.

30
Q

What are the anion inhibitors? None bold

A
  1. perchlorate (ClO4-), pertechnetate (TcO4-), and thiocyanate (SCN-).
31
Q

What is the MOA for the anion inhibitors?

A
  1. competitively inhibits iodide transport mechanism blocking iodide uptake.
32
Q

While limited, therapeutic uses do exist for anion inhibitors of the thyroid. What is one?

A

block thyroidal reuptake of iodide in patients with iodide-induced hyperthyroidism (e.g., amiodarone-induced hyperthyroidism).

33
Q

What is the MOA of potassium iodide?

A
  1. inhibit iodine organification and hormone release (possibly inhibition of thyroglobulin proteolysis); decrease size and vascularity of hyperplastic gland.
34
Q

What are three therapeutic uses for potassium iodide?

A
  1. Thyroid storm – improvement in symptoms within 2-7 days.
  2. Preoperative reduction of hyperplastic gland.
  3. Block thyroidal uptake of radioactive isotopes of iodine in a radiation emergency or other exposure to radioactive iodine.
35
Q

What is Radioactive Iodine (131I) used for?

How does it do this?

A

Thyroid ablation

effect depends on emission of β rays. Within a few weeks, destruction of thyroid parenchyma evidenced by epithelial swelling and necrosis, follicular disruption, edema, and leukocyte infiltration.

36
Q

What are some contraindications to thyroid ablation?

A

pregnancy or breast-feeding: Crosses placenta and excreted in breast milk, destroys fetal or infant thyroid gland.

37
Q

In what cases would we use B-blockers in thyroid disease?

A
  1. Cause clinical improvement of hyperthyroid symptoms but do not typically alter thyroid hormone levels (exception: high doses of propranolol may inhibit peripheral conversion of T4 to T3, lowering T3 levels ~20%).
38
Q

How and when should levothyroxine be administered?

A
  1. Administer levothyroxine on an empty stomach, 60 minutes before meals, 4 hours after meals, or at bedtime. Due to many drug interactions/effects separate drug administration times.
39
Q

What toxicities can arise from thyroxine in children?

A
  1. Children – restlessness, insomnia, accelerated bone maturation and growth.
40
Q

What toxicities can arise from thyroxine tx in adults?

A
  1. Adults – increased nervousness, heat intolerance, episodes of palpitations and tachycardia, or unexplained weight loss.
41
Q

Chronic overtreatment with T4 can result in what toxic effect, especially in the elderly?

A

Atrial fibrillation

osteoporosis acceleration

42
Q

What is the end stage of untreated hypothyroidism?

A

Myxedema coma

43
Q

If a patient presents with the following, what should you suspect?

What should you administer?

progressive weakness, stupor, hypothermia, hypoventilation, hypoglycemia, hyponatremia, water intoxication, shock,

A

Consider Myxedema coma - Admit to ICU and initiate large loading dose of levothyroxine via IV followed by daily maintenance doses.

44
Q

How should you approach tx of a hypothyroid patient with coronary artery disease?

A

Cautiously, since low levels of thyroxine are cardio protective against increasing demands which could result in angina, A fib, or MI.

45
Q

What is the treatment protocol for a thyroid storm?

A
  1. β-blocker to control severe cardiac manifestations (or calcium-channel blocker if contraindicated).
  2. Potassium iodide to prevent release of thyroid hormones from gland.
  3. PTU to block hormone synthesis.
  4. Hydrocortisone IV to protect against shock (also blocks peripheral conversion of T4 to T3).
  5. Supportive therapy to control fever, heart failure, or underlying disease states.
  6. In rare instances where above measures fail, oral bile acid sequestrants, plasmapheresis, or peritoneal dialysis may lower circulating thyroxine.
46
Q
A

Endocrine II - Exam 2 (16 decks)

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