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ER II Exam 2 > Thyroid and Anti-Thyroid Drugs > Flashcards

Thyroid and Anti-Thyroid Drugs Flashcards

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1
Q

What are the 4 thyroid drugs?

A
  • Levothyroxine [T4]
  • Liothyroxine [T3]
  • Liotrix [a 4:1 ratio of T4:T3]
  • Thyroid desiccated
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2
Q

What are the 4 anti-thyroid agents?

A
  • Radioactive iodine (131I) sodium
  • Methimazole
  • Potassium iodide
  • Propylthiouracil [PTU]
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3
Q

Which iodide transport enzyme controls the flow of iodide across the apical membrane of the thyroid follicular cell?

A

Pendrin

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4
Q

Where is oral T4 best absorbed within the GI tract?

A

Duodenum and ileum

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5
Q

T4 and T3 absorption may be affected by what underlying condition?

A

Myxedema w/ ileus but NOT by mild hypothyroidism

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6
Q

How does the half-life and clearance of T4 and T3 change in a hyperthyroid vs. hypothyroid state?

A
  • Hyperthyroid = T4 and T3 clearance is ↑ and half-life ↓
  • Hypothyroid = T4 and T3 clearance is ↓ and half-life ↑
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7
Q

Which 6 agents inhibit 5’-deiodinase, blocking T4 to T3 conversion and increasing reverse T3 levels, and may be given in pt’s experiencing thyroid storm?

A
  • Radiocontrast agents: iopanoic acid and ipodate
  • Amiodarone
  • β-blockers
  • Corticosteroids
  • PTU
  • Flavanoids
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8
Q

List 9 drugs/agents that decrease T4 absorption?

A
  • Antacids (aluminum hydroxide, calcium carbonate)
  • Ferrous sulfate
  • Cholestyramine
  • Colestipol
  • Ciprofloxacin
  • PPI’s
  • Bran, Soy, and Coffee
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9
Q

List 7 drugs which induce hepatic CYP450s and increase the metabolism of T4 and T3?

A
  • Rifampin
  • Rifabutin
  • Phenobarbital
  • Phenytoin
  • Protease inhibitors
  • Carbamazepine
  • Imatinib
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10
Q

List 5 agents that are responsible for the induction of autoimmune thyroid diseas w/ hypo- or hyperthyroidism.

A
  • Interferon-α
  • Interferon-β
  • Interleukin-2
  • Lithium
  • Amiodarone
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11
Q

How long after administering thyroid hormone does it take to see the effects and why?

A

Lag time of hours or days due effects at the level of gene transcription

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12
Q

After T3 enters the nucleus and binds the thyroid receptor (TR) what occurs?

A
  • Corepressor is released and coactivator binds to the TR
  • Homodimer separates, and TR binds to RXR (retinoid X receptor)
  • Gene transcription ensues
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13
Q

Even though T3 is 3-4x more potent than T4, why is it not recommended for routine replacement therapy?

A
  • Short 1/2 life (requires multiple daily doses)
  • Higher cost
  • Difficulty w/ monitoring its adequacy of replacement
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14
Q

What are preparations of T3 best used for clinically?

A

Short-term suppression of TSH

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15
Q

What is the absorption, bioavailability, metabolism, half-life, and dosing like for the anti-thyroid drug, PTU?

A
  • Rapidly absorbed, peak serum after 1 hour
  • 50-80% bioavailability (incomplete absorption and/or large first-pass effect)
  • Renal excretion (virtually all metabolites in 24 hrs)
  • Half-life = 1.5 hours
  • 3-4 doses/day (compared to 1x/day for Methimazole)
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16
Q

What is the absorption, bioavailability, metabolism, half-life, and dosing like for the anti-thyroid drug, Methimazole?

A
  • Completely absorbed
  • Slower renal excretion than PTU (65% dose recovered - 48 hrs)
  • Half-life = 6 hrs
  • Once daily dosing
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17
Q

Why are the anti-thyroid drugs, PTU and Methimazole, generally not recommended in pregnancy; which drug should be given if therapy is requied?

A
  • Can cross the placenta and become concentrated in fetal thyroid
  • PTU is recommended in first trimester
  • Methimazole is drug of choice in second and third trimester
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18
Q

What is the main MOA of both PTU and Methimazole?

A
  • Inhibit thyroidal peroxidase-catalyzed rxns

- Blocks iodide organification

  • Inhibits coupling of MIT and DIT to form T3 and T4
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19
Q

How does the fall in T3 concentration with PTU + iodine differ from that of Methimazole + iodine?

A

PTU blocks peripheral conversion of T4 –> T3; significantly greater fall in [T3] and T3:T4 ratio

20
Q

What effect to PTU and Methimazole have on thyroid gland iodide uptake?

A
  • Do NOT block thyroid gland iodide uptake
  • Act to inhibit hormone synthesis, rather than release
21
Q

How long must therapy with PTU or Methimazole be given before stores of T4 and T3 are depleted?

A

3-4 weeks of therapy

22
Q

What are the most common AE’s associated with PTU or Methimazole?

A
  • Maculopapular pruritic rash, at times accompanied by:
  • Fever + nausea + GI distress
23
Q

What are some of the rare AE’s associated with PTU or Methimazole; which is more specific to each?

A
  • Urticarial rash + Vasculitis + Lupus-like rxn
  • LAD
  • Hypoprothrombinemia
  • Acute arthralgia
  • Hepatitis (more common w/ PTU)
  • Cholestatic jaundice (more common w/ methimazole)
24
Q

What is the most serious AE associated with PTU or Methimazole; who is most at risk and how is this condition reversed?

A
  • Agranulocytosis (granulocyte count <500 cells/mm3)
  • Risk ↑ in older pt’s and those receiving high-dose methimazole
  • Reversed w/ drug discontinuation and CSF’s
25
Q

What is the MOA of the monovalent anions perchlorate, pertechnetate, and thiocyanate as anti-thyroid agents?

A

Block thyroid gland uptake of iodide by competitively inhibiting the iodide transport mechanism

26
Q

What is the MOA of the anti-thyroid agent, Potassium Iodide?

A
  • Inhibit organification and hormone release
  • ↓ the size and vascularity of hyperplastic thyroid gland
27
Q

What are the 3 clinical uses of the anti-thyroid agent, Potassium Iodide?

A

1) Thyroid storm - thyrotoxic sx’s improve rapidly (within 2-7 days)
2) Preoperative reduction of hyperplastic thyroid
3) Block thyroidal uptake of radioactive isotopes of iodine in a radiation emergency or other exposure to radioactive iodine

28
Q

Although uncommon, what are some of the AE’s which may be seen with the anti-thyroid agent, Potassium Iodide?

A
  • Acneiform rash
  • Swollen salivary glands
  • Mucous membrane ulcerations
  • Conjunctivitis
  • Metallic taste
29
Q

Who should you avoid giving the anti-thyroid agent, Potassium Iodide?

A

Pregnant women, since iodides can cross the placenta and cause fetal goiter

30
Q

What effect does radioactive iodinde (131I) have on the thyroid?

A

β-ray radiation causes destruction of thyroid parenchyma, evidenced by epithelial swelling, follicular disruption, edema, and leukocyte infiltration

31
Q

What is radioactive iodinde (131I) used for and what are the advantages of using it?

A
  • For tx of thyrotoxicosis
  • Advantages = ease of administration, effectiveness, low expense, and absence of pain
32
Q

Which β-blockers are effective adjunctive agents in the management of thyrotoxicosis and which is most commonly used?

A
  • Those w/o sympathomimetic activity (i.e., metoprolol, propranolol, and atenolol)
  • Propranolol is most commonly used
33
Q

What effect do β-blockers have on thyroid levels?

A
  • Improve hyperthyroid sx’s, but typically do not alter levels
  • High doses of propranolol have been shown to reduce T3 through blockade of peripheral conversion of T4 –> T3
34
Q

Radioactive iodine 131I is contraindicated in whom?

A

Women who are pregnant or breast feeding

35
Q

Which anti-thyroid drugs are considered safe in women who are breast feeding?

A

The thiomides —> PTU and Methimazole

36
Q

How do adults differ from infants/children in the amount of T4 needed per body weight?

A

Infants/children require MORE T4 per body weight than adults

37
Q

How should T4 be given and how long does it take to reach steady state levels?

A
  • Given on empty stomach (due to interactions with foods and drugs)
  • Takes 6-8 weeks to reach steady-state levels
38
Q

How is hypothyroidism managed in someone with myxedema coma as far as route of administration and dosing?

A
  • Give T4 via IV due to poor absorption in pt’s w/ myxedema coma
  • Large loading dose of T4 followed by smaller IV dosing
39
Q

How should a patient with myxedema and coronary artery disease be managed with T4?

A

Correction of myxedema with T4 must be done cautiously to avoid provoking arrhythmia, angina, or acute MI (sx’s of elevated T4)

40
Q

Why is management of hypothyroidism in pt’s trying to get pregnant and those currently pregnant so important?

A
  • Hypothyroid women are typically infertile until restoration of normal thyroid levels
  • Maintenance of normal levels is crucial due to fetal brain development dependence of maternal T4
41
Q

When is anti-thyroid drug therapy most useful for Grave’s disease and what are the preferred agents?

A
  • Most useful in young pt’s w/ small glands and mild disease
  • Methimazole or PTU administered until remission (12-18 mo. of tx)
  • Methimazole is preferable to PTU (EXCEPT in pregnancy) due to once-daily dosing
42
Q

When is a thyroidectomy the preferred tx for Grave’s disease and what % of these pt’s will require thyroid supplementation?

A
  • Tx of choice for pt’s w/ very large glands or multinodular goiter
  • 80-90% will require thyroid supplementation
43
Q

When is radioactive iodine the preferred tx for Grave’s disease; what about in pt’s w/ underlying heart disease, severe toxicosis, and the elderly?

A
  • Preferred tx for most pt’s >21 years of age
  • In pt’s w/ underlying heart disease, severe thyrotoxicosis, or elderly tx w/ anti-thyroids until pt is euthyroid is preferable
  • 80% will develop hypothyroidism and require replacement therapy
44
Q

What are the adjunct drugs which can be added to anti-thyroid therapy in pt with Graves?

A
  • β-blockers w/o intrinsic sympathomimetic activity may be helpful in controlling tachycardia, HTN, and atrial fibrillation
  • If β-blocker is contraindicated can give the CCB, diltiazem, for management of tachycardia
45
Q

Which drugs are indicated for treating thyroid storm (thyrotoxic crisis) and why is each given?

A
  • β-blockers to control the arrhythmia
  • Potassium iodide to prevent release of thyroid hormones from thyroid gland
  • PTU or methimazole to block hormone synthesis
  • IV hydrocortisone to protect against shock and to block conversion of T4 to T3 in peripheral tissues/blood
  • Supportive therapy to control any underlying issues
46
Q

In the rare situation where anti-thyroid agents are inadequate in controlling thyroid storm, what can be done?

A

Plasmapheresis or peritoneal dialysis may be used to lower levels of circulating T4

ER II Exam 2 (15 decks)

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