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Pharmacology- Test 5 > Thyroid Drugs > Flashcards

Thyroid Drugs Flashcards

1
Q

What is the most suitable preparation (most used drug) to treat hypothyroidism?

A

Levothyroxine (T4)

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2
Q

T/F Long-term replacement therapy is needed for the treatment of hypothyroidism?

A

TRUE

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3
Q

What are the limitations to dosing for treatment of hypothyroidism?

A

Physiologic doses can mimic hyperthyroidism:

  • cardiovascular effects
  • weight loss
  • osteoporosis
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4
Q

What are the dosing changes associated with treatment of hypothyroidism?

A

Dose changes are made slowly until a steady state level is reached

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5
Q

What are the 2 drugs that are treatments for hypothyroidism?

A

(1) Levo-thyroxine (T4)

2) Liothyronine (triiodothyronine/T3

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6
Q

Which one of the hypothyroidism drugs is preferred? Why? (5)

A

Levo-thyroxine is preferred:

  • longer half-life (less dosing)
  • synthetic T4 will convert to T3 (in liver)
  • low cost
  • easy to monitor in serum
  • no immediate CV effects (T3 has immediate CV effects)
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7
Q

Which hypothyroid drug is more potent?

A

Liothyronine (Triiodothyronine, T3)

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8
Q

T/F Liothyronine is an active hormone.

A

TRUE

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9
Q

When would you take Liothyronine?

A
  • In patients with severe hypothyroid

- In patients in a coma; they will be given IV T3 until patient is stabilized and then they will be maintained on T4

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10
Q

What are the possible etiologies of hyperthyroidism? (4)

A

(1) Graves’ disease
(2) Toxic nodular goiter
(3) Subacute thyroiditis
(4) Postpartum thyroiditis

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11
Q

What is the rationale in the treatment of hyperthyroidism?

A

To destroy hyperactive cells or directly inhibit thyroid hormone synthesis/release

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12
Q

What are the drugs that are used to treat hyperthyroidism?

A

(1) Thioamide drugs
(2) 131I
(3) K iodide

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13
Q

What are the therapeutic goals in the treatment of hyperthyroidism?

A

(1) Control symptoms of thyrotoxicosis
(2) Reach euthyroid state
(3) Decrease auto-antibody levels (Graves’ disease)

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14
Q

What are the Thioamide drugs?

A

(1) Propylthiouracil (PTU)

(2) Methimazole

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15
Q

Methimazole: Mechanism of Action

A
  • Directly inhibit peroxidase enzyme in T4/T3 biosynthesis
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16
Q

Propylthiouracil (PTU): Mechanism of Action

A
  • Directly inhibits peroxidase enzyme in T4/T3 biosynthesis

- Also inhibits deiodination of T4 to T4 in the liver.

17
Q

T/F When treated with PTU, blood levels of T4 decline more rapidly than T3.

A

FALSE; because PTU inhibits the deiodination of T4 to T3, blood levels of T3 decline more rapidly

18
Q

Thioamide drugs: Effects

A

Slow onset, 2-4 weeks to become euthyroid

19
Q

Why is there a slow onset for Thioamide drugs?

A

because humans store T3 and T4 and it takes a while for the continued release of preformed T3 and T4 to deplete

20
Q

Thioamide drugs: Toxicity

A
  • Both drugs are well tolerated

- Skin rash is sometimes seen

21
Q

What is the purpose of Thioamide drugs? Limitation?

A
  • To take the patient off the medication once at a euthyroid state in hopes that they will remain in the euthyroid state
  • Limitation: high relapse rate in Graves’ disease due to continued autoantibody presence/production
    ~if immune system is still active and they’re producing antibodies to the TSH receptor they they’re going to become hyperthyroid again
22
Q

Graves’ disease: Emphasis of relapse (from treatment)

A

Emphasis is given to the concept that relapse signifies persistence of a greater or lesser concentration of TSH receptor antibodies in the blood

23
Q

What would happen if treament is stopped given:

(1) High titer TSH-R Ab levels?
(2) Lower level TSH-R Ab levels?
(3) No longer measurable TSH-R Ab levels?

A

(1) There will be a quick bounce back up to hyperthyroid levels. You would need to resume treatment and hopefully the immune system will settle down and you would try and take them off at a different time
(2) There will be a delayed response back to hyperthyroidism. You would need to resume treatment and hopefully the immune system will settle down completely and you would try to take them off again at a different time
(3) There will be the patient in euthyroid state.

24
Q

Why is “permanent” remission not a good phrase for Graves’ disease?

A

There can be something that triggers the immune system at a later date that can activate the TSH-R Ab to produce another hyperthyroid state

25
Q

Radioactive Iodine: Mechanism

A
  • Active uptake exclusively into thyroid follicle cells
  • Localized tissue distruction
  • Safe
26
Q

Radioactive Iodine: Cautions

A
  • Children: thyroid cancer
  • Elderly: transient hyperthyroidism
  • Should not be used in pregnancy
27
Q

Radioactive Iodine: Complications

A

(1) Transient hyperthyroidism

(2) Permanent Hypothyroidism

28
Q

Potassium Iodide (KI): Mechanism of Action

A
  • “Paradoxical” inhibition of iodine uptake
  • Inhibition of peroxidase enzyme
  • Inhibition of proteolytic release of T4/T3 in the thyroid cell
29
Q

What is the only agent to inhibit relesase of T4/T3?

A

KI

30
Q

Which drug decreases the size and vascularity of the thyroid gland?

A

KI

31
Q

Propranolol: Mechanism of Action

A
  • Symptomatic control of B-adrenergic action

- ALSO inhibits T4 to T3 conversion in the liver

32
Q

T/F Other B-adrenergic drugs like atenolol, alprenolol, and metoprolol have similar activity.

A

FALSE; only have SLIGHT activity

33
Q

Iodinated Radiocontrast Media (Ipodate): Mechanism of Action

A
  • Inhibits T4 deiodination and rapidly decreases T3 concentrations
34
Q

What is the main use of Ipodate?

A

To visualize the gall bladder

Pharmacology- Test 5 (6 decks)

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