Thyroid Drugs Flashcards
(34 cards)
What is the most suitable preparation (most used drug) to treat hypothyroidism?
Levothyroxine (T4)
T/F Long-term replacement therapy is needed for the treatment of hypothyroidism?
TRUE
What are the limitations to dosing for treatment of hypothyroidism?
Physiologic doses can mimic hyperthyroidism:
- cardiovascular effects
- weight loss
- osteoporosis
What are the dosing changes associated with treatment of hypothyroidism?
Dose changes are made slowly until a steady state level is reached
What are the 2 drugs that are treatments for hypothyroidism?
(1) Levo-thyroxine (T4)
2) Liothyronine (triiodothyronine/T3
Which one of the hypothyroidism drugs is preferred? Why? (5)
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)
Which hypothyroid drug is more potent?
Liothyronine (Triiodothyronine, T3)
T/F Liothyronine is an active hormone.
TRUE
When would you take Liothyronine?
- 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
What are the possible etiologies of hyperthyroidism? (4)
(1) Graves’ disease
(2) Toxic nodular goiter
(3) Subacute thyroiditis
(4) Postpartum thyroiditis
What is the rationale in the treatment of hyperthyroidism?
To destroy hyperactive cells or directly inhibit thyroid hormone synthesis/release
What are the drugs that are used to treat hyperthyroidism?
(1) Thioamide drugs
(2) 131I
(3) K iodide
What are the therapeutic goals in the treatment of hyperthyroidism?
(1) Control symptoms of thyrotoxicosis
(2) Reach euthyroid state
(3) Decrease auto-antibody levels (Graves’ disease)
What are the Thioamide drugs?
(1) Propylthiouracil (PTU)
(2) Methimazole
Methimazole: Mechanism of Action
- Directly inhibit peroxidase enzyme in T4/T3 biosynthesis
Propylthiouracil (PTU): Mechanism of Action
- Directly inhibits peroxidase enzyme in T4/T3 biosynthesis
- Also inhibits deiodination of T4 to T4 in the liver.
T/F When treated with PTU, blood levels of T4 decline more rapidly than T3.
FALSE; because PTU inhibits the deiodination of T4 to T3, blood levels of T3 decline more rapidly
Thioamide drugs: Effects
Slow onset, 2-4 weeks to become euthyroid
Why is there a slow onset for Thioamide drugs?
because humans store T3 and T4 and it takes a while for the continued release of preformed T3 and T4 to deplete
Thioamide drugs: Toxicity
- Both drugs are well tolerated
- Skin rash is sometimes seen
What is the purpose of Thioamide drugs? Limitation?
- 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
Graves’ disease: Emphasis of relapse (from treatment)
Emphasis is given to the concept that relapse signifies persistence of a greater or lesser concentration of TSH receptor antibodies in the blood
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?
(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.
Why is “permanent” remission not a good phrase for Graves’ disease?
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
