Thyroid & Antithyroid Drugs Flashcards
Drugs for treatment of hypothyroidism
Levothyroxine (T4)
Liothyronine (T3)
Liotrix (T4 and T3)
Drug of choice for treatment of Grave’s disease (due to longer half-life and lower adverse effect profile)
Methimazole
Drug of choice for treatment of thyroid storm, because of it’s additional action to prevent peripheral conversion of T4->T3
Propylthiouracil (PTU)
MOA of antithyroid drugs (PTU and methimazole)
Irreversibly inhibit the peroxidase enzyme. The content of thyroglobulin gradually decreases due to:
- The continued secretion and inhibition of synthesis
- Suppression of hormone secretion
- PTU (ONLY!!) prevents peripheral conversion of T4 -> T3
Explain why antithyroid drugs are goitrogenic.
There is a compensatory increase in TSH secretion with continued decrease of thyroid hormone synthesis and secretion.
*NB: because of this, it is necessary to administer T4 to prevent goiter.
Adverse effects of PTU and methimazole
Most common: Rash
Other: Nausea, headache, pain/stiffness of joints. Mild, transient leukopenia is common in children.
Most serious: Agranulocytosis
Monovalent anions that competitively inhibit the iodide/sodium pump (symport).
Perchlorate, thiocyanate, fluoborate
High doses of perchlorate can cause?
Fatal aplastic anemia
Mood stabilizer that inhibits thyroid hormone secretion and may interfere with Ca2+ metabolism
Lithium
MOA of iodide (aka Lugol’s solution, potassium iodide)
Primary MOA at therapeutic doses is inhibition of T3/T4 release.
High concentrations will decrease (but not ABOLISH) thyroid hormone synthesis through inhibition of iodine organification.
Reduce size and vascularity of thyroid gland
Used in diagnosis of thyroid function and as means of definitive treatment of hyperthyroidism
Radioactive iodine (131-I)
Which particles of 131-I cause necrosis of the thyroid gland?
Beta particles
Which particles of 131-I pass through soft tissues and can be detected by an external counter?
Gamma particles
Control thyrotoxic symptoms associated with increased sensitivity to catecholamines; useful in thyrotoxic crisis.
Beta blockers: propranolol, metoprolol, atenolol
Beta blocker that has the additional effect of preventing the peripheral conversion of T4 –> T3 at high doses through inhibition of hepatic 5’-deiodinase I
Propranolol
Contraindications for the use of beta blockers in thyroid disease
Cardiac failure, bronchial asthma
Control tachycardia and decrease the incidence of supra ventricular arrhythmias in thyroid storm; not used with beta blockers
CCBs (verapamil and diltiazem appear to be the most effective)
MOA of glucocorticoids in thyrotoxic crisis
- Decrease peripheral conversion of T4 to T3; increase the conversion of T4 to rT3.
- Inhibit TSH secretion, decrease plasma TBG levels, inhibit iodide uptake and T4/T3 release
MOA of cholestyramine and other bile acid-binding resins in thyrotoxic crisis
Bind thyroid hormone conjugates secreted in bile and prevent their enterohepatic recycling.
