treatment thyroid, toxic goitre, carbimazole, thyrotoxicosis

1. Anti thyroid medications
Nuwan Gunapala
Registrar WD 21/40B

2. Overview
 Thyroid physiology
 Treatment options
◦ Thyoamides
◦ Iodide
◦ Steroids
◦ Lithium
◦ Other drugs

3. Thyroid physiology
 Thyroid hormones are iodine
containing amino acids
 Dietary Iodide are absorbed and
transfer in to thyroid.
 Some of iodide secret via bile and
reabsorb through enterohepatic
circulation
 Iodide enters to thyrocytes via sodium
iodide symporter

4.  Iodide enters to colloid through apical
membrane via a transporter called
pendrin
 Thyroid peroxidase enzyme located at
apical membrane of thyrocytes convert
iodide to iodine and attach it to globulin -
iodotyrosines
 Iodotyrosines condensed to form tri and
tetra iodotyrosines – thyroid peroxidase
 When there is a need these T4 and T3
molecules released in to blood.

6. Thyoamides
 Mechanism of action
◦ Inhibit thyroid peroxidase and prevents
organification of iodine and condensation
of iodotyrosines
 Propylthiouracyl also inhibit peripheral
conversion of T3

7. Thioamides
 Carbimazole
 Methimazole
 Propylthiouracil
 Methylthiouracil

8. Characteristics of thioamides
 Results appear later – 3 to 4 wks
symptoms relieved and 3 to 4 mts
BMR normalize
 Long term results in thyroid
hyperplasia
 Methimazole is potent 10 times as
propylthiouracil
 Propylthiouracil is preferable in pregnancy:
◦ It crosses the placenta less readily
◦ Is not secreted in breast milk

9.  Propylthiouracil has an early onset of
action, so use in thyroid storm

10. Adverse reactions
1. Long-term use leads to thyroid hyperplasia;
2. Pruritic maculopapular rash is the most common
adverse reaction
3. The severe adverse reaction is agranulocytosis

11. Iodide
 In pharmacologic doses the major action
is to inhibit hormone release(Wolff–
Chaikoff effect)
 Improvement in thyrotoxic symptoms
occurs within 2 -7 days, after that escape
mechanism
 Decrease of size & vascularity of the
hyperplastic gland
 Iodides in pregnancy should be avoided,
since they cross the placenta and can
cause fetal goiter

12. Clinical use
Treatment of hyperthyroidism
1. Operation preparation
2. Thyroid crisis.
Adverse reactions
1.Rash
2. Swollen salivary glands, mucous
membrane ulcerations

13. Lithium
 Reduce secretion of thyroglobulin in to
colloid
 Also reduce release of hormones from
throglobulin in to circulation
 Indications
◦ elevation of transaminases
◦ agranulocytosis
◦ allergic reaction
◦ resistance to propylthiouracil therapy

14. Steroides
 Corticosteroids reduce T4 to
T3 conversion and possibly affect the
autoimmune process in Graves’
disease
 Use in Graves disease and thyroid
storm
 Also use in graves eye disease

15. Other drugs
 Amioderone
 Barbiturates accelerate T4 breakdown
(by enzyme induction) and are also
sedative
 Because thyrotoxic patients have an
increased thyroid hormone
enterohepatic circulation,
cholesteramine has a role in treatment

16. Symptoms controlling drugs
 Propranolol will control tachycardia,
hypertension, and atrial fibrillation
 Diltiazem, can control tachycardia in
patients in whom beta-blockers are
contraindicated