ANTI-THYROID DRUGS

Rx for HYPOthyroidism
CLASS EXAMPLES INDICATION M.O.A SIDE EFFECTS
T4 L- thyroxine -Hypothyroidism -Absorption of oral T4 is Rapid increase of dose
(Tetraiodo-L- (levothyroxine sodium) incomplete and variable. /high dose therapy:
thyronine) thyroxine deficiency -It is 99.9% bound to plasma
T4 is the less active from any cause. proteins; -> angina, heart failure,
precursor of T3 “Replacement - mainly to thyroxine-binding tachycardia, atrial
therapy” globulin (TBG) fibrillation
-T4 passes in to the -T4 is converted to the active
cells of target organ IMPORTANT: form; T3 in tissues. Especially in the elderly
and combines with Treatment must be -T4 is deiodinated and conjugated and in ischaemic heart
specific nuclear life-long in the liver and excreted in bile disease
receptors. and urine.
Main Causes: t 1/2, depends on the thyroid -start with a low dose;
These receptors are Autoimmune status of the person 12.5-25
found in most (Hashimoto) micrograms/day
tissues. thyroiditis, 1o thyroid *7 days in euthyroid subjects,
failure *14 days in hypothyroism Over dose of thyroxine
-They induce protein Symptoms: Reversible *3 days in hyperthyroidism -> features similar to
synthesis (growth slowing of body thyrotoxicosis
retardation and short functions, lethargy, -With regular dosing, the steady (finger tremors,
stature in children tiredness, BMR, state plasma concentration is tachycardia)
with untreated appetite, CO, dry achieved only after 4-5
hypothyroidism) skin, cold intolerance, weeks.(t1/2x 5) Certain drugs interfere
wt, constipation with absorption –
-Increase the basal *Dosage form; T4 sodium tablets *sucralfate,
metabolic rate and -Cretinism (neonatal *strength of tablets; in *cholestyramine resin
O2 consumption. hypothyroidism) micrograms(50ug, 100ug/tablet) *iron/calcium/ mineral
-hypo at any age *Store tablets <250C; preferably supplements
-T4 causes -Myxoedema in the refrigerator *aluminium hydroxide
proliferation of beta -Autoimmune *Once a day therapy in the *Some soy products
adrenergic receptors thyroiditis morning. Before breakfast; for *Phenytoin/
particularly in the -Subclinical (no better absorption and better carbamazepine/
CVS. features) bioavailability. rifampicin enhances
- therefore there is hypothyroidism excretion through
increased sensitivity *Elderly and in patients with IHD effect on liver enzymes
to catecholamines Dx: Low free thyroxin + start with 12.5-25ug/day.
(epinephrine and TSH **Increase the dose gradually ->This may necessitate
norepinephrine) every 2- 4 weeks an increase in the dose

T3 Liothyronine sodium -Hypothyroidism -Is about 5 times as biologically associated with more
(Triiodo- L- (Na salt of T3) -Severe active as T4 adverse effect
thyronine) hypothyroidism -Its binding to plasma proteins is (hence, uses is
Less protein bound (hypothyroid coma) weaker than T4 uncommon)
 faster action than -T ½ is 2 days in euthyroid subjects
T4 Used only when a -It is mainly used to manage
quicker onset of action severe hypothyroidism;
T3 is the major is needed e.g. impending coma or coma;
mediator of myxodema coma administered IV or through a
physiological effects nasogastric tube (a high dose).
-Used (together with
hydrocortisone)

Liotrix Constituent of many Expensive with no Mimics ratio of normal thyroid

commercial thyroid special advantage secretion
hormone in fixed
ratio of 4:1 (T4:T3)
Rx of HYPERthyroidism
CLASS EXAMPLES INDICATION M.O.A SIDE EFFECTS
1. Inhibitors of Propylthiouracil 1. Management of *Inhibit iodine organification -Nausea
hormone “Graves” disease: an -> blocking thyroxine peroxidase -Taste disturbance
synthesis *Inhibits peripheral autoimmunedisorder which promotes coupling of I- -Pruritic rash
(Thionamides) deiodination of T4 to T3 characterized by with Tyrosine  MIT and with -vasculitis
*Reserved for pts
Inhibits: remissions and MIT DIT) -arthralgia
->oxidation of intolerant of carbimazole
exacerbations. *Immunosupressive -cholestatic jaundice
iodide (1/10th activity of
2. Hyperthyroidism Hepatitis
->Iodination of methimazole)
*High agranulocytosis due to toxic multi *accumulate in the thyroid -lymphadenopathy
tyrosine
(report any fever/ sore nodular goitre: proir to Onset of effect ~ 3-4 wks (time - hypo
(organification)
->Coupling of throat which tend to surgery for depletion of preformed prothrombinaemia
iodotyrosines precede this) 3. Management of hormone) - Agranulocytosis +
thyroid crisis (severe ->Although t 1/2 is short; 2-4 hrs, Neutropenia
Methimazole hyperthyroidism/ ->High intrathyroidal (most dangerous
thyroid storm) concentration of all thionamides -> sore throat+fever)
*not bound to plasma 4. Adjuvant therapy for 30-40 hrs prolong their
proteins and is with radio iodine duration of action Cross sensitivity b/wn
metabolised in the liver therapy ->Hence a single daily dose is propylthiouracil and
and excreted in urine methimazole ~ 50%
adequate (once a day therapy).
Carbimazole ->Do not block the release of
*All are given p.o. stored thyroid hormones
*Drug of choice in
*Rapidly absorbed ->Hence clinical effects are seen
Grave’s
*Converted in vivo to
from the gut only after7-10days (when
methimazole-1st pass met preformed T4 is depleted)
(rapidly and completely)

2. Inhibitors of Perchlorates Anion Inhibitors: Competitively inhibits the uptake Causes aplastic
iodide trapping (Thiocyanates/ Nitrates) Potassium perchlorate of iodine anaemia (rarely used)

3. Inhibitors of Iodine, iodides of K & *Short term Rx only -Action not clear -Adverse reactions to
hormone Na, organic iodides (antithyroid effect -Inhibits organification and iodide (iodism) is rare
release drops) hormone release and reversed by
*Inhibit all aspects of T4 *Quick (2-7 days) -Decreases size and vascularity of withdrawal
formation + release effect  useful in gland (smaller) ->rash, swollen salivary
thyroid storm -useful pre-thyroidectomy (10 glands, conjunctivitis,
days prior) rhinorhoea, drug fever,
-Reduces conversion of T4 to T3 metalic taste
Inhibit thyrotropin action

4. Agent that I131, I 125, I 123 1.Relapse of Graves Concentrated by thyroid ->Eventual
destroy thyroid disease following Emits beta rays which destroy hypothyroidism:
tissue thionamide therapy thryoid tissue within few weeks -> identify early and
2.In patients who *cytotoxic effect is restricted to treat with thyroxine
develop cells of thyroid follicles ->c/i: pregnancy and in
agranulocytosis *Does not damage the breast feeding
following thionamide parathyroid
therapy *Given p.o (syrup)
3.To treat some types *single dose (8wks for full effect)
of thyroid carcinoma * Stabilise Pt first with
with metastasis Carbimazole before 131I
*Stop Carbimazole 3-4/7 b4 131I
Rx

5. β blockers Propanolol (non- 3. Before and after radio 1. In newly diagnosed, until thyroid c/i: asthma
only as short selective) iodine therapy function test results are available for
term adjuvant 4. To treat thyroid crisis confirmation.
therapy (“thyroid storm”) 2. Concurrently with the
commencement of thionamides until
their action is well established