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Anti Thyroid
Anti Thyroid
Thioamides
Iodides
Radioiodine
receptor blocking agents
THIOAMIDES
Thioamides decreases thyroid hormone
formation
Thioamides (Propylthiouracil,
methimazole and carbimazole)
prevents formation of thyroid
hormone from iodide and tyrosine.
THIOAMIDES
Mechanism of action:
These agents are actively concentrated by the thyroid
gland against a concentration gradient.
Their primary effect is to inhibit thyroid hormone
synthesis by interfering with thyroperoxidase (TPO)
mediated iodination of tyrosine residues in thyroglobulin.
Partly block the coupling of two iodinated tyrosines (DIT
and MIT) to form thyroxine (T4 ) or triiodothyronine (T3 ).
THIOAMIDES
Thioamide (rarely, thionamide) are the most important
class of antithyroid compounds in clinical practice used
in nondestructive therapy of hyperthyroidism.
These agents are potent inhibitors of TPO, which is
responsible for the iodination of tyrosine residues of
thyroglobulin and the coupling of iodotyrosine residues
to form iodothyronines.
The most clinically useful thioamides are thioureylenes
(=N-CS-N=), which are five- or six- membered
structures.
6-Propyl-2-thiouracil
Used to manage
hyperthyroidism which is due
to an overactive thyroid gland
(Grave's disease).
Ethyl 3-methyl-2thioimidazoline-1carboxylate
Structure-activity relationships
The C2 thioketo/ thioenol group and an
unsubstituted N1 position are essential for
activity of six membered thioamides.
The enolic hydroxyl group at C4 in PTU and the
presence of alkyl group at C5 and C6 enhance the
inhibitory potency.
6-Propyl-2-thiouracil
Structure-activity relationships
Structure-activity relationships
Efforts to improve the taste and
decrease the rate of release of
methimazole led to the development
of carbimazole.
Carbimazole, the pro-drug derivative
of methimazole, gives rise to
methimazole in vivo and is used in
the same dosage.
IODIDES
Iodides in High Concentrations Decrease
Thyroid Activity and Thyroid Gland Size.
When iodides are present in the blood in high
concentration (100 times the normal plasma
level: 0.6 to 0.8 g/lit), most activities of the
thyroid gland are decreased.
Reduce the rate of iodide trapping
Decrease its blood supply
It also lowers the elevated BMR.
Net effect is the reduction of size of thyroid gland
IODIDES
It also has been suggested that excess iodide might
change the conformation of thyroglobulin, making
the protein less susceptible to thyroidal proteolysis.
Iodide, as Lugol's solution (Strong Iodine Solution
USP) or as saturated potassium iodide solution, is
administered for approximately 2 weeks to ensure
decreased vascularity and firming of the gland.
Lugols solution contains 5% iodine (5 grams in 100
mL) and 10% potassium iodide (10 grams in 100
mL).
RADIOACTIVE IODIDE
Definitive treatment: given primarily to destroy the hyper
functioning thyroid tissue.
Available as Sodium iodide I 131 (Na131I)
Radioiodine is an oral medication and given as single dose.
Patients taking radioiodine therapy, few required more than
one dose.
Usual dose: 100 to 200 Ci per gram of weight of thyroid
gland.
RADIOACTIVE IODIDE
Radioiodine is taken by the follicular cell in the
same way as iodine and beta emission of
radioiodine causes necrosis and decrease the
activity of thyroid tissue.
The cell necrosis induced by radioiodine occurs
gradually.
May elapse hyperthyroidism (after 6-18 weeks or
later of the treatment) before a hypothyroid or
euthyroid state is achieved.
RADIOACTIVE IODIDE
Pregnancy: Sodium iodide I 131 has been shown to cause harm to a
developing fetus. Use in pregnant women should be avoided.
Nursing mother: Iodine is excreted in breast milk. Therefore,
formula feedings for infants are strongly recommended for nursing
women requiring sodium iodide I 131 treatment.
The side effects commonly seen with sodium iodide I 131 treatment
are mild with the smaller doses given for hyperthyroidism but may
be more severe with the larger doses given for thyroid cancer.
Sodium iodide I 131 may cause suppression of the bone marrow,
resulting in anemia, and reductions in white blood cells and
platelets.
Increased risk of death from cardiovascular