A detail description on Anti-thyroid drugs, its classification and disorders.

1. ANTI-THYROID
DRUGS
Komal Chandrapaxi
VP22PHARM0200009
M.Pharm 2ndsem.

2. CONTENTS
 Introduction
 Thyroid Hormones
 Synthesis, Storage and Release
 Thyroid Disorders
 Classification of Thyroid Drugs
 References

3. INTRODUCTION
 Its is a butterfly shapes gland that is situated
on the front of the neck.
 It has two side lobes, connected by a bridge in
the middle.
 Brownish red in color, rich with blood vessels.
Functions:
Thyroid secretes hormones, collectively called
thyroid hormones.
Thyroid hormones influencing- Metabolism,
body temperature and growth/development. Fig.no. 1 - Thyroid Gland

4. THYROID HORMONES
 Thyroid gland secrets 3 main hormones:
Thyroxine(T4) Important for growth and Both are considered
development as thyroid hormone
Triidothyronine(T3)
Calcitonine - Important for control of plasma Ca2
 Thyroxine is secreted in more amounts compared to triiodothyronine.
 The tissue of the thyroid gland is composed mostly of thyroid follicles.
 The follicles are made up of a central cavity filled with a sticky fluid called
colloid.

5.  Between the follicles single or small groups cells; parafollicular
cells, also called as c-cells which secrete the calcitonin hormone.
Fig.no.2 – Microscopic structure of thyroid gland

6. SYNTHESIS, RELEASE OF HORMONES
 The thyroid hormones are synthesized and stored in the thyroid
follicles as a part of “thyroglobulin” molecule, which is a
glycoprotein synthesized by thyroid cells.
 This involves the following processes-
a) Iodine uptake
b) Oxidation and iodination
c) Coupling
d) Storage and release
e) Peripheral conversion of T4 to T3

7. Fig.no.3 – Synthesis, storage and release of thyroid hormone

8. THYROID DISORDERS

9. HYPERTHYROIDISM
 Thyrotoxicosis
 Overproduction of thyroid hormones
Grave’s disease (most common)
Toxic nodular goiter
CAUSES
Fig.no.4 - Symptoms

10. Fig.no.5 – Grave’s disease and Goiter

11. HYPOTHYROIDISM
 Insufficiency in the amount of thyroid hormone in the body
 PRIMARY HYPOTHYROIDISM:
Thyroid gland failure despite proper stimulation from the pituitary.
 SECONDARY HYPOTHYROIDISM:
Failure of the pituitary to produce TSH to stimulate the thyroid
gland.
 TERTIARY HYPOTHYROIDISM:
Failure of the hypothalamus.

12.  Hashimoto’s thyroiditis
 Congenital hypothyroidism Fig.no.6 - Hashimoto’s thyroiditis
 Myxoedema
Fig.no.7 - Critinism
CAUSES

13. TREATMENT OF HYPERTHYROIDISM
Fig.no.8 – Classification of Anti-thyroid drugs

14.  The thioamide antithyroid (class1) and ionic inhibitors(class2) are
also called goitrogens.
 Because, if given in excess they cause enlargement of thyroid by
feedback release of TSH.

15. Fig.no.9 – Action of Drugs

16. • The thioamide hormone synthesis inhibitors are called “anti-thyroid drugs”.
• Antithyroid drugs bind to thyroid peroxidase and prevent oxidation of
iodide/iodotyrosyl residues.
1)Inhibit iodination of tyrosine residues in thyroglobuline.
2) Inhibit coupling of iodotyrosine residues to form T3 and T4.
• Simply this class drug decreases the output of thyroid hormone from the
gland so decreases the sign and symptoms of thyrotoxicosis.
• Propyl Thiouracil- Inhibit conversion of T4-T3- Mostly in type 1st diabetes
mellitus- but methamizole & Carbamazole not have this action
 Inhibit hormone synthesis (Thioamides)

17. Pharmacokinetics :
• Administered orally.
• T ½ is 6-15hrs.
• Carbimazole is converted to its active
metabolite, i.e; methimazole.
• Cross placenta barrier and and also
appear in the milk.
• Propylthiouracil(PTU) – highly protein
bound, metabolized in liver and
excreted in urine.
Adverse Effects :
• High does: Causes excess
TSH production and
Enlargement of thyroid gland
(Goiter).
• Other side effects: GI
intolerance, Skin rashes,
joint pain.
• Graying or loss of hair, loss
of taste, fever & liver
damage.

18.  Inhibit hormone release (Iodine and Iodides)
• It is the fastest acting thyroid inhibitor.
• Iodine is covered in to iodide (I-) and due to negative feedback
mechanism iodide inhibit release of thyroid hormone.
• Within 1-2 days of starting of treatment causes inhibition of
secretion of thyroid hormone.
• Iodine mostly orally in solution with potassium Iodide( Lugols
iodine)
• Within daily administration, peak effects are seen in 10-15 days.

19. Adverse Effects :
• Acute reaction- Only in people
sensitive to iodine.
Symptoms like- joint pain, swelling
of lips, fever, angio-edema.
• Long term use- can cause
goiter.
Uses :
• Treatment of thyrotoxic crisis –
Thyroid storm.
• Preoperative preparation – for
thyroidetomy in Grave’s disease.

20.  Destroy thyroid tissue (Radioactive Iodine)
• I-131 is the only isotope used in treatment of thyrotoxicosis
• Half life – 8days, available as sodium salt; given orally.
• One of the advantage of radioactive iodine is it produce necrosis of cell
(affected thyroid follicular cell) without damaging neighboring tissue.
• Average therapeutic dose – 3to6m curie.
Side effects :
Hypothyroidism
Increase risk of thyroid cancer
Very slow response observed for treatment with I-131

21. Mechanism of Action :
The isotope emit
both (β) & gama (δ) radiations
Have shorter range
Penetrate tissue
upto 0.5-2mm
Pyknosis and
necrosis by
fibrosis
Pass through
tissue without
damage

22. REFERENCES
 Tripathi KD; Essential of Medical Pharmacology; Eight edition;
Jaypee brothers Medical Publisher Pvt. Ltd; New Delhi; Page.no.
267-279.
 Katzung Bertram G and Masters Susan B; Basic and Clinical
Pharmacology; 12th edition; MC Graw Hill Medical; NewYork;
Page.no. 681-696.
 Shanbhag V Tara; Pharmacology for Medical Graduates; Third
Edition; RELX India Pvt.Ltd; New Delhi; Page.no. 340-346
 www.google.com

23. THANK YOU