Anti-Thyroid Drugs and Its Applications.pptx

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

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

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: T hyroid gland failure despite proper stimulation from the pituitary. SECONDARY HYPOTHYROIDISM: F ailure of the pituitary to produce TSH to stimulate the thyroid gland. TERTIARY HYPOTHYROIDISM: F ailure 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. I odine 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. O ne 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; 12 th 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

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