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anti-thyroiddrugs.pptx
1.
2. ⦁ Thyroid gland – Wharton in 1656
⦁ Physiological significance was recognized by Graves
and Basedow.
⦁ Isolation and Crystallisation of Thyroxine(T4) –
Kendall in 1915.
⦁ Antithyroid drugs were developed as derivatives of
Thiourea which was disovered to cause goiter in rats.
3. ⦁ Thiourea was the 1st drug used in man,followed by
Thiouracil – Introduced byAstwood in 1951.
⦁ T3 --- detected ,isolated,and synthesized by Gross and
PittRivers in 1952.
4. ⦁ It is due to excessive secretion of thyroid hormones.
⦁ The two main cause are
⦁ 1. Graves’disease
⦁ 2. Toxic nodular goiter
5. ⦁ An autoimmune disorder;
⦁ Here, the IgG get bind to TSH receptor and mimic TSH
and secrete the hormones,
⦁ This lead to increase the thyroid level in the patients
⦁ Due to feed back effect the TSH level get low which
cause swelling of periorbital tissue.
6. ⦁ It produce thyroid hormone dependent of TSH, mostly
occure to nontoxic goiter
⦁ Occular changes are generally absent.
10. ⦁ Three general categories into which most of the agents
can be assigned:
⦁ Thioureylenes include all the compounds currently
used clinically
⦁ Aniline derivatives, of which the sulfonamides make
up the largest number, embrace a few substances that
have been found to inhibit thyroid hormone synthesis
⦁ Polyhydric phenols, such as resorcinol, which have
caused goiter in humans when applied to abraded skin.
11. ⦁ Inhibit hormone synthesis by inhibiting peroxidase.
⦁ Propylthiouracil also inhibits peripheral de-iodination
of T4 and T3.
⦁ Methimazole is more potent and longer acting than
propylthiouracil.
⦁ Slow in onset ~ 4 weeks.
⦁ Thiocarbamide group – essential for anti thyroid
activity
12. ⦁ Well absorbed orally, widely distributed
⦁ highly plasma protein bound
⦁ t1/2 = 1 – 10hrs
⦁ Partly metabolized in the liver and the thyroid gland ;
Carbimazole is converted to its active metabolite,
Methimazole.
⦁ Cross placental barrier and are secreted in breast milk
⦁ excreted in the urine unchanged
13. ⦁ Common adverse effects includes maculopapular rash,
GI side effects, arthralgia.
⦁ Hypothyroidism
⦁ Rare – exfoliative dermatitis, vasculitis ,lupus-like
reaction…
⦁ Severe hepatitis – seen with propylthiouracil
Agranulocytosis ( reversible) – dangerous complication
14. ⦁ USES:
⦁ 1) Non-operative therapy of hyperthyroidism.
⦁ 2) Preoperative therapy of hyperthyroidism: combined
with iodide.
⦁ 3) Thyrotoxic crisis: combined with propanalol,larger
dose of iodide…
15.
16. ⦁ Iodine – oldest and fastest acing agent. - paradoxical
effect on thyroid gland.
⦁ Iodides blocks the organification and release, through
inhibition of proteolysis.
⦁ It decrease the size and vascularity – used before
surgery.
⦁ Jod-Basedow phenomenon in susceptible individuals
⦁ It is an ideal agent for the treatment of severe
thyrotoxicosis and preoperatively.
17. ⦁ 1) Preoperative therapy of hyperthyroidism: combined
with thiourea derivatives
⦁ 2) Thyrotoxic crisis: combined with thiourea
derivatives(PTU)
⦁ 3) Prophylaxis of endemic goiter.
18. 1) Acute effects:
hypersensitivity to iodine. Manifestations are
swelling of lips, eyelids, angioedema of larynx, fever,
joint pain, petechial hemorrhages.
19. ⦁ 2) Chronic intoxication (iodism)
⦁ Others – salivary gland inflammation and acne.
⦁ Long term use of high doses – Hypothyroidsm and
goiter
⦁ Chronic use in pregnancy avoided – fetal/infantile
goiter
20.
21. ⦁ I-131 is the only isotope used in treatment of
thyrotoxicosis while others are used in diagnosis.
⦁ Administered as sodium salts of I–131 orally.
⦁ t1/2 – 8 days
⦁ Therapeutic effect depends on emission of beta rays –
destroys the thyroid gland.
22. ⦁ Most common indication – hyperthyroidism due to
Grave’s disease and Toxic Nodular Goiter.
⦁ Indicated in elderly patients, allergy to thioamides,
recurrent hyperthyroidism and in patients with systemic
diseases contraindicating surgery.
⦁ Average therapeutic dose- 3-6m curie
23. ⦁ Simple,inexpensive
⦁ No surgical risk ,scar or injury to parathyroids and
nerves
⦁ Contol of hyperthyroidism is permanent
24. ⦁ Focal soreness in the neck
⦁ Hypothyroidism
⦁ Damage to fetal thyroid
⦁ Thyroid carcinoma,Leukemia..
⦁ Radiation induced genetic damage
25.
26. ⦁ Monovalent ions like perchlorate, pertechnetate,
thiocyanate ,nitrates inhibit the iodide trapping by the
thyroid gland.
⦁ Anion inhibitors are uncommon in use because of
serious toxicity.
⦁ These are effective in iodine induced hyperthyroidism
27.
28. ⦁ Lithium is known to inhibit synthesis and release of
thyroid hormones.
⦁ Amiodarone – inhibits peripheral conversion of T4
toT3.
⦁ Antiepileptic drugs /Rifampicin – enhance hormone
metabolism.
⦁ Sulphonamides, PAS – inhibits iodination and coupling
reaction.
29.
30. ⦁ Occurs in about 0.2 – 0.4% of all pregnancies
⦁ Due to Grave’s Disease (common), Toxic nodules,
Thyroiditis…
⦁ RISK –
Fetal and Neonatal Hyperthyroidism
The drug mainly used is Methimazole due to its lower
hepatotoxic potential.