Hyperthyroidism is caused by excess thyroid hormone production. Treatment aims to normalize thyroid hormone levels, minimize symptoms, and provide individualized therapy based on disease severity and patient factors. Treatment options include antithyroid medications, radioactive iodine, surgery, and beta blockers. Antithyroid drugs work by inhibiting thyroid hormone synthesis and are given for 12-24 months to induce remission. Radioactive iodine is the treatment of choice for Graves' disease and destroys overactive thyroid cells with radiation. Surgery may be considered for large goiters or lack of drug treatment response. Therapy for thyroid storm involves rapidly suppressing hormone levels along with antiadrenergic and corticosteroid treatment.

1. Hyperthyroidism
Dr. Chavan P. R.
Pharm D

2. DEFINITION
 Thyrotoxicosis is any syndrome
caused by excess thyroid hormone
and can be related to excess hormone
production (hyperthyroidism).

3. Etiology

4. PATHOPHYSIOLOGY

5. CLINICAL PRESENTATION

6. DIAGNOSIS

7. Thyroid level chart

8. DESIRED OUTCOME
 To normalize the production of thyroid
hormone
 Minimize symptoms and long-term
consequences
 Provide individualized therapy based on
the type and severity of disease, patient
age and gender, existence of
nonthyroidal conditions, and response to
previous therapy

9. NONPHARMACOLOGIC
THERAPY
 Surgical removal of the thyroid gland should be
considered in patients with a large gland (>80 g), severe
ophthalmopathy, or a lack of remission on antithyroid
drug treatment.
 If thyroidectomy is planned, propylthiouracil (PTU) or
methimazole (MMI) is usually given until the patient is
biochemically euthyroid (usually 6 to 8 weeks), followed
by the addition of iodides (500 mg/day) for 10 to 14 days
before surgery to decrease the vascularity of the gland.
Levothyroxine may be added to maintain the euthyroid
state while the thionamides are continued.
 Complication of surgery: 1.Hypothyroidism, 2.Recurrent
laryngeal nerve injury, 3.Airway obstruction, 4.Wound

12. Treatment

13. Mechanisms of antithyroid drugs

14. Thioureas (Thionamides)
o Propylthiouracil(PTU) and Methimazole
*Mechanism of action
 PTU and methimazole block thyroid hormone synthesis
by inhibiting the peroxidase enzyme system of the
thyroid, preventing oxidation of trapped iodide and by
inhibiting coupling of MIT and DIT to form T4 and T3.
 PTU (but not methimazole) also inhibits peripheral
conversion of T4 to T3.
*Initial dose
 Usual initial doses include PTU300 to 600 mg daily
(usually in three or four divided doses) or methimazole
30 to 60 mgdaily given in three divided doses.
 Evidence exists that both drugs can be given as a
single daily dose.

15. *Maintenance dose
 Typical daily maintenance doses are PTU 50 to
300 mg and methimazole 5 to 30 mg.
 Continue therapy for 12 to 24 months to induce
long-term remission.
 Improvement in symptoms and laboratory
abnormalities should occur within 4 to 8 weeks, at
which time a tapering regimen to maintenance
doses can be started.
*Monitoring
 Monitor patients every 6 to 12 months after
remission.

16. Adverse effects
 Agranulocytosis (with fever, malaise,
gingivitis, or pharyngeal infection,
 Aplastic anemia,
 Lupus-like syndrome,
 Polymyositis,
 GI intolerance,
 Hepatotoxicity,
 Hypoprothrombinemia
 Pruritic maculopapular rashes,
 Arthralgias, fever, and
 Benign transient leukopenia (white blood cell
count

17. Iodides
*Mechanism of action
 Acutely blocks thyroid hormone release, inhibit thyroid
hormone biosynthesis by interfering with intrathyroidal
iodide use, and decreases size and vascularity of the
gland.
*Dosage form
 Potassium iodide is available as a saturated solution
(SSKI, 38 mg iodide per drop) or as Lugol`s solution,
containing 6.3 mg of iodide per drop.
*Dose
 Typical starting dose of SSKI is 3 to 10 drops daily (120–
400 mg) in water or juice. Whenused to prepare a patient
for surgery, it should be administered 7 to 14 days
preoperatively. Symptom improve occur within 2-7 days of

18. Adverse effects
 Hypersensitivity reactions (skin
rashes, drug fever, rhinitis,
conjunctivitis),
 Salivary gland swelling,
 “iodism” (metallic taste, burning mouth
and throat, sore teeth and gums,
symptomsof a head cold, and
sometimes stomach upset and
diarrhea), and
 Gynecomastia.

19. Adrenergic Blockers
o Propranolol and Nadolol
*β-Blockers are used to ameliorate thyrotoxic
symptoms such as palpitations, anxiety, tremor, and
heat intolerance, they have no effect on peripheral
thyrotoxicosis or prevent thyroid storm.
*β-Blockers are usually used as adjunctive therapy with
antithyroid drugs and RAI or iodide.
The only conditions for which β-blockers are primary
therapy for thyrotoxicosis are those associated with
thyroiditis.
*Initial Dose
 Propranolol dose 20 to 40 mg orally four times daily
is effective for most patients (heart rate

20. Contraindications
1.Decompensated heart failure
2.Sinus bradycardia.
3.Concomitant therapy with monoamine
oxidase inhibitors or tricyclic
antidepressants.
4.Patients with spontaneous hypoglycemia.
 Centrally acting sympatholytic (eg, clonidine)
and calcium channel antagonists (eg,
diltiazem) may be useful for symptom control
when contraindications to β-blockade exist.

21. Adverse effects
 Nausea,
 Vomiting,
 Anxiety,
 Insomnia,
 Lightheadedness,
 Bradycardia, and
 Hematologic disturbances.

22. Radioactive Iodine
* Mechanism
 Sodium iodide–131 is an oral liquid that
concentrates in the thyroid and initially
disrupts hormone synthesis by
incorporating into thyroid hormones and
thyroglobulin.
*Uses:
 Agent of choice for Graves’ disease,
toxic autonomous nodules, and toxic
multinodular goiters.

23. *Dose:
 The goal of therapy is to destroy overactive thyroid
cells, and a single dose of 4000 to 8000 rad (40–80
Gy) results in a euthyroid state in 60% of patients at 6
months or sooner.
 A second dose of RAI should be given 6 months after
the first RAI treatment if the patient remains
hyperthyroid.
 Patients with cardiac disease and elderly patients are
often treated with thionamides prior to RAI ablation
because thyroid hormone levels transiently increase
after RAI treatment due to release of preformed
thyroid hormone.
 Antithyroid drugs are not routinely used after RAI
because their use is associated with a higher
incidence of posttreatment recurrence or persistent
hyperthyroidism.

24. * Adverse effects:
• Hypothyroidism commonly occurs
months to years after RAI.
• The acute, shortterm side effects
include mild thyroidal tenderness
and dysphagia.
*Contraindication:
• Pregnancy is an absolute
contraindication to use of RAI.

25. Treatment of Thyroid Storm
 Initiate the following therapeutic
measures promptly:
(1) Suppression of thyroid hormone
formation and secretion.
(2) Antiadrenergic therapy.
(3) Administration of corticosteroids.
(4) Treatment of associated
complications or coexisting factors
that may have precipitated the storm.

26.  Iodides, which rapidly block the release of preformed thyroid
hormone, should be administered after a thionamide is
initiated to inhibit iodide utilization by the overactive gland.
 Antiadrenergic therapy with the short-acting agent esmolol is
preferred because it can be used in patients with pulmonary
disease or at risk for cardiac failure and because its effects
can be rapidly reversed.
 Corticosteroids are generally recommended, but there is no
convincing evidence of adrenocortical insufficiency in thyroid
storm; their benefits may be attributed to their antipyretic
action and stabilization of blood pressure (BP).
 General supportive measures, including acetaminophen as an
antipyretic (avoid aspirin or other nonsteroidal anti-
inflammatory drugs, which may displace bound thyroid
hormone), fluid and electrolyte replacement, sedatives,
digoxin, antiarrhythmics, insulin, and antibiotics should be

27. PREGNANCY
 PTU is considered the drug of choice during
the first trimester of pregnancy
 To prevent fetal goiter and suppression of
fetal thyroid function, PTU is usually
prescribed in daily doses of 300 mg or less
and tapered to 50 to 150 mg daily after 4 to 6
weeks.
 PTU doses of less than 200 mg daily are
unlikely to produce fetal goiter.
 During the second and third trimesters, MMI
is thought to be the drug of choice because of
the greater risk of hepatotoxicity with PTU.

28. Neonatal and Pediatric
Hyperthyroidism
 The disease is usually expressed 7 to 10
days postpartum and treatment with
antithyroid drugs (PTU 5 to 10 mg/kg/day or
MMI 0.5 to 1 mg/kg/day) may be needed for
as long as 8 to 12 weeks until the antibody is
cleared.
 Iodide (potassium iodide one drop per day or
Lugol’s solution one to three drops per day)
and sodium iodate may be used for the first
few days to acutely inhibit hormone release.
 Childhood hyperthyroidism has classically
been managed with either PTU or MMI.

29. EVALUATION OF
THERAPEUTIC OUTCOMES
 Evaluation on a monthly basis until patient
reach a euthyroid condition.
 Note of Clinical signs of continuing
thyrotoxicosis or the development of
hypothyroidism
 After t4 replacement is initiated, the goal is to
maintain both the free t4 level and the TSH
concentration in the normal range.
 Once a stable dose of t4 is identified, the
patient may be followed every 6 to 12
months.

30. Thank you