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  • Image not available. The molecular biology of the thyroid hormones and their receptors has provided an in-depth understanding of the various mutations that give rise to hyper- and hypothyroidism.
  • Image not available. Thyrotoxicosis is most commonly caused by Graves's disease, which is an autoimmune disorder in which thyroid-stimulating antibody (TSAb) directed against the thyrotropin receptor elicits the same biologic response as thyroid-stimulating hormone (TSH).
  • Image not available. Hyperthyroidism may be treated with antithyroid drugs such as propylthiouracil (PTU) or methimazole (MMI), radioactive iodine (RAI: 131I), or surgical removal of the thyroid gland; selection of the initial treatment approach is based on patient characteristics such as age, concurrent physiology (e.g., pregnancy), comorbidities (e.g., chronic obstructive lung disease), and convenience.
  • Image not available. PTU and MMI reduce the synthesis of thyroid hormones and are similar in efficacy and adverse effects, but their dosing ranges differ by 10-fold.
  • Image not available. Response to PTU and MMI is seen in 4 to 6 weeks with a maximal response in 4 to 6 months; treatment usually continues for 1 to 2 years, and therapy is monitored by clinical signs and symptoms and by measuring the serum concentrations of TSH and free thyroxine (T4).
  • Image not available. Many patients choose to have ablative therapy with 131I rather than undergo repeated courses of PTU or MMI; most patients receiving RAI eventually become hypothyroid and require thyroid hormone supplementation.
  • Image not available.Adjunctive therapy with β-blockers controls the adrenergic symptoms of thyrotoxicosis but does not correct the underlying disorder; iodine may also be used adjunctively in preparation for surgery and acutely for thyroid storm.
  • Image not available. Hypothyroidism is most often due to an autoimmune disorder known as Hashimoto's thyroiditis, and the drug of choice for replacement therapy is levothyroxine.
  • Image not available. Monitoring of levothyroxine replacement therapy is achieved by observing clinical signs and symptoms and by measuring the TSH (elevated for underreplacement, suppressed for overreplacement).

Upon completion of the chapter, the reader will be able to:

  • 1. Describe the signs and symptoms of hyperthyroidism and hypothyroidism.
  • 2. Outline the changes seen in thyroid function tests (free and total triiodothyronine [T3] and thyroxine [T4], force-time integral [FTI] and thyroid-stimulating hormone [TSH]) and the radioactive iodine uptake (RAIU) scan in hyperthyroidism and hypothyroidism.
  • 3. Describe the mode of action, patient selection, maintenance and maximal doses, drug interactions, and adverse effects for thionamides, radioactive iodine (RAI), ?-blockers, and iodides.
  • 4. Outline the treatment for thyroid storm and Graves ophthalmopathy.
  • 5. Compare and contrast the products available for thyroid supplementation in hypothyroidism; describe the drug of choice.
  • 6. Outline the starting and maintenance doses and adverse effects for levothyroxine as well as the end point and monitoring of therapy.
  • 7. Describe the diagnosis, prognosis, and treatment of thyroid carcinoma.

Thyroid hormones affect the function of virtually every organ system. In the child, thyroid hormone is critical for normal growth and development. In the adult, the major role of thyroid hormone is to maintain metabolic stability. Substantial reservoirs of thyroid hormone in ...

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