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KEY CONCEPTS

KEY CONCEPTS

  • image Thyrotoxicosis is most commonly caused by Graves’ 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 Hyperthyroidism may be treated with antithyroid drugs such as methimazole (MMI) or propylthiouracil (PTU), radioactive iodine (RAI: sodium iodide-131 [131I]), or surgical removal of the thyroid gland; selection of the initial treatment approach is based on patient characteristics such as age, concurrent physiology (eg, pregnancy), comorbidities (eg, chronic obstructive lung disease), and convenience.

  • image MMI and PTU reduce the synthesis of thyroid hormones and are similar in efficacy, although their dosing ranges differ by 20-fold. Overall, PTU has a greater incidence of side effects. Agranulocytosis is a rare but severe adverse effect associated with both medications.

  • image Response to MMI and PTU is seen in 4 to 6 weeks and therefore β-blocker therapy may be concurrently initiated to reduce adrenergic symptoms. Maximal response is typically seen 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 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 Many patients choose to have ablative therapy with 131I rather than undergo repeated courses of MMI or PTU treatment; most patients receiving RAI eventually become hypothyroid and require thyroid hormone supplementation.

  • image Hypothyroidism is most often due to an autoimmune disorder known as Hashimoto's thyroiditis.

  • image The drug of choice for replacement therapy in hypothyroidism is levothyroxine.

  • image Studies of combination therapy with levothyroxine and liothyronine have not shown reproducible benefits. This approach to the treatment of hypothyroidism requires further study.

  • image Monitoring of levothyroxine replacement therapy is achieved by observing clinical signs and symptoms and by measuring the serum TSH level. An elevated TSH indicates under-replacement; a suppressed TSH indicates over-replacement.

PATIENT CARE PROCESS

Patient Care Process for the Management of Hyperthyroidism

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Collect

  • Patient characteristics (eg, age, race, sex, pregnancy status)

  • Patient history (past medical, family, social) including patient signs and symptoms: warm, smooth, moist skin, palpitations, exophthalmos, pretibial myxedema, and unusually fine hair; anxiety, tremor, heat intolerance, tachycardia, weight loss, and menstrual disturbances (see Clinical Presentation Box)

  • Current medications (including over-the-counter [OTC] and herbal medication use)

  • Objective data

    • Heart rate, blood pressure (BP), weight, and body mass index (BMI)

    • Labs (eg, FT4, TT3, TSH, thyroid-stimulating antibodies; serum electrolytes, Scr, ALT)

    • Other diagnostic tests when indicated (eg, thyroid ultrasound, RAIU scan)

Assess

  • Cause of hyperthyroidism (see Table 92-3)

  • Current medications that may contribute to or worsen hyperthyroidism

  • Current medications that may interact with antithyroid therapy

  • Appropriateness and effectiveness of current antithyroid regimen

Plan*

  • Drug therapy regimen including specific antithyroid therapy, dose, and duration (see Table ...

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