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INTRODUCTION

Key Clinical Questions

  • image How does one interpret thyroid function tests in the inpatient setting?

  • image How can one distinguish nonthyroidal illness from other thyroid conditions?

  • image How does myxedema coma differ from a normal hypothyroid state and how is it treated?

  • image What characterizes thyroid storm and how is it distinct from thyrotoxicosis?

  • image How is thyroid storm treated?

Thyroid disease is important to hospitalists for two reasons. Rarely, patients are admitted to the hospital with myxedema coma or thyrotoxicosis, conditions that must be recognized early, as prompt diagnosis and treatment reduce patient morbidity and mortality. More often, patients have thyroid function tests performed in the hospital because of nonspecific symptoms such as fatigue, weight loss, and palpitations, and the hospitalist has to distinguish between true thyroid disease and nonthyroidal illness syndrome (euthyroid sick syndrome). To understand the diagnosis and treatment of thyroid disease, it is necessary to review the normal physiology of thyroid hormone.

THYROID HORMONE PHYSIOLOGY AND TESTING

Thyroid hormone usually refers to both thyroxine (T4) and triiodothyronine (T3). The thyroid synthesizes primarily T4, but also synthesizes T3. T3 is thought to be the biologically active form of the hormone; T4, which has a longer half-life, functions as a prohormone. Eighty percent of T3 is produced by deiodination of the tyrosine rings of T4 by tissue deiodinases. Both type 1 and 2 deiodinases convert T4 to T3. In contrast, type 3 deiodinase converts T4 to inactive reverse T3 (rT3), and also inactivates T3.

T4 and T3 gain access to cells by transporters which are still being elucidated. T3 acts mainly in the nucleus, binding to thyroid hormone receptors to regulate gene expression. This genomic action accounts for many physiologic effects of T3, including thermogenesis, decreased systemic vascular resistance, and increased cardiac chronotropy and inotropy.

T3 feeds back at the level of the hypothalamus and pituitary to regulate thyrotropin-releasing hormone and thyroid-­stimulating hormone (TSH) synthesis and secretion, respectively. Thyroid-­stimulating hormone governs the amount of thyroid hormone synthesized by the thyroid gland. Thyroid-stimulating hormone is a heterodimeric glycoprotein hormone that can be measured by rapid, sensitive, and reliable immunoassays in the laboratory. A suppressed TSH demonstrates excessive thyroid hormone and hyperthyroidism, while an elevated TSH indicates inadequate thyroid hormone and hypothyroidism (Figure 152-1).

Figure 152-1

Algorithm for thyroid function tests. This algorithm does not apply in patients with hypothalamic-pituitary disease, serious illness, or those who are taking certain medications such as amiodarone, glucocorticoids, and dopamine.

In certain clinical scenarios, including patients with central hypothyroidism (secondary hypothyroidism) due to hypothalamic-pituitary dysfunction, patients treated with medications such as dopamine and glucocorticoids, and patients who ...

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