How does one interpret thyroid function tests in the inpatient setting?
How can one distinguish nonthyroidal illness from other thyroid conditions?
How does myxedema coma differ from a normal hypothyroid state and how is it treated?
What characterizes thyroid storm and how is it distinct from thyrotoxicosis?
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 usually refers to both thyroxine (T4) and triiodothyronine (T3). The thyroid synthesizes primarily T4, but can also synthesize T3. T3 is felt 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 a family of deiodinases, which are expressed in a variety of tissues. Both the type 1 and 2 deiodinases convert T4 to T3. In contrast, the type 3 deiodinase converts T4 to inactive reverse T3 (rT3) and also inactivates T3.
Both T4 and T3 likely gain access to cells by a variety of transporters that are still being elucidated. T3 acts mainly in the nucleus, binding to thyroid hormone receptors (TRs) to regulate gene expression. This genomic action accounts for many of T3's physiologic effects including thermogenesis, decreased systemic vascular resistance, and increased cardiac chronotropy and inotropy. T3 and the TR may also act directly in the cytoplasm on other cell signaling pathways that influence physiologic function.
T3 feeds back at the level of the hypothalamus and pituitary to regulate thyrotropin-releasing hormone (TRH) and thyroid stimulating hormone (TSH) synthesis and secretion respectively. TSH governs the amount of thyroid hormone synthesized by the thyroid gland. TSH 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 150-1).
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.