Introduction

Disorders of the thyroid gland result primarily from autoimmune processes that stimulate the overproduction of thyroid hormones (thyrotoxicosis) or cause glandular destruction and underproduction of thyroid hormones (hypothyroidism). Neoplastic processes in the thyroid gland can lead to benign nodules or thyroid cancer.

Thyroidal production of the hormones thyroxine (T₄) and triiodothyronine (T₃) is controlled via a classic endocrine feedback loop (see Fig. 171-1 Diagram of Pituitary Axes). Some T₃ is secreted by the thyroid, but most is produced by deiodination of T₄ in peripheral tissues. Both T₄ and T₃ are bound to carrier proteins (thyroid-binding globulin [TBG], transthyretin [binds T₄], and albumin) in the circulation. Increased levels of total T₄ and T₃ with normal free levels are seen in states of increased carrier proteins (pregnancy, estrogens, cirrhosis, hepatitis, and inherited disorders). Conversely, decreased total T₄ and T₃ levels with normal free levels are seen in severe systemic illness, chronic liver disease, and nephrosis.