Synthesis of thyroglobulin. The precursor of thyroglobulin is synthesized in the rER of the follicular epithelial cells. Thyroglobulin is posttranslationally glycosylated in the rER and the Golgi apparatus before it is packaged into vesicles and secreted by exocytosis into the lumen of the follicle.
2.
Resorption, diffusion, and oxidation of iodide. Follicular epithelial cells actively transport iodide from the 758 The most common symptom of thyroid disease is a goiter, the enlargement of the thyroid gland. It may indicate either hypothyroidism or hyperthyroidism. Hypothyroidism can be caused by insufficient dietary iodine (iodine-defciency goiter, endemic goiter) or by one of several inherited autoimmune diseases, such as autoimmune thyroiditis (Hashimoto’s thyroiditis). Autoimmune thyroiditis is characterized by the presence of abnormal autoimmunoglobulins directed against thyroglobu-lin (TgAb), thyroid peroxidase (TPOAb), and the TSH recep-tor (TSHAb). The results are thyroid cell apoptosis and follicular destruction. The low levels of circulating thyroid hormone stimulate release of excessive amounts of TSH, which cause hypertrophy of the thyroid through synthesis of more thyroglobulin. Adult hypothyroidism, formerly called myxedema (due to the puffy appearance of the skin) is char-acterized by mental and physical sluggishness. The edema that occurs in the severe stages of hypothyroidism is caused by the accumulation of large amounts of hyaluronan in the extracellular matrix of the connective tissue of the dermis. In hyperthyroidism (toxic goiter or Graves’ dis-ease), excessive amounts of thyroid hormones are re-leased into the circulation. Individuals with Graves’ disease have detectable levels of autoantibodies. These abnormal immunoglobulins (IgG) bind to the TSH receptors on the follicular cells and stimulate adenylate cyclase activity. As a result, increased levels of cAMP in follicular cells lead to continuous stimulation of the cells and increased thyroid hormone secretion. Because of negative feedback, the lev-els of TSH in the circulation are usually normal. However, under such stimulation the thyroid gland undergoes hyper-trophy, and the thyroid hormone is secreted at abnormally high rates, causing increased metabolism. Most of the clin-ical futures are associated with increased metabolic rate and increased sympathetic nerve activities. These include weight loss, excessive sweating, tachycardia, and nervous-ness. Noticeable features include protrusion of the eyeballs and retraction of the eyelids, resulting from increased sym-pathetic activity and increased deposition of extracellular matrix in the adipose tissue located behind the eyeball (Fig. F21.4.1a). The thyroid gland is enlarged. Microscopic features include the presence of columnar follicular cells lin-ing the thyroid follicles. Because of the high utilization of col-loid, the follicle tends to be depleted in the areas of contact with the apical surface of follicular cells (Fig. F21.4.1b). The treatment for Graves’ disease is either surgical to remove the thyroid gland or radiotherapy by ingestion of radioactive iodine (131I), which destroys most active follicular cells.