Production and secretion of PRL are predominantly under inhibitory control by the hypothalamus. Thus disruption of the pituitary stalk and the hypothalamohypophyseal portal vessels (e.g., secondary to surgery or physical trauma) results in an increase in PRL levels but a decrease in ACTH, TSH, FSH, LH, and GH. PRL circulates unbound to serum proteins and thus has a relatively short half-life of about 20 minutes. Normal basal serum concentrations are similar in men and women. Release of PRL is normally under tonic inhibition by the hypothalamus. This is exerted by dopaminergic tracts that secrete dopamine in the median eminence. There is also evidence for existence of a prolactin-releasing factor (PRF). The exact nature of this compound is not known, although many factors, including TRH and hormones in the glucagon family (secretin, glucagon, VIP, and gastric inhibitory polypeptide [GIP]) can stimulate release of PRL.
PRL is one of the many hormones released in response to stress. Surgery, fear, stimuli causing arousal, and exercise are
Upon completion of this chapter the student should be able to answer the following questions: 1.
Describe the anatomy and histology of the thyroid gland, including the structure of the thyroid follicle.
2.
Explain how thyroid hormones are synthesized within the thyroid gland, including the processes of iodine uptake, iodination of tyrosine residues in thyroglobulin by thyroid peroxidase/dual oxidase, and coupling to form T4 and T3.
3.
Describe the process of endocytosis by which thyroglobulin is retrieved from the follicle lumen and processed to yield T3 and T4, which are secreted into the circulation.
4.
Diagram the hypothalamic-pituitary-thyroid axis to show how TSH regulates thyroid function and how thyroid hormones feed back to regulate the axis. List examples of how central input can alter the set point of the axis.
5.
Discuss the role of thyroid-binding proteins in the transport and stability of thyroid hormones, and the role of peripheral deiodinases in the activation of T4 to T3 or inactivation to reverse T3. Contrast the cellular location and function of the D1 and D2 deiodinases.
6.
Describe the mechanisms of thyroid hormone action, including the nature and location of the thyroid hormone receptor and its ability to either repress or activate target gene transcription.
7.
Discuss the actions of thyroid hormone during development, especially on the central nervous system (CNS) and skeleton, including the consequences of severe hypothyroidism.
8.
Describe the effects of thyroid hormone on basal metabolic rate and thermogenesis, on the cardiovascular system (heart rate, cardiac output, systemic vascular resistance), and on other organ systems (skin, skeletal muscle, digestive tract).
he thyroid gland produces the prohormone tetraiodothyronine (T4, also called thyroxine) and the active hormone triiodothyronine (T3). Synthesis of T4 and T3 requires iodine, which can be a limiting factor in some parts of the world. Much of T3 is also made by peripheral conversion of T4 to T3. Thyroid hormone acts primarily through a nuclear receptor that regulates gene transcription. T3 is critical for normal brain and bone development and has broad effects on metabolism and cardiovascular function in adults.
Anatomy and Histology of the Thyroid Gland
The thyroid gland is composed of right and left lobes that sit anterolateral to the trachea (