Iatrogenic causes include ablation of the pituitary by surgery or radiation http://ebooksmedicine.net • Other, less common causes of anterior pituitary hypo-function include inflammatory lesions such as sarcoidosis or tuberculosis, trauma, and metastatic tumors involving the pituitary
The clinical manifestations of anterior pituitary hypo-function depend on the specific hormones that are lacking. In children, growth failure (pituitary dwarfism) may occur as a result of growth hormone deficiency. Gonadotropin or gonadotropin-releasing hormone (GnRH) deficiency leads to amenorrhea and infertility in women and to decreased libido, impotence, and loss of pubic and axillary hair in men. TSH and ACTH deficiencies result in hypothyroidism and hypoadrenalism, respectively (discussed later). Prolactin deficiency results in failure of postpartum lactation. The anterior pituitary also is a rich source of MSH, synthesized from the same precursor molecule that produces ACTH; therefore, one of the manifestations of hypopituitarism is pallor of skin from loss of stimulatory effects of MSH on melanocytes.
The posterior pituitary, or neurohypophysis, is composed of modified glial cells (termed pituicytes) and axonal processes extending from nerve cell bodies in the supraoptic and paraventricular nuclei of the hypothalamus. The hypothalamic neurons produce two peptides: anti-diuretic hormone (ADH) and oxytocin. They are stored in axon terminals in the neurohypophysis and released into the circulation in response to appropriate stimuli. ADH is a nonapeptide hormone synthesized predominantly in the supraoptic nucleus. In response to several different stimuli, including increased plasma osmotic pressure, left atrial distention, exercise, and certain emotional states, ADH is released from axon terminals in the neurohypophysis into the general circulation. The hormone acts on the collecting tubules of the kidney to promote the resorption of free water. Oxytocin stimulates the contraction of smooth muscle in the pregnant uterus and of muscle surrounding the lactiferous ducts of the mammary glands. Impairment of oxytocin synthesis and release has not been associated with significant clinical abnormalities.
The clinically important posterior pituitary syndromes involve ADH underor overproduction.
ADH deficiency causes diabetes insipidus, a condition characterized by excessive urination (polyuria) due to an inability of the kidney to resorb water properly from the urine. Diabetes insipidus can result from several causes, including head trauma, neoplasms, and inflammatory disorders of the hypothalamus and pituitary, and from surgical procedures involving the hypothalamus or pituitary. The condition sometimes arises spontaneously (idiopathic). Diabetes insipidus from ADH deficiency is designated central, to differentiate it from nephrogenic diabetes insipidus, which is caused by renal tubular unresponsiveness to circulating ADH. The clinical manifestations of both diseases are similar and include the excretion of large volumes of dilute urine with an inappropriately low specific gravity. Serum sodium and osmolality are increased as a result of excessive renal loss of free water, resulting in thirst and polydipsia. Patients who can drink water generally compensate for urinary losses, but patients who are obtunded, bedridden, or otherwise limited in their ability to obtain water may develop life-threatening dehydration.