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USMLE – Hypothyroidism

Hypothyroidism is caused by any structural or functional derangement that interferes with the production of adequate levels of thyroid hormone. It can result from a defect anywhere in the cisco 640-816 hypothalamic-pituitary-thyroid axis. As in the case of hyperthyroidism, this disorder is divided into primary and secondary categories, depending on whether the hypothyroidism arises from an intrinsic abnormality in the thyroid or occurs as a result of hypothalamic or pituitary disease. The causes of hypothyroidism can be divided into several categories.

Primary hypothyroidism accounts for the vast majority of cases of hypothyroidism. The most common cause of hypothyroidism in iodine-sufficient areas of the world is chronic autoimmune thyroiditis, or Hashimoto thyroiditis. This condition is variously reported to cause 15 to 60% of cases of hypothyroidism. Both cellular and humoral factors contribute to the thyroid injury and hypothyroidism in chronic autoimmune thyroiditis.


Hypothyroidism can follow thyroid surgery or radiation, be drug induced, or occur as a result of an infiltrative disorder. Cisco 642-104  A large resection of the gland (total thyroidectomy) for the treatment of hyperthyroidism or excision of a primary neoplasm is a common cause of hypothyroidism. The gland may also be ablated by radiation, whether in the form of radioiodine administered for the treatment of hyperthyroidism, or exogenous irradiation, such as external radiation therapy to the neck. Drugs given intentionally to decrease thyroid secretion (e.g., methimazole and propylthiouracil) can cause hypothyroidism, as can agents used to treat nonthyroid conditions (e.g., lithium). Finally, infiltrative diseases such as hemochromatosis, amyloid, and sarcoid are rare causes of hypothyroidism.

Secondary hypothyroidism is that caused by TSH deficiency, and tertiary (central) hypothyroidism is caused by TRH deficiency. Secondary hypothyroidism can result from any of the causes of hypopituitarism, frequently a pituitary tumor; other causes include postpartum pituitary necrosis, trauma, and nonpituitary tumors. Tertiary (central) hypothyroidism can be caused by any disorder that damages the hypothalamus or interferes with hypothalamic-pituitary portal blood flow, thereby preventing delivery of TRH to the pituitary. This can result from hypothalamic damage from tumors, trauma, radiation therapy, or infiltrative diseases. Classic clinical manifestations of hypothyroidism include cretinism and myxedema.

Lillian Thompson By Lillian Thompson

USMLE – Hyperthyroidism

Thyrotoxicosis is a hypermetabolic state caused by elevated levels of free T3 and T4. It is often referred to as hyperthyroidism because it is caused most commonly by hyperfunction of the thyroid gland. When these elevated levels arise from hyperfunction of the thyroid, as occurs in Graves disease, the thyrotoxicosis may correctly be called hyperthyroidism. When the increased hormone levels reflect excessive leakage of hormone out of a nonhyperactive gland, however, it is properly referred to as thyrotoxicosis. Long usage often equates these terms. By either name, the syndrome is manifested by nervousness, palpitations, rapid pulse, fatigability, muscular weakness, weight loss with good appetite, diarrhea, heat intolerance, warm skin, excessive perspiration, emotional lability, menstrual changes, a fine tremor of the hand (particularly when outstretched), eye changes, and variable enlargement of the thyroid gland. Thyrotoxicosis can be caused by a variety of disorders:

- Diffuse hyperplasia of the thyroid associated with Graves disease (accounts for 85% of cases)

- Ingestion of exogenous thyroid hormone (administered for hypothyroidism)

- Hyperfunctional multinodular goiter

- Hyperfunctional adenoma of the thyroid

- Thyroiditis

The terms primary and secondary hyperthyroidism are sometimes used to designate hyperthyroidism arising from an intrinsic thyroid abnormality and that arising from processes outside of the thyroid, such as a TSH-secreting pituitary tumor. Less common causes of secondary hyperthyroidism include secretion of excessive amounts of thyroid hormone by ectopic thyroid arising in ovarian teratomas (struma ovarii).


The clinical manifestations of hyperthyroidism include changes referable to the hypermetabolic state induced by excess thyroid hormone as well as those related to over activity of the sympathetic nervous system. Excessive levels of thyroid hormone result in an increase in the basal metabolic rate. Cardiac manifestations are among the earliest and most consistent features of hyperthyroidism. Patients with hyperthyroidism can have an increase in cardiac output, owing to both increased cardiac contractility and increased peripheral oxygen requirements. Tachycardia, palpitations, and cardiomegaly are common. Arrhythmias, particularly atrial fibrillation, occur frequently and are more common in older patients. The basis for these arrhythmias is not clear. Congestive heart failure may develop, particularly in elderly patients with preexisting cardiac disease. Myocardial changes, such as foci of lymphocytic and eosinophilic infiltration, mild fibrosis in the interstitium, fatty changes in myofibers, and an increase in size and number of mitochondria, have been described. These changes are not frequent, and other possible concomitant pathogeneses have not been rigorously ruled out, so debate continues about so-called thyrotoxic cardiomyopathy.

Other findings throughout the body include atrophy and fatty infiltration of skeletal muscle, sometimes with focal interstitial lymphocytic infiltrates; minimal fatty changes in the liver, sometimes accompanied by mild periportal fibrosis and a mild lymphocytic infiltrate; osteoporosis; and generalized lymphoid hyperplasia with lymphadenopathy.

Ocular changes often call attention to hyperthyroidism. A wide, staring gaze and lid lag are present because of sympathetic over stimulation of the levator palpebrae superioris. Only patients with Graves disease have ophthalmopathy.

In the neuromuscular system, over activity of the sympathetic nervous system produces tremor, hyperactivity, emotional lability, anxiety, inability to concentrate, and insomnia. Proximal muscle weakness is common with decreased muscle mass.

The skin of thyrotoxic patients tends to be warm, moist, and flushed because of increased blood flow and peripheral vasodilation to increase heat loss. Sweating is increased because of higher levels of calorigenesis. Infiltrative dermopathy is seen only in Graves hyperthyroidism.

In the gastrointestinal system, increased gut motility results from increased sympathetic activity. There is an increase in appetite and hyperphagia. Despite the increase in appetite, weight loss occurs primarily as a result of increased energy expenditure but also increased bowel motility.

The skeletal system is also affected in hyperthyroidism. Thyroid hormone stimulates bone resorption, resulting in increased porosity of cortical bone and reduced volume of trabecular bone. The net effect is osteoporosis and an increased risk of fractures in patients with chronic hyperthyroidism.

A diagnosis of hyperthyroidism is made using both clinical and laboratory findings. Determining the serum TSH concentration, in conjunction with a measurement of unbound (free) T4, provides the best initial screen for cases of suspected hyperthyroidism. Free T4 levels are usually increased. TSH levels are extremely sensitive to free T4 levels and are thus decreased to low levels in patients with primary hyperthyroidism (i.e., hyperthyroidism owing to intrinsic thyroid disease). TSH levels, however, are not a reliable indicator of thyroid function in patients with thyrotoxicosis caused by hypothalamic or primary pituitary disease (e.g., TSH-secreting pituitary adenomas). Determining TSH levels after the injection of TRH (TRH stimulation test) is used in the evaluation of cases of suspected hyperthyroidism with equivocal changes in the baseline serum TSH level. A normal rise in TSH after administration of TRH excludes secondary hyperthyroidism. Measurement of radioactive iodine uptake provides an additional direct indication of the level of activity within the thyroid gland. An unusual variant of hyperthyroidism is T3-hyperthyroidism, or T3-thyrotoxicosis, in which serum TSH is low and circulating levels of free T3 are high, but free T4 is normal. This results from an increase in thyroidal T3 secretion and increased extrathyroidal conversion of T4 to T3 and can be seen in Graves disease or any form of primary hyperthyroidism. The therapeutic options for hyperthyroidism include multiple medications, each of which has a different mechanism of action. Typically, these include a beta-blocker, to control symptoms induced by increased adrenergic tone; a thionamide, to block new hormone synthesis; an iodine solution, to block the release of thyroid hormone; and agents that inhibit peripheral conversion of T4 to T3. Radioiodine, which is incorporated into thyroid tissues, resulting in ablation of thyroid function over a period of 6 to 18 weeks. may also be used.

Lillian Thompson By Lillian Thompson

USMLE – Normal Thyroid Gland

The thyroid gland is unique among the organs of the endocrine system because of its size and superficial location. It consists of two bulky lateral lobes connected by a relatively thin isthmus, usually located below and anterior to the larynx. Normal variants in the structure of the thyroid gland include the presence of a pyramidal lobe above the isthmus.

The thyroid gland develops embryologically from an evagination of the developing pharyngeal epithelium that descends to its normal position in the anterior neck. This pattern of descent explains the occasional presence of thyroid tissue in atypical locations. Incomplete descent may lead to the formation of the thyroid at loci abnormally high in the neck, producing a lingual or aberrant subhyoid thyroid. Excessive descent leads to substernal thyroid glands. Malformations of branchial pouch differentiation may result in intrathyroidal sites of the thymus or parathyroid glands. The implication of these deviations becomes evident in the patient who has a total thyroidectomy and subsequently develops hypoparathyroidism.

The weight of the normal adult thyroid is approximately 15 to 20 gm. The thyroid has a rich intraglandular capillary network that is supplied by the superior and inferior thyroidal arteries. Nerve fibers from the cervical sympathetic ganglia indirectly influence thyroid secretion by acting on the blood vessels. The thyroid is divided into lobules composed of about 20 to 40 evenly dispersed follicles. The follicles range from uniform to variable in size and are lined by Cisco 642-104  cuboidal-to-low columnar epithelium, which is filled with thyroglobulin. In response to trophic factors from the hypothalamus, TSH is released by thyrotrophs in the anterior pituitary into the circulation. TSH acts on the thyroid, causing the follicular epithelial cells of the thyroid to pinocytize colloid and ultimately convert thyroglobulin into thyroxine (T4) and lesser amounts of triiodothyronine (T3). T4 and T3 are released into the systemic circulation, where most of these peptides are reversibly bound to circulating plasma proteins, such as thyroxine binding globulin (TBG), for transport to peripheral tissues. The binding proteins serve to maintain the serum free T3 and T4 concentrations within narrow limits, yet ensure that the hormones are readily available to the tissues. The unbound T3 and T4 enter cells and interact with nuclear receptors, which change gene expression and ultimately up-regulate 640-822 certification carbohydrate and lipid catabolism and stimulate protein synthesis in a wide range of cells. The net effect of these processes is an increase in the basal metabolic rate.


The thyroid gland is one of the most responsive organs in the body. The gland responds to many stimuli and is in a constant state of adaptation. During puberty, pregnancy, and physiologic stress from any source, the gland increases in size and becomes more active. This functional lability is reflected in transient hyperplasia of the thyroidal epithelium. At this time, thyroglobulin is resorbed, and the follicular cells become tall and columnar, sometimes forming small infolded buds or papillae. When the stress abates, involution occurs; that is, the height of the epithelium falls, colloid accumulates, and the follicular cells resume their normal size and architecture. Failure of this normal balance between hyperplasia and involution may produce major or minor deviations from the usual histologic pattern.

The function of the thyroid gland can be inhibited by a variety of chemical agents, collectively referred to as goitrogens. Because they suppress T3 and T4 synthesis, the level of TSH increases, and subsequent hyperplastic enlargement of the gland (goiter) follows. The antithyroid agent propylthiouracil inhibits the oxidation of iodide and blocks production of the thyroid hormones. Iodide, when given to patients with thyroid hyperfunction, also blocks the release of thyroid hormones but through different mechanisms. Iodides in large doses inhibit proteolysis of thyroglobulin. Thus, thyroid hormone is synthesized and incorporated within increasing amounts of colloid, but it is not released into the blood.

In the interfollicular stroma, the thyroid gland also contains a population of para follicular cells, or C cells, which synthesize and secrete the hormone calcitonin. This hormone promotes the absorption of calcium by the skeletal system and inhibits the resorption of bone by osteoclasts.

Diseases of the thyroid are of great importance because most are amenable to medical or surgical management. They include conditions associated with excessive release of thyroid hormones (hyperthyroidism), those associated with thyroid hormone deficiency (hypothyroidism), and mass lesions of the thyroid.

Lillian Thompson By Lillian Thompson

Hypothalamic Suprasellar Tumors

Neoplasms in this location may induce hypofunction or hyperfunction of the anterior pituitary, diabetes insipidus, or combinations of these manifestations. The most commonly implicated lesions are gliomas (sometimes arising in the chiasm) and craniopharyngiomas. The craniopharyngioma is thought to be derived from vestigial remnants of Rathke pouch. These slow-growing tumors account for 1% to 5% of intracranial tumors; some of these lesions arise within the sella, but most are suprasellar. Although they occur most commonly during childhood and adolescence, about 50% present clinically after age 20. Children usually come to clinical attention because of endocrine deficiencies such as growth retardation, whereas adults usually present with visual disturbances. Pituitary hormonal deficiencies, including diabetes insipidus, are common.

Craniopharyngiomas average 3 to 4 cm in diameter; they may be encapsulated and. solid but more commonly are cystic and sometimes multiloculated. More than three fourths of these tumors contain sufficient calcification to be visualized radiographically. In their strategic location, they often encroach on the optic chiasm or cranial nerves and not infrequently bulge into the floor of the third ventricle and base of the brain. Two histologic forms can be distinguished – adamantinomatous and papillary.


The adamantinomatous craniopharyngioma consists of nests or cords of stratified squamous or columnar epithelium embedded. in a spongy reticulum. Often the nests of squamous cells gradually merge into a peripheral layer of columnar cells. Keratin formation is seen, and this form of the tumor is frequently calcified. Additional features typical of adamantinomatous craniopharyngioma include cholesterol-rich cyst contents, fibrosis, and chronic inflammatory reaction. These tumors extend fingerlets of epithelium into adjacent brain, where they elicit a brisk glial reaction.

The papillary craniopharyngioma usually lacks the keratin, calcification, and cyst content. The squamous cells of the solid sections of the tumor do not have the columnar sheet at the periphery and do not typically generate a spongy reticulum in the internal layers.

Lillian Thompson By Lillian Thompson

USMLE – Posterior Pituitary Syndromes

The posterior pituitary is composed of modified glial cells (designated pituicytes) and axonal processes extending from nerve cell bodies in the supraoptic and paraventricular nuclei of the hypothalamus. These neurons produce two peptides: ADH and oxytocin. The hormones are stored in axon terminals in the posterior pituitary and are released into the circulation in response to appropriate stimuli. Oxytocin stimulates contraction of the uterine smooth muscle cells in the gravid uterus and cells surrounding the lactiferous ducts of the mammary glands. Inappropriate oxytocin secretion has not been associated with clinical abnormalities. ADH is a nonapeptide hormone synthesized predominantly in the supraoptic nucleus. In response to a number of different stimuli, including increased plasma oncotic pressure, left atrial distention, exercise, and certain emotional states, ADH is released from the axon terminals in the neurohypophysis into the general circulation. The clinically relevant posterior pituitary syndromes involve ADH and include diabetes insipidus and secretion of inappropriately high levels of ADH. Glial tumors can also arise, rarely, from the pituicytes.


Diabetes insipidus: ADH deficiency causes diabetes insipidus, a condition characterized by excessive urination (polyuria) owing to an inability of the kidney to resorb water properly from the urine. It can result from a variety of processes, including head trauma, tumors, and inflammatory disorders of tile hypothalamus and pituitary as well as surgical procedures involving these organs. The condition can arise spontaneously, in the absence of an underlying disorder. The clinical manifestations include the excretion of large volumes of dilute urine with an inappropriately low specific gravity. Serum sodium and osmolality are increased owing to excessive renal loss of free water, resulting in thirst and polydipsia. Patients who can drink water can generally compensate for urinary losses; patients who are obtunded, bedridden, or otherwise limited in their ability to obtain water may develop life-threatening dehydration.

Syndrome of inappropriate ADH (SIADH) secretion: ADH excess causes resorption of excessive amounts of free water, resulting in hyponatremia. The most frequent causes of SIADH include the secretion of ectopic ADH by malignant neoplasms (particularly small cell carcinomas of the lung), non-neoplastic diseases of the lung, and local injury to the hypothalamus or posterior pituitary (or both). The clinical manifestations of SIADH are dominated by hyponatremia, cerebral edema, and resultant neurologic dysfunction. Although total body water is increased, blood volume remains normal, and peripheral edema does not develop.

Lillian Thompson By Lillian Thompson

USMLE – Hypopituitarism

Hypopituitarism refers to decreased secretion of pituitary hormones, which can result from diseases of the hypothalamus or of the pituitary. Hypofunction of the anterior pituitary occurs when approximately 75% of the parenchyma is lost or absent. This may be congenital or the result of a variety of acquired abnormalities that are intrinsic to the pituitary. Most cases of hypofunction arise from destructive processes directly involving the anterior pituitary, such as tumors, ischemic necrosis of the pituitary, and the empty sella syndrome, although other mechanisms have been identified.

Tumors and other mass lesions: Pituitary adenomas, other benign tumors arising within the sella, primary and metastatic malignancies, and cysts can induce hypopituitarism. Any mass lesion in the sellae can cause damage by exerting pressure on adjacent pituitary cells.

Pituitary surgery or radiation: Surgical excision of a pituitary adenoma may inadvertently extend to nonadenomatous pituitary. If sufficient normal tissue is removed, hypopituitarism may ensue. Radiation of the pituitary, used to prevent regrowth of residual tumor after surgery, exposes the nonadenomatous pituitary to the same radiation.

Rathke cleft cyst: These cysts, lined by ciliated cuboidal epithelium with occasional goblet cells and anterior pituitary cells, can accumulate proteinaceous fluid and expand causing symptoms.

Pituitary apoplexy: This is a sudden hemorrhage into the pituitary gland, often occurring into a pituitary adenoma. In its most dramatic presentation, apoplexy causes the sudden onset of excruciating headache, diplopia owing to pressure on the oculomotor nerves, and hypopituitarism.


Ischemic necrosis of the pituitary and Sheehan syndrome: Ischemic necrosis of the anterior pituitary is an important cause of pituitary insufficiency. In general, the anterior pituitary tolerates ischemia reasonably well; loss of as much as half to the anterior parenchyma can occur without clinical consequence. With damage to 75% or more, however, evidence of hypopituitarism develops. Sheehan syndrome, or postpartum necrosis of the anterior pituitary, is the most common form of clinically significant ischemic necrosis of the anterior pituitary. During pregnancy, the anterior pituitary enlarges to almost twice its normal size. This physiologic expansion of the gland is not accompanied by an increase in blood supply from the low-pressure venous system, and hence there is relative anoxia of the pituitary. Thus, sudden infarction of the anterior lobe precipitated by obstetric hemorrhage or shock may occur. Sudden systemic hypotension precipitates vasospasm of the vessels and thus ischemic necrosis of much of the anterior lobe. The posterior pituitary, because it receives its blood directly from arterial branches, is much less susceptible to ischemic injury in this setting and is therefore usually not affected. Pituitary necrosis may also be encountered in other conditions, such as disseminated intravascular coagulation and (more rarely) sickle cell anemia, elevated intracranial pressure, traumatic injury, and shock of any origin. Whatever the pathogenesis, the infarcted adenohypophysis at the outset appears soft, pale, and ischemic or hemorrhagic. Over time, the ischemic area is resorbed and replaced by fibrous tissue. In some long-standing cases, the gland scars down to a fibrous nubbin weighing less than 0.1 gm, attached to the wall of an empty sella.

Empty sella syndrome: Any condition that destroys part or all of the pituitary gland, such as ablation of the pituitary by surgery or radiation, can result in an empty sella. The empty sella syndrome refers to the presence of an enlarged, empty sella turcica that is not filled with pituitary tissue. There are two types: (1) In a primary empty sella, there is a defect in the diaphragma sellae that allows the arachnoidea mater and cerebrospinal fluid to herniate into the sella, resulting in expansion of the sella and compression of the pituitary. Classically the affected patients are obese women with a history of multiple pregnancies. The empty sella syndrome may be associated with visual field defects and occasionally with endocrine anomalies, such as hyperprolactinemia owing to interruption of inhibitory hypothalamic effects. Only rarely is it associated with hypopituitarism because sufficient functioning parenchyma is maintained. (2) In a secondary empty sella, a mass, such as a pituitary adenoma, enlarges the sella but then is removed by surgery or radiation. Hypopituitarism can result from the treatment or spontaneous infarction.

Genetic defects: Rare congenital deficiencies of one or more pituitary hormones have been recognized in children. A defect has been identified in a gene that encodes pit-1, a transcription factor that is important in the expression of pituitary-specific genes, such as GH, prolactin, and TSH. The defective form of the protein can bind to the DNA response element but does not activate the target genes. Consequently, children born with this deficiency cannot synthesize these hormones.

Less frequently, disorders that interfere with the delivery of pituitary hormone-releasing factors from the hypothalamus, such as hypothalamic tumors, may also cause hypofunction of the anterior pituitary. Any disease involving the hypothalamus can alter secretion of one or more of the hypothalamic hormones that influence secretion of the corresponding pituitary hormones. In contrast to diseases that involve the pituitary directly, any of these conditions can also diminish the secretion of ADH, resulting in diabetes insipidus. Such hypothalamic lesions are:

Tumors include benign lesions that arise in the hypothalamus, such as craniopharyngiomas, and malignant tumors that metastasize to that site, such as breast and lung carcinomas. Hypothalamic hormone deficiency can ensue when brain or nasopharyngeal tumors are treated with radiation.

Infiltrative disorders and infections, such as sarcoidosis or tuberculous meningitis, can cause deficiencies of anterior pituitary hormones and diabetes insipidus.

The clinical manifestations of anterior pituitary hypofunction depend on the nature and extent of the causative process as well as the type and degree of hormonal insufficiency. These changes are related to decreased function of the adrenal cortex, thyroid, and gonads. Additional alterations of hypopituitarism include pallor, as a result of loss of melanocyte-stimulating hormone (MSH) atrophy of the genitalia with resultant amenorrhea, impotence, and loss of libido; and loss of pubic and axillary hair.

Lillian Thompson By Lillian Thompson

USMLE – Other Anterior Pituitary Adenomas

Pituitary adenomas may elaborate more than one hormone. Somatotroph adenomas commonly contain immunoreactive prolactin. In some tumors, designated mixed adenomas, more than one cell population is present.640-822 certification  In other cases, a single cell type is apparently capable of synthesizing more than one hormone. A few comments are made about several of the less frequent functioning tumors.

Gonadotroph (LH-producing and FSH-producing) adenomas constitute 10 to 15% of pituitary adenomas. These tumors can be difficult to recognize because they secrete hormones inefficiently and variably, and the secretory products usually do not cause a recognizable clinical syndrome. Gonadotroph adenomas are most frequently found in middle-aged men and women when they become large enough to cause neurologic symptoms, such as impaired vision, headaches, diplopia, or pituitary apoplexy. Pituitary hormone deficiencies can also be found, most commonly impaired secretion of LH. This causes decreased energy and libido in men (due to reduced testosterone) and amenorrhea in premenopausal women. The neoplasms are basophilic or chromophobic and can reach substantial size before they are detected.


Thyrotroph (TSH-producing) adenomas are rare, accounting for approximately 1% of all pituitary adenomas. Thyrotroph adenomas are chromophobic or basophilic and are a rare cause of hyperthyroidism.

A substantial number of pituitary adenomas generate no detectable hormonal product and are designated null cell adenomas. These nonfunctional tumors account for approximately 20% of all pituitary adenomas. These tumors are either chromophobic or contain cells with granular, eosinophilic cytoplasm. In contrast to the hormonally active tumors, the granular cytoplasm in such tumors is due largely to the presence of numerous mitochondria, whereas secretory granules are infrequent. Patients with null cell adenomas typically present with mass effects. These lesions may also compromise the residual anterior pituitary sufficiently to produce hypopituitarism. This may occur as a result of gradual enlargement of the adenoma or after642-104 dumps  abrupt enlargement of the tumor because of acute hemorrhage (pituitary apoplexy).

Pituitary carcinomas are quite rare, and most are not functional. These malignant tumors range from well differentiated, resembling somewhat atypical adenomas, to poorly differentiated, with variable degrees of pleomorphism and the features characteristic of carcinomas in other locations. The diagnosis of carcinoma requires the demonstration of metastases, usually to lymph nodes, bone, liver, and sometimes elsewhere.

Lillian Thompson By Lillian Thompson

USMLE – Corticotroph Cell Adenomas

Corticotroph adenomas are usually small micro adenomas at the time of diagnosis. These tumors are basophilic or chromophobic and stain positively with periodic acid Schiff (PAS) stains because of the presence of carbohydrate in the ACTH precursor molecule.

Excess production of ACTH by the corticotroph adenoma leads to adrenal hypersecretion of cortisol and the development of hypercortisolism (also known as Cushing syndrome). It can be caused by a wide variety of conditions in addition to ACTH-producing pituitary tumors. When the hypercortisolism is due to excessive production of ACTH by the pituitary, the process is designated Cushing disease. Large destructive adenomas can develop in patients after surgical removal of the adrenal glands for treatment of Cushing syndrome. This condition, known as Nelson syndrome, occurs in most cases because of a loss of the inhibitory effect of adrenal corticosteroids on a preexisting corticotroph microadenoma. Because the adrenals are absent in patients with this disorder, hypercortisolism does not develop. In contrast, patients present with mass effects of the pituitary tumor. In addition, there can be hyperpigmentation because of the stimulatory effect of other products of the ACTH precursor molecule on melanocytes.

Lillian Thompson By Lillian Thompson

USMLE – Growth Hormone (Somoatotroph Cell) Adenomas

GH-secreting tumors are the second most common type of functioning pituitary adenoma. These tumors, similar to other pituitary adenomas, arise from a monoclonal expansion of a single cell that has undergone somatic mutation. 40% of somatotroph cell adenomas express an oncogene (gsp), which is a mutant GTPase deficient alpha subunit of the G protein, Gs. Somatotroph cell adenomas may be quite large by the time they come to clinical attention because the manifestations of excessive GH may be subtle. Histologically, GH-containing adenomas are composed of granulated cells, which appear acidophilic or chromophobic in routine sections. Immunocytochemical stains demonstrate GH within the cytoplasm of the neoplastic cells. In addition, small amounts of immunoreactive prolactin are often present.

Persistent hypersecretion of GH stimulates the hepatic secretion of insulin-like growth factor-I (IGF-I), which causes many of the clinical manifestations. If a somatotrophic adenoma appears in children before the epiphyses have closed, the elevated levels of GH result in gigantism. This is characterized by a generalized increase in body size, with disproportionately long arms and legs. If the increased levels of GH are present after closure of the epiphyses, patients develop acromegaly. In this condition, growth is most conspicuous in skin and soft tissues; viscera (thyroid, heart, liver, and adrenals); and bones of the face, hands, and feet. Bone density may be increased (hyperostosis) in both the spine and the hips. Enlargement of the jaw results in its protrusion (prognathism), with broadening of the lower face. The hands and feet are enlarged with broad, sausage-like fingers. In most instances, gigantism is also accompanied by evidence of acromegaly. These changes develop for decades before being recognized, hence the opportunity for the adenomas to reach substantial size. GH excess is also correlated with a variety of other disturbances, including gonadal dysfunction, diabetes mellitus, generalized muscle weakness, hypertension, arthritis, congestive heart failure, and an increased risk of gastrointestinal cancers. Prolactin can be demonstrated in a substantial fraction of GH-producing adenomas and in some cases may be released in sufficient quantities to produce hyperprolactinemia.


The goals of treatment are to restore GH levels to normal and to decrease symptoms referable to a pituitary mass lesion, while not causing hypopituitarism. To achieve these goals, the tumor can be removed surgically by a transsphenoidal approach or destroyed by radiation therapy, or GH secretion can be reduced by drug therapy. When effective control of GH hypersecretion is achieved, the characteristic tissue overgrowth and related symptoms gradually recede, and the metabolic abnormalities improve.

Lillian Thompson By Lillian Thompson