Chapter 40 - Disorders of Endocrine Function
The role of iodine in proper thyroid gland function relates to which of the following?
Oxidation to iodide Coupling to molecular tyrosine Trapping of dietary iodine in thyroid cells The ability of iodine to neutralize dietary salt Follicular cells of the thyroid gland trap dietary iodine, oxidize it to iodide, and couple it to molecules of the amino acid, tyrosine. These iodotyrosines are then combined to form T4 and T3. The role of iodine in proper thyroid gland function does not involve retention of iodide in renal tubules or the ability of iodine to neutralize dietary salt.
Low serum levels of which hormone is helpful in differentiating between primary or secondary causes of hypothyroidism?
Thyroid-stimulating hormone (TSH) TSH levels are helpful in differentiating between primary (high TSH) and secondary (low TSH) causes of hypothyroidism. Low serum T3 or T4 levels do not confirm the diagnosis of hypothyroidism. Medically speaking, hypothyroidism refers to a deficiency of the thyroid hormone thyroxine.
The conditions of pituitary gigantism in children and acromegaly in adults are produced by excessive levels of
growth hormone. Growth hormone excess in children, before skeletal epiphyses close, leads to rapid growth, resulting in "pituitary gigantism." In adults, excessive growth hormone causes bony growth that occurs at the short bones, such as the hands and feet, the brow, and the mandible. The thyroid hormone, antidiuretic hormone, and corticosteroid are not related to either gigantism or acromegaly.
Cushing syndrome differs from Cushing disease in that the term Cushing syndrome is used only to describe
hypercortisolism manifestations, regardless of cause. Cushing syndrome is used to describe the clinical features of hypercortisolism, regardless of cause, whereas Cushing disease is the diagnosis reserved for pituitary-dependent conditions. Cushing syndrome is used to describe the clinical features of hypercortisolism not a specific cause.
When damage occurs to the antidiuretic hormone (ADH)-producing cells in the hypothalamus from head trauma, intracranial tumors, or neurosurgery, what disorder is suggested by a large diuresis of very dilute urine?
Diabetes insipidus ADH acts directly on the renal collecting ducts and distal tubules, increasing membrane permeability to water that is characteristic of diabetes insipidus. Kidney damage would not likely result from causes described in the question nor would it result in a large diuresis of very dilute urine. Diabetes mellitus is related to insufficient insulin not ADH disfunction. Adrenogenital syndrome is a group of disorders caused by adrenocortical hyperplasia or malignant tumors, resulting in abnormal secretion of adrenocortical hormones and characterized by masculinization of women, feminization of men, or precocious sexual development in children.
Syndrome of inappropriate antidiuretic hormone (SIAHD) secretion can be attributed to which of the following?
Malignant lung disorders Nonmalignant lung disorders Ectopic production of antidiuretic hormone has been noted in association with several types of tumors, the most common of which are primary lung malignancies, although nonmalignant lung disorders are also capable of ADH synthesis. Ectopic production of antidiuretic hormone has not been noted in association with renal disorders, an overactive adrenal cortex, or a hyperactive posterior pituitary gland.
A patient diagnosed with hormonal resistance can present with which assessment datum?
No response to exogenous hormone replacement Lack of normal hormonal action Normal hormone levels Elevated hormone levels The absence of response to exogenous hormone replacement and a lack of normal hormonal action is characteristic of hormone resistance. Diminished hormonal action in the presence of normal or high hormonal levels is most likely to have genetic or acquired hormone resistance. Decreased hormone levels are not characteristic of hormonal resistance.
A severely hypertensive patient presents with the classic triad of headache, tachycardia, and diaphoresis, and laboratory tests show excessive circulating catecholamine levels. Which rare, but treatable, disorder is suspected?
Pheochromocytoma A pheochromocytoma is a catecholamine-secreting tumor that is usually located in the adrenal medulla and presents a classic triad of symptoms (headache, tachycardia, and diaphoresis) that result from effects of the massive circulating catecholamine levels on the sympathetic nervous system. Adrenal cortical hypertension and hypertrophy or hypotrophy of the adrenal gland do not present with these symptoms.
The secretion of the appropriate amount of free thyroid hormones in circulating body fluid is regulated by the feedback interaction between which hormone sources?
Pituitary Hypothalamus Thyroid Secretion of thyroid hormone is regulated by the hypothalamic-pituitary-thyroid feedback system. The adrenal medulla and the parathyroid are not involved.
If the cause of hypercortisolism is an adrenal tumor, which option is indicated?
Unilateral removal of the affected gland Unilateral adrenalectomy is indicated if hypercortisolism is caused by an adrenal tumor. Adrenalin administration would exacerbate the problem. Bilateral removal of adrenal glands is rarely performed today because it requires lifelong glucocorticoid and mineralocorticoid replacement. Glucocorticoid, but not mineralocorticoid, hormone replacement would not be appropriate therapy.
In adrenocortical insufficiency, such as Addison disease, the most severe manifestations are the result of
an insufficient amount of circulating cortisol. The most severe clinical manifestations of adrenocortical insufficiency occur because of inadequate levels of circulating cortisol. Addison disease is not significantly related to amounts of T4 and T3 or to the renin-angiotensin system. Hyposecretion of all the adrenocortical hormones may occur in Addison disease, but that is not a cause of the most severe manifestations of Addison disease.
The origin of congenital adrenal hyperplasia occurs when circulating cortisol levels
are insufficient to provide negative feedback to the anterior pituitary gland. Adrenal hyperplasia occurs when enzymes needed for cortisol production are lacking and cannot produce adequate cortisol levels to provide negative feedback to the anterior pituitary gland. Adrenocorticotropic hormone (ACTH) secretion continues uncontrolled and results in adrenal hypertrophy and androgen overproduction. Normal cortisol levels would not be characteristic of congenital adrenal hyperplasia. High cortisol levels that stimulate ACTH activity would not be characteristic of congenital adrenal hyperplasia. Adrenal glands proliferate with normal ACTH levels would not be characteristic of congenital adrenal hyperplasia.
The uncontrolled hormone production in acromegaly and gigantism is most often the result of
benign somatotropic tumor in the pituitary gland. Growth hormone excess is nearly always caused by uncontrolled production of the hormone by a benign somatotropic tumor in the pituitary gland. Growth hormone stimulates the liver to produce insulin-like growth factor (IGF)-1, and these two hormones act in concert to cause unregulated growth of soft and bony tissues. The uncontrolled hormone production in acromegaly and gigantism is not most often the result of pituitary response to excessive calcium intake, asymptomatic hypercalcemia, or hyperparathyroidism.
The pituitary gland produces a hormone that is a potent anabolic agent that causes the development of all tissues of the body that are capable of responding to it. This hormone is called
growth hormone (GH). The hormones produced by the anterior pituitary gland have direct actions on other endocrine glands in the body, with the exception of GH. GH promotes increased mitosis and cellular growth, increases the rate of protein synthesis, decreases protein catabolism, slows the rate of carbohydrate utilization, and mobilizes fats for energy use. Luteinizing hormone (LH) and follicle-stimulating hormone (FSH) are involved with female reproduction. Thyroid-stimulating hormone (TSH) is not involved in the process described in the question.
Children who have midline craniocerebral defects, nystagmus, retinal abnormalities, and other midline or midfacial abnormalities (e.g., cleft lip or palate) should be evaluated for deficiencies in
growth hormone. Deficiencies in growth hormone can lead to congenital malformations of cranial development. T3 and T4 hormone, parathyroid hormone, and corticosteroid hormone deficiencies are not currently connected with congenital malformations of the cranium.
The pathology of syndrome of inappropriate antidiuretic hormone (SIADH) secretion, leading to dilution of serum and an excess of water relative to solute, produces
hyponatremia and swelling of cells and neural compression. SIADH leads to hyponatremia when free water is inappropriately conserved and "dilutes" the serum to a sodium concentration below the normal range. When an excess of water is present, relative to solute, cells swell, causing profound effects of cellular swelling on neurons. The pathology of syndrome of inappropriate antidiuretic hormone (SIADH) secretion does not result in the shrinking of cells and neuron tissue, hypokalemia and cardiac dysrhythmias, or hemoconcentration and high hemoglobin/hematocrit.
Changes in urine osmolality seen in syndrome of inappropriate antidiuretic hormone (SIADH) secretion cause
increased water retention without sodium. Increased water reabsorption in renal tubules raises urine osmolality but dilutes serum, causing serum osmolality to fall. Changes in urine osmolality do not result in an increase in serum osmolality. With this pathology, despite increased water retention, the patient does not become edematous. Changes in urine osmolality do not result in an increase in water retention with sodium.
An enlarged thyroid gland produces a colloid goiter when
lack of iodine prevents T4 and T3 but without stopping thyroglobulin formation. Lack of iodine prevents production of both T4 and T3 but does not stop the formation of thyroglobulin. Insufficient T4 and T3 allow excessive quantities of thyroid-stimulating hormone to be secreted, and this in turn causes the thyroid cells to secrete tremendous amounts of thyroglobulin (colloid) into the follicles, producing a goiter. A colloid goiter is not the result of a lack of iodine preventing the formation of thyroid-stimulating hormone without stopping T4 and T3 production; excessive iodine suppressing thyroid-stimulating hormone, T4, and T3 formation; or insufficient dietary iodine being replaced with iodized salt.
The most significant regulator of antidiuretic hormone (ADH) release is
osmotic pressure of plasma. Specialized neurons called osmoreceptors, found in the hypothalamus, respond to changes in osmotic pressure by means of a set point. When body fluids become too concentrated, ADH is released and more water is reabsorbed in the kidneys. Body mass index is not a significant regulator of ADH release. Rate pressure product is not a significant regulator of ADH, but rather an indicator of the oxygen requirements of the heart. Serum pH is not a significant regulator of ADH release.
If annual development assessment shows a child to have growth hormone deficiencies, treatment alternatives include
pharmacologic agents that affect growth hormone secretion. Many pharmacologic agents are available that stimulate growth hormone secretion in children; these include insulin, arginine, levodopa, and clonidine. Childhood growth deficiencies are not treated with parathyroid preparations, are not always related to tumors, and are not generally terminal in nature.
