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hypoadrenalism, distinguishing it from primary adrenal disease Metyrapone testing is unnecessary Deficiency of epinephrine occurs with secondary adrenal insufficiency, since high local concentrations of cortisol are required to induce the production of the enzyme phenylethanolamine N-methyltransferase (PNMT) that catalyzes the conversion of norepinephrine to epinephrine in the adrenal medulla The diagnosis of GH deficiency is made difficult by the pulsatile nature of GH secretion and individual variability GH deficiency is present in 96% of patients with three or more other pituitary hormone deficiencies The insulin hypoglycemia test, long considered the gold standard, is actually unreliable, cumbersome, and uncomfortable; it is contraindicated in the elderly, in patients with cardiovascular or cerebrovascular disease, and in patients with any history of seizures, an abnormal electroencephalogram (EEG), or recent brain surgery Other GH stimulation tests require the administration of intravenous arginine and growth hormone releasing hormone (GHRH) and oral carbidopa and levodopa (combination) in patients pretreated with propranolol or estrogen However, these tests do not discriminate well between normal individuals and patients with presumed GH deficiency (patients with three or more other pituitary hormone deficiencies) Also, normal overweight adults (body mass index [BMI] 25 kg/m2) typically have blunted peak GH levels (below 20 ng/mL) after arginine-GHRH administration Serum insulin-like growth factor (IGF-I) levels are in the normal range in about 50% of adults with GH deficiency However, very low levels of IGF-I (< 84 mcg/L) are indicative of GH deficiency except in conditions that naturally suppress serum IGF-I (eg, malnutrition, prolonged fasting, oral estrogen, hypothyroidism, uncontrolled diabetes mellitus, liver failure) In GH deficiency, exercise-stimulated serum GH levels usually fail to rise and remain at < 5 ng/mL; however, by age 40 years, most normal adults have lost their GH response to exercise The differential diagnosis of GH deficiency is congenital GH resistance with deficiency of IGF-I; at its worst, IGF-I deficiency results in Laron dwarfism that is resistant to GH therapy Because hemochromatosis can cause hypopituitarism, in patients with hypopituitarism without an established etiology, it is prudent to screen for hemochromatosis with a serum iron and transferrin saturation or ferritin.

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ops in patients receiving high-dose methadone or chronic intrathecal infusion of opioids; both GH deficiency and secondary adrenal insufficiency occur in 15% of such patients Secondary adrenal insufficiency may persist for many months following high-dose corticosteroid therapy Severe illness causes functional suppression of TSH and T4 Hyperthyroxinemia reversibly suppresses TSH Administration of triiodothyronine (Cytomel) suppresses TSH and T4 Bexarotene, used to treat cutaneous T cell lymphoma, suppresses TSH secretion, resulting in temporary central hypothyroidism Corticosteroids or megestrol treatment reversibly suppresses endogenous ACTH and cortisol secretion

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Patients with destructive lesions (eg, tumors) may develop complications related to them or to surgery or radiation therapy Among patients with craniopharyngiomas, diabetes insipidus is found in 16% preoperatively and in 60% postoperatively Hyponatremia often presents abruptly during the first 2 weeks following pituitary surgery Visual field impairment may occur Hypothalamic damage may result in morbid obesity as well as cognitive and emotional problems Conventional radiation therapy results in an increased incidence of small vessel ischemic strokes and second tumors Patients with untreated hypoadrenalism and a stressful illness may become febrile and die in shock and coma Adults with GH deficiency have experienced an increased cardiovascular morbidity Rarely, acute hemorrhage may occur in large pituitary tumors, manifested by rapid loss of vision, headache, and evidence of acute pituitary failure (pituitary apoplexy) requiring emergency decompression of the sella

Transsphenoidal removal of pituitary tumors will sometimes reverse hypopituitarism Postoperative hyponatremia often occurs; serum sodium must be checked frequently for 2 weeks after pituitary surgery Hypogonadism due to PRL excess usually resolves during treatment with dopamine agonists Endocrine substitution therapy must be given before, during, and, often, permanently after such procedures GH-secreting tumors may respond to octreotide (see section on acromegaly) Radiation therapy with x-ray, gamma knife, or heavy particles may be necessary but increases the likelihood of hypopituitarism The mainstay of substitution therapy for pituitary insufficiency remains lifetime hormone replacement

namespace Example_4_5_ _ _ _Ternary_Operator { class ValuesProgram { static void Main( ) { int valueOne = 10; int valueTwo = 20; int maxValue = valueOne > valueTwo valueOne : valueTwo; Console.WriteLine("ValueOne: {0}, valueTwo: {1}, maxValue: {2}", valueOne, valueTwo, maxValue); } } }

MRI provides the best visualization of pituitary tumors Thickening of the pituitary stalk can also be caused by sarcoidosis or hypophysitis

Launch Project Builder, select File Create New Project, and select one of the AppleScript Studio project templates. Open the Resource folder using the discloser triangle and double-click on the project s MainMenu.nib file to open the file in Interface Builder. Construct your application s user interface and name each interface component you wish to access from your scripts (more on this later). Create new script-based handlers for interface actions. The development environment creates these handlers and adds them to the main AppleScript of the application. Move back to Project Builder and fill in each handler with AppleScript code that responds to interface actions.

Reversible hypogonadotropic hypogonadism may occur with serious illness, malnutrition, or anorexia nervosa The clinical situation and the presence of normal adrenal and thyroid function allow ready distinction from hypopituitarism Profound hypogonadotropic hypogonadism develops in men who receive gonadotropin-releasing hormone (GnRH) therapy for prostate cancer; it usually persists following cessation of therapy Hypogonadotropic hypogonadism usually devel-

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