best java barcode library 1 Pituitary hormones in Objective-C

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Table 26 1 Pituitary hormones
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Anterior pituitary Growth hormone (GH)1 Prolactin (PRL) Adrenocorticotropic hormone (ACTH) Thyroid-stimulating hormone (TSH) Luteinizing hormone (LH)2 Follicle-stimulating hormone (FSH) Posterior pituitary Arginine vasopressin (AVP)3 Oxytocin
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GH closely resembles human placental lactogen (hPL) LH closely resembles human chorionic gonadotropin (hCG) 3 AVP is identical with antidiuretic hormone (ADH)
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dominant, or X-linked recessive trait Some of these patients exhibit benign pituitary enlargement that may regress spontaneously Kallmann s syndrome is the most common cause of congenital isolated gonadotropin deficiency It is usually sporadic but may be familial Three different genetic inheritance patterns can occur: X-linked recessive (Kal 1), autosomal dominant (Kal 2), or autosomal recessive (Kal 3) Kallmann s syndrome has an incidence of 1:10,000 males and 1:50,000 females It is associated with hyposmia caused by hypoplasia of the olfactory bulbs In Kallmann s syndrome, about 50% of patients have unilateral renal agenesis; some patients may also exhibit cryptorchidism, sensorineural deafness, cerebellar dysfunction, bilateral synkinesis, nystagmus, cleft lip, or higharched palate
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Clinical Findings
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Manifestations of hypopituitarism vary depending on which specific hormones are lacking and whether their deficiency is partial or complete
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A Symptoms and Signs
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Gonadotropin deficiency includes loss of luteinizing hormone (LH) and follicle-stimulating hormone (FSH), which causes hypogonadism and infertility Patients with isolated gonadotropin deficiency may seek medical attention for delayed adolescence (See also discussion of primary amenorrhea) Congenital gonadotropin deficiency in males may be associated with congenital micropenis or cryptorchism Hypogonadotropic hypogonadism is also seen in patients with congenital adrenal hypoplasia, a rare X-linked disorder caused by a mutation in the DAX-1 gene Adrenal insufficiency caused by failure to form the permanent zone of the adrenal cortex can present during infancy or childhood in boys with DAX-1 gene mutations Boys who survive beyond childhood usually do not enter puberty as a result of hypogonadotropic hypogonadism However, hypogonadotropic hypogonadism and subtle signs of adrenal failure can present in adulthood in males with partial loss-of-function mutations in DAX-1 In acquired gonadotropin deficiency, both men and women lose axillary, pubic, and body hair gradually, particu-
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B Laboratory Findings
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The fasting blood glucose may be low Hyponatremia is often present Hyperkalemia usually does not occur, since aldosterone production is not affected The free tetraiodothyronine (thyroxine, T4) level is low, and TSH is not elevated Plasma levels of sex steroids (testosterone and estradiol) are low or low normal, as are the serum gonadotropins as well Elevated prolactin (PRL) levels are found in patients with prolactinomas, acromegaly, and hypothalamic disease ACTH deficiency causes functional atrophy of the adrenal cortex within 2 weeks of pituitary damage Therefore, the diagnosis of secondary hypoadrenalism may be confirmed by holding any corticosteroid medication on the day of the test and by administering cosyntropin (synthetic ACTH1 24), 025 mg (intramuscularly or intravenously); blood is drawn 30 60 minutes after the injection A serum cortisol of 20 mcg/dL (550 nmol/mL), random or stimulated, rules out the diagnosis A baseline ACTH level is low or normal in secondary
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Endocrine Disorders
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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