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Tumor adrenal

Hyperaldosteronism is a syndrome caused by excessive secretion of aldosterone. It is characterized by renal loss of potassium. Sodium reabsorption in the kidney is increased and accompanied by an increase in extracellular fluid. Clinically, an increased blood pressure (hypertension) is observed. Primary hyperaldosteronism is caused by aldosterone-producing, benign adrenal tumors (Conn s syndrome). Secondary hyperaldosteronism is caused by activation of the renin-angiotensin-aldosterone system. Various dtugs, in particular diuretics, cause or exaggerate secondary peadosteronism. [Pg.606]

G, alpha Insertions/dele- syndrome fibrous dysplasia of bone cafe-au-lait skin lesions sexual precocity pituitary, thyroid, or adrenal tumors Albright s hereditary with constitutive cAMP production Inactivating G a (86-89)... [Pg.87]

Aerosol - Chronic feeding of ribavirin to rats at doses of 16 to 100 mg/kg/day (estimated human equivalent of 2.3 to 14.3 mg/kg/day, based on body surface area adjustment for adults) suggest that ribavirin may induce benign mammary, pancreatic, pituitary, and adrenal tumors. [Pg.1780]

Spironolactone Block cytoplasmic aldosterone receptors in collecting tubules of nephron possible membrane effect Increased salt and water excretion reduces remodeling reduces mortality Chronic heart failure aldosteronism (cirrhosis, adrenal tumor) hypertension Oral duration 24-72 h (slow onset and offset) Toxicity Hyperkalemia, antiandrogen actions... [Pg.314]

Waalkes MP, Ward JM, Liu J, Diwan B (2003) Transplacental carcinogenicity of inorganic arsenic in the drinking water Induction of hepatic, ovarian, pulmonary and adrenal tumors in mice. Toxicol Appl Pharmacol, 186 7-17. [Pg.303]

Several relatively common disorders result in aldosterone secretion abnormalities and aberrations of electrolyte status. In Addison s disease, the adrenal cortex is often destroyed through autoimmune processes. One of the effects is a lack of aldosterone secretion and decreased Na+ retention by the patient. In a typical Addison s disease patient, serum [Na+] and [CL] are 128 and 96 meq/L, respectively (see Table 16.2 for normal values). Potassium levels are elevated, 6 meq/L or higher, because the Na+ reabsorption system of the kidney, which is under aldosterone control, moves K+ into the urine just as it moves Na+ back into plasma. Thus, if more Na+ is excreted, more K+ is reabsorbed. Bicarbonate remains relatively normal. The opposite situation prevails in Cushing s disease, however, in which an overproduction of adrenocorticosteroids, especially cortisol, is present. Glucocorticoids have mild mineralocorticoid activities, but ACTH also increases aldosterone secretion. This may be caused by an oversecretion of ACTH by a tumor or by adrenal hyperplasia or tumors. Serum sodium in Cushing s disease is slightly elevated, [K+] is below normal (hypokalemia), and metabolic alkalosis is present. The patient is usually hypertensive. A more severe electrolyte abnormality is seen in Conn s syndrome or primary aldosteronism, usually caused by an adrenal tumor. Increased blood aldosterone levels result in the urinary loss of K+ and H+, retention of Na+ (hypernatremia), alkalosis, and profound hypertension. [Pg.403]

According to the classical view of metabolism the hormones are synthesized as free steroids in endocrine tissues and prepared for excretion in urine by peripheral metabolism and conjugation. This view had to be modified upon the isolation of dehydroepiandrosterone sulfate from adrenal tumor [307]. Thus dehydroepiandrosterone sulfate, a steroid conjugate, was shown to be secreted by the adrenal tissue. Isotopic methods also pointed in the same direction. Lieberman et al. [304], using... [Pg.20]

Cushing s syndrome is caused by the hypersecretion of cortisol by cells in the adrenal cortex. Hypersecretion can be due to overstimulation of cortisol-releasing mechanisms by excess ACTH, a pituitary hormone. Cushing s can result from pituitary or adrenal tumors. It is further characterized by obesity, a rounded face, muscle weakness, a tendency to bruise easily, and numerous other complications. [Pg.294]

Spironolactone has been used as a potassium-sparing diuretic in cardiac failure and in the management of ascites and edema associated with hepatic cirrhosis with secondary hyperaldosteronism. It is also used to treat hyperaldosteronism due to adrenal tumors or adrenal hyperplasia. It has a weak positive inotropic effect and a modest antihypertensive effect, in keeping with its natriuretic action. [Pg.3176]

Adrenal tumor Alcoholism Angina pectoris Cardiac arrhythmia CNS degenerative disease Cushing s disease Coronary insufficiency Delirium ... [Pg.90]

Hydrocortisone is also u.scd during postoperative recovery alter surgery For Cushing s syndrome—exce.ssive adrenal. secretion oF glucocorticoids. Cushing s syndrome can be caused by bilateral adrenal hyperplasia or adrenal tumors and is treated by surgical removal oF the tumors or re.section oF hyperpla.stic adrenal gland(s). [Pg.810]

Metyrosine (23, a-methyl-L-tyrosine), a norepinephrine biosynthesis inhibitor, is in limited clinical use to help control hypertensive episodes and other symptoms of catecholamine overproduction in patients with the rare adrenal tumor pheochromocytoma (10). Metyrosine, a competitive inhibitor of tyrosine hydroxylase, inhibits the production of catecholamines by the tumor. Although metyrosine is useful in treating hypertension caused by excess catecholamine biosynthesis... [Pg.15]

Interpretation In normal subjects, plasma ACTH concentrations peak 30 minutes after CRH injection (80 7pg/mL at 0930 hr 29 2.6pg/mL at 2030 hr), and serum cortisol peaks at 60 minutes (13 Ijig/dL at 1000 17 0.7p.g/dL at 2100 hr). Patients with pituitary ACTH deficiency (secondary adrenal insufficiency) have decreased ACTH and cortisol responses. Patients with hypothalamic disease have prolonged ACTH responses and subnormal cortisol responses. Most patients with Cushing s syndrome caused by adrenal tumors or nonendocrine ACTH-producing tumors do not respond to CRH. Most patients with Cushing s syndrome respond with a normal or excessive increase in ACTH. Responses are usually normal in patients with depression. [Pg.2017]

Interpretation In normal subjects, 11-deoxycortisol increases from <1 (ig/dL to >7 tg/dL after metyrapone stimulation, and ACTH values exceed 150pg/mL. No response or impaired response may be seen in pituitary or hypothalamic disease combined with inadequate enzyme blockade (plasma cortisol >3 )Xg/dL) or with Cushing s syndrome caused by adrenal tumors or nonendocrine ACTH-secreting tumors. Exaggerated responses may be seen in pituitary Cushing s syndrome. [Pg.2018]

Although subnormal basal plasma concentrations of DHEA-S occur in primary, secondary, and tertiary forms of adrenal insufficiency, measurement is of little value in the diagnosis of adrenal insufficiency low concentrations of adrenal androgens are normally observed in children and in the elderly. Patients with human immunodeficiency virus (HIV) infection have been shown to have reduced concentrations of DHEA-S. DHEA-S concentrations are usually determined in the management of women with hirsutism or in patients suspected of having adrenal tumors. ... [Pg.2024]

Normal Ciiishing s Syndrome Adrenal Tumor Ectopic ACTH Syndrome... [Pg.2026]

Nonfunctioning Adrenocortical Tumors Approximately 2% of the population have an adrenal tumor most of these tumors are nonfunctioning and are sometimes called incidentalomas. They are found when CT scans of the abdomen are performed that can easily detect tumors 1 cm in diameter or 5 g in weight. No virilizing tumors smaller than 1 cm in diameter have been reported. Carcinomas are usually more than 30 g in weight. [Pg.2030]

Sloan DA, Schwartz RW, McGrath PC, Kenady DE. Diagnosis and management of adrenal tumors, Curr Opin Oncol 1996 8 30-6. [Pg.2049]

Late-onset adrenal hyperplasia Cushing s syndrome Virilizing adrenal tumors Adrenocorticoid insufficiency Thyroid disorders Hypothyroidism Hyperthyroidism Pituitary disorders... [Pg.2115]

Classical congenital hyperplasia 21-Hydroxylase deficiency 11-Hydroxylase deficiency 3P-Hydroxysteroid dehydrogenase deficiency Adult or attenuated adrenal hyperplasia Androgen-producing adrenal tumors... [Pg.2116]


See other pages where Tumor adrenal is mentioned: [Pg.545]    [Pg.818]    [Pg.217]    [Pg.694]    [Pg.698]    [Pg.66]    [Pg.732]    [Pg.336]    [Pg.250]    [Pg.884]    [Pg.243]    [Pg.426]    [Pg.426]    [Pg.916]    [Pg.370]    [Pg.172]    [Pg.1540]    [Pg.285]    [Pg.545]    [Pg.818]    [Pg.21]    [Pg.469]    [Pg.2017]    [Pg.2026]    [Pg.2026]    [Pg.2026]    [Pg.2027]    [Pg.2027]    [Pg.2029]    [Pg.2131]   
See also in sourсe #XX -- [ Pg.2029 , Pg.2030 , Pg.2031 , Pg.2032 , Pg.2033 , Pg.2034 , Pg.2035 , Pg.2036 , Pg.2037 , Pg.2038 ]




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Adrenal cortex tumors

Adrenal cortical tumor

Adrenal gland tumors

Adrenal medulla tumors

Adrenalitis

Adrene

Aldosterone-producing adrenal tumor

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