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Diseases » Adrenal adenoma, familial » Diagnosis

Diagnosis of Adrenal adenoma, familial

Adrenal adenoma, familial Diagnosis: Book Excerpts

Diagnostic Tests for Adrenal adenoma, familial: Online Medical Books

16 MEDICAL BOOKS ONLINE! Review excerpts from medical books online, free, without registration, for more information about diagnostis of Adrenal adenoma, familial.

Adrenal hypofunction: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

Diagnosis requires demonstration of decreased corticosteroid concentrations in plasma and an accurate classification of adrenal hypofunction as primary or secondary. If secondary adrenal hypofunction is suspected, the metyrapone test is indicated. This test requires oral or I.V. administration of metyrapone, which blocks cortisol production and should stimulate the release of corticotropin from the hypothalamic-pituitary system. In adrenal hypofunction, the hypothalamic-pituitary system responds normally, and plasma reveals high levels of corticotropin; however, plasma levels of cortisol precursor and urinary concentrations of 17-hydroxycorticosteroids don’t rise.

If either primary or secondary adrenal hypofunction is suspected, a short corticotropin stimulation test may be done. If both corticotropin and cortisol are low, the long corticotropin test may be done. The test involves I.V. administration of corticotropin over 6 to 8 hours, after samples have been obtained to determine baseline plasma cortisol and 24-hour urine cortisol levels. In adrenal hypofunction, plasma and urine cortisol levels fail to rise normally in response to corticotropin; in secondary hypofunction, repeated doses of corticotropin over successive days produce a gradual increase in cortisol levels until normal values are reached.

In a patient with typical addisonian symptoms, the following laboratory findings strongly suggest acute adrenal hypofunction:

❑ decreased cortisol levels in plasma (less than 10 mcg/dl in the morning, with lower levels in the evening); however, this test is time-consuming, and emergency therapy shouldn’t be postponed for test results

❑ decreased serum sodium and fasting blood glucose levels

❑ increased serum potassium and blood urea nitrogen levels

❑ elevated hematocrit and lymphocyte and eosinophil counts

❑ X-rays showing a small heart and adrenal calcification.

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Source: Professional Guide to Diseases (Eighth Edition), 2005

Hyperaldosteronism: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

Persistently low serum potassium levels in a nonedematous patient who isn’t taking diuretics, who doesn’t have obvious GI losses (from vomiting or diarrhea), and who has a normal sodium intake, suggest hyperaldosteronism. If hypokalemia develops in a hypertensive patient shortly after starting treatment with potassium-wasting diuretics (such as thiazides), and if it persists after the diuretic has been discontinued and potassium replacement therapy has been instituted, evaluation for hyperaldosteronism is necessary.

CONFIRMING DIAGNOSIS A low plasma renin level that fails to increase appropriately during volume depletion (upright posture, sodium depletion) and a high plasma aldosterone level during volume expansion by salt loading confirm primary hyperaldosteronism in a hypertensive patient without edema.

The serum bicarbonate level is often elevated, with ensuing alkalosis due to hydrogen and potassium ion loss in the distal renal tubules. Other tests show markedly increased urinary aldosterone levels, increased plasma aldosterone levels and, in secondary hyperaldosteronism, increased plasma renin levels.

A suppression test is useful to differentiate between primary and secondary hyperaldosteronism. During this test, the patient receives oral desoxycorticosterone for 3 days while plasma aldosterone levels and urinary metabolites are continuously measured. These levels decrease in secondary hyperaldosteronism but remain the same in primary hyperaldosteronism. Simultaneously, renin levels are low in primary hyperaldosteronism and high in secondary hyperaldosteronism.

Other helpful diagnostic evidence includes an increase in plasma volume of 30% to 50% above normal, electrocardiogram signs of hypokalemia (ST-segment depression and U waves), chest X-ray showing left ventricular hypertrophy from chronic hypertension, and localization of the tumor by adrenal angiography or computed tomography scan.

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Source: Professional Guide to Diseases (Eighth Edition), 2005

Adrenal hypofunction: Diagnosis
(Handbook of Diseases)

The diagnosis of adrenal insufficiency should be made only with corticotropin stimulation testing to assess adrenal reserve capacity.

The corticotropin stimulation test involves I.M. or I.V. administration of cosyntropin with samples obtained 60 minutes later. Cortisol levels should be greater than 18 µg/dl. If the result is abnormal, primary and secondary adrenal insufficiency can be distinguished by measuring aldosterone levels from the same blood sample. With secondary adrenal insufficiency, the aldosterone level is normal (greater than or equal to 5 ng/dl). Baseline plasma cortisol levels may also be obtained. With Addison’s disease, plasma and urine cortisol levels fail to rise normally in response to corticotropin; with secondary hypofunction, repeated doses of corticotropin over successive days produce a gradual increase in cortisol levels until normal values are reached.

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Source: Handbook of Diseases, 2003