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Diseases » Conn's syndrome » Diagnosis

Diagnosis of Conn's syndrome

Conn's syndrome Diagnosis: Book Excerpts

Diagnostic Tests for Conn's syndrome: Online Medical Books

16 MEDICAL BOOKS ONLINE! Review excerpts from medical books online, free, without registration, for more information about diagnostis of Conn's syndrome.

ALKALOSIS (INCREASED PH): Ask the following questions:
(Algorithmic Diagnosis of Symptoms and Signs)

What is the bicarbonate level? If this is elevated, the patient has a metabolic alkalosis. If this is decreased, the patient has a respiratory alkalosis associated with salicylate intoxication or hyperventilation syndrome.
Has the patient been vomiting? If so, look for gastric outlet obstruction, intestinal obstruction, and other causes of vomiting. If there is no history of vomiting, the alkalosis may be due to diuretics, Cushing's disease, or chronic antacid use.

DIAGNOSTIC WORKUP

The workup of alkalosis should include a CBC, chemistry panel, urinalysis, electrolytes, arterial blood gas analysis, flat plate of the abdomen, chest x-ray, and consultation with an endocrinologist.

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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

ALKALOSIS (INCREASED PH): Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

Taking a drug history and noting hyperventilation or vomiting during the clinical evaluation will assist in the diagnosis. Serial electrolytes, arterial blood gases, and drug screen are first-line laboratory tests to assist in the diagnosis.

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Source: Differential Diagnosis in Primary Care, 2007

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