Hyperaldosteronism
Hyperaldosteronism: Excerpt from Professional Guide to Diseases (Eighth Edition)
In hyperaldosteronism (Conn’s syndrome), hypersecretion of the mineralocorticoid aldosterone by the adrenal cortex causes excessive reabsorption of sodium and water, and excessive renal excretion of potassium.
Causes and incidence
Hyperaldosteronism may be primary (uncommon) or secondary. In 70% of patients, hyperaldosteronism results from a benign aldosterone-producing adrenal adenoma. In 15% to 30% of patients, the cause is unknown; rarely, the cause is bilateral adrenocortical hyperplasia (in children) or carcinoma. Incidence is three times higher in females than in males and is highest between ages 30 and 50.
In primary hyperaldosteronism, chronic aldosterone excess is independent of the renin-angiotensin system and, in fact, suppresses plasma renin activity. This aldosterone excess enhances sodium reabsorption by the kidneys, which leads to mild hypernatremia and, simultaneously, hypokalemia and increased extracellular fluid (ECF) volume. Expansion of intravascular fluid volume also occurs and results in volume-dependent hypertension and increased cardiac output. Excessive ingestion of English black licorice or licorice-like substances can produce a syndrome similar to primary hyperaldosteronism due to the mineralocorticoid action of glycyrrhizic acid.
Secondary hyperaldosteronism results from an extra-adrenal abnormality that stimulates the adrenal gland to increase production of aldosterone. For example, conditions that reduce renal blood flow (renal artery stenosis) and ECF volume or produce a sodium deficit activate the renin-angiotensin system and, subsequently, increase aldosterone secretion. Thus, secondary hyperaldosteronism may result from conditions that induce hypertension through increased renin production (such as Wilms’tumor), ingestion of hormonal contraceptives, and pregnancy.
However, secondary hyperaldosteronism may also result from disorders unrelated to hypertension, which may or may not cause edema. For example, nephrotic syndrome, hepatic cirrhosis with ascites, and heart failure commonly induce edema, whereas Bartter’s syndrome and salt-losing nephritis don’t.
Signs and symptoms
Most clinical effects of hyperaldosteronism result from hypokalemia, which increases neuromuscular irritability and produces muscle weakness; intermittent, flaccid paralysis; fatigue; headaches; paresthesia; and, possibly, tetany (resulting from metabolic alkalosis), which can lead to hypocalcemia.
Diabetes mellitus is common, perhaps because hypokalemia interferes with normal insulin secretion. Hypertension and its accompanying complications are also common. Other characteristic findings include visual disturbances and loss of renal concentrating ability, resulting in nocturnal polyuria and polydipsia. Azotemia indicates chronic potassium depletion nephropathy.
Diagnosis
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.
Treatment
Although treatment of primary hyperaldosteronism may include unilateral adrenalectomy, administration of a potassium-sparing diuretic — spironolactone — and sodium restriction may control hyperaldosteronism without surgery. For bilateral adrenal hyperplasia, spironolactone is the drug of choice. Treatment of secondary hyperaldosteronism must include correction of the underlying cause.
Special considerations
Patient care includes careful monitoring and recording of urine output, blood pressure, weight, and serum potassium levels.
❑ Watch for signs of tetany (muscle twitching, Chvostek’s sign) and for hypokalemia-induced cardiac arrhythmias, paresthesia, or weakness. Give potassium replacement, as ordered, and keep calcium gluconate I.V. available.
❑ Ask the dietitian to provide a low-sodium, high-potassium diet.
❑ After adrenalectomy, watch for weakness, hyponatremia, rising serum potassium levels, and signs of adrenal hypofunction, especially hypotension.
❑ If the patient is taking spironolactone, advise him to watch for signs of hyperkalemia. Tell him that impotence and gynecomastia may follow long-term use.
❑ Tell the patient who must take steroid hormone replacement to wear a medical identification bracelet.
Book Source Details
- Book Title: Professional Guide to Diseases (Eighth Edition)
- Author(s): Springhouse
- Year of Publication: 2005
- Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2005 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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