Hyperaldosteronism
In hyperaldosteronism, the adrenal cortex hypersecretes the mineralocorticoid aldosterone, causing excessive reabsorption of sodium and water and excessive renal excretion of potassium.
The disorder may be classified as primary, resulting from a stimulus inside the adrenal gland, or secondary, resulting from an extra–adrenal stimulus. Incidence of hyperaldosteronism is two times greater in females than in males and highest between ages 30 and 50.
Causes
Primary hyperaldosteronism (Conn’s syndrome) is uncommon. In 70% of patients, it results from a small, unilateral aldosterone–producing adrenal adenoma. In the remaining 30%, the cause is either unclear, adrenocortical hyperplasia (in children), or carcinoma. Excessive ingestion of English black licorice or a similar substance can produce a syndrome similar to primary hyperaldosteronism due to the mineralocorticoid action of glycyrrhizic acid, which is present in licorice.
Secondary hyperaldosteronism results from extra–adrenal pathology, which stimulates the adrenal gland to increase production of aldosterone. For example, conditions that reduce renal blood flow (renal artery stenosis) and extracellular fluid volume or that produce a sodium deficit activate
the renin–angiotensin–aldosterone system and, subsequently, increase aldosterone secretion. Thus, secondary hyperaldosteronism may result from conditions that induce hypertension through increased renin production (such as Wilms’ tumor), from ingestion of oral contraceptives, and from pregnancy. However, this type may also result from disorders unrelated to hypertension that may or may not cause edema. For example, nephrotic syndrome, hepatic cirrhosis with ascites, and heart failure commonly induce edema; Bartter’s syndrome and salt–losing nephritis don’t.
the renin–angiotensin–aldosterone system and, subsequently, increase aldosterone secretion. Thus, secondary hyperaldosteronism may result from conditions that induce hypertension through increased renin production (such as Wilms’ tumor), from ingestion of oral contraceptives, and from pregnancy. However, this type may also result from disorders unrelated to hypertension that may or may not cause edema. For example, nephrotic syndrome, hepatic cirrhosis with ascites, and heart failure commonly induce edema; Bartter’s syndrome and salt–losing nephritis don’t.
Complications
Hyperaldosteronism can produce neuromuscular irritability, tetany, paresthesia, and seizures. Cardiac complications include arrhythmias, ischemic heart disease, left ventricular hypertrophy, heart failure, and death. Metabolic alkalosis, nephropathy, and azotemia may also occur.
Assessment
The patient may complain of headache, visual disturbances, muscle weakness, fatigue, polyuria, and polydipsia. Inspection may detect intermittent flaccid paralysis, resulting from hypokalemia and, possibly, tetany, which may be caused by metabolic alkalosis and lead to hypocalcemia. Secondary hyperaldosteronism rarely occurs without edema.
Palpation may reveal a weak pulse, signs of muscle tonicity, and positive Chvostek’s and Trousseau’s signs. Auscultation of the apical pulse may detect cardiac arrhythmias. Auscultation of blood pressure reveals hypertension.
