HYPERALDOSTERONISM

Hyperaldosteronism may be primary or secondary

PRIMARY HYPERALDOSTERONISM

Aetiology

« Adrenal adenoma

• Adrenal hyperplasia

Primary hyperaldosteronism due to adrenal adenoma is termed Conn’s syndrome.

Pathophysiology

Aldosterone is secreted from the zona glomerulosa of the adrenal gland in response to stimulation by angiotensin II.

Following are the sequence of events

• The enzyme renin is secreted by the kidneys in response to decreased renal perfusion pressure or flow

• Renin causes the formation of angiotensin I from angiotensinogen (an alpha 2 globulin)

• Angiotensin I is inactive but is converted to active form angiotensin II by the Angiotensin-converting enzyme.

• Angiotensin II causes power vasoconstriction & stimulation of aldosterone from the adrenal gland.

• Aldosterone causes sodium retention and potassium loss, resulting in an increase in blood pressure.

Clinical features

The usual presentation is with hypertension and hypokalaemia.

Hypertension may be severe and associated with renal and retinal damage.

Muscle weakness

Paraesthesias

Tetany

Headache

Polyuria

Polydipsia.

Investigations

Serum electrolytes – hypokalaemia

Plasma aldosterone – elevated

• CT Scan or MRI – for differentiation of adenoma from hyperplasia.

Management

• Adenoma – surgical removal

Hyperplasia – aldosterone antagonists e.g. spironolactone

SECONDARY HYPERALDOSTERONISM

Raised levels of aldosterone are present due to:

• Liver cirrhosis

• Nephrotic syndrome

– CCF with excessive diuretic therapy