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Which of the following are causes of metabolic alkalosis with hypokalaemia?

True / False

Spironolactone Incorrect answer selected

Conn's syndrome Correct

Pyloric stenosis Correct

Small bowel villous adenoma Incorrect answer selected

Addison's disease Correct

Explanation

Potassium regulation and plasma pH are regulated in ways that are intrinsically linked. Aldosterone is a major regulatory hormone, particularly affecting the distal convoluted tubule to increase sodium reabsorption and enhance potassium secretion. As more sodium is reabsorbed than potassium secreted, the net lumenal negative charge causes chloride and water to follow sodium. Water then follows sodium and chloride by osmosis.

Spironolactone is an aldosterone antagonist and hence associated with hyperkalaemia, that is, it mimics type four renal tubular acidosis. Furosemide enhances lumenal potassium, chloride and sodium loss in the thick loop of Henle; attempts to reabsorb sodium in the distal convoluted tubule result in increased urine proton loss and hence alkalosis.

Acid/bicarbonate and potassium loss may also occur within the gastrointestinal tract. Loss of H+ and K+ cations through projectile vomiting gives rise to the classical biochemical findings of pyloric stenosis, namely hypokalaemia, hypochloraemia, metabolic alkalosis, assuming there is no associated shock.

Conn's syndrome is of a solitary, aldosterone-secreting adrenal adenoma and is a cause of primary hyperaldosteronism, hence it produces a similar picture of normal/high-ish sodium (true hypernatraemia is rare due to compensatory escape mechanisms), hypokalaemia, volume overload and arterial hypertension.

Addison's disease produces aldosterone deficiency, hence there is hyponatraemia, hyperkalaemia and volume depletion.

Reference:

Anaesthesia UK. Sodium, potassium and the anaesthetist.

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