Why Addison disease causes high potassium, low sodium and hypotension

Trace the electrolyte pattern to missing aldosterone

Aldosterone acts on the distal nephron to reabsorb sodium and, in exchange, secrete potassium and hydrogen ions into the urine. In primary adrenal insufficiency, the adrenal cortex itself is damaged, so aldosterone falls. Sodium escapes in urine, sweat and gut secretions, and potassium accumulates because the kidney cannot excrete it efficiently.

Water follows the lost sodium, so circulating volume shrinks. The result is the classic laboratory pattern of low sodium, high potassium and a raised BUN from reduced kidney perfusion. The raised BUN reflects dehydration rather than primary kidney disease in most cases. The salt craving many patients describe is the body's attempt to replace sodium.

Gastrointestinal symptoms make the pattern worse. Nausea, vomiting and diarrhoea are common in adrenal insufficiency, and each adds further fluid and sodium loss while reducing the patient's ability to replace them by mouth. The nurse should treat new vomiting in a patient with Addison disease as a reason for earlier review rather than a minor complaint, because oral replacement may no longer be absorbed.

Connect hypotension and collapse to volume and cortisol loss

Volume depletion from sodium wasting lowers blood pressure, and it often drops further on standing, producing dizziness and falls. Cortisol normally supports vascular tone and the response to stress hormones, so its absence makes hypotension worse and harder to correct with fluid alone. Weakness and fatigue reflect both problems.

During infection, surgery, injury or abrupt stopping of steroid therapy, the body needs far more cortisol than a failing adrenal gland can supply. That mismatch can trigger adrenal crisis, with profound hypotension, vomiting, abdominal pain and shock. Recognising the early electrolyte and blood pressure pattern helps the nurse anticipate this danger.

Explain hypoglycaemia, water handling and skin darkening

Cortisol helps the liver make glucose from protein during fasting and stress. When cortisol is missing, blood glucose can fall, especially with poor intake or illness. Cortisol is also needed to excrete a water load normally, so its lack adds to dilutional hyponatraemia on top of sodium loss.

In primary disease, low cortisol removes negative feedback, so the pituitary releases large amounts of ACTH. ACTH and a related peptide stimulate pigment cells, darkening skin creases, scars, pressure points, lips and the lining of the mouth. In secondary adrenal insufficiency, from pituitary failure, ACTH is low, pigmentation does not occur and electrolytes are often near normal because aldosterone is relatively preserved.

Translate the mechanism into assessment and nursing actions

Monitor orthostatic blood pressure, heart rate, weight, intake and output, and signs of dehydration. Trend sodium, potassium and glucose, and watch the cardiac monitor for peaked T waves or rhythm changes when potassium is high. Assess for confusion, nausea and abdominal pain, which can signal worsening toward crisis.

Give prescribed hormone replacement on time and report missed doses or vomiting that prevents oral intake. Teach patients that steroid needs rise during illness, that sick-day plans come from the prescriber, and that they should carry identification stating they have adrenal insufficiency. Encourage them not to stop replacement suddenly.

Work a hypothetical exam-style scenario

Imagine a patient with known Addison disease admitted with gastroenteritis who has been unable to keep tablets down. Blood pressure is low and falls further on sitting up, potassium is high, sodium is low and glucose is borderline. Options are to give oral fluids and recheck tomorrow, restrict salt, notify the provider urgently about possible adrenal crisis, or encourage ambulation.

Urgent notification is best, because missed replacement plus illness has produced the full pattern of aldosterone and cortisol deficiency with worsening hypotension. Oral fluids alone are inadequate when vomiting continues. Salt restriction worsens sodium loss. Ambulation risks falls from orthostatic hypotension. The provider directs parenteral treatment under local protocol.

Sources and further reading

MSD Manual Professional: Addison Disease. Sodium loss and potassium retention from aldosterone deficiency, cortisol effects, ACTH-driven pigmentation, lab pattern and primary versus secondary differences.

NIDDK: Symptoms and Causes of Adrenal Insufficiency and Addison's Disease. Salt craving, orthostatic dizziness, low blood glucose, skin darkening and the risk of adrenal crisis.