Mineralocorticoids are responsible for balancing sodium, potassium, and water. In Addisons disease the level of sodium decreases and potassium increases. Low sodium (hyponatremia) can lead to vomiting, diarrhea, weight loss and weakness. High potassium (hyperkalemia) mainly effects the heart causing changes in the rhythm and contraction.

Glucocorticoids stimulate the breakdown and utilization of sugars by the body. They effect protein and fat metabolism, help maintain blood pressure, and suppress inflammation. A deficiency of glucocorticoids can produce intestinal signs including vomiting, diarrhea, abdominal pain and weight loss; and generalized signs including loss of energy, weakness, and depression.

Hypoadrenocortism can be caused by any mechanism which damages the adrenal gland. In many cases unknown underlying causes stimulate the immune system to attack the adrenal gland (idiopathic adrenal insufficiency). Less commonly infections and tumors can be involved.

Clinical signs of Addisons disease are often vague and include loss of appetite (anorexia), loss of energy, weakness which can reach the point of collapse, vomiting, mild diarrhea, abdominal pain, depression, incoordination, behavioral changes, and fluctuating temperature. Episodes of clinical signs may come and go until they eventually reach a crisis.

Because of this wide range of symptoms diagnosis relies on laboratory testing. General screening blood tests may reveal a decrease in the ratio between sodium and potassium. More specific testing measures the changes in cortisol levels in the blood in response to stimulation with Adrenocorticotrophin (ACTH), the hormone produced by the brain to trigger excretion by the adrenal glands. In normal animals cortisol will increase significantly following an injection of ACTH whereas little or no increase is seen in cases of Addisons disease. Changes in the heart can be detected using an Electrocardiogram (ECG). One of the most common findings is a large "spiked" T wave.

Collapsed patients are treated with intravenous saline (sodium chloride) to correct the sodium deficiency, glucocorticoids (e.g. prednisolone) and mineralocorticoids (e.g. fludrocortisone). Response to treatment is usually seen within 2 hours with the animal being able to stand.

Long term therapy involves continuing doses of the glucocorticoids and mineralocorticoids.