Diminished hormone production from the cortex of the adrenal gland. In all species, injury to the gland may occur from hemorrhage, mineralization, amyloid deposition, or invasion by infectious agents but clinical signs of insufficiency rarely occur except in the dog.
- immune-mediated h. — see primary hypoadrenocorticism (below).
- primary h. — occurs most often in dogs, usually the result of an idiopathic atrophy of the adrenal glands involving all layers of the cortex. Immune-mediated mechanisms are suspected. The clinical effects are related to insufficient production of mineralocorticoids causing hyponatremia, hypochloremia and hyperkalemia. Hypovolemia, prerenal azotemia and cardiac conduction abnormalities lead to weakness, vomiting, diarrhea and bradycardia. Deficiency of glucocorticoids may also cause hypoglycemia. Called also Addison's disease, immune-mediated hypoadrenocorticism.
- secondary h. — lesions of the pituitary and, more commonly in dogs, the long-term administration of corticosteroids which causes a reduced secretion of ACTH and leads to reduced synthesis and low blood levels of glucocorticoids. Mineralocorticoid levels remain normal.
