potassium) are severe, the resulting hypovolemia, prerenal azotemia, and cardiac arrhythmias may result in an Addisonian crisis. In severe cases, the patient may be presented in shock and moribund. Addisonian crisis must be differentiated from other life-threatening disorders such as diabetic ketoacidosis, necrotizing pancreatitis, and septic peritonitis. Causes The adrenal glands are located above the kidneys. The adrenal outer layer, or cortex, has three layers; each produces a specific type of steroid. Primary Primary adrenocortical insufficiency is the more common form of hypoadrenocorticism. All layers of the adrenal gland stop functioning; the problem is with the adrenal gland. This causes a deficiency of both mineralocorticoid and glucocorticoid secretion. Most cases are classified as idiopathic, although immune-mediated adrenocortical destruction is a likely cause. Bilateral destruction of the adrenal cortex by neoplasia (e.g. lymphosarcoma), granulomatous disease, or arterial thrombosis can also cause primary adrenocortical insufficiency. The destruction is progressive, although variable in rate, ultimately leading to complete loss of adrenocorotical function. A partial deficiency syndrome may occur initially, with signs manifested only during times of stress (e.g., boarding, travel, surgery). Secondary In secondary hypoadrenocorticism the problem is not in the adrenal gland but in the pituitary gland. Usually, the anterior portion of the pituitary gland produces a hormone, adrenocorticotropic hormone (ACTH), that signals the zona fasciculata and zona reticularis to produce their steroids. When the pituitary is unable to produce ACTH, these zones stop production of their hormones. The zona glomerulosa is not controlled by ACTH, and remains able to produce a normal amount of mineralocorticoids. A dog with secondary hypoadrenocorticism only needs to have medication to replace the glucocorticoid steroid cortisol. One dog in every 42 diagnosed with hypoadrenocorticism has the secondary form of the disease where mineralocorticoid production remains intact. Secondary adrenocortical insufficiency involves only a deficiency of glucocorticoid secretion. Destructive lesions (e.g. neoplasia, inflammation) in the pituitary gland or hypothalamus and chronic administration of exogenous glucocorticoids or megestrol acetate (cats) are the most common causes. Drug induced Drug induced (iatrogenic) hypoadrenocorticism is caused during abrupt cessation of a steroid medication. During steroid treatment, the adrenal glands do not function fully. The body senses the levels of the exogenous steroids in the system and therefore does not signal for additional production. The usual protocol for stopping steroid medications is not to eliminate them suddenly, but to withdraw from them gradually in a "tapering off" process, which allows the production to