The adrenal gland is made up of two parts, the cortex and the medulla. The adrenal cortex produces hormones necessary for normal body functioning; deficiency of these hormones results in adrenal insufficiency. The cortex is responsible for producing glucocorticoids, mineralocorticoids, and androgens. Destruction or dysfunction of the adrenal cortex mainly causes glucocorticoid and mineralocorticoid deficiency. Primary adrenal insufficiency is also known as autoimmune adrenalitis or Addison disease.

Adrenal insufficiency ranges from mild nonspecific symptoms to life-threatening shock conditions. Due to its vague symptoms and varying degree of clinical presentation, a clinician must maintain a high level of suspicion for this disease. The decreasing or suppressed adrenal function may be masked until stress or illness triggers an adrenal crisis.

Adrenal insufficiency can be classified into primary, secondary, and tertiary causes. Primary adrenal insufficiency occurs when there is a pathology affecting the adrenal gland itself. Secondary adrenal insufficiency results from a decreased level of adrenocorticotrophin hormone (ACTH) released from the pituitary gland, and tertiary adrenal insufficiency results from a decreased level of corticotrophin-releasing hormone (CRH) released from the hypothalamus.

An important distinction in these patients is the presence of mineralocorticoid deficiency. Those with secondary or tertiary adrenal insufficiency will typically have preserved mineralocorticoid function due to the separate feedback systems. Mineralocorticoid levels are regulated by the renin-angiotensin system that is independent of hypothalamic or pituitary signals.

Another important distinction is the acute versus chronic nature of the disease. Acute adrenal insufficiency patients often present in a critically ill state, while chronic presentation can be insidious.