Hypoadrenocorticism Insidious and Deadly

The hypothalamic-pituitary-adrenal axis is a key player in the maintenance of protein metabolism, mineral and acid-base homeostasis, immune function, blood pressure, gastrointestinal function, erythropoiesis, and mentation. Hypoadrenocorticism (Addison’s disease) can result from either lack of cortisol production from the adrenal glands, or result from lack of CRF or ACTH stimuli from the hypothalamus or pituitary glands. The majority of cases of hypoadrenocorticism in dogs result from immune-mediated lymphocytic plasmacytic destruction of the adrenal cortex. Adrenocortical destruction typically results in a lack of both glucocorticoid from the zona fasciculata and lack of mineralocorticoid production from the zona glomerulosa. However, in some dogs, destruction of the zona fasciculata can occur before destruction of the zona glomerulosa, resulting in clinical signs of glucocorticoid deficiency alone before clinical signs associated with loss of mineralocorticoids. This is known as “atypical primary hypoadrenocorticism”. Secondary adrenocortical deficiency (“secondary Addison’s”) is associated with a loss of either corticotropin releasing factor (CRF) from the hypothalamus, or lack of production or release of adrenocorticotropic hormone (ACTH) from the posterior pituitary gland. In secondary adrenocortical deficiency, loss of trophic stimulation of the zona fasciculata results in a loss of glucocorticoid (cortisol) release and spares the zona glomerulosa. Thus, mineralocorticoid activity is maintained. Secondary hypoadrenocorticism has been described following craniocerebral trauma, or can occur spontaneously ...