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Hypoadrenocorticism in Dogs and Cats

Patty Lathan, VMD, DACVIM (SAIM)
Mississippi State University, College of Veterinary Medicine, Mississippi State, MS, USA

Hypoadrenocorticism in Dogs pituitary and hypothalamus, such that ACTH and CRH
production are decreased when adequate cortisol con-
Etiology/Pathophysiology centrations are present.
Most naturally occurring cases of primary hypoadren-
Primary hypoadrenocorticism (Addison disease, HOAC) ocorticism in dogs are idiopathic, likely due to immune‐
results from the destruction of >90% of the adrenal cor- mediated destruction of the adrenal cortex. Rarely,
tex. Clinical signs are due to both cortisol and aldoster- infiltration of the adrenal cortex by fungus, neoplasia,
one deficiency in the majority of patients, although some other granulomatous disease, or amyloidosis has been
patients only have signs of cortisol deficiency (atypical reported. Trauma, hemorrhage, and infarction may also
hypoadrenocorticism). lead to Addison disease, as can drugs used to treat hyper-
Aldosterone is the major mineralocorticoid secreted adrenocorticism. Although proper use of mitotane usu-
by the outermost layer of the adrenal cortex, the zona glo- ally leads to necrosis of only the zonae fasciculata and
merulosa. Its main activities are the conservation of reticularis, improper monitoring, or use in a particularly
sodium and water, and excretion of potassium and hydro- sensitive patient, can result in destruction of all three
gen ions (acid), from the distal renal tubules. Aldosterone layers of the cortex, causing both cortisol and aldoster-
secretion is primarily regulated by the renin‐angiotensin‐ one deficiency. Trilostane is an enzyme inhibitor that
aldosterone system, but secretion can also be stimulated decreases cortisol concentrations, but also decreases
by hyperkalemia. In patients with hypoadrenocorticism aldosterone concentrations to a lesser extent. It can lead
and subsequent aldosterone deficiency, hyperkalemia, to cortisol deficiency and, occasionally, aldosterone
hyponatremia, and hypovolemia are common. deficiency. Additionally, trilostane has been reported to
Cortisol is the major glucocorticoid produced by the cause idiosyncratic adrenocortical necrosis, resulting in
innermost layers of the adrenal cortex, the zonae fascicu- both cortisol and aldosterone deficiency.
lata and reticularis. Its functions include stimulation of Secondary hypoadrenocorticism can be caused by
gluconeogenesis and erythropoiesis, suppression of the either a pituitary lesion, resulting in ACTH deficiency, or
inflammatory response, and maintenance of gastrointes- iatrogenically. Iatrogenic secondary hypoadrenocorti-
tinal mucosal integrity. Cortisol also helps the body deal cism is caused by abrupt cessation of exogenous gluco-
with stress. In dogs with HOAC, cortisol deficiency often corticoids following long‐term use. Long‐term use of
results in lethargy, gastrointestinal signs, hypoglycemia, glucocorticoids suppresses production of ACTH.
and anemia. Without the trophic effects of ACTH, the zonae fascicu-
Cortisol release is regulated by the hypothalamic‐ lata and reticularis atrophy. When the exogenous gluco-
pituitary‐adrenal axis (HPAA). During times of stress corticoid is abruptly discontinued (not tapered), ACTH
(emotional, physiologic, other), corticotropin‐releasing production occurs, but the adrenal cortex is atrophied
hormone (CRH) is secreted from the hypothalamus, and incapable of producing adequate amounts of corti-
and stimulates the release of adrenocorticotropic sol. Thus, signs of cortisol deficiency occur. Aldosterone
hormone (ACTH) from the pituitary gland. ACTH then deficiency is not present in cases of secondary hypoad-
stimulates cortisol secretion from the adrenal cortex. renocorticism, since ACTH has little regulatory control
Cortisol has a negative feedback effect on both the of aldosterone production.

Clinical Small Animal Internal Medicine Volume I, First Edition. Edited by David S. Bruyette.
© 2020 John Wiley & Sons, Inc. Published 2020 by John Wiley & Sons, Inc.
Companion website: www.wiley.com/go/bruyette/clinical