NAVLE Endocrine

Feline Hypoadrenocorticism Study Guide

Feline hypoadrenocorticism (Addison's disease) is a rare but life-threatening endocrine disorder resulting from inadequate production of adrenocortical hormones, primarily glucocorticoids (cortisol) and mineralocorticoids (aldosterone).

Overview and Clinical Importance

Feline hypoadrenocorticism (Addison's disease) is a rare but life-threatening endocrine disorder resulting from inadequate production of adrenocortical hormones, primarily glucocorticoids (cortisol) and mineralocorticoids (aldosterone). With only approximately 48 documented cases in the veterinary literature since 1983, this condition remains significantly rarer in cats than in dogs. However, its waxing and waning clinical signs often mimic more common feline diseases, earning it the nickname "the great pretender." Early recognition is crucial as untreated cases can progress to life-threatening Addisonian crisis.

Zone Hormone Produced Primary Function
Zona Glomerulosa Aldosterone (mineralocorticoid) Sodium retention, potassium excretion, fluid balance
Zona Fasciculata Cortisol (glucocorticoid) Glucose metabolism, stress response, immune modulation
Zona Reticularis Androgens (DHEA, androstenedione) Sex hormone precursors

Adrenal Gland Anatomy and Physiology

Adrenal Gland Structure

The feline adrenal glands are paired, small triangular organs located craniomedial to each kidney in the retroperitoneal space. Each gland consists of two distinct functional regions: the outer adrenal cortex (comprising approximately 80-90% of the gland) and the inner adrenal medulla. The cortex is further divided into three zones, each producing specific hormones.

Hypothalamic-Pituitary-Adrenal (HPA) Axis

Cortisol secretion is regulated by the HPA axis through a negative feedback loop. Corticotropin-releasing hormone (CRH) is released from the hypothalamus, stimulating the anterior pituitary to release adrenocorticotropic hormone (ACTH). ACTH then acts on the adrenal cortex to stimulate cortisol production. Elevated cortisol levels provide negative feedback to both the hypothalamus and pituitary, completing the regulatory loop.

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