NAVLE Endocrine

Feline Hyperadrenocorticism Study Guide

Hyperadrenocorticism (HAC), also known as Cushing's syndrome or hypercortisolism, is a rare but clinically significant endocrinopathy in cats caused by chronic excessive cortisol production.

Overview and Clinical Importance

Hyperadrenocorticism (HAC), also known as Cushing's syndrome or hypercortisolism, is a rare but clinically significant endocrinopathy in cats caused by chronic excessive cortisol production. Unlike dogs where HAC is relatively common, feline HAC accounts for fewer than 200 cases reported in veterinary literature, making it an uncommonly tested but high-yield topic on the NAVLE.

The clinical importance of recognizing feline HAC lies in its unique presentation compared to canine HAC, the strong association with concurrent diabetes mellitus (80-90% of cases), and the distinctive clinical sign of extreme skin fragility that occurs in approximately one-third of affected cats. Failure to recognize this condition often leads to poor diabetic regulation and progressive deterioration.

High-YieldWhen you see an older cat with poorly controlled or insulin-resistant diabetes mellitus combined with dermatologic abnormalities (especially skin fragility), always consider hyperadrenocorticism as a differential diagnosis.
Type Prevalence Mechanism
Pituitary-Dependent HAC (PDH) 75-85% of cases Pituitary adenoma (usually benign) secretes excess ACTH causing bilateral adrenal hyperplasia
Adrenal-Dependent HAC (ADH) 15-25% of cases Functional adrenal tumor (50% adenoma, 50% carcinoma) autonomously secretes cortisol; contralateral gland atrophies
Iatrogenic HAC Rare in cats Chronic exogenous glucocorticoid administration; cats are relatively resistant compared to dogs

Etiology and Pathophysiology

Normal HPA Axis Function

The hypothalamic-pituitary-adrenal (HPA) axis regulates cortisol production through a cascade of hormonal signals. The hypothalamus releases corticotropin-releasing hormone (CRH), which stimulates the anterior pituitary to secrete adrenocorticotropic hormone (ACTH). ACTH then acts on the zona fasciculata of the adrenal cortex to produce cortisol. Elevated cortisol levels normally suppress CRH and ACTH through negative feedback.

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