Hyperadrenocorticism (Cushing's Syndrome) in Dogs

Hyperadrenocorticism (Cushing's Syndrome) in Dogs

By: Dr. Douglas Brum

Section: Information In-depth

The adrenal glands are small endocrine organs located near the kidneys. They are comprised of two major parts:

  • The adrenal cortex (outer layer)
  • The adrenal medulla (inner layer)

    The adrenal cortex is further divided into three regions, each of which makes a different type of steroid hormone.

  • The outermost region of the adrenal cortex produces a hormone called aldosterone that is important in regulation of salt and waterFresh Flow Pet Fountain
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  • The mid-region produces cortisone, which has many important biological functions. Excessive cortisone production results in many of the clinical symptoms of Cushing's syndrome.

  • The inner region of the adrenal cortex produces sex hormones.

    The adrenal medulla produces catecholamine hormones such as epinephrine that help the body respond to sudden emergencies.

    Normally, control centers in the brain regulate the production of cortisone by the adrenal cortex.
    The hypothalamic region of the brain secretes a hormone called corticotrophin-releasing hormone (CRH), which in turn stimulates the pituitary gland to produce adrenocorticotropic hormone (ACTH). ACTH stimulates the production of cortisone by the adrenal cortex. High circulating concentrations of cortisone normally suppress ACTH production by the pituitary gland thus maintaining normal blood concentrations of cortisone by means of a "feed-back" mechanism. In dogs with Cushing's syndrome, abnormally high blood concentrations of cortisone occur as a result of a pituitary tumor that produces abnormally high concentrations of ACTH or by an adrenal tumor that produces abnormally high concentrations of cortisone. An understanding of the body's normal "feed-back" mechanism helps your veterinarian diagnose Cushing's syndrome and identify the underlying cause (pituitary tumor vs. adrenal tumor).

    Other Diseases

    Several other diseases may produce symptoms similar to those of Cushing's syndrome. Such disorders include:

  • Iatrogenic Cushing's disease. Animals that are receiving chronic (long term) oral, injectable, or even topical steroid preparations like ear drops or eye drops may have the same clinical signs as a true cushingoid dog. A slow withdrawal of the steroids will lead to a resolution of the clinical signs.

  • Diabetes mellitus is caused by inadequate production of insulin by the pancreas. As a result, abnormally high blood glucose concentration (hyperglycemia) and spillage of glucose into the urine (glucosuria) occur. Increased water consumption (polydipsia), increased appetite (polyphagia), and increased urination (polyuria) are common signs of diabetes mellitus.

  • Diabetes insipidus results from deficient production of anti-diuretic hormone (ADH) or failure of the kidney to respond to anti-diuretic hormone. This hormone is responsible for facilitating production of concentrated urine by the kidneys. Failure of this mechanism leads to increased urinations (polyuria) and increased water consumption (polydipsia).

  • Hypothyroidism results in decreased production of thyroid hormone and may lead to obesity, lethargy, muscle weakness and high blood cholesterol concentration. These clinical findings may be confused with hyperadrenocorticism.

  • Kidney disease may lead to increased urinations and increased water consumption.

  • Liver disease may result in abnormally high blood concentrations of liver enzymes such as alkaline phosphatase, liver enlargement and increased thirst. These findings may be confused with Cushing's syndrome.

  • Dogs with disorders of growth hormone may develop clinical symptoms that may be confused with Cushing's syndrome.

  • Dogs treated with phenobarbital for control of epilepsy may develop increased water consumption, increased urinations, increased appetite, and abnormally high blood concentrations of liver enzymes. These findings may be confused with Cushing's syndrome.

  • Iatrogenic Cushing's syndrome can result from long-term oral or topical administration of cortisone-like drugs (prednisolone, dexamethasone) may result in clinical and laboratory features similar to those observed in dogs with naturally-occurring hyperadrenocorticism.

     
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