Clinical Signs:
  • ·Polyuria/Polydipsia (PU/PD): Occurs in 80-85% of cases and refers to excessive urination and excessive drinking. The mechanism is due to effects of corticosteroids on antidiuretic hormone (ADH) levels. (ADH, secreted from the pituitary gland, is responsible for most of the resorption and thus conservation of fluid from the kidneys before fluid becomes voidable urine). It is believed that excessive levels of cortisol (the primary adrenal glucocorticoid) interferes with the release of ADH; in the relative absence of ADH, fluid is lost in the urine...and enhancement of thirst mechanisms are invoked to replace this loss.
  • Polyphagia: occurs is 90-90% of cases and refers to excess appetite. The mechanism is not known. However, most owners assume that if their dog's appetite is good, the dog feels good and does not require medical attention. WRONG!
  • Pot Bellied Appearance: occurs in 90-95% of affected dogs. The cause is thought to be a combination of reduced abdominal muscle strength from glucocorticoid-enhanced muscle protein breakdown, concurrent enlargement of abdominal organs...especially the liver (in many but not all animals), mobilization of fat stores and resultant deposition of fat into the abdominal space and a chronically full/enlarged urine bladder. (Click on Pot belly picture, at top)
  • Muscle Weakness/Lameness/Lethargy: occurs in 75-80% of cases and is the result weakness due to muscle protein breakdown. Lameness, in some cases, occurs due to weakening of skeletal and skeletal support structures containing protein elements. For example, some cases of knee injury, e.g. anterior cruciate ligament rupture or luxations of the patella (knee cap) are due to weakening of these structures caused by glucocorticoid-induced protein wasting. Lethargy may also result from related respiratory deficiencies (see below) and secondary hypothyroidism (see below). Poor oxygenation-->poor tissue energy production; low thyroid hormone levels result in reduced metabolic rates--->
    --->decreased energy.
  • Osteoporosis: seen in about 15% of cases, refers to decreased calcification of boney matrix. Glucocorticoids increase calcium excretion in the urine and decrease absorption from the gastrointestinal tract. Calcium is, therefore,leeched from the bone to maintain normal blood and tissue calcium levels.
  • · Panting: a fairly common occurence...The mechanisms inducing dogs to pant are mulifactorial.

a) Increased deposition of fat over the thorax...less room for the lungs to expand

b) Abdominal organ enlargement (especially the liver which is right against the diaphragm muscle) and fat accumulation place pressure on the diaphragm (already weakened by protein breakdown) interfering with its function in respiration

c) Weakening of all muscles of respiration due to glucocorticoid-induced muscle protein breakdown; the animal is unable to expand the chest and lungs adequately during individual respirations and attempts to compensate via increasing the frequency of repirations.

d) Pickwickian syndrome: When the ventilations are inadequate and animals are cyanotic (bluish membranes due to unoxygenated red blood cells) despite panting and resting to reduce oxygen consumption by tissues, the body tries to compensate in other ways: by increasing the red blood cell mass (to carry the remaining oxygen more efficiently), and increasing the heart workload (to pump the blood more efficiently to the tissues). Often these efforts fail and the animal develops heart failure in addition. And panting continues hopelessly...

e) In some breeds there are concurrent cardiac and respiratory problems that are exacerbated by decreased respiratory depth and increased frequency.

f) Thromboembolism: hyperadrenocorticism predisposes to thromboembolus (blot clot) formation. A clot in a lung can result in acute (life-threatening) respiratory distress or chronically poor perfusion of the affected area of the lung, with compensatory panting to overide inefficient oxygenation by the affected lung. Interestingly, development of a pulmonary thrombus seems to occur more frequently in animals undergoing treatment for hyperadrenocorticism!

  • Reproductive Effects: in animals that are sexually intact: In males, testicles become small and soft; in females, there is failure to enter estrus cycle.
    In spayed females: there is sometimes enlargement of the clitoris due to increased levels of sex steroids (androgens) from the adrenal gland.
  • Pseudomyotonia. Occurs in less than 1% of effected animals and refers to involuntary contraction of certain muscle groups. Usually the dog is noted to have a "stiff" gait in the hind legs. (click on "Stance Pictures" above)
  • Hypothyroidism: The excessive glucorticoids "feedback" to the pituitary gland...some of this may leak into and inhibit the portions of the gland responsible for TSH release. Additionally, glucocorticoids affect the metabolism of thyroxin, and interfere with the conversion of T4 to T3. It is not unusual to mistakenly assume that the primary problem is hypothyroidism, rather than hyperadrenocorticism as there are many clinical similarities between the diseases..especially the skin abnormalities. (More about Hypothyroidism elsewhere on this site.)
  • Immune Suppression: corticosteroids, at high levels, are immunosuppressive. Hence, animals are more susceptible to infections. Interestingly, the labwork often fails to indicate the presence of infection, such as elevated white blood cells, because the production of these is suppressed! Affected animals can not mount a fever either. Hence awareness of the possibility of infection is mandated even in the absence of supporting laboratory data.
  • Urinary Tract Calculi: Rarely the excessive excretion of calcium in the urine that occurs with hyperadrenocorticism may result in calcium-containing crystals or more problematic, urinary tract stones.
  • Skin Issues: (click on Alopecia and Calcinosis pictures, at top of page)

a) Alopecia, often bilateral and symmetrical. Also, clipped hair fails to grow back.

b) Poor wound healing (probably due, in part to protein breakdown...rather than synthesis). Sometimes striae are seen...these are fragile scars representing areas of poor healing. Elective surgeries should be avoided until the disease is treated!

c) Thin fragile skin...again, due to protein breakdown. Often the skin is also wrinkled and the underlying blood vessels are easily visualized.

d) Bruising. The thin, fragile skin of affected animals is easily bruised.

e) Pyoderma...bacterial infection of the skin are common, and there is often accompanying odor (due to seborrheic changes) and pruritis (itching). These animals are prone to skin and other infections due to ongoing immune system suppression. With chronic inflammation, pigment changes (hyperpigmentation) may also be seen.

f) Striations (striae): these represent fragile, thin scars from poor wound healing.

g) Calcinosis cutis: abnormal soft tissue composition predisposes to soft tissue mineralization in the form of calcium deposits. In the skin, these are chalky areas of firmness most often seen on the face, neck, back, belly and groin. Other sites of potential soft tissue mineralization are liver, kidney, trachea stomach and the aorta.

  • Hypertension: occurs in about 50% of cases. Mechanisms are related to the effect(s) of corticosteroids on the blood pressure regulatory enzyme system (renin-angiotensin activation), enhances sensitivity of the natural vascular blood pressure sensors, suppression of vasodilating prostaglandins. In addition, many cases of hyperadrenocorticism have concurrent hyperaldosteronism. Aldosterone is another adrenal hormone involved in the retension of salt and water, in exchange for potassium secretion. The net result of aldosterone influence is elevated blood pressure. More about hypertension can be found elsewhere on this website.
  • Congestive Heart Failure: The conditions which predispose to hypertension also increase the work load for the heart. Although the heart compensates in many ways, the additional fluid volumes and added elevated blood pressure can push the system into congestive heart failure.
  • Pancreatitis: there is a consistent association of pancreatitis and glucorticoid excess in some dogs. Not all dogs with hyperadrenocorticism develop pancreatitis, though.

  • Diabetes: The use and abuse (natural or iatrogenic) of corticosteroids has been implicated in the precipitation of diabetes mellitus in some animals. More about diabetes can be found elsewhere on this website.

  • Anorexia, Vomiting, Abdominal pain-ulcers,Bloodly diarrhea, Weight loss: Corticosteroid alter the availability of protectorant prostaglandin molecules, affecting the integrity of the gastrointestinal tract. Ulcers from excessive serum levels of adrenal corticosteroids...or non-judicious use of corticosteroid-containing medications are possible.

  • Behavioral Changes: Due to potential effects on the cortical regions of the central nervous system, animals may sometimes become hyperactive, aggressive and even experience rage , OR they may become depressed.

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