Cushing’s Disease

As Finlay is currently undergoing medication for Cushings, we’re going to keep this “health issue” prominently placed. It is a disease which is becoming more and more common, but equally very easily over-looked by dog owners. Hopefully reading, and re-reading this article will help you understand what to look out for. If you currently have any doubts about the health of your dog, please don’t hesitate to make an appointment with your Vet. Articles like these throughout the web are only provided as “information” – the only place you can get the right help is by talking with your Vet. (article originally posted in November 2011)

Tara with CushingsCushing’s Disease in Scottish Terriers

Cushing’s Disease in Scottish Terriers (and other breeds) is a common endocrinological disorder in dogs. In humans though, CD is rare. The clinical presentation of CD is however, is highly similar between both dogs and humans with characteristic signs such as abdominal obesity, weight gain, fatigue, muscle atrophy, and skin changes.

Harvey Cushing M.D. (8 April 1869 – 7 October 1939) was the first to discover the problems caused by the malfunction of the pituitary gland and in his report of 1912 termed it “polyglandular syndrome” later to become more famously known as: “Cushing’s Syndrome.”

Cushing’s Disease in Scottish Terriers and other dogs, is probably very easily overlooked by many Scottie dog owners as it is usually only associated with the elder Scottie and we therefore tend to think that it is the onset of old age.

You may already be familiar with Cushings Syndrome, but the details below will give you some vital information. Reprinted with kind permission from

Feline-Adrenal-GlandCushing’s disease (hyperadrenocorticism) in dogs is a condition that results from the chronic overproduction of too much glucocorticoid in the body. In the normal dog, the pituitary gland produces a hormone called ACTH, which stimulates the adrenal gland to produce the glucocorticoid hormones necessary for the function of many systems in the body. If something goes wrong in the pituitary gland or adrenal gland and too much glucocorticoid is produced, then Cushing’s disease develops. This is a very complicated disease with a wide range of symptoms and causes. This article will try to give a concise description of the disease, its symptoms, how it is diagnosed, and its treatment.

Who gets Cushing’s disease?

Cushing’s disease is considered a disease of middle age and older dogs and cats. It is much more common in dogs. This disease is similar in cats except that in cats up to 80% also have concurrent diabetes mellitus. This article will refer to the problem as it occurs in dogs. The usual age of contracting the disease is around six or seven years with a range of two to sixteen years. There is equal distribution between males and females and there does not appear to be an increase of the disease in any one breed.

What are the symptoms of Cushing’s disease in dogs?

For dogs ultimately diagnosed with Cushing’s disease, hair loss was one of the most common reasons the owners first brought their dog in for evaluation.

As a result of the chronically elevated glucocorticoids (steroids), the affected dogs develop a classic combination of dramatic clinical signs and lesions. The disease progresses slowly. A study showed that most dogs had at least one symptom of the disease from one to six years before the disease was diagnosed. Because the symptoms occur so gradually, the owner often attributes the changes to “old age.” Some dogs will have only one symptom, while others may have many.

Increased Water Consumption and Urination: The most common symptom is increased consumption of water and the resultant increased urination (polyuria/polydipsia). The dogs drink between two and ten times the normal amount of water and the resultant increase in urination follows. This symptom is present in over 85% of all animals with Cushing’s disease. Previously housebroken animals may begin to have accidents because their bladders fill quickly with the overproduction of urine.

Increase in Appetite: Increase in appetite (polyphagia) is another common clinical symptom that shows up in around 80% of the affected animals. Dogs may begin stealing food, getting into the garbage, begging continuously, and become very protective of their food. Despite having other symptoms, the owner may feel that the dog is okay because of his good appetite.

tfh_cushingsAbdominal Enlargement: Abdominal enlargement is a common symptom in up to 80% of the affected dogs. The potbellied appearance is a result of the shifting of fat to the abdominal area and a weakening and wasting of muscle mass in the abdomen.

Hair Loss and Thin Skin: Hair loss and thinning of the skin are also common symptoms in dogs with Cushing’s disease. It is estimated that between 50% and 90% of the affected animals develop these symptoms. Hair loss (alopecia) is one of the most common reasons that owners bring their dog in for evaluation. The hair loss usually starts over the areas of wear such as the elbows and progresses to the flanks and abdomen until eventually only the head and extremities have hair. The skin may also become thin and be easily damaged and slow to heal.

Increased panting, recurrent urinary tract infections, or losses in reproductive ability are other symptoms often noted with this disease.

Cushing’s Disease has two forms

There are two different distinct forms of the disease. There is pituitary dependent hyperadrenocorticism (PDH) and there is an adrenal-based disease.

Pituitary dependent hyperadrenocorticism: PDH involves the oversecretion of ACTH by the pituitary gland. ACTH is a hormone that stimulates the adrenal gland to produce glucocorticoids. The pituitary gland is most likely overproducing ACTH because of a pituitary tumor. The PDH form of the disease is responsible for around 80% of the cases of canine Cushing’s disease.

Adrenal-based hyperadrenocorticism: The adrenal-based form of the disease is usually a result of an adrenal tumor that causes an oversecretion of glucocorticoids. Adrenal tumors are responsible for around 20% of the cases of Cushing’s disease. There is also a form of the disease called “iatrogenic” Cushing’s disease that occurs as a result of giving the animal high doses of steroids. In this form of the disease, symptoms of Cushing’s disease will go away once the steroids are discontinued.


It is recommended that any dog suspected of having Cushing’s disease should have a complete blood count, chemistry profile, and urinalysis performed as a routine part of the evaluation.

Cushing’s disease can present with a variety of symptoms and may also be involved with several different disease processes. Therefore, it is recommended that any dog suspected of having Cushing’s disease should have acomplete blood count (CBC)blood chemistry panel, andurinalysis performed as a routine part of the evaluation. Common abnormalities in these tests include increases in alkaline phosphatase, and ALT (liver enzymes), increased cholesterol, decreased BUN (a kidney function test), and dilute urine (low specific gravity).

There are several different tests that can be performed to get a definitive diagnosis of Cushing’s disease. Many times the veterinarian may perform more than one test to help confirm the diagnosis or to determine which form of the disease is present. A diagnosis of Cushing’s disease, however, should never be made on the basis of laboratory tests alone. The dog needs to be showing symptoms of the disease, and have a medical history consistent with the diagnosis.

The three most common “screening” tests are the urine cortisol:creatinine ratio, the low dose dexamethasone suppression test, and ultrasound.

Urine Cortisol:Creatinine Ratio: In this test, the owner generally collects a urine sample at home (where the animal is not stressed). The sample is sent by the veterinarian to a special laboratory for testing. Most dogs with Cushing’s disease have an abnormal result. However, there are other diseases that can also cause abnormal results. So if this test is abnormal, further diagnostic testing should be performed.

Low Dose Dexamethasone Suppression Test: The low dose dexamethasone suppression test is useful in diagnosing Cushing’s disease in dogs. When given low doses of dexamethasone, normal dogs show a marked decrease in blood cortisol levels when tested 8 hours later. Most dogs (more than 90%) with Cushing’s disease do not have a decrease in cortisol level after being given dexamethasone. The results can sometimes help determine which type of disease is present.

ACTH Stimulation Test: This is another test that is commonly used in the diagnosis of Cushing’s disease today. It will not distinguish between the two types of hyperadrenocorticism, but it may aid in the diagnosis in difficult cases. It is also used to evaluate the effectiveness of therapy.

Abdominal Ultrasound: Abdominal ultrasound is helpful in three respects. First, it is a good test to evaluate all of the abdominal organs in the dog. Secondly, it is used to study the size and shape of the adrenal glands. The adrenal glands in pituitary dependent hyperadrenocorticism are usually normal in size or enlarged. If a tumor is present however, one adrenal gland is often abnormally large or of uneven shape. Finally, if a tumor is suspected, ultrasound can help identify any metastasis to other organs.

High Dose Dexamethasone Suppression Test: This blood test, which is not used often, may help to is used to distinguish between pituitary dependent hyperadrenocorticism and adrenal-based hyperadrenocorticism.


Treatment consists of several different options. Depending on the type of disease, surgery can be performed. If an adrenal tumor is identified, then surgical removal may be a viable option. There are several different forms of tumors that can invade the adrenal gland and their treatment will be based on the particular tumor type.

Non surgical treatment is the most often used treatment for most cases of canine Cushing’s disease. About 80% of the cases of Cushing’s disease in the dog are of the pituitary type, and since both the adrenal and the pituitary type will respond effectively to some of the oral treatments, many veterinarians do not perform the diagnostics necessary to distinguish between the two different forms. There are currently several different oral medications being used to treat canine Cushing’s disease.

Nonsurgical treatment is the most common treatment for canine Cushing’s disease.

Lysodren: Until recently, Lysodren (also known as mitotane, and o,p’-DDD) was the only treatment available for pituitary dependent Cushing’s disease. It is convenient to use and is relatively inexpensive and is still probably the most widely used treatment. The downside of this drug is that it can have some serious side effects and regular blood-monitoring needs to be performed. During the initial phases of the therapy, the dog must be very carefully monitored, and there must be close communication between the veterinarian and the owner.

The use of Lysodren is somewhat like chemotherapy. It works by destroying cells of the adrenal gland that produce the corticosteroid hormones. As the number of corticosteroid-producing cells is reduced, even though the pituitary gland continues to produce excess ACTH, the adrenal gland is less able to respond, so the amount of glucocorticoid being produced is reduced. The problems arise when too much of the adrenal cortex is killed off. The animals may then need to be placed on prednisone, either short or long term. The Lysodren is initially given daily while the animal is being monitored for a decrease in the symptoms (water consumption, appetite). On the 8th or 9th day of the initial therapy, the dog needs to be examined and an ACTH stimulation test is performed to determine if the drug is working. If the goal is achieved, maintenance therapy is started. If the goal has not been reached, then the dog generally remains on the daily medication for 3 to 7 additional days and is rechecked until the proper results are achieved. If the dog becomes lethargic, vomits, or has diarrhea, or if the treatment does not work by 30 days, then the treatment plan is reevaluated. If treatment is successful, then symptoms should resolve within 4 to 6 months. A certain percentage of dogs will relapse and need to undergo the daily therapy again at some point in their lives. If a dog ever becomes ill while on Lysodren, the Lysodren should be stopped immediately and the dog should be examined by a veterinarian. If the therapy is successful, the dog will need to be on Lysodren for the rest of his life.

Trilostane: Trilostane is a newer treatment that is used to treat some dogs with Cushing’s disease. It is more expensive, but may be an alternative treatment for dogs with adrenal tumors. As with Lysodren, the dog is reexamined repeatedly during the initial phase of treatment, and ACTH stimulation tests are performed. In many cases, after several months of therapy the dose needs to be increased.

Ketoconazole: Ketoconazole is an oral antifungal agent that has been used extensively since the mid 80s. One of the side effects of ketoconazole is that it interferes with the synthesis of steroid hormones. It therefore gained some popularity as a treatment for Cushing’s disease. However, it is rarely used today.

L-deprenyl (Anipryl)L-deprenyl (Anipryl) has been advocated for the treatment of Cushing’s disease in dogs, but its effectiveness has come into question.


Cushing’s disease is a disease that affects middle age to older dogs. The affected animal has a characteristic presentation including increased water consumption and resulting increased urination, increased appetite, hair loss, and a potbellied appearance. There are several diagnostic tests available, as well as several treatments.

References and further reading

Bonagura, J. Kirk’s Current Veterinary Therapy XII. W.B. Saunders Co. Philadelphia, PA; 2000.

Feldman, EC. An update on the diagnosis of Cushing’s Syndrome in Dogs. Presented at the Wisconsin Veterinary Medical Association Convention, Madison, Wisconsin, October 2005.

Feldman, EC. Treatment of hyperadrenocorticism in dogs. Presented at the Wisconsin Veterinary Medical Association Convention, Madison, Wisconsin, October 2005.

Ramsey I, Neiger R. Canine hyperadrenocorticism. In: Bonagura JD, Twedt DC (eds.) Kirk’s Current Veterinary Therapy XIV. WB Saunders Co, Philadelphia, PA 2009:2224-227.

© 2011 Foster & Smith, Inc.
Reprinted as a courtesy and with permission from (
On-line store at
Free pet supply catalog: 1-800-323-4208

Craniomandibular Osteopathy


87724235-101106152903What is craniomandibular osteopathy?Craniomandibular osteopathy (CMO) is a bone disease of growing dogs. It affects the bones of the skull, including the mandible (lower jaw), tympanic bullae (bone surrounding the middle ear) and temporal region (bone of the skull, which forms a joint with the lower jaw called the temporomandibular joint). The lesions are bilateral, and consist of irregular enlargements of the affected bones.What causes craniomandibular osteopathy and which breeds does it affect?The cause of CMO is unknown. It is not cancerous or caused by inflammation. It is an inherited condition in West Highland white terriers, and also occurs more commonly in other terrier breeds including the Scottish, Cairn, and Boston. It has also been reported in the Boxer, Labrador Retriever, Great Dane, and Doberman Pinscher.What are the signs of craniomandibular osteopathy?West Highland white terrier (Westie)The signs of disease usually occur between 4 and 8 months of age. There is swelling of the jaws, difficulty eating, and pain on opening the mouth; sometimes there is actually an inability to open the mouth. Dogs may drool and be depressed. Often the body temperature will fluctuate over time, with fever occurring in phases every 10-14 days. In severely affected dogs, the masticatory muscles (those involved in chewing) may atrophy and there may be lymphadenopathy (swollen glands).

Radiographs (x-rays) of affected dogs demonstrate irregular thickenings of the various facial bones. It may be necessary to sedate or lightly anesthetize the dog to obtain good radiographs, since it is a painful condition and the dog may not lie quietly.

How is craniomandibular osteopathy diagnosed?

A veterinarian can generally make the diagnosis through obtaining a good medical history, physical examination, and radiographs. In dog breeds that are rarely affected, biopsies may be necessary to distinguish it from other diseases causing similar lesions such as neoplasia,osteomyelitis, and hypertrophic osteodystrophy.

What is the treatment of craniomandibular osteopathy?

Currently, there is no treatment that will alter the progression of the disease. Therapy is usually targeted at making the dog more comfortable through the use of pain relievers and anti-inflammatory drugs such as prednisone. Proper nutrition must be provided, and in severe cases, it may be necessary to place a gastrostomy (stomach) tube.

What is the prognosis for dogs with craniomandibular osteopathy?

The abnormal bone growth slows as the dog ages and usually stops by one year of age. At that point, the lesions often regress, though some dogs may have permanent difficulties with eating and using the mouth. If the lesions affect the temporomandibular joint, permanent inability to move the jaw may result. In some cases, surgery can partially correct this problem.

How is craniomandibular osteopathy prevented?

Since it is an inherited condition in West Highland white terriers, those dogs with the disease, or with parents or siblings with the disease, should not be bred. Since it may be inherited in other terrier breeds as well, breeders should avoid breeding affected dogs.

References and Further Reading
Johnson, KA; Watson, ADJ. Skeletal diseases. In Ettinger, S. (ed). Textbook of Veterinary Internal Medicine. W.B. Saunders Co. Philadelphia, PA; 2000.Riser, WH; Newton, CD. Craniomandibular osteopathy., JK. Diseases affecting developing bone. In Birchard, SJ; Sherding, RG (eds.) Saunders Manual of Small Animal Practice. W.B. Saunders Co. Philadelphia, PA; 1994.
© 2011 Foster & Smith, Inc.
Reprinted as a courtesy and with permission from (
On-line store at
Free pet supply catalog: 1-800-323-4208

Addison’s Disease

P1050349Although Addison’s disease can be a very serious disease the changes it causes can be very subtle in the early stages. The signs of the disease are variable and often vague. It is important to get an early diagnosis because, with treatment, affected animals can lead a normal and full life.

Addison’s Disease, named after the 19th century English Physician, Thomas Addison who identified and described it as such:

the failure of the body to produce enough of the hormome “cortisol” and in some cases the hormone “aldosterone”. The disease is sometimes termed “hypoadrenocorticism” or “hypocortisolemia”.

Cortisol is extremely vital to health and the amount produced by the adrenal glands is precisely balanced. Cortisol’s most important job is to help the body respond to stress. Therefore if the adrenal glands are damaged in any way, the dogs body will be unable to produce enough cortisol and may become ill at times of stress.

Aldosterone helps to maintain the blood pressure, water and salt balance in the body but helping the kidneys to remain sodium and excrete potassium. When Aldosterone production falls too low, the kidneys are not able to regulate salt and water balance thus causing blood volume and pressure to drop.

It is the body’s own immune system that causes the gradual destruction of the outer layer of the adrenal glands.

The following is an article from the PetEducation website:

Addison’s disease in dogs is also known as hypoadrenocorticism. It is a disease that results from the reduction in corticosteroid secretion from the adrenal gland. The adrenal gland is a small gland located near the kidney that secretes several different substances that help regulate normal body functions. Some of the most important products that it secretes are called glucocorticoids and mineralocorticoids. There is another disease called Cushing’s disease (hyperadrenocorticism) that occurs when the adrenal gland produces too much of these hormones. Addison’s disease is not as common as Cushing’s disease, but it still occurs with regular frequency in the dog population. It is difficult to recognize initially, but once it is diagnosed, it can be successfully treated.

Glucocorticoids and Mineralocorticoids
The adrenal gland produces both glucocorticoids and mineralocorticoids. Glucocorticoids such as cortisol have an effect on sugar, fat, and protein metabolism. They are partially responsible for the reaction known as fight or flight response during stressful periods. Mineralocorticoids such as aldosterone have an influence on the electrolytes sodium and potassium in the body. They help regulate these electrolytes particularly in stressful situations. When the adrenal glands do not function adequately, these hormones are not produced at sufficient levels and the metabolism and electrolyte balance of the animal create the symptoms and complications of Addison’s disease.

Who gets Addison’s disease and what are the symptoms?
Addison’s is primarily a disease of young to middle-aged female dogs, however, a dog of any age and either sex can develop the disease. It does not appear to be more common in any one particular breed. Cats can develop this disease, but it is extremely rare. The symptoms of Addison’s disease are very vague and many animals may have symptoms for a long time before the disease is diagnosed. Some of the more common symptoms include lethargy, anorexia, vomiting, and muscle weakness. The symptoms may wax and wane, further complicating the diagnosis. The other presentation for this disease is an episode called an ‘Addisonian crisis.’ In this scenario, the animal collapses in a state of shock due to an imbalance of electrolytes and metabolism during a period of stress. This episode may be the first time the owner suspects disease and may be fatal, if not treated promptly.

What causes the adrenal glands to stop producing corticoids?
There are several different reasons the adrenal glands may fail. By far, the most common is destruction of the glands by the body. This process where the body attacks and kills its own tissue is known as ‘immune mediated destruction.’ Other causes can be infections in the gland from granulomatous diseases such as histoplasmosis or blastomycosis, or through other means such as infarcts, tumors, or amyloidosis of the gland. Another cause of Addison’s can be the failure of the pituitary gland to secrete ACTH, which is a hormone that stimulates the adrenal gland to work. The hypothalamus can also stop producing CRH, which is a hormone that controls the adrenal gland. Failure of the pituitary gland or hypothalamus is usually a result of a tumor, inflammation, or injury.

How is hypoadrenocorticism diagnosed?
Diagnosis is of Addison’s disease in dogs is confirmed by a blood test called the ACTH stimulation test. However, because the disease is not very common and has a wide variety of symptoms, the ACTH test is usually done after several other tests are used to rule out more common diseases.

If the animal comes into the hospital in an Addisonian crisis with electrolyte imbalances, and responds to therapy, then a presumptive diagnosis of Addison’s disease is made and once the animal recovers, the diagnosis can be confirmed with an ACTH stimulation test.

If however, the animal presents with a history of weight loss, lethargy, or muscle weakness, which are the symptoms of many diseases, a chemistry profile and blood count are usually performed first to look at a number of body systems. Dogs with Addison’s disease often have elevated blood urea nitrogen (BUN) and an elevated creatinine, as well as decreased blood glucose. The blood count may show a chronic anemia. If the blood work supports the diagnosis of Addison’s disease, then an ACTH challenge test is performed.

In an ACTH challenge test, the dog is given an injection of the adrenal stimulating hormone ACTH. A normal dog will respond by having an increase in blood cortisol. If a dog with Addison’s disease is given ACTH, the dog will not have an increase in blood cortisol and the diagnosis of Addison’s disease is confirmed.

How is Addison’s disease treated?
Once the disease is diagnosed, the treatment is fairly straightforward. The standard treatment involves replacing the mineralocorticoids and glucocorticoids in the body. The drugs most commonly used to accomplish this are Florinef (fludrocortisone). Florinef is usually given twice a day. Initially, the blood sodium and potassium levels are monitored to help obtain the correct dose. After the animal is regulated, then the levels are rechecked 2 to 3 times a year and adjustments in dosing are made as needed.

A newer option in the treatment of Addison’s disease is a drug called DOCP. The injection is long acting and only needs to be given once every 25 days. DOCP has been intensively tested and been shown to provide better electrolyte regulation than Florinef. Some animals on DOCP may also need to be placed on a low maintenance dose of prednisone.

References and Further Reading
Herrtage M. Hypoadrenocorticism. In: Ettinger SJ, Feldman EC (eds.) Textbook of Veterinary Internal Medicine. WB Saunders Co, Philadelphia, PA 2005:1612-1622.

Kintzer PP, Peterson ME. Hypoadrenocorticism. In: Bonagura JD, Twedt DC (eds.) Kirk’s Current Veterinary Therapy XIV. WB Saunders Co, Philadelphia, PA 2009:231-235.

© 2011 Foster & Smith, Inc.
Reprinted as a courtesy and with permission from (
On-line store at
Free pet supply catalog: 1-800-323-4208

If you think your Scottie is displaying any of these symptoms, or you are worried about his health, please do not hesitate in making an appointment to see your own Vet. The Health pages within this website are merely for information and not advice.