dwerten
06-23-2009, 09:08 AM
Here is a 2001 article from the Whole Dog Journal. According to this article, Addison's is uncommong in yorkies.....
Addison’s Disease: Averting An Adrenal Crisis
This glandular disorder itself may be rare, but the symptoms it gives rise to are not—successful treatment depends on early diagnosis and immediate veterinary intervention
By Arnold Plotnick, M.S., D.V.M., Dip. ACVIM, Dip. ABVP
First published in DOG WORLD Magazine, Vol. 86, No. 6, June 2001, p. 54.
Reprinted with permission.
Doug Hess is a free-lance photographer who lives and works in Washington, D.C. The summer of 2000 was hectic for Hess, as his workload began to pick up. He sometimes can’t remember the details of every photo shoot, but, when it comes to his beloved West Highland White Terrier, he remembers the events of last August very clearly.
“I came home from the studio for lunch, like I do every day. Tipper, my 6-year-old Westie, was waiting for me. I hooked her leash onto her collar and off we went to the park, as usual,” he recalls. “About 10 minutes after we started walking, Tipper suddenly collapsed on the sidewalk! Fortunately, my veterinarian’s office was only two blocks away, and Tipper only weighs about 18 pounds. I called ahead on my cell phone to let them know I was coming, and then I whisked her there in a heartbeat.”
When Hess arrived at the veterinary office, they were ready for him. “They took me and Tipper into an exam room right away. Tipper was conscious, but too weak to stand. My vet examined her and asked me a million questions,” he remembers. “He asked about her appetite, her thirst, whether she had done any vomiting or had any diarrhea in the recent past, if she could have gotten into the garbage or come into contact with any poisons or toxins. All I could do was tell him no, that she was fine and had been perfectly fine up until the collapse.”
During her physical examination, Tipper’s pulse was weak, her heart rate was slow and her gums were a bit pale. Other than that, everything else seemed pretty normal. “The vet pressed on her gums, which made them blanch and turn white. Then he counted how long it took for the color to return. It took three or four seconds. He said that was too long.”
An intravenous catheter was placed in Tipper’s right front leg, and blood was obtained for some blood tests, which they sent to an outside laboratory. “The vet said that it looked like she was in shock, although the slow heart rate was unusual,” Hess says. “Most dogs, if they’re in shock, will have [a weak pulse] and a rapid heart rate. The vet said it was odd. He thought maybe she had been stung by a bee or bitten by some kind of insect while we were walking, and she had a sudden allergic reaction.”
Tipper was given intravenous fluids at a rapid rate and dexamethasone, a steroid, which is standard therapy for a shock-type allergic reaction. Hess recalls, with amazement, what happened next. About five minutes after receiving the steroid injection and the intravenous fluids, Tipper stood up, started wagging her tail and tried to jump off the table. “She was ready to get going back to the park!” Hess says. “But I went along with my vet’s recommendation, and I let them keep her overnight for observation.”
The next day, Hess called to find out how Tipper was doing. “They said she was doing great, eating and barking and wanting to play,” he says. “Typical Tipper. But they wanted to talk to me about the blood test results that had arrived that morning. That made me kind of nervous.”
Hess zipped over to the veterinary office on his lunch hour to pick up Tipper. The vet told him he wanted to keep Tipper for one more day to do another test. Hess asked if anything was wrong, and the vet said the blood tests were suggestive of an adrenal gland disorder, but another test would be needed to be 100 percent sure.
The doctor’s suspicions were confirmed when the test results came back three days later. “He called me at home and told me the news: ‘Tipper has Addison’s disease.’ ”
What Is Addison’s Disease?
Early anatomists had been aware of the adrenal glands for years; however, it wasn’t until 1849 that Thomas Addison described a syndrome in humans that he associated with the dysfunction of the adrenal glands. At that time, no therapy was available, and patients with the disorder died from their illness. The first reported canine case of Addison’s disease was described 104 years later, in 1953. It is a rare disease in dogs, and it has been estimated that, on average, a small-animal practice with two veterinarians, each seeing 1,500 dogs per year, should expect to diagnose one case of Addison’s disease a year.
In dogs, Addison’s disease, also known as hypoadrenocorticism, is an uncommon but treatable glandular disorder. It tends to occur in young to middle-age female dogs. Although it has been diagnosed in very young dogs (5 weeks) and very old dogs (15 years), the average age at diagnosis is 4.3 to 5.4 years. Females constitute 70 percent to 75 percent of all reported cases. Primary Addison’s disease occurs as a result of atrophy or destruction of the outer portion (the cortex) of the adrenal glands. The adrenal cortex secretes several hormones.
Primary Addison’s disease occurs when two of these hormones, cortisol and aldosterone, become deficient as the adrenal cortices begin to fail. A much less common form of Addison’s disease (secondary Addison’s disease) occurs when the pituitary gland, located in the brain, fails to secrete adequate amounts of the hormone that signals the adrenal gland to make the proper hormones. Primary Addison’s is the most common form of the disease and is known simply as Addison’s. It occurs as a result of inadequate hormone production and is a product of the immune system destroying both adrenal cortices.
The most common clinical and historical signs seen in dogs with Addison’s disease are lethargy, depression, poor appetite, vomiting, weakness, weight loss, dehydration, diarrhea, collapse, excessive thirst, excessive urination, a weak pulse and a slow heart rate. Capillary refill time, measured by timing how long it takes for blanched gums to return to their pink color, is a measure of how well the heart is perfusing the tissues with blood, and is usually prolonged in Addison’s disease.
Unfortunately, no set of signs is overly suggestive of the disorder, and the signs listed also may be present in a variety of more common conditions such as kidney disease, gastrointestinal disease and various infectious diseases. One important diagnostic clue is a history of waxing and waning illness that seems to become worse when the animal is stressed and responds to nonspecific therapy such as intravenous fluids and rest.
The vague signs and the response to nonspecific supportive care make Addison’s disease difficult to diagnose unless the veterinarian has a high degree of suspicion at the outset. Many times, a diagnosis is achieved only after a dog is brought to the veterinary hospital in a full-blown adrenal crisis. At that point, careful questioning of the owner often reveals that indeed, some of the clinical signs listed above had been present for weeks or months preceding the crisis, but they were of a degree mild enough that it did not concern the owner.
A Compound Diagnosis
Routine bloodwork often shows abnormalities that can be suggestive of an adrenal disorder such as Addison’s disease. The classic abnormalities are an elevated potassium level (hyperkalemia), a low sodium level (hyponatremia), elevated kidney parameters (azotemia), bicarbonate levels that are mildly to moderately below the low end of the labs predetermined reference range (metabolic acidosis), and the absence of what is called a “stress leukogram.”
Dogs, when they are sick, are considered to be physiologically “stressed.” The normal adrenal gland releases cortisol in response to such stress, and this causes the white blood cell panel to take on a characteristic pattern, which is commonly called a stress leukogram. Because dogs with Addison’s disease cannot produce cortisol, they cannot mount a stress response. The white blood cell picture will appear normal, instead of taking on the appearance of a stress leukogram. It is easy for a veterinarian to recognize a stress leukogram; however, it takes an astute clinician to look at a normal white blood cell panel and realize that a normal leukogram is abnormal for a dog that is sick. The high potassium and low sodium are a result of inadequate secretion of aldosterone, the other adrenal hormone that is usually deficient in dogs with Addison’s disease.
Addison’s Disease: Averting An Adrenal Crisis
This glandular disorder itself may be rare, but the symptoms it gives rise to are not—successful treatment depends on early diagnosis and immediate veterinary intervention
By Arnold Plotnick, M.S., D.V.M., Dip. ACVIM, Dip. ABVP
First published in DOG WORLD Magazine, Vol. 86, No. 6, June 2001, p. 54.
Reprinted with permission.
Doug Hess is a free-lance photographer who lives and works in Washington, D.C. The summer of 2000 was hectic for Hess, as his workload began to pick up. He sometimes can’t remember the details of every photo shoot, but, when it comes to his beloved West Highland White Terrier, he remembers the events of last August very clearly.
“I came home from the studio for lunch, like I do every day. Tipper, my 6-year-old Westie, was waiting for me. I hooked her leash onto her collar and off we went to the park, as usual,” he recalls. “About 10 minutes after we started walking, Tipper suddenly collapsed on the sidewalk! Fortunately, my veterinarian’s office was only two blocks away, and Tipper only weighs about 18 pounds. I called ahead on my cell phone to let them know I was coming, and then I whisked her there in a heartbeat.”
When Hess arrived at the veterinary office, they were ready for him. “They took me and Tipper into an exam room right away. Tipper was conscious, but too weak to stand. My vet examined her and asked me a million questions,” he remembers. “He asked about her appetite, her thirst, whether she had done any vomiting or had any diarrhea in the recent past, if she could have gotten into the garbage or come into contact with any poisons or toxins. All I could do was tell him no, that she was fine and had been perfectly fine up until the collapse.”
During her physical examination, Tipper’s pulse was weak, her heart rate was slow and her gums were a bit pale. Other than that, everything else seemed pretty normal. “The vet pressed on her gums, which made them blanch and turn white. Then he counted how long it took for the color to return. It took three or four seconds. He said that was too long.”
An intravenous catheter was placed in Tipper’s right front leg, and blood was obtained for some blood tests, which they sent to an outside laboratory. “The vet said that it looked like she was in shock, although the slow heart rate was unusual,” Hess says. “Most dogs, if they’re in shock, will have [a weak pulse] and a rapid heart rate. The vet said it was odd. He thought maybe she had been stung by a bee or bitten by some kind of insect while we were walking, and she had a sudden allergic reaction.”
Tipper was given intravenous fluids at a rapid rate and dexamethasone, a steroid, which is standard therapy for a shock-type allergic reaction. Hess recalls, with amazement, what happened next. About five minutes after receiving the steroid injection and the intravenous fluids, Tipper stood up, started wagging her tail and tried to jump off the table. “She was ready to get going back to the park!” Hess says. “But I went along with my vet’s recommendation, and I let them keep her overnight for observation.”
The next day, Hess called to find out how Tipper was doing. “They said she was doing great, eating and barking and wanting to play,” he says. “Typical Tipper. But they wanted to talk to me about the blood test results that had arrived that morning. That made me kind of nervous.”
Hess zipped over to the veterinary office on his lunch hour to pick up Tipper. The vet told him he wanted to keep Tipper for one more day to do another test. Hess asked if anything was wrong, and the vet said the blood tests were suggestive of an adrenal gland disorder, but another test would be needed to be 100 percent sure.
The doctor’s suspicions were confirmed when the test results came back three days later. “He called me at home and told me the news: ‘Tipper has Addison’s disease.’ ”
What Is Addison’s Disease?
Early anatomists had been aware of the adrenal glands for years; however, it wasn’t until 1849 that Thomas Addison described a syndrome in humans that he associated with the dysfunction of the adrenal glands. At that time, no therapy was available, and patients with the disorder died from their illness. The first reported canine case of Addison’s disease was described 104 years later, in 1953. It is a rare disease in dogs, and it has been estimated that, on average, a small-animal practice with two veterinarians, each seeing 1,500 dogs per year, should expect to diagnose one case of Addison’s disease a year.
In dogs, Addison’s disease, also known as hypoadrenocorticism, is an uncommon but treatable glandular disorder. It tends to occur in young to middle-age female dogs. Although it has been diagnosed in very young dogs (5 weeks) and very old dogs (15 years), the average age at diagnosis is 4.3 to 5.4 years. Females constitute 70 percent to 75 percent of all reported cases. Primary Addison’s disease occurs as a result of atrophy or destruction of the outer portion (the cortex) of the adrenal glands. The adrenal cortex secretes several hormones.
Primary Addison’s disease occurs when two of these hormones, cortisol and aldosterone, become deficient as the adrenal cortices begin to fail. A much less common form of Addison’s disease (secondary Addison’s disease) occurs when the pituitary gland, located in the brain, fails to secrete adequate amounts of the hormone that signals the adrenal gland to make the proper hormones. Primary Addison’s is the most common form of the disease and is known simply as Addison’s. It occurs as a result of inadequate hormone production and is a product of the immune system destroying both adrenal cortices.
The most common clinical and historical signs seen in dogs with Addison’s disease are lethargy, depression, poor appetite, vomiting, weakness, weight loss, dehydration, diarrhea, collapse, excessive thirst, excessive urination, a weak pulse and a slow heart rate. Capillary refill time, measured by timing how long it takes for blanched gums to return to their pink color, is a measure of how well the heart is perfusing the tissues with blood, and is usually prolonged in Addison’s disease.
Unfortunately, no set of signs is overly suggestive of the disorder, and the signs listed also may be present in a variety of more common conditions such as kidney disease, gastrointestinal disease and various infectious diseases. One important diagnostic clue is a history of waxing and waning illness that seems to become worse when the animal is stressed and responds to nonspecific therapy such as intravenous fluids and rest.
The vague signs and the response to nonspecific supportive care make Addison’s disease difficult to diagnose unless the veterinarian has a high degree of suspicion at the outset. Many times, a diagnosis is achieved only after a dog is brought to the veterinary hospital in a full-blown adrenal crisis. At that point, careful questioning of the owner often reveals that indeed, some of the clinical signs listed above had been present for weeks or months preceding the crisis, but they were of a degree mild enough that it did not concern the owner.
A Compound Diagnosis
Routine bloodwork often shows abnormalities that can be suggestive of an adrenal disorder such as Addison’s disease. The classic abnormalities are an elevated potassium level (hyperkalemia), a low sodium level (hyponatremia), elevated kidney parameters (azotemia), bicarbonate levels that are mildly to moderately below the low end of the labs predetermined reference range (metabolic acidosis), and the absence of what is called a “stress leukogram.”
Dogs, when they are sick, are considered to be physiologically “stressed.” The normal adrenal gland releases cortisol in response to such stress, and this causes the white blood cell panel to take on a characteristic pattern, which is commonly called a stress leukogram. Because dogs with Addison’s disease cannot produce cortisol, they cannot mount a stress response. The white blood cell picture will appear normal, instead of taking on the appearance of a stress leukogram. It is easy for a veterinarian to recognize a stress leukogram; however, it takes an astute clinician to look at a normal white blood cell panel and realize that a normal leukogram is abnormal for a dog that is sick. The high potassium and low sodium are a result of inadequate secretion of aldosterone, the other adrenal hormone that is usually deficient in dogs with Addison’s disease.