addison s disease merck vet manual

50 bpm) that predisposes to weakness or circulatory collapse after minimal exertion. A progressive decrease in blood volume contributes to hypotension, weakness, and microcardia. Increased excretion of water by the kidneys, because of decreased reabsorption of sodium and chloride, results in progressive dehydration and hemoconcentration. Emesis, diarrhea, and anorexia are common and contribute to the animal’s deterioration. Weight loss is frequently severe. Similar clinical signs are seen in cats with hypoadrenocorticism. Decreased gluconeogenesis and increased sensitivity to insulin contribute to the development of moderate hypoglycemia. In some dogs, hyperpigmentation of the skin is seen because of the lack of negative feedback on the pituitary gland and increased ACTH release. Atypical Addison disease has been reported in dogs and is associated with hypocortisolemia with normal electrolytes. Clinical signs are similar to those seen in dogs with both glucocorticoid and mineralocorticoid insufficiency. The adrenal cortex is reduced to one-tenth or less of its normal thickness and consists primarily of the adrenal capsule. The adrenal medulla is relatively more prominent and, with the capsule, makes up the bulk of the remaining adrenal glands. After obtaining a baseline blood sample, ACTH (gel or synthetic) is administered. Gel preparations are administered IM, and a second blood sample is obtained 2 hours later. Synthetic preparations are administered IM or IV with a second blood sample 1 hour later.Urine output should be assessed to determine whether the dog is becoming anuric. Fluids should be continued, at a rate appropriate to match ongoing losses, until the clinical signs and laboratory abnormalities have resolved. Electrolytes, renal function, and glucose should be monitored regularly to assess response to therapy. Serum electrolytes should be monitored weekly until the proper dose is determined.

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Which one of the following effects is LEAST likely to be caused by the release of endogenous glucocorticoids? Isolated aldosterone insufficiency appears to be very rare, whereas isolated glucocorticoid insufficiency is likely underdiagnosed given the lack of electrolyte abnormalities. The clinical signs of hypoadrenocorticism are often vague, may wax and wane over time, are rarely pathognomonic, and may be present for days, weeks, or months before diagnosis. Diagnosis depends on an accurate history, physical examination, and screening laboratory tests (CBC, chemistry panel, urinalysis). Confirmation requires adrenal function testing using the ACTH stimulation test. Treatment is highly successful but often lifelong. The disease may be familial in Standard Poodles, West Highland White Terriers, Great Danes, Bearded Collies, Portuguese Water Dogs, and a variety of other breeds. The cause of primary adrenocortical failure usually is unknown, although most cases probably result from an autoimmune process. Other causes include destruction of the adrenal gland by granulomatous disease, metastatic tumor, hemorrhage, infarction, adrenolytic agents ( mitotane ), or adrenal enzyme inhibitors (trilostane). Isolated glucocorticoid insufficiency is more commonly seen in older dogs with vague GI signs, weight loss, normal electrolyte concentrations, hypoalbuminemia and hypocholesterolemia. Although hypoadrenocorticism is seen in dogs of any breed, sex, or age, idiopathic adrenocortical insufficiency is most common in young, female adult dogs. This may be related to its suspected immune-mediated pathogenesis. Potassium excretion by the kidneys is reduced and results in a progressive increase in serum potassium levels. Hyponatremia and hypochloremia result from renal tubular loss. Severe hyperkalemia may result in bradycardia and an irregular heart rate with changes in the ECG. Some dogs develop a pronounced bradycardia (heart rate ?

Less common (10% to 15% of cases) is a tumor in the adrenal glands themselves. Longterm use of corticosteroid drugs (for example, to decrease inflammation or treat an immune disorder) can also cause signs of Cushing disease (see Disorders of the Pituitary Gland in Dogs: Cushing Disease ). It is most common in young to middle-aged dogs. The cause is usually not known, but an autoimmune condition in which the body destroys some of its own tissue is likely. The adrenal gland can also be destroyed by other conditions, including medications used to treat Cushing disease and cancer in other parts of the body. Secretion of aldosterone, the main mineralocorticoid hormone, is reduced, which affects the levels of potassium, sodium, and chloride in the blood. Potassium gradually builds up in the blood and, in severe cases, may cause the heart to slow down or beat irregularly. Some dogs have such a slow heart rate (50 beats per minute or lower) that they can become weak or go into shock. Decreased production of glucocorticoids (such as cortisol) results in moderately low blood sugar. Dogs with atypical Addison disease can have low blood levels of cortisol but normal levels of sodium, potassium, and chloride. Weight loss is often severe. Although signs can be hard to identify while Addison disease is developing, severe consequences, such as shock and evidence of kidney failure, can develop suddenly. The condition may be inherited in Standard Poodles, West Highland White Terriers, Great Danes, Bearded Collies, Portuguese Water Dogs, and a variety of other breeds. Although the disease can be seen in any breed, sex, or age, it is most common in young, female, adult dogs. The diagnosis is confirmed by specific evaluation of adrenal function. This is done by measuring the level of cortisol in the blood, treating the dog with adrenocorticotropin (a hormone that stimulates the adrenal gland in healthy animals), and then measuring the level of cortisol in the blood a second time.

Some dogs (especially dogs on DOCP) also require daily oral glucocorticoid therapy to adequately control clinical signs. Dogs with atypical Addison disease require only replacement doses of prednisone, although it is recommended that electrolytes be monitored every 3 mo for the first year after diagnosis.Supportive therapy and rest are indicated in cases of chronic Addison disease. Therefore, the clinician must always consider the diagnosis in patients with the appropriate signalment and clinical signs. From developing new therapies that treat and prevent disease to helping people in need, we are committed to improving health and well-being around the world. The Merck Veterinary Manual was first published in 1955 as a service to the community. The legacy of this great resource continues as the Merck Veterinary Manual in the US and Canada and the MSD Manual outside of North America. The owner also states that the dog has gained weight but is eating, drinking, urinating, and defecating normally. Of the following conditions, which is the most likely explanation? The adrenal gland has 2 parts—the cortex and the medulla. The outer layer produces the mineralocorticoids, which help to control the body’s balance of sodium and potassium salts. The middle layer produces glucocorticoids, which are involved in metabolizing nutrients as well as in reducing inflammation and immune responses. The inner layer produces sex hormones such as estrogen, progesterone, and androgens. It releases epinephrine (sometimes also called adrenaline) and norepinephrine, both of which increase heart output, blood pressure, and blood glucose, and slow digestion. The signs result primarily from chronic excess of the hormone cortisol. Increased cortisol levels in dogs may result from one of several mechanisms. The most common cause (85% to 90% of cases) is a tumor in the pituitary gland. The pituitary tumor produces a hormone that triggers excessive development of the adrenal gland.

The remainder result from destruction of the adrenal gland by granuloma (eg, tuberculosis, histoplasmosis ), tumor, amyloidosis, hemorrhage, or inflammatory necrosis. Hypoadrenocorticism can also result from administration of drugs that block corticosteroid synthesis (eg, ketoconazole, the anesthetic etomidate ). In children, the most common cause of primary adrenal insufficiency is congenital adrenal hyperplasia, but other genetic disorders are being increasingly recognized as causes. A low serum concentration of sodium ( hyponatremia ) and a high concentration of potassium ( hyperkalemia ) result. However, when adrenal insufficiency is caused by inadequate adrenocorticotropic hormone (ACTH) production ( secondary adrenal insufficiency ), electrolyte levels are often normal or only mildly deranged, and the circulatory problems are less severe. In the absence of cortisol, insufficient carbohydrate is formed from protein; hypoglycemia and decreased liver glycogen result. Weakness follows, due in part to deficient neuromuscular function. Resistance to infection, trauma, and other stress is decreased. Myocardial weakness and dehydration reduce cardiac output, and circulatory failure can occur. Thus, adrenal insufficiency secondary to pituitary failure does not cause hyperpigmentation. Black freckles are common on the forehead, face, neck, and shoulders. Bluish black discolorations of the areolae and mucous membranes of the lips, mouth, rectum, and vagina occur. Decreased tolerance to cold, with hypometabolism, may be noted. Dizziness and syncope may occur. Weight loss, dehydration, and hypotension are characteristic of the later stages of Addison disease. Shock and fever may be the only signs. Peutz-Jeghers syndrome is characterized by pigmentation of the buccal and rectal mucosa. Frequently, hyperpigmentation occurs with vitiligo, which may indicate Addison disease, although other diseases can cause this association.

Affected dogs have low baseline cortisol levels, and there is little response to administration of adrenocorticotropin. Hormone replacement treatment can often be started while the pet is being stabilized. Laboratory values are monitored regularly to assess response to treatment and adjust doses if needed. For longterm treatment, replacement hormones can be given by mouth or injection. Lifelong treatment is necessary. Often, there are no signs, and the tumor is found by chance during treatment for other conditions. When signs are present, they may include increased thirst and urination, increased heart rate, restlessness, and a distended abdomen. Diagnosis is often made based on signs and ultrasonography. Treatment involves surgery (if feasible) and management of high blood pressure. Other tumors in the adrenal glands, such as neuroblastomas and ganglioneuromas, can develop from nerve cells. From developing new therapies that treat and prevent disease to helping people in need, we are committed to improving health and well-being around the world. Which of the following is an uncommon symptom of this disorder? In the top right panel, hyperpigmentation of the palmar creases is visible in a patient with Addison disease. In the bottom left panel hyperpigmented macules of the gums are visible in this patient with Addison disease.It causes various symptoms, including hypotension and hyperpigmentation, and can lead to adrenal crisis with cardiovascular collapse. Diagnosis is clinical and by finding elevated plasma adrenocorticotropic hormone (ACTH) with low plasma cortisol. Treatment depends on the cause but generally includes hydrocortisone and sometimes other hormones. Other causes include trauma, surgery, and sodium loss due to excessive sweating. Even with treatment, Addison disease may cause a slight increase in mortality. It is not clear whether this increase is due to mistreated adrenal crises or long-term complications of inadvertent over-replacement.

Some clinicians tend to give too little fludrocortisone in an effort to avoid use of antihypertensives. If nausea and vomiting preclude oral therapy, parenteral therapy is necessary. Patients should be instructed when to take supplemental prednisone or hydrocortisone and taught to self-administer parenteral hydrocortisone for urgent situations. A preloaded syringe with 100 mg hydrocortisone should be available to the patient. A bracelet or wallet card giving the diagnosis and corticosteroid dose may help in case of adrenal crisis that renders the patient unable to communicate. Immediate intravascular volume expansion is done by giving 1 L of a 5% dextrose in 0.9% saline solution over 1 to 2 hours. Additional 0.9% saline is given IV until hypotension, dehydration, and hyponatremia have been corrected. Serum potassium may fall during rehydration, requiring replacement. Mineralocorticoids are not required when high-dose hydrocortisone is given. When illness is less acute, hydrocortisone 50 or 100 mg IM every 6 hours can be given. Restoration of blood pressure and general improvement should occur within 1 hour after the initial dose of hydrocortisone. Inotropic agents may be needed until the effects of hydrocortisone are achieved. Maintenance oral doses of hydrocortisone (15 to 30 mg) and fludrocortisone (0.1 mg) are given daily thereafter, as described above. Recovery depends on treatment of the underlying cause (eg, infection, trauma, metabolic stress) and adequate hydrocortisone therapy. Complications of corticosteroid therapy may include psychotic reactions. If psychotic reactions occur, then the hydrocortisone dose can be reduced to the lowest level consistent with maintaining blood pressure and good cardiovascular function. Antipsychotics may be temporarily required, but use should not be prolonged. From developing new therapies that treat and prevent disease to helping people in need, we are committed to improving health and well-being around the world.

The Merck Manual was first published in 1899 as a service to the community. The legacy of this great resource continues as the Merck Manual in the US and Canada and the MSD Manual outside of North America. Learn more about our commitment to Global Medical Knowledge. The authors identify the function of the adrenal cortex, forms of the disease, diagnostics, acute therapy, and long-term maintenance. An overall low disease prevalence combined with vague clinical signs and nonspecific clinicopathologic abnormalities makes diagnosis challenging. Ultimately, specialized laboratory testing is required for definitive diagnosis. Each functional zone of the cortex is responsible for the synthesis of a specific hormone. Less common causes of adrenocortical destruction include: 1,2 Mineralocorticoids are spared because ACTH does not directly influence their release. Rarely, congenital defects of the pituitary gland, such as a cystic Rathke’s pouch, neoplasia, or trauma9 affecting the hypothalamus or pituitary gland, result in secondary hypoadrenocorticism. The syndrome is typically transient, and adrenal function normalizes following correction of the underlying condition. Critically ill patients exhibiting refractory hypotension despite aggressive fluid therapy and the use of pressor agents should be evaluated for CIRCI. With the exception of the ACTH stimulation test—which has narrow values that define hypoadrenocorticism—there is a vast continuum of potential findings on the initial screening tests. The Addisonian crisis is the life-threatening culmination of combined hormone deficiencies that can be fatal if not appropriately treated. The serum biochemical profile may reveal hypoglycemia, eosinophilia, lymphocytosis, hypercalcemia, hypocholesterolemia, hyperphosphatemia, hypochloremia, and elevated liver enzymes. 10 Anemia—from chronic disease or gastrointestinal (GI) bleeding—may be identified, although relative polycythemia may also result from dehydration.

Most myopathies that cause weakness can be differentiated by their distribution, lack of abnormal pigmentation, and characteristic laboratory findings. In contrast, patients with hypoglycemia due to oversecretion of insulin can have attacks at any time, usually have increased appetite with weight gain, and have normal adrenal function. Unlike those with Addison disease, these patients are not likely to have hyperpigmentation, hyperkalemia, and increased BUN. It is important to note that ACTH levels within the normal range are inappropriate when cortisol levels are very low. If time is too short (eg, emergency surgery), the patient is given hydrocortisone empirically (eg, 100 mg IV or IM), and provocative testing is done subsequently. Secondary adrenal insufficiency is diagnosed by a prolonged ACTH stimulation test, glucagon stimulation test, or insulin tolerance test. In the glucagon stimulation tests, plasma ACTH and cortisol levels fail to rise in response to glucagon in patients with secondary adrenal insufficiency. The insulin tolerance test is not recommended in patients suspected of having severe adrenal insufficiency. Some authorities believe that in patients with suspected secondary adrenal insufficiency, a low-dose ACTH stimulation test using 1 mcg IV instead of the standard 250 mcg-dose should be done because such patients may react normally to the higher dose. Patients taking glucocorticoid supplements or spironolactone should not take them on the day of the test. However, because pituitary failure may cause adrenal atrophy (and hence failure to respond to ACTH), the patient may need to be primed with long-acting ACTH 1 mg IM once a day for 3 days before the ACTH stimulation test if pituitary disease is suspected. Cosyntropin 1 mg IM is given, and cortisol is measured at intervals for 24 hours, typically at 1, 6, 12, and 24 hours.

Results for the first hour are similar for both the short (sampling stopped after 1 hour) and prolonged tests, but in Addison disease there is no further rise beyond 60 minutes. In secondary and tertiary adrenal insufficiency, cortisol levels continue to rise for ? 24 hours. Only in cases of prolonged adrenal atrophy is adrenal priming (with long-acting ACTH) necessary. The simple short test is usually done initially, because a normal response obviates the need for further investigation. If ACTH stimulation testing is done, elevated ACTH levels together with low cortisol levels confirm the diagnosis. Adrenal autoantibodies can be assessed. In patients with autoimmune disease, the adrenals are atrophied, whereas in patients with tuberculosis or other granulomas, the adrenals are enlarged (initially) with frequent calcification. Bilateral adrenal hyperplasia, particularly in children and young adults, suggests a genetic enzyme defect. Thus, hydrocortisone (identical to cortisol) is given in 2 or 3 divided doses with a typical total daily dose of 15 to 30 mg. One regimen gives half the total in the morning, and the remaining half split between lunchtime and early evening (eg, 10 mg, 5 mg, 5 mg). Others give two thirds in the morning and one third in the evening. Doses immediately before bed should generally be avoided because they may cause insomnia. Alternatively, prednisone 5 mg orally in the morning and possibly an additional 2.5 mg orally in the evening may be used. Additionally, fludrocortisone 0.1 to 0.2 mg orally once a day is recommended to replace aldosterone. The easiest way to adjust the fludrocortisone dosage is to ensure that the renin level is within the normal range and that blood pressure and serum potassium level are normal. In some patients, fludrocortisone causes hypertension, which is treated by reducing the dosage or starting a nondiuretic antihypertensive.

Depending on the degree of vomiting and diarrhea, hypoalbuminemia, hypoglobulinemia, or acidemia may be identified. Azotemia in the presence of an inappropriately low specific gravity (typically Patients with atypical hypoadrenocorticism are more likely to exhibit hypoalbuminemia, hypocholesterolemia, and anemia on routine bloodwork ( Table 3 ). 7 In the hands of experienced ultrasonographers, the adrenal glands may appear thin and short when compared with adrenal glands in healthy dogs; 18 however, in a few cases of hypoadrenocorticism, normal size adrenal glands have been reported. 14 Proceed cautiously if the serum sodium concentration is Additionally, to correct life-threatening hyperkalemia: Studies have shown that DOCP administered to healthy dogs at these doses does not produce adverse effects. 24 Rarely, some patients may experience GI signs secondary to glucocorticoid withdrawal following abrupt cessation of steroid therapy. To avoid signs of adrenal insufficiency, it is recommended to taper steroids to physiologic replacement doses over several weeks. In patients that meet the criteria of CIRCI and display refractory hypotension (despite aggressive medical management), we suggest the use of supplemental glucocorticoids at doses similar to those used in an Addisonian crisis ( Table 4 ). Following resolution of critical illness, corticosteroid therapy may be tapered and discontinued depending on the patient’s clinical response. A repeat ACTH stimulation test can be performed 4 to 6 weeks following discontinuation of steroid therapy to document adrenal recovery. It is not uncommon for veterinarians to successfully extend the dosing interval. If finances are of concern, after the first dose, it is reasonable to attempt incremental lowering of the subsequent DOCP doses by approximately 25%. Clients can also be taught to administer DOCP at home, which has potential cost savings.

Once patients are well regulated, evaluate them at least 2 times each year, with a physical examination and routine bloodwork. Although canine hypoadrenocorticism is serious and, sometimes, life-threatening, early identification and proper treatment can result in an excellent long-term prognosis in most patients. 27 Canine and Feline Endocrinology and Reproduction, 3rd ed. St. Louis: WB Saunders, 2004. pp 394-439. Addison’s disease due to bilateral adrenal malignancy in a dog. J Small Anim Pract 2010; 51(6):333-336. Clinical, immunological, and genetic features of autoimmune primary adrenal insufficiency: Observations from a Norwegian registry. J Clin Endocrinol Metab 2009; 94(12):4882-4890. Lancet 1992; 339:1559-1562. Analysis of P450 side-chain cleavage enzyme autoantibodies in dogs affected with hypoadrenocorticism (abstract). J Vet Intern Med 2014; 28:1027. Glucocorticoid deficient hypoadrenocorticism in dogs: 18 cases (1986-1995).Comparison of classic hypoadrenocorticism with glucocorticoid-deficient hypoadrenocorticism in dogs: 46 cases (1985-2005).J Vet Intern Me d 2014; 28(1):154-159. Secondary hypoadrenocorticism associated with craniocerebral trauma in a dog.Pretreatment clinical and laboratory findings in dogs with hypoadrenocorticism: 225 cases (1979-1993).Genetic evaluation of Addison’s disease in the Portuguese Water Dog. BMC Vet Res 2006; 2:15. Heritability and complex segregation analysis of hypoadrenocorticism in the standard poodle. J Small Anim Pract 2003; 44:8-12. Inheritance of hypoadrenocorticism in bearded collies. Am J Vet Res 2002; 63:643-647. Abnormalities in serum electrolyte concentrations in dogs with hypoadrenocorticism. J Vet Intern Med 2007; 21(6):1168-1173. White blood cell count and the sodium to potassium ratio to screen for hypoadrenocorticism in dogs. J Vet Intern Med 2011; 25(6):1351-1356. Radiographic findings in dogs with naturally-occurring primary hypoadrenocorticism.Small Anim Pract 1995; 36(3):132-135.

Ultrasonographic evaluation of adrenal glands in dogs with primary hypoadrenocorticism or mimicking diseases. Vet Rec 2010; 167(6):207-210. Use of basal serum or plasma cortisol concentrations to rule out a diagnosis of hypoadrenocorticism in dogs: 123 cases (2000-2005).Intramuscular administration of a low dose of ACTH for ACTH stimulation testing in dogs.Relative adrenal insufficiency in dogs with sepsis. J Vet Intern Med 2007; 21(2):226-231. Pituitary-adrenal function in dogs with acute critical illness.Vet Clin North Am Small Anim Pract 2011; 41(4):767-782. Toxicity of desoxycorticosterone pivalate given at high doses to clinically normal beagles for six months. Am J Vet Res 1993; 54(11):1954-1961. Subcutaneous administration of desoxycorticosterone pivalate for the treatment of canine hypoadrenocorticism.Lower initial dose desoxycorticosterone pivalate for treatment of canine primary hypoadrenocorticism. Aust Vet J 2013; 91(3):77-82. J Vet Intern Med 1997; 11(2):43-49 She received her DVM from University of California—Davis and completed a small animal internship at VCA West Los Angeles Animal Hospital. He received his DVM from University of Missouri and completed an internship at Purdue University and residency in internal medicine at University of California—Davis. He then became a staff internist at West Los Angeles Veterinary Medical Group and member of the Department of Comparative Medicine at Stanford University. These dog training tips will help you get started.Here are 15 breeds with notable smarts.For some pet experts, these “invisible fences” are a source of controversy. Find out if an electric dog fence is the right choice for your pet.It’s often referred to as the great imitator by veterinarians because its clinical signs are often very vague and can mimic other conditions.

But while getting to a diagnosis may be frustrating, the good news is that with lifelong treatment, most dogs with Addison’s disease have an excellent prognosis and the condition shouldn’t have any impact on your dog’s life expectancy. Dogs have two small adrenal glands that are located near their kidneys, and these glands produce two important hormones: In other words, the dog’s immune system attacks the adrenal tissue by mistake. The Merck Veterinary Manual notes that other conditions can damage the adrenal glands as well and trigger the condition, including medications used to treat Cushing’s disease (a condition caused by too much cortisol) and cancer in other parts of the body. Several breeds are more prone to the condition, including standard poodles, West Highland white terriers, Great Danes, bearded collies, and Portuguese water dogs. They include: Signs of an Addisonian crisis include severe vomiting and diarrhea, shock, and collapse. It’s a multi-step process: The veterinarian first measures the amount of cortisol in the dog’s blood before giving him an injection of a hormone called adrenocorticotropin. In healthy dogs, this hormone is able to stimulate the adrenal gland. Then, the veterinarian measures the level of cortisol in the dog’s blood a second time. If the dog has Addison’s disease, his cortisol levels will be low both times it’s measured. The adrenocorticotropin will have little to no effect. Once the patient is stable, long-term hormone replacement treatment can begin. Entriken says this usually involves either a desoxycorticosterone pivalate (DOCP) injection every three to four weeks or a dose of fludrocortisone acetate by mouth daily to correct the aldosterone deficit. A common steroid called prednisone is often prescribed to replace cortisol, and it must be given every day by mouth as well. In fact, clinical signs can appear and worsen when stressed. “Particular attention should be paid to avoiding stressful situations,” he says.

As the pet owner, you are the expert on what makes your dog feel stressed, but common causes include being boarded, moving, and having house guests. But with therapy, most dogs have an excellent long-term prognosis and are able to live long, active lives. A close partnership between you and your veterinary office is the best way to keep your pet healthy. Check here for information, cautions and concerns, as well as possible side effects. Very little snail bait is required to cause poisoning (less than a teaspoon per 10 pounds of body weight). What foods and supplements are best sources of vitamin C for your guinea pig? If you're interested in learning more about a broader look at veterinary medicine, the veterinarians, the clients, and the patients, VetzInsight is a great learning experience. Any reliance you place on such information is strictly at your own risk. Addison’s disease occurs when the adrenal glands fail to produce the hormones that they are in charge of in the body. These steroids play a large role in regulating your dog’s internal organs and body systems. Without them, your dog’s body deteriorates, leading to serious complications and even death. Veterinarians suspect that most of these cases result from an autoimmune process. Addison’s disease can also be caused by destruction of the adrenal gland, either by a metastatic tumor, hemorrhage, infarction, granulomatous disease, adrenolytic agents like the drug mitotane, or a drug like trilostane that inhibits adrenal enzymes. This leads to a wide range of symptoms and in acute cases of Addison’s disease, death. There are, however, some breeds that appear to be predisposed to the disease: It has been called the great imitator. In general, dogs with Addison’s may experience recurrent bouts of gastroenteritis, poor appetite, slow loss of body condition, and an inability to respond appropriately to stress. It's important to note that the symptoms of Addison's disease may wax and wane.