Cushings disease in dogs
Kathsgrdn
5 years ago
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Newbie to this forum. My baby has Cushings!
Comments (14)Trilostane is very recently available in the US for treatment of Cushings with less side effects than lysodren. Well, except for the very low risk of sudden death. But other than that, it is a reversible non-cytotoxic drug that doesn't carry the risk of making your dog Addisonian like lysodren can. Some vets use trilostane in conjunction with ketoconazole (an anti-fungal drug) to increase the bioavailability of the trilostane and reduce the dose. As far as behavior changes, most dogs don't have that many except the already mentioned increased hunger, thirst, and perhaps panting and lethargy. I've heard a few people say that their dog got aggressive or had other odd personality changes with Cushings in the untreated stage, but that seems rare. Once treated and stable, it seems all those signs go away. As far as pain and quality of life go, I think it depends on how well the disease is being managed. Most seem like happy dogs, unless they go into a Addisonian crisis. Then they are pretty darn miserable until their cortisol levels are fixed. But that is pretty easy to do. If they are accidently made permanently Addisonian, that is treatable too. I guess it would be a big problem if your dog was hard to medicate for some reason, because treating either Cushings or Addisons is usually a lifelong ordeal. Another issue would be if your dog get stressed at the vets or resented frequent blood draws. I think the biggest issue in treating Cushings is the expense and inconvenience to the owner, because the dog must be pilled, monitored at home carefully, and the drug dose must be monitored closely requiring many blood draws and trips to the vet. This isn't a type of disease where you just give some pills for a couple of weeks and it goes away. It's generally life long. So it requires a lot of committment from the owner. But dogs are well worth the effort IMHO. Their quality of life is much improved with treatment....See MoreAtypical Cushings & Chronic Kidney Disease
Comments (4)Assuming the correct diagnoses, a dog with chronic renal disease showing azotemia (high BUN and/or creatinine) has already lost 75% of renal function. A non-azotemic dog with low urine specific gravity has lost 66% of renal function, IF that specific gravity is 100% caused by the renal disease. Unfortunately, having lost that much renal function does shorten a dog's life. The 2 diseases aren't really related as far as cause, but they can have devastating effects on each other. Factors that increase morbidity in renal disease are hypertension, proteinuria, hyperphosphatemia. Proteinuria is an effect of kidney disease, but it also causes further kidney damage. Proteinuria is also an effect of Cushings, which of course also aggravates the renal disease. A low protein diet is necessary to decrease the amount of protein going to the kidneys, and therefore reduces the damage. Cushings can also cause hypertension, which damages the kidneys. And in typical cushings, you increase the risk for diabetes mellitus which can also cause kidney damage. So lots of intertwining effects on both of those diseases. Having both also makes diagnosis and management a challenge as it's difficult to know if the symptoms are caused by lack of management on the renal issue or lack of management on the cushings issue. No easy way to sort that out. Now all that is based on your typical hyperadrenocorticism, not atypical cushings. I don't know that anyone knows enough about atypical cushings to make any correlations. My major concern is adding lysodren to a dog with pre-existing renal disease. That may be a dangerous combo, especially when lysodren isn't used for atypical cushings. If there were some clear indication for it, I might play that game. But the cortisol is not high then I can't think of a good reason to play in that neck of the woods without clear indication. Especially if the medication isn't controlling the symptoms which may be all due to worsening kidney disease (which is made even worse with the lysodren). The diet recommendations for kidney disease are based on monitoring proteinuria, hyperphosphatemia, hypertension, and other parameters. In some cases, all the dog needs is a quality senior diet. Some vets prefer a heart diet such as H/D with its moderate protein restriction as opposed to K/D. Others go with the Purina renal formula. Treating proteinuria specifically usually requires an ACE inhibitor such as enalapril or benazapril. Sometimes the ACE inhibitor is also enough to treat hypertension, other times you need to add amlopidine or other medication. Lots of things can be affected by both diseases, and frequent monitoring and adjusting the treatment protocol is warranted. Oh, and both diseases predispose dogs to UTIs, so routine urine cultures are also needed. Hope that helps a bit. It's probably as confusing to you as it is to me and anyone else who reads it. But you unfortunately have an interesting case in your Gracie. I hope things can be worked out best for her....See Moremanaging bowel disease in my dog
Comments (1)I'm sorry about your dog. My Max didn't have bowel disease but he did have liver cancer. He stopped eating because of it, and we had to put him to sleep. My Max, your typical Lab, had never missed a meal in his life before the cancer, and we knew that when he refused to eat it was because he was miserable. Most dogs with bowel disease eat; I think it is the cancer that is making her feel bad. Is she on pred to help control the bowel disease? It would also stimulate her appetite......See Morecushings.... thoughts???
Comments (20)Since having cushing's disease is a permanent ovedose of steroids, I am copying the drug information for glucocorticoids from a veterinary drug handbook. By looking at the effects glucocorticoids have, you may better be able to understand your dog's condition. EFFECRS OF GLUCOCORTICOIDS Cardiovascular System: Glucocorticoids can reduce capillary permeability and enhance vasoconstriction. A relatively clinically insignificant positive inotropic effect can occur after glucocorticoid administration. Increased blood pressure can result from both the drugs' vasoconstrictive properties and increased blood volume that may be produced. Cells: Glucocorticoids inhibit fibroblast proliferation, macrophage response to migration inhibiting factor, sensitization of lymphocytes and the cellular response to mediators of inflammation. Glucocorticoids stabilize lysosomal membranes. CNS/Autonomic Nervous System: Glucocorticoids can lower seizure threshold, alter mood and behavior, diminish the response to pyrogens, stimulate appetite and maintain alpha rhythm. Glucocorticoids are necessary for normal adrenergic receptor sensitivity. Endocrine System: When animals are not stressed, glucocorticoids will suppress the release of ACTH from the anterior pituitary, thereby reducing or preventing the release of endogenous corticosteroids. Stress factors (e.g., renal disease, liver disease, diabetes) may sometimes nullify the suppressing aspects of exogenously administered steroids. Release of thyroid-stimulating hormone (TSH), follicle-stimulating hormone (FSH), prolactin and luteinizing hormone (LH) may all be reduced when glucocorticoids are administered at pharmacological doses. Conversion of thyroxine (T4) to triiodothyronine (T3) may be reduced by glucocorticoids; and plasma levels of parathyroid hormone increased. Glucocorticoids may inhibit osteoblast function. Vasopressin (ADH) activity is reduced at the renal tubules and diuresis may occur. Glucocorticoids inhibit insulin binding to insulin-receptors and the post-receptor effects of insulin. Hematopoietic System: Glucocorticoids can increase the numbers of circulating platelets, neutrophils and red blood cells, but platelet aggregation is inhibited. Decreased amounts of lymphocytes (peripheral), monocytes and eosinophils are seen as glucocorticoids can sequester these cells into the lungs and spleen and prompt decreased release from the bone marrow. Removal of old red blood cells is diminished. Glucocorticoids can cause involution of lymphoid tissue. GI Tract and Hepatic System: Glucocorticoids increase the secretion of gastric acid, pepsin and trypsin. They alter the structure of mucin and decrease mucosal cell proliferation. Iron salts and calcium absorption are decreased while fat absorption is increased. Hepatic changes can include increased fat and glycogen deposits within hepatocytes, increased serum levels of alanine aminotransferase (ALT) and gamma-glutamyl transpeptidase (GGT). Significant increases can be seen in serum alkaline phosphatase levels. Glucocorticoids can cause minor increases in BSP (bromosulfophthalein) retention time. Immune System (also see Cells and Hematopoietic System): Glucocorticoids can decrease circulating levels of T-lymphocytes; inhibit lymphokines; inhibit neutrophil, macrophage, and monocyte migration; reduce production of interferon; inhibit phagocytosis and chemotaxis; antigen processing; and diminish intracellular killing. Specific acquired immunity is affected less than nonspecific immune responses. Glucocorticoids can also antagonize the complement cascade and mask the clinical signs of infection. Mast cells are decreased in number and histamine synthesis is suppressed. Many of these effects only occur at high or very high doses and there are species differences in response. Metabolic effects: Glucocorticoids stimulate gluconeogenesis. Lipogenesis is enhanced in certain areas of the body (e.g., abdomen) and adipose tissue can be redistributed away from the extremities to the trunk. Fatty acids are mobilized from tissues and their oxidation is increased. Plasma levels of triglycerides, cholesterol and glycerol are increased. Protein is mobilized from most areas of the body (not the liver). Musculoskeletal: Glucocorticoids may cause muscular weakness (also caused if there is a lack of glucocorticoids), atrophy, and osteoporosis. Bone growth can be inhibited via growth hormone and somatomedin inhibition, increased calcium excretion and inhibition of vitamin D activation. Resorption of bone can be enhanced. Fibrocartilage growth is also inhibited. Ophthalmic: Prolonged corticosteroid use (both systemic or topically to the eye) can cause increased intraocular pressure and glaucoma, cataracts and exophthalmos. Renal, Fluid, & Electrolytes: Glucocorticoids can increase potassium and calcium excretion; sodium and chloride reabsorption and extracellular fluid volume. Hypokalemia and/or hypocalcemia occur rarely. Diuresis may occur following glucocorticoid administration. Skin: Thinning of dermal tissue and skin atrophy can be seen with glucocorticoid therapy. Hair follicles can become distended and alopecia may occur. Adverse effects are generally associated with long-term administration of these drugs, especially if given at high dosages or not on an alternate day regimen. Effects generally are manifested as symptoms of hyperadrenocorticism. Many of the potential effects, adverse and otherwise, are outlined above in the Pharmacology section. In dogs, polydipsia (PD), polyphagia (PP) and polyuria (PU), may all be seen with short-term "burst" therapy as well as with alternate-day maintenance therapy on days when the drug is given. Adverse effects in dogs can include dull, dry haircoat, weight gain, panting, vomiting, diarrhea, elevated liver enzymes, pancreatitis, GI ulceration, lipidemias, activation or worsening of diabetes mellitus, muscle wasting and behavioral changes (depression, lethargy, viciousness). With the exception of PU/PD/PP, adverse effects associated with antiinflammatory therapy are relatively uncommon. Adverse effects associated with immunosuppressive doses are more common and potentially more severe. As far as evaluating quality of like, ask yourself what are 5 things your dog used to love (food, walks, swimming, whatever). Then ask yourself if she is still able to enjoy those things. If not, then her quality of life is diminished. I don't believe that dogs with Cushings are painful, but I think they can become uncomfortable. Cushings makes animals more prone to other conditions which can be painful, such as UTIs, pancreatitis, etc. I hope this helps a bit. Personally I think if you are questioning her quality of life, then it is probably diminished. But whether or not it has diminished to an unacceptable level is a decision only you and your family can make, since you know your dog better than anyone else....See MoreKathsgrdn
5 years agoKathsgrdn
5 years ago
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