The Cause Of Mammary Gland Tumors
Neoplastic diseases are the result of an uncontrolled growth of abnormal cells subsequently forming a tissue mass. Mammary gland tumors are neoplastic tumors of the mammary glands. These tumors are more common in canine and feline female animals and rarely occur in large domestic animals. Mice are also affected by mammary gland tumors. Although the incidence of mammary gland tumors are more often seen in female canines than female felines, the malignancy rate is higher in felines. The cause of mammary gland tumors in mice can be from an oncornavirus (retrovirus). Hormones may be a cause of mammary gland tumors in canines and felines. In the feline species, hormone therapies (estrogen, progesterone) may increase the risk of mammary gland tumors. Most often in felines, mammary gland tumors are malignant. They have the potential to metastasize to other organs in the body. Bacterial infection may develop. Weight loss and muscle wasting may also occur. Clinical signs seen in felines with mammary gland tumors are a firm nodule or mass are palpated in the mammary chain. Lymph nodes may be enlarged. The mammary ducts may be secreting fluid or
…show more content…
bleeding. The cat may be excessively grooming the area. Lethargy, weight loss and no interest in food may be seen. Diagnostic tests include a fine-needle aspirate to collect fluid from the mass and perform a cytologic examination. An incisional biopsy should also be performed to confirm findings. Thoracic radiographs, an abdominal ultrasound and lymph node aspirates assist with the stage of the tumor and the treatment plan. The surgical treatment recommended for felines with mammary gland tumors is radical mastectomy of the mammary chain because of the high incidence of malignancy. Treatment with chemotherapy is warranted for felines where the disease has metastasized. Radiation therapy helps to provide relief from pain for non-removable tumors and inhibit growth of microscopic cells. NSAIDS and opioids are prescribed for pain management. Intact felines may be more likely to acquire mammary gland tumors. To reduce the risk of this disease, ovariohysterectomy (spaying) is recommended as the increase in sex hormone production contributes to mammary gland tumors. It is important to realize most mammary gland tumors in felines are malignant and aggressive surgical intervention may be the best course of treatment. Early intervention in the form of ovariohysterectomy is a good defense against this form of tumor. Any suspicious lump or mass of the mammary area should be examined by a veterinary professional.
Metabolic Diseases Metabolic diseases are any disease that occurs when failure of normal metabolism causes the body to have too much or too little of an essential substance. This results in the body’s inability to eliminate or breakdown substances within the body. Addison’s disease (hypoadrenocorticism) is a metabolic disease where the adrenal glands fail to secrete glucocorticoids (cortisol) and mineralcorticoids (aldosterone). Addison’s disease can arise from the gland or it can be the result of a hormone that tells the gland to secrete the corticoids. Primary and atypical Addison’s disease can be the result of immune mediated damage to the adrenal glands and secondary Addison’s disease results from the failure of stimulation of ACTH (adrenocorticotropic hormone) from the pituitary to the adrenal glands. Addison’s disease primarily affects canines and is occasionally seen in felines and equines. Female dogs under the age of seven are more affected by this disease. Clinical signs of Addison’s disease in canines include vomiting, retching, and lethargy. Additionally, diarrhea, weakness, and shaking may be seen. Weight loss, abdominal pain, dehydration, weak pulse and decreased capillary refill time can also be present. An Adisonian crisis is a life threatening state where collapse, bradycardia, weak pulse and abdominal pain are seen. Clinical signs of Addison’s disease may be vague because they are similar to symptoms of other diseases and can wax and wane. Because of this, diagnostic testing is important. Diagnostic tests for Addison’s disease will involve a serum chemistry panel.
The result of a sodium/potassium electrolyte ratio of less than 25:1 along with increased levels of BUN, calcium and creatinine and a decrease in blood glucose and albumin concentrations may lead to a diagnosis of Addison’s disease. However, since electrolyte levels may not affect Addison’s disease an ACTH stimulation test provides a definitive diagnosis by testing the dog’s adrenal glands to produce cortisol. In this test, initially a blood sample is taken and the cortisol level is measured. The dog is then injected with synthetic ACTH (Cortrosyn®) to stimulate the adrenal glands to produce cortisol. In one hour a blood sample is taken and the cortisol level is measured. Addison’s disease is diagnosed if the dog has no or low response to this
stimulation. Chronic management and treatment for the Addisonian canine patient will involve a glucocorticoid supplementation (prednisolone or prednisone) and a mineralocorticoid supplementation (fludrocortisone or Percorten®-V). Therapy with glucocorticoid supplementation involves daily dosing of a medication for the dog’s entire life. Higher doses are initially prescribed tapering down to a maintenance dose. Clinical signs exhibited by the dog determine this maintenance dose. If the dose is too high, the dog will exhibit signs of excessive drinking, urinating and an increase in appetite. If the dose is too low, the dog will exhibit signs of inappetence, vomiting and diarrhea. During times of stress, the dose will have to be increased to meet the demand of the body’s inability to produce additional glucocorticoids. Therapy with a mineralocorticoid supplementation will involve periodic testing of electrolyte levels to determine the frequency and dose of the medication. Fludrocortisone is a daily oral medication and Percorten®-V is an injectable medication that is administered approximately every 25 days. Acute crisis management will involve hospitalization. Intravenous fluid administration along with higher doses of glucocorticoids may be required. Proper medical management and prompt attention during an acute crisis will provide the Addisonian’s patient with a normal quality of life. Addison’s disease in the canine patient can be controlled with proper medical treatment. Dogs with Addison’s disease are more susceptible to infection, notably urinary tract infections. Urinalysis should be performed as part of the patient’s regular bi-annual physical exam. Electrolytes should be examined periodically. Signs for acute illness include vomiting, diarrhea, weakness and collapse and should be treated as an emergency.
Toxic Diseases A toxic disease is the result of the ingestion, absorption or inhalation of a substance that is poisonous and causes damage to organs, tissues and cells. Additionally, overexposure to any particular substance can also be considered a toxin. Ethylene glycol is a clear, odorless and sweet solvent found in radiator fluid, antifreeze and brake fluid. Puddles of this solvent can be found in garages and under cars. In colder temperatures, animals tend to seek out the warmth from recently turned off car engines. The sweet tasting solvent is ingested by the animal and results in ethylene glycol toxicosis. All animals are susceptible to ethylene glycol toxicosis with canines and felines being affected more often. Ethylene glycol is absorbed rapidly. The animal’s body metabolizes ethylene glycol, further breaking it down to oxalic acid and binding it to blood in the body. It then forms calcium oxalate crystals in the kidneys resulting in toxic levels of BUN and creatinine concluding in renal failure. Severe kidney failure results sooner in cats than in dogs. Symptoms in feline patients with ethylene glycol toxicosis within the first 12 hours include vomiting, ataxia (drunken appearance), muscle twitching, rapid eyeball movement and p/u, p/d (increased urination and drinking). Symptoms occurring 12-24 hours post exposure include lack of urine production, low body temperature, vomiting, seizures, drooling, inappetence and painful kidneys. This later stage is when renal failure is developing. The body metabolizes ethylene glycol, breaking it down to oxalic acid and binding it to blood in the body. It then forms calcium oxylate crystals in the kidneys resulting in toxic levels of BUN and creatinine concluding in renal failure. Diagnostic tests used to diagnose ethylene glycol toxicosis in felines include a urinalysis to reveal calcium oxylate crystals and isosthenuria (the inability to concentrate or dilute urine). A commercial test kit utilizing serum or plasma is available however testing must be performed within 12 hours after exposure. Limitations exist in feline patients with this test because the animal’s sensitivity to ethylene glycol may result in false-negative results due to the kit’s control levels based on canine parameters. Collectively, diagnostic tests in additional to clinical signs should be taken into consideration when evaluating possible ethylene glycol poisoning. Treatments for ethylene glycol toxicosis in felines include the induction of emesis if within the first two hours of ingestion. This is contraindicated if the cat is exhibiting signs of reduced consciousness because of the risk of aspiration. To inhibit the metabolism of ethylene glycol, an IV ethanol solution can be administered, however, this method must be monitored constantly and can have serious effects on the kidneys (metabolic acidosis) and CNS depression. Fomepizole, used as an antidote for ethylene glycol poisoning in dogs, can be used in cats but in higher doses. Fomepizole treatment is administered intravenously. Gastric lavage may be useful but treatment must be within the first hour of ingestion. Fluid therapy is vital for correction of fluid deficits. Proper storage and disposal of solvents containing ethylene glycol are crucial in the prevention of poisoning from ingestion of this toxic substance. Promptly clean up spills from automobile fluids and keep animals away from areas where automobile fluids are being drained. Tightly cap storage containers containing ethylene glycol solvents. An animal that is provided with fresh water at all times, will not be thirsty and may not seek other sources of drinking water that could be contaminated. If ethylene glycol ingestion is suspected, seek immediate veterinary attention for the animal.
bleeding. The cat may be excessively grooming the area. Lethargy, weight loss and no interest in food may be seen. Diagnostic tests include a fine-needle aspirate to collect fluid from the mass and perform a cytologic examination. An incisional biopsy should also be performed to confirm findings. Thoracic radiographs, an abdominal ultrasound and lymph node aspirates assist with the stage of the tumor and the treatment plan. The surgical treatment recommended for felines with mammary gland tumors is radical mastectomy of the mammary chain because of the high incidence of malignancy. Treatment with chemotherapy is warranted for felines where the disease has metastasized. Radiation therapy helps to provide relief from pain for non-removable tumors and inhibit growth of microscopic cells. NSAIDS and opioids are prescribed for pain management. Intact felines may be more likely to acquire mammary gland tumors. To reduce the risk of this disease, ovariohysterectomy (spaying) is recommended as the increase in sex hormone production contributes to mammary gland tumors. It is important to realize most mammary gland tumors in felines are malignant and aggressive surgical intervention may be the best course of treatment. Early intervention in the form of ovariohysterectomy is a good defense against this form of tumor. Any suspicious lump or mass of the mammary area should be examined by a veterinary professional.
Metabolic Diseases Metabolic diseases are any disease that occurs when failure of normal metabolism causes the body to have too much or too little of an essential substance. This results in the body’s inability to eliminate or breakdown substances within the body. Addison’s disease (hypoadrenocorticism) is a metabolic disease where the adrenal glands fail to secrete glucocorticoids (cortisol) and mineralcorticoids (aldosterone). Addison’s disease can arise from the gland or it can be the result of a hormone that tells the gland to secrete the corticoids. Primary and atypical Addison’s disease can be the result of immune mediated damage to the adrenal glands and secondary Addison’s disease results from the failure of stimulation of ACTH (adrenocorticotropic hormone) from the pituitary to the adrenal glands. Addison’s disease primarily affects canines and is occasionally seen in felines and equines. Female dogs under the age of seven are more affected by this disease. Clinical signs of Addison’s disease in canines include vomiting, retching, and lethargy. Additionally, diarrhea, weakness, and shaking may be seen. Weight loss, abdominal pain, dehydration, weak pulse and decreased capillary refill time can also be present. An Adisonian crisis is a life threatening state where collapse, bradycardia, weak pulse and abdominal pain are seen. Clinical signs of Addison’s disease may be vague because they are similar to symptoms of other diseases and can wax and wane. Because of this, diagnostic testing is important. Diagnostic tests for Addison’s disease will involve a serum chemistry panel.
The result of a sodium/potassium electrolyte ratio of less than 25:1 along with increased levels of BUN, calcium and creatinine and a decrease in blood glucose and albumin concentrations may lead to a diagnosis of Addison’s disease. However, since electrolyte levels may not affect Addison’s disease an ACTH stimulation test provides a definitive diagnosis by testing the dog’s adrenal glands to produce cortisol. In this test, initially a blood sample is taken and the cortisol level is measured. The dog is then injected with synthetic ACTH (Cortrosyn®) to stimulate the adrenal glands to produce cortisol. In one hour a blood sample is taken and the cortisol level is measured. Addison’s disease is diagnosed if the dog has no or low response to this
stimulation. Chronic management and treatment for the Addisonian canine patient will involve a glucocorticoid supplementation (prednisolone or prednisone) and a mineralocorticoid supplementation (fludrocortisone or Percorten®-V). Therapy with glucocorticoid supplementation involves daily dosing of a medication for the dog’s entire life. Higher doses are initially prescribed tapering down to a maintenance dose. Clinical signs exhibited by the dog determine this maintenance dose. If the dose is too high, the dog will exhibit signs of excessive drinking, urinating and an increase in appetite. If the dose is too low, the dog will exhibit signs of inappetence, vomiting and diarrhea. During times of stress, the dose will have to be increased to meet the demand of the body’s inability to produce additional glucocorticoids. Therapy with a mineralocorticoid supplementation will involve periodic testing of electrolyte levels to determine the frequency and dose of the medication. Fludrocortisone is a daily oral medication and Percorten®-V is an injectable medication that is administered approximately every 25 days. Acute crisis management will involve hospitalization. Intravenous fluid administration along with higher doses of glucocorticoids may be required. Proper medical management and prompt attention during an acute crisis will provide the Addisonian’s patient with a normal quality of life. Addison’s disease in the canine patient can be controlled with proper medical treatment. Dogs with Addison’s disease are more susceptible to infection, notably urinary tract infections. Urinalysis should be performed as part of the patient’s regular bi-annual physical exam. Electrolytes should be examined periodically. Signs for acute illness include vomiting, diarrhea, weakness and collapse and should be treated as an emergency.
Toxic Diseases A toxic disease is the result of the ingestion, absorption or inhalation of a substance that is poisonous and causes damage to organs, tissues and cells. Additionally, overexposure to any particular substance can also be considered a toxin. Ethylene glycol is a clear, odorless and sweet solvent found in radiator fluid, antifreeze and brake fluid. Puddles of this solvent can be found in garages and under cars. In colder temperatures, animals tend to seek out the warmth from recently turned off car engines. The sweet tasting solvent is ingested by the animal and results in ethylene glycol toxicosis. All animals are susceptible to ethylene glycol toxicosis with canines and felines being affected more often. Ethylene glycol is absorbed rapidly. The animal’s body metabolizes ethylene glycol, further breaking it down to oxalic acid and binding it to blood in the body. It then forms calcium oxalate crystals in the kidneys resulting in toxic levels of BUN and creatinine concluding in renal failure. Severe kidney failure results sooner in cats than in dogs. Symptoms in feline patients with ethylene glycol toxicosis within the first 12 hours include vomiting, ataxia (drunken appearance), muscle twitching, rapid eyeball movement and p/u, p/d (increased urination and drinking). Symptoms occurring 12-24 hours post exposure include lack of urine production, low body temperature, vomiting, seizures, drooling, inappetence and painful kidneys. This later stage is when renal failure is developing. The body metabolizes ethylene glycol, breaking it down to oxalic acid and binding it to blood in the body. It then forms calcium oxylate crystals in the kidneys resulting in toxic levels of BUN and creatinine concluding in renal failure. Diagnostic tests used to diagnose ethylene glycol toxicosis in felines include a urinalysis to reveal calcium oxylate crystals and isosthenuria (the inability to concentrate or dilute urine). A commercial test kit utilizing serum or plasma is available however testing must be performed within 12 hours after exposure. Limitations exist in feline patients with this test because the animal’s sensitivity to ethylene glycol may result in false-negative results due to the kit’s control levels based on canine parameters. Collectively, diagnostic tests in additional to clinical signs should be taken into consideration when evaluating possible ethylene glycol poisoning. Treatments for ethylene glycol toxicosis in felines include the induction of emesis if within the first two hours of ingestion. This is contraindicated if the cat is exhibiting signs of reduced consciousness because of the risk of aspiration. To inhibit the metabolism of ethylene glycol, an IV ethanol solution can be administered, however, this method must be monitored constantly and can have serious effects on the kidneys (metabolic acidosis) and CNS depression. Fomepizole, used as an antidote for ethylene glycol poisoning in dogs, can be used in cats but in higher doses. Fomepizole treatment is administered intravenously. Gastric lavage may be useful but treatment must be within the first hour of ingestion. Fluid therapy is vital for correction of fluid deficits. Proper storage and disposal of solvents containing ethylene glycol are crucial in the prevention of poisoning from ingestion of this toxic substance. Promptly clean up spills from automobile fluids and keep animals away from areas where automobile fluids are being drained. Tightly cap storage containers containing ethylene glycol solvents. An animal that is provided with fresh water at all times, will not be thirsty and may not seek other sources of drinking water that could be contaminated. If ethylene glycol ingestion is suspected, seek immediate veterinary attention for the animal.