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Ulcer prevention in pets

Ulcer prevention in pets

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Clients may report seeing melena if there has been large-scale bleeding, but not seeing melena doesn't exclude the possibility of gastrointestinal bleeding. Other clinical signs associated with gastric ulcers include anorexia, weight loss, increased salivation, and abdominal pain.

Abdominal pain in some animals could be a reflection of peritonitis from a perforation, or near perforation. Clinical signs attributed to underlying disease e. It is also important to understand that there may be no overt clinical signs directly suggestive of gastric ulcers, likely making the incidence of gastric ulceration in dogs and cats underestimated.

Mucous membrane pallor may be seen if bleeding is severe, and the presence of masses in animals with other features suggestive of ulcers should prompt at least needle cytology to exclude a mast cell tumor as the primary cause of an ulcer.

There are no pathognomonic clinical pathology abnormalities seen in patients with gastric ulcers, but several that can be highly suggestive in a patient with other supportive historical and physical examination findings.

Anemia, which can be regenerative or non-regenerative, will be seen in some animals. Some patients may have microcytosis and hypochromasia neither evident without indices or examination of a blood smearwith or without anemia, suggestive of iron deficiency if there has been chronic gastric bleeding.

Inflammatory leukograms are possible reflecting the inflammation that often accompanies ulcers. Platelet numbers are usually normal, but can vary depending on the underlying cause of ulcers; chronic ulcers may be associated with thrombocytosis. Serum biochemistry abnormalities will be variable and sometimes reflect the underlying cause and severity of the gastric ulcer.

Increases in liver enzyme activity and abnormalities in the indirect indicators of hepatic function decreases in one or more of albumin, cholesterol, BUN and glucose may be seen in patients with ulcers attributed to liver disease; cholestatic liver diseases may be accompanied by hypercholesterolemia.

Albumin and globulin concentrations may be decreased as a consequence of intraluminal bleeding, and in some patients, an increase in BUN without an increase in creatinine may be seen with large-scale gastric hemorrhage. Results of a urinalysis don't overtly suggest the presence of an ulcer, but could be important to rule out urinary tract causes of, or contributions to, anemia or hypoalbuminemia; results of a urinalysis could also suggest the presence of liver disease e.

low urine specific gravity and biurate crystals. Patients with suspected, or confirmed, gastric ulcers without any other identified risk factor may be candidates for measurement of fasting serum gastrin concentrations to rule out gastrinomas.

Patients with gastric ulcers can have chronic, low-grade blood loss that is not overtly apparent. For patients that do not have overt signs of gastrointestinal bleeding, but for which bleeding is suspected as a cause of anemia or microcytosis, a fecal occult blood test can help confirm the intestinal tract as a site of blood loss.

Substantial amounts of blood in the proximal intestinal tract are needed to produce melena, so normal stools do not at all exclude gastrointestinal hemorrhage in the suspect patient as noted previously above. The initial suspicion of gastric ulcers is usually aroused by the presence of compatible clinical signs and laboratory abnormalities, particularly in a patient that has an identifiable risk factor in the history e.

NSAID or glucocorticoid administration or laboratory data base liver disease or renal failure. However, few patients actually have a definitive diagnosis established, but are instead empirically treated. Definitive diagnosis of gastric ulcers is made by visualization of the ulcer, usually by endoscopic examination, or during gastrotomy.

An advantage to endoscopic or surgical diagnosis is the potential for biopsy of tissue in and around the ulcer to examine for primary gastric diseases, especially neoplasia, when other risk factors for gastric ulcers do not exist. Strongly supportive findings for ulcers can be generated from contrast radiography or abdominal ultrasonography.

Filling defects, gastric wall thickening, and prolonged retention of contrast material in the stomach are features that can be seen in some, but not all, patients with gastric ulcers during contrast radiography. Ultrasonographic findings supportive of gastric ulcers include gastric wall thickening, which is often focal, the detection of a mucosal crater that may have tiny bubbles within it, disruption of the normal layering of the gastric wall, and gastric hypomotility.

Several of these ultrasonographic findings can be seen with other gastric diseases e. gastric neoplasia and aren't specific for gastric ulcers.

Key to treatment of gastric ulcers is identification and elimination, whenever possible, of underlying diseases or risk factors. In the majority of patients, treatment will also entail administration of drugs that reduce gastric acid secretion, and that provide mucosal protection in the face of an ulcer.

The most commonly used class of drugs to reduce acid secretion is the H2 receptor blockers which include famotidine, ranitidine and cimetidine. Proton pump inhibitors such as omeprazole are also appropriate for treatment of gastric ulcers, but have been more favored for patients with difficult to treat ulcers or with difficult to treat primary causes e.

some gastrinomas. Administration of synthetic PGE2 analogs such as misoprostol can also be of benefit, particularly for patients with NSAID-induced ulcers.

Sucralfate is an appropriate medication to give to patients with confirmed, or suspected ulcers. In an acid environment, sucralfate attains a gel-like consistency that fosters drug binding to ulcer beds protecting them from additional acid-injury. Sucralfate can also promote local production of prostaglandins and enhance the protective properties of mucus.

Coupled with the fact that sucralfate carries a low risk of drug-induced side effects occasional constipationit is recommended for virtually all ulcer patients.

One does need to be aware that sucralfate can interfere with the absorption of other drugs. Patients with life-threatening hemorrhage, or medically intractable ulcers, are candidates for surgical resection of ulcers.

Excised tissue should be submitted for histopathological examination to exclude gastric neoplasia as a primary cause of the ulcer. For patients with unavoidable risk factors, administration of PGE2 analogs can be helpful in reducing the risk of developing gastric ulcers.

Several studies in dogs document the protective benefits of misoprostol administration to prevent NSAID-induced ulcers. H2 blockers are commonly given to patients with mast cell tumors, renal failure or hepatic disease to prevent gastric ulcers. Because cimetidine can alter the metabolism of other drugs, and usually requires administration every 8 hours, the author favors other H2 blockers for patients with liver disease, or that are receiving other drugs.

Prevention of glucocorticoid-induced ulcers remains problematic in small animal practice. While it seems common to administer H2 blockers to patients receiving high-doses glucocorticoids, H2 blockers have not been proven to prevent the development of gastric ulcers in dogs or cats.

The prognosis for patients with gastric ulcers varies with the underlying etiology. The prognosis is good for patients that have correctable underlying risk factors or diseases e.

drug-induced ulcers, hypoadrenocorticismbut can be poor if the underlying disease cannot be reversed e. chronic renal failure or unresectable neoplasia.

Fox LE, Rosenthal RC, Twedt DC et al. Plasma histamine and gastrin concentrations in 17 dogs with mast cell tumors. Vet Intern Med. Liptak JM, Hunt GB, Barrs VRD, et al. Gastroduodenal ulceration in cats: eight cases and a review of the literature.

J Feline Med Surgery ; Penninck D, Matz M, Tidwell A. Ultrasonography of gastric ulceration in the dog. Vet Radiol Ultrasound ; A clinical trial is launched for a novel drug that could extend healthy lifespan in senior dogs. The first canine patient has been dosed in the study that aims to demonstrate an increase in longevity and quality of life in dogs treated with LOY Learn how technology can help interpret it for you.

Known as "The Street Vet," Kwane Stewart, DVM, has a passion for providing care to pets living with homeless individuals. Podcast CE: New guidelines in the management of canine parvovirus. Dermatology expert stresses importance of cytology and cultures.

: Ulcer prevention in pets

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Some exclusions apply. Oversized products are not included. There are many different ways to prevent decubitus ulcers from forming. These specialized surfaces include foam devices, air-filled devices, inflatable airbeds or even water beds that have the ability to be heated.

Placing a dog in deep straw may also provide excellent support and avoid ulcers. However, all incisions must be healed or covered if this method is used.

One of the best types of padded bedding for recumbent dogs is a thick, egg-crate foam rubber pad with a vinyl covering. A sheepskin cover on the mat allows some air circulation under the animal, and wicks urine away from the skin.

Using a sling for 2 to 4 hours a day can help keep pressure off the acromion of the scapula, tuber coxae, and greater trochanter, especially in large dogs. Dog wheelchairs, like www. These devices support the pelvic area in paraparetic or paraplegic dogs, thereby keeping pressure off the bony prominences of the hindquarters, stimulating neural response, maintaining muscle tone, improving circulation, respiratory system health and even mental health as it provides mobility.

During these times, isotonic muscle activity is occurring. Placement of limbs in correct physiological position helps stretch the muscles and tendons appropriately to prevent contracture. Slings can also be used to support the full body, hind end only, or thoracic end only as needed. Animals in any water tank should be adequately supported to prevent aspiration of water or stress associated with fear of drowning.

Bandages with splints can also be very helpful in preventing pressure sores. Diagnosis of gastric ulceration is often presumed from clinical signs and laboratory corroboration of blood in the stool or vomitus but can be diagnosed definitively via direct observation with an endoscope or surgical exploration with or without biopsy and full histopathological examination of the retrieved tissues.

A complete blood count CBS , biochemistry profile serum chemistry analysis , and urinalysis are typically employed to help differentiate primary gastrointestinal disease from other causes and can identify secondary problems.

Additional testing, including liver function testing or testing for specific diseases, may be helpful as well. X-rays, unfortunately, are not often helpful. Ultrasound can be useful but can't definitively confirm the presence of ulceration. There is no known breed predisposition for gastric ulceration.

Some potentially causative conditions, however, have been associated with a breed predisposition in dogs. Gastric dilatation volvulus , Addison's disease , and inflammatory bowel disease are among these. Treatment of gastric ulceration may be undertaken via drug therapy. A class of medications referred to as gastroprotectants are commonly employed to help reduce gastric acid production, alleviate inflammation, reduce pain, and generally help the body heal itself.

Emergency surgery may be indicated in cases of suspected or confirmed perforation or imminent perforation. It's worth noting that the prognosis for gastric perforation patients tends to be poor. Treatment of the underlying cause, if identifiable, is always crucial to the long-term success of gastric ulcer therapy.

Surgical exploration alone typically involves costs that are nearly identical to that for endoscopy. The cost of treatment depends greatly on the severity of the disease. However, the reality is that because many of these patients aren't identified until they're very, very sick, few patients fall under this category.

Treatment of causative diseases can prove very expensive as well. Their expenses may be considered separately under articles describing these disease entities, their treatments, and their costs.

Prevention isn't generally considered a feature of this particular disease's overall landscape. Like bed sores in a human being, these ulcers are a serious concern with any pet that is immobilized for extended periods of time. Older dogs and disabled pets are prone to lying still for long periods of time and without muscle mass to protect them, ulcers and sores can form.

Pets with loss of feeling or sensation in their limbs are also at risk for developing sores. And in older, weaker pets who are unable to gently sit or lie down, but instead drop heavily on the floor.

Causing repeated trauma to a specific area, like an elbow or hip. Ulcers and pressure wounds can affect any dog breed at any age however, most commonly occurs in larger breed dogs. Bed sore wounds are fairly obvious to the naked eye and most commonly occur on the boniest parts of a dog such as hips, elbows, hocks, knees, chest or side of the legs.

Pressure sores are a chronic condition that is difficult to treat and harder to heal. Pay attention to these symptoms:.

Any open wounds that are red or purple, seeping pus, or smell require immediate veterinary care. If you suspect your dog is experiencing any of these symptoms, see your Veterinarian immediately.

Once formed, pressure wounds are extremely difficult to treat , and prevention is key. An active dog is a happy dog! Support your dog with a lifting harness by helping them to stand or gently lower themselves to the ground.

Slings and lifting harnesses are designed to support your pet and can be used to lift the full body or just the rear or front end. Lifting harnesses are a quick, easy way to get your dog back on their feet and can help make potty breaks a breeze. And they are also a great way to get your dog upright and moving again!

Regular massage helps alleviate muscle cramping and provides neural stimulation to the spinal cord. Soft bedding that is thick and well-padded will prevent future trauma. If you your dog is mobility challenged or prone to laying down for extended periods of time, your pet should be physically turned or change its position every two to three hours.

Not only do decubital ulcers cause pain and disfigurement, the condition can become chronic and expensive to treat. And if left untreated they can possibly become life threatening. To prevent ulcers, your pet requires meticulous care of their hair and skin over and around the boniest parts of your dog.

Keep at risk areas clean, dry and free of urine or feces.

Gastric ulcer disease in dogs and cats (Proceedings) In addition, warm whirlpool baths, frequent sponge baths and clipping the perineal and abdominal area help keep the area clean, especially in incontinent dogs. Jamie Freyer, DVM. If treatment for an existing ulcer is required, there are a number of nursing interventions that can be implemented to help avoid a prolonged painful and debilitating recovery. These animals may require:. pressure sore.
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A recent study of gastric ulcers in cats found systemic mast cell tumors the most common cause of ulcers in that study population. Gastric ulcers also develop when protective forces break down. Alterations in mucosal blood flow are a common risk factor for the development of gastric ulcers, and can result from many different processes.

Administration of non-steroidal anti-inflammatory drugs NSAIDs and glucocorticoids decrease local prostaglandin production thereby reducing mucosal blood flow, limiting the epithelium's capacity to protect itself from the injurious effects of acid.

Recent investigations in other species on the effects of NSAIDs have suggested that this class of drugs can also impair ulcer healing through inhibition of angiogenesis necessary for granulation tissue formation in the ulcer bed and epithelial proliferation.

Hypovolemia, shock, vascular thrombosis, or other processes that interrupt gastric blood flow e. Other diseases associated with ulcers can disrupt normal mucosal architecture, and likely also alter blood flow; examples include gastric neoplasms and inflammatory stomach diseases.

For some of the diseases that are associated with ulcers, for example liver disease and hypoadrenocorticism in dogs, the mechanisms contributing to ulcer formation are not well-characterized, but are still likely to involve aberrations in mucosal protective functions.

The most common clinical sign of gastric ulcers in dogs and cats is vomiting, which may or may not have blood in it. Blood in the vomitus can appear fresh, or digested to create the classic "coffee grounds" appearance. It must be pointed out that the appearance of fresh or digested blood in vomitus does not definitively indicate that an ulcer is the source of blood as blood emanating from the nasopharynx or esophagus could be swallowed and vomited.

Clients may report seeing melena if there has been large-scale bleeding, but not seeing melena doesn't exclude the possibility of gastrointestinal bleeding. Other clinical signs associated with gastric ulcers include anorexia, weight loss, increased salivation, and abdominal pain.

Abdominal pain in some animals could be a reflection of peritonitis from a perforation, or near perforation. Clinical signs attributed to underlying disease e. It is also important to understand that there may be no overt clinical signs directly suggestive of gastric ulcers, likely making the incidence of gastric ulceration in dogs and cats underestimated.

Mucous membrane pallor may be seen if bleeding is severe, and the presence of masses in animals with other features suggestive of ulcers should prompt at least needle cytology to exclude a mast cell tumor as the primary cause of an ulcer. There are no pathognomonic clinical pathology abnormalities seen in patients with gastric ulcers, but several that can be highly suggestive in a patient with other supportive historical and physical examination findings.

Anemia, which can be regenerative or non-regenerative, will be seen in some animals. Some patients may have microcytosis and hypochromasia neither evident without indices or examination of a blood smear , with or without anemia, suggestive of iron deficiency if there has been chronic gastric bleeding.

Inflammatory leukograms are possible reflecting the inflammation that often accompanies ulcers. Platelet numbers are usually normal, but can vary depending on the underlying cause of ulcers; chronic ulcers may be associated with thrombocytosis.

Serum biochemistry abnormalities will be variable and sometimes reflect the underlying cause and severity of the gastric ulcer.

Increases in liver enzyme activity and abnormalities in the indirect indicators of hepatic function decreases in one or more of albumin, cholesterol, BUN and glucose may be seen in patients with ulcers attributed to liver disease; cholestatic liver diseases may be accompanied by hypercholesterolemia.

Albumin and globulin concentrations may be decreased as a consequence of intraluminal bleeding, and in some patients, an increase in BUN without an increase in creatinine may be seen with large-scale gastric hemorrhage.

Results of a urinalysis don't overtly suggest the presence of an ulcer, but could be important to rule out urinary tract causes of, or contributions to, anemia or hypoalbuminemia; results of a urinalysis could also suggest the presence of liver disease e.

low urine specific gravity and biurate crystals. Patients with suspected, or confirmed, gastric ulcers without any other identified risk factor may be candidates for measurement of fasting serum gastrin concentrations to rule out gastrinomas.

Patients with gastric ulcers can have chronic, low-grade blood loss that is not overtly apparent. For patients that do not have overt signs of gastrointestinal bleeding, but for which bleeding is suspected as a cause of anemia or microcytosis, a fecal occult blood test can help confirm the intestinal tract as a site of blood loss.

Substantial amounts of blood in the proximal intestinal tract are needed to produce melena, so normal stools do not at all exclude gastrointestinal hemorrhage in the suspect patient as noted previously above. The initial suspicion of gastric ulcers is usually aroused by the presence of compatible clinical signs and laboratory abnormalities, particularly in a patient that has an identifiable risk factor in the history e.

NSAID or glucocorticoid administration or laboratory data base liver disease or renal failure. However, few patients actually have a definitive diagnosis established, but are instead empirically treated. Definitive diagnosis of gastric ulcers is made by visualization of the ulcer, usually by endoscopic examination, or during gastrotomy.

An advantage to endoscopic or surgical diagnosis is the potential for biopsy of tissue in and around the ulcer to examine for primary gastric diseases, especially neoplasia, when other risk factors for gastric ulcers do not exist.

Strongly supportive findings for ulcers can be generated from contrast radiography or abdominal ultrasonography. Filling defects, gastric wall thickening, and prolonged retention of contrast material in the stomach are features that can be seen in some, but not all, patients with gastric ulcers during contrast radiography.

Ultrasonographic findings supportive of gastric ulcers include gastric wall thickening, which is often focal, the detection of a mucosal crater that may have tiny bubbles within it, disruption of the normal layering of the gastric wall, and gastric hypomotility.

Several of these ultrasonographic findings can be seen with other gastric diseases e. gastric neoplasia and aren't specific for gastric ulcers. Key to treatment of gastric ulcers is identification and elimination, whenever possible, of underlying diseases or risk factors.

In the majority of patients, treatment will also entail administration of drugs that reduce gastric acid secretion, and that provide mucosal protection in the face of an ulcer. The most commonly used class of drugs to reduce acid secretion is the H2 receptor blockers which include famotidine, ranitidine and cimetidine.

Proton pump inhibitors such as omeprazole are also appropriate for treatment of gastric ulcers, but have been more favored for patients with difficult to treat ulcers or with difficult to treat primary causes e.

some gastrinomas. Administration of synthetic PGE2 analogs such as misoprostol can also be of benefit, particularly for patients with NSAID-induced ulcers. Sucralfate is an appropriate medication to give to patients with confirmed, or suspected ulcers.

In an acid environment, sucralfate attains a gel-like consistency that fosters drug binding to ulcer beds protecting them from additional acid-injury.

Sucralfate can also promote local production of prostaglandins and enhance the protective properties of mucus. Coupled with the fact that sucralfate carries a low risk of drug-induced side effects occasional constipation , it is recommended for virtually all ulcer patients.

One does need to be aware that sucralfate can interfere with the absorption of other drugs. Patients with life-threatening hemorrhage, or medically intractable ulcers, are candidates for surgical resection of ulcers. Excised tissue should be submitted for histopathological examination to exclude gastric neoplasia as a primary cause of the ulcer.

For patients with unavoidable risk factors, administration of PGE2 analogs can be helpful in reducing the risk of developing gastric ulcers. Several studies in dogs document the protective benefits of misoprostol administration to prevent NSAID-induced ulcers. H2 blockers are commonly given to patients with mast cell tumors, renal failure or hepatic disease to prevent gastric ulcers.

Because cimetidine can alter the metabolism of other drugs, and usually requires administration every 8 hours, the author favors other H2 blockers for patients with liver disease, or that are receiving other drugs. Prevention of glucocorticoid-induced ulcers remains problematic in small animal practice.

While it seems common to administer H2 blockers to patients receiving high-doses glucocorticoids, H2 blockers have not been proven to prevent the development of gastric ulcers in dogs or cats. The signs of kidney disease can be exactly the same as that of ulceration, so treatment for both is usually started.

Mast cell tumors are common in Boxers and other breeds. They secrete histamine responsible for allergic reactions , which increases gastric acid secretion and predisposes to ulcers.

Gastrinomas are tumors found in the stomach and will also release large amounts of gastric acid. Other, less common causes. These include liver disease, inflammatory bowel disease, foreign bodies, and ingestion of caustic materials.

If your dog has symptoms of gastric ulceration, the first step is consulting with your veterinarian. A thorough physical exam and diagnostics are needed to rule out many of the above causes. This will include a nose-to-tail physical and bloodwork such as a complete blood count and a chemistry panel.

Findings may include anemia and low proteins from blood loss though the ulcer and an elevated blood urea nitrogen BUN. In some cases, white blood cell counts may be elevated in response to inflammation.

Other tests that your veterinarian may be able to do include a barium study and abdominal ultrasound. In a barium study, a large amount of bright contrast is given to a dog by mouth. Radiographs are taken immediately and then at various predetermined intervals.

The barium shows up bright white on x-ray. It can show defects in the stomach. Ultrasound can also be used to evaluate for ulcers, although they can be very difficult to see. If a stomach mass such as a gastrinoma is causing the ulceration, then ultrasound may be able to identify it.

Specialized testing can more definitively diagnose an ulcer. Generally, you must be referred to a specialist for an endoscopy, which will be done under anesthesia.

Frequently small samples are taken biopsy for definitive diagnosis. The results can take one to two weeks. Treatment for gastric ulceration depends on the underlying cause. If one is not found, then general treatment includes antacids, a bland diet, and gastroprotectants such as sucralfate.

The major classes of antacids are proton pump inhibitors PPIs and H2 blockers. Both work in slightly different ways to lower gastric acid production. Famotidine Pepcid is an H2 blocker, while omeprazole and pantoprazole are PPIs.

Carafate sucralfate is another drug frequently used in the management of ulcers. It is a soothing agent that coats ulcerated areas. It is given as a tablet dissolved in water a slurry. It can be give up to three times a day for relief of discomfort.

Other approaches may include a bland diet such as boiled chicken and rice. Probiotics can be added to food to maintain normal GI flora populations.

Slippery elm and ginger may have some positive effects on GI ulcers, as well. Perforated stomach ulcers are severe, life-threatening emergencies. A perforation occurs when the ulcer has eroded completely through all four layers of the stomach or intestine.

This allows leakage of bacteria-laden stomach and intestinal fluid into the abdominal cavity, leading to massive inflammation, infection, and sepsis. Treatment for perforated ulcers includes stabilization of shock and infection followed by surgery to repair the ulcers.

Prognosis varies and depends on the underlying cause. For uncomplicated ulcers and ulcers related to H. pylori, prognosis is good with appropriate treatment. It is important to know that they can recur. Discontinuation of NSAIDs and steroids when possible will improve the prognosis for cases related to these medications.

In the case of perforated ulcers, prognosis is guarded. Really interesting information. Our female labrador is on NSAIDs for arthritis, and now Omeperazole for reflux and suspected ulcers. Very helpful, thanks! Very informative article. My 17 month old Rottweiler was diagnosed with pancreatitis and was on 4 different meds, 2 of which you stated in the article.

She had several of the same symptoms, after following the Drs. orders for 5 days she now has to be on special food. I wonder if the pancreatitis will return. We rushed her to the vet as soon as the symptoms started.

NSAIDS are sometimes used along with other drugs, such as corticosteroids, that increase the risk of gastric inflammation. Metabolic disease states, such as hyperadrenocorticism and liver diseases, may also increase the risk. Stomach cancer is yet another cause, but relatively uncommon in dogs.

Symptoms of gastric ulcers in dogs The clinical signs in dogs are similar to those of humans, but may manifest differently. Clinical signs noticed by pet parents may include:. Diagnosis of gastric ulcers in dogs These signs might raise a suspicion of significant inflammation but further confirmation is necessary to diagnose a gastric ulcer.

While there are no diagnostic blood tests, blood tests should still be run to determine if other diseases are present. The only confirmatory ulcer test is to look directly at the lining of the stomach.

Endoscopy is the least invasive method of visualizing an ulcer and confirming a diagnosis. Treatment of gastric ulcers in dogs The primary method of treatment is removal of the causes.

Discontinuation of NSAIDS and glucocorticoids is critical. Lowering levels of gastric acid is also important.

Ulcer prevention in pets -

Anemia, which can be regenerative or non-regenerative, will be seen in some animals. Some patients may have microcytosis and hypochromasia neither evident without indices or examination of a blood smear , with or without anemia, suggestive of iron deficiency if there has been chronic gastric bleeding.

Inflammatory leukograms are possible reflecting the inflammation that often accompanies ulcers. Platelet numbers are usually normal, but can vary depending on the underlying cause of ulcers; chronic ulcers may be associated with thrombocytosis. Serum biochemistry abnormalities will be variable and sometimes reflect the underlying cause and severity of the gastric ulcer.

Increases in liver enzyme activity and abnormalities in the indirect indicators of hepatic function decreases in one or more of albumin, cholesterol, BUN and glucose may be seen in patients with ulcers attributed to liver disease; cholestatic liver diseases may be accompanied by hypercholesterolemia.

Albumin and globulin concentrations may be decreased as a consequence of intraluminal bleeding, and in some patients, an increase in BUN without an increase in creatinine may be seen with large-scale gastric hemorrhage. Results of a urinalysis don't overtly suggest the presence of an ulcer, but could be important to rule out urinary tract causes of, or contributions to, anemia or hypoalbuminemia; results of a urinalysis could also suggest the presence of liver disease e.

low urine specific gravity and biurate crystals. Patients with suspected, or confirmed, gastric ulcers without any other identified risk factor may be candidates for measurement of fasting serum gastrin concentrations to rule out gastrinomas. Patients with gastric ulcers can have chronic, low-grade blood loss that is not overtly apparent.

For patients that do not have overt signs of gastrointestinal bleeding, but for which bleeding is suspected as a cause of anemia or microcytosis, a fecal occult blood test can help confirm the intestinal tract as a site of blood loss. Substantial amounts of blood in the proximal intestinal tract are needed to produce melena, so normal stools do not at all exclude gastrointestinal hemorrhage in the suspect patient as noted previously above.

The initial suspicion of gastric ulcers is usually aroused by the presence of compatible clinical signs and laboratory abnormalities, particularly in a patient that has an identifiable risk factor in the history e. NSAID or glucocorticoid administration or laboratory data base liver disease or renal failure.

However, few patients actually have a definitive diagnosis established, but are instead empirically treated. Definitive diagnosis of gastric ulcers is made by visualization of the ulcer, usually by endoscopic examination, or during gastrotomy.

An advantage to endoscopic or surgical diagnosis is the potential for biopsy of tissue in and around the ulcer to examine for primary gastric diseases, especially neoplasia, when other risk factors for gastric ulcers do not exist. Strongly supportive findings for ulcers can be generated from contrast radiography or abdominal ultrasonography.

Filling defects, gastric wall thickening, and prolonged retention of contrast material in the stomach are features that can be seen in some, but not all, patients with gastric ulcers during contrast radiography.

Ultrasonographic findings supportive of gastric ulcers include gastric wall thickening, which is often focal, the detection of a mucosal crater that may have tiny bubbles within it, disruption of the normal layering of the gastric wall, and gastric hypomotility. Several of these ultrasonographic findings can be seen with other gastric diseases e.

gastric neoplasia and aren't specific for gastric ulcers. Key to treatment of gastric ulcers is identification and elimination, whenever possible, of underlying diseases or risk factors. In the majority of patients, treatment will also entail administration of drugs that reduce gastric acid secretion, and that provide mucosal protection in the face of an ulcer.

The most commonly used class of drugs to reduce acid secretion is the H2 receptor blockers which include famotidine, ranitidine and cimetidine. Proton pump inhibitors such as omeprazole are also appropriate for treatment of gastric ulcers, but have been more favored for patients with difficult to treat ulcers or with difficult to treat primary causes e.

some gastrinomas. Administration of synthetic PGE2 analogs such as misoprostol can also be of benefit, particularly for patients with NSAID-induced ulcers. Sucralfate is an appropriate medication to give to patients with confirmed, or suspected ulcers. In an acid environment, sucralfate attains a gel-like consistency that fosters drug binding to ulcer beds protecting them from additional acid-injury.

Sucralfate can also promote local production of prostaglandins and enhance the protective properties of mucus. Coupled with the fact that sucralfate carries a low risk of drug-induced side effects occasional constipation , it is recommended for virtually all ulcer patients.

One does need to be aware that sucralfate can interfere with the absorption of other drugs. Patients with life-threatening hemorrhage, or medically intractable ulcers, are candidates for surgical resection of ulcers. Excised tissue should be submitted for histopathological examination to exclude gastric neoplasia as a primary cause of the ulcer.

For patients with unavoidable risk factors, administration of PGE2 analogs can be helpful in reducing the risk of developing gastric ulcers. Several studies in dogs document the protective benefits of misoprostol administration to prevent NSAID-induced ulcers. H2 blockers are commonly given to patients with mast cell tumors, renal failure or hepatic disease to prevent gastric ulcers.

Because cimetidine can alter the metabolism of other drugs, and usually requires administration every 8 hours, the author favors other H2 blockers for patients with liver disease, or that are receiving other drugs. Prevention of glucocorticoid-induced ulcers remains problematic in small animal practice.

While it seems common to administer H2 blockers to patients receiving high-doses glucocorticoids, H2 blockers have not been proven to prevent the development of gastric ulcers in dogs or cats.

The prognosis for patients with gastric ulcers varies with the underlying etiology. The prognosis is good for patients that have correctable underlying risk factors or diseases e. drug-induced ulcers, hypoadrenocorticism , but can be poor if the underlying disease cannot be reversed e.

chronic renal failure or unresectable neoplasia. Fox LE, Rosenthal RC, Twedt DC et al. Plasma histamine and gastrin concentrations in 17 dogs with mast cell tumors.

Vet Intern Med. Liptak JM, Hunt GB, Barrs VRD, et al. Gastroduodenal ulceration in cats: eight cases and a review of the literature.

J Feline Med Surgery ; Penninck D, Matz M, Tidwell A. Ultrasonography of gastric ulceration in the dog. Vet Radiol Ultrasound ; A clinical trial is launched for a novel drug that could extend healthy lifespan in senior dogs. The first canine patient has been dosed in the study that aims to demonstrate an increase in longevity and quality of life in dogs treated with LOY Learn how technology can help interpret it for you.

Known as "The Street Vet," Kwane Stewart, DVM, has a passion for providing care to pets living with homeless individuals.

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At the New York Vet Show, Dr Andrew Rosenberg shares why these tests are key in dermatologic diagnostics. Fetch Coastal lecturer Liza Wysong, BAS, RVT, VTS CP-CF, SAIM , describes the discrepancies of this disease in dog and cat patients and the importance of an individualized approach.

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Animal Welfare. CBD in Pets. Clinical Pathology. Equine Medicine. Feline Medicine. Fish Medicine. Food Animals. Infectious Diseases. Internal Medicine. One Health. Pain Management. Poultry Medicine. Preventive Medicine. Respiratory Medicine. Shelter Medicine. Important: Steroids and NSAIDs should almost never be used in combination.

There are rare cases such as autoimmune diseases where high doses of steroids will be used with very low doses of aspirin, but these are specific conditions. In most cases, the two should never be administered together. Doing so significantly increases the risk of life-threatening ulcers.

It is also crucial to remember not to administer over-the-counter products to your dogs. Ibuprofen, naproxen, meloxicam, ketorolac, and aspirin are all human NSAIDs.

These can be extremely toxic to dogs, leading to gastric ulceration and kidney failure. Endocrine disorders. If your dog has either of these conditions, your veterinarian should be on the lookout for gastric ulcers.

Acute and chronic kidney disease. As kidneys fail, the body loses its ability to rid itself of toxins. Gastric acid levels go up, leading to ulcers. The signs of kidney disease can be exactly the same as that of ulceration, so treatment for both is usually started.

Mast cell tumors are common in Boxers and other breeds. They secrete histamine responsible for allergic reactions , which increases gastric acid secretion and predisposes to ulcers. Gastrinomas are tumors found in the stomach and will also release large amounts of gastric acid.

Other, less common causes. These include liver disease, inflammatory bowel disease, foreign bodies, and ingestion of caustic materials. If your dog has symptoms of gastric ulceration, the first step is consulting with your veterinarian. A thorough physical exam and diagnostics are needed to rule out many of the above causes.

This will include a nose-to-tail physical and bloodwork such as a complete blood count and a chemistry panel. Findings may include anemia and low proteins from blood loss though the ulcer and an elevated blood urea nitrogen BUN.

In some cases, white blood cell counts may be elevated in response to inflammation. Other tests that your veterinarian may be able to do include a barium study and abdominal ultrasound. In a barium study, a large amount of bright contrast is given to a dog by mouth.

Radiographs are taken immediately and then at various predetermined intervals. The barium shows up bright white on x-ray. It can show defects in the stomach. Ultrasound can also be used to evaluate for ulcers, although they can be very difficult to see.

If a stomach mass such as a gastrinoma is causing the ulceration, then ultrasound may be able to identify it. Specialized testing can more definitively diagnose an ulcer. Generally, you must be referred to a specialist for an endoscopy, which will be done under anesthesia.

Frequently small samples are taken biopsy for definitive diagnosis. The results can take one to two weeks. Treatment for gastric ulceration depends on the underlying cause. If one is not found, then general treatment includes antacids, a bland diet, and gastroprotectants such as sucralfate.

The major classes of antacids are proton pump inhibitors PPIs and H2 blockers. Both work in slightly different ways to lower gastric acid production.

Famotidine Pepcid is an H2 blocker, while omeprazole and pantoprazole are PPIs. Carafate sucralfate is another drug frequently used in the management of ulcers. It is a soothing agent that coats ulcerated areas.

It is given as a tablet dissolved in water a slurry. It can be give up to three times a day for relief of discomfort.

Other approaches may include a bland diet such as boiled chicken and rice. Probiotics can be added to food to maintain normal GI flora populations. Slippery elm and ginger may have some positive effects on GI ulcers, as well.

Perforated stomach ulcers are severe, life-threatening emergencies. A perforation occurs when the ulcer has eroded completely through all four layers of the stomach or intestine.

This allows leakage of bacteria-laden stomach and intestinal fluid into the abdominal cavity, leading to massive inflammation, infection, and sepsis. Treatment for perforated ulcers includes stabilization of shock and infection followed by surgery to repair the ulcers.

Prognosis varies and depends on the underlying cause. For uncomplicated ulcers and ulcers related to H. pylori, prognosis is good with appropriate treatment. It is important to know that they can recur. Discontinuation of NSAIDs and steroids when possible will improve the prognosis for cases related to these medications.

In the case of perforated ulcers, prognosis is guarded. Really interesting information. Our female labrador is on NSAIDs for arthritis, and now Omeperazole for reflux and suspected ulcers. Very helpful, thanks! Very informative article. My 17 month old Rottweiler was diagnosed with pancreatitis and was on 4 different meds, 2 of which you stated in the article.

She had several of the same symptoms, after following the Drs. orders for 5 days she now has to be on special food. I wonder if the pancreatitis will return.

We rushed her to the vet as soon as the symptoms started. Anyone have some advice to keep her healthy, please let me know. Our dog was diagnosed with pancreatitis as well. I also have veterinarian proscribed probiotics if I see any changes in her poo.

I have a five-year-old Boerboel who for the last three years has had weekly episodes of hypersalivation with lots of licking, belching, and drooling. These episodes frequently last for up to four hours during which time she loses a ridiculous amount of fluid through salivation.

She has a great appetite, her poo is light-colored and consistent from day to day, and she never seems to be in pain. They seem more frequent during the winter months, than the summer months. Anybody have any suggestions? My almost 11 year old Lab has had similar symptoms on and off. He drips tons of saliva and licks his lips.

We thought it may be triggered by stress but it seems to occur more frequently after a meal. Today we brought him to the vet to get a full blood work up and check his pancreas.

We are awaiting the results. In the meantime, the vet has prescribed omeprazol and misoprostol to treat a possible ulcer. Good luck with Mavis.

Gastro duodenal ulcers preventikn ulcers are relatively Ulcer prevention in pets in humans, inn potentially in dogs. Subjective symptoms are Amplitude training adaptations recognized and Ulcer prevention in pets discomfort heartburn sends people reaching for antacids and ln blocking Organic herbs and spices. Using special instruments called endoscopes, doctors can easily see the lining of a stomach and small intestine to confirm an ulcer. While we tend to blame stress and anxiety for these ulcers, there is also an infectious component Helicobacter pylori to gastric ulcers in humans. Smoking and alcohol consumption can also play a role in people. In dogs, the primary culprit is Non Steroidal Anti-Inflammatory Drugs NSAIDS. Preventoon stomach Ulcer prevention in pets a key initial role in digestion through its mixing actions, preventtion through the secretion of gastric Ulcer prevention in pets and pepsin, which are important for the activation Ulcfr key Body composition testing enzymes. The gastric epithelium is remarkably resistant to the deleterious effects of low pH because of the presence of a number of protective forces that prevent acid-induced injury. Secretion of gastric acid is under control of central and peripheral neurological and hormonal stimuli. Peripherally, the important mediators of gastric acid secretion are acetylcholine, gastrin and histamine. Gastrin is released from G cells in the antral mucosa, and histamine is secreted by enterochromaffin cells in the gastric glands.

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