Gastroenterology Flashcards
What is regurgitation?
Expulsion of food/water from pharynx/ esophagus. May be difficult to differentiate from vomiting or expectoration (respiratory tract expulsion) characteristics of regurgitation: no prodromal signs, no retching, no bile, can occur due to dysmotility of pharynx/esophagus or physical obstruction, can ask owner to record video. Causes - congenital - vasulcar ring anomaly, megaoesophagus, hiatal hernia. Acquired obstructive causes - foreign body, stricture, neoplasia, Intraluminal:carcinoma, leiomyoma, sarcoma. B) Extraluminal: thyroid carcinoma, pulmonary carcinoma, mediastinal lymphoma. Acquired causes of Dysmotility - esophagitis; gastroesophageal reflux, foreign body, caustic ingestion, recurrent vomiting, focal or generalised myasthenia gravis, hypadrenocorticism, myopathy/neuropathy = a) botulism, tetanus, lead, idiopathic, dysautonomia.
What is dysphagia?
difficulty eating/swallowing
May include/exaggerated swallowing, food or water falling out of the mouth, gagging when swallowing. Causes: oral pain: bone/teeth fracture, dental disease/abscess, inflammation of oral pharyngeal tissues, oropharyngeal mass: tumour, granuloma, foreign body, nasopharyngeal polyp. Trauma: to bone or soft tissue structures, neuromuscular diseasE: focal myasthenia, masticatory myositis, TMJ disease, cricopharyngeal achalasia, tick paralysis, rabies, tetanus, botulism, CNS disease.
What is vomiting?
Differentiate from regurgitation: prodromal signs might be present (hypersalivation, nausea, lip smacking) , retching, abdominal effort is component, bile may be present. Causes: dietary indescretion/acute gastroenteritis/foreign body, gastric dilatation or volvulus, infectious enteritis, parvovirus, haemorrhagic gastroenteritis, parasitic, toxic ingestion, side effects of drugs, gastric ulcer, pyometra, diabetic ketoacidosis/ketosis, pancreatitis, peritonitis, hepatopathy, uraemia, hypadrenocorticism, seticaemia, inflammatory bowel disease, pancreatitis, neoplasia, benign yloric stenosis, gastric antral mucosal hypertrophy, colitis, uraemia, hypoadrenocorticism, hepatopathy, diabetic ketoacidosis, hyperthyroidism, dysautonomia. Diagnostic plan: haematology/biochem/urinalysis/radiographs/parvo snap test/ PLI/ cortisol/ fecal analysis/ biopsies/ treatment trial.
What is hematemesis?
Blood in vomitus. May be frank or digested blood. Causes; gastroduodenal ulceration, NSAIDS, corticosteroid associated, sepsis/shock, neoplasia increasing gastric acidity: mast cell tumour, gastrinoma, neoplasia: adenocarcinoma, lymphoma, leiomyoma, yosarcoma, haemorrhagic gastroenteritis, foreign body, pancreatitis, uraemia, hepatopathy, hypoadrenocorticism, coagulopathy.
What is diarrhoea?
May be small or large bowel. Small bowel - weight loss, polyphagia, fecal volume increased, may see melena, vomiting. Large bowel diarrhoea - increased faecel frequency, may see mucous, hematochezia, dyschezia, occasionally vomiting with severe signs. Often times may present with mixed small and large signs. Causes: Dietary indiscretion, gastroenteritis, infectious - roundworms, hookworms, whipworms, salmonella, clostridia, campylobacter, E. coli, parvovirus, coronavirus, giardia, tritricomonas, coccidia, intussusception, Food responsive, dietary desponsive, inflammatory bowel disease, lymphangiectasia, neoplasia: lymphoma, adenocarcinoma, leiomyoma/sarcoma, histiocytic ulcerative colitis: boxers and french bulldogs, gunal, pancreatitis, hypoadrenocorticism, uraemia, hpetopathy, exocrine pancreatic insufficiency.
What is melena/hematochezia?
melena digested blood in faeces, source could be anywhere from oral to small intestine. Hematochezia is frank blood. source is distal colon/rectum. Causes - parvovirus, parasitic, haemorrhagic gastroenteritis, inflammatory bowel disease, neoplasia, ingested from oral, perianal fistulas, foreign body/trauma, uraemic ulceration, hepatopathy/portal hypertension, pancreatitis, coagulopathy.
Describe the diagnostic tests that can be done with GI disease
Haematology - mild to moderate neutrophilia may be present with chronic inflammatory conditions. anaemia of chronic inflammatory disease may be present with chronic inflammatory conditions. blood loss anaemia may be present with chorinc GI blood loss in ulceration neoplasia intestinal parasitism or IBD. eosinophilia may be present with intestinal parasitism or some forms of iBD. Albumin may be increased with dehydration,, albumin may be decreased with GI protein loss which can be a manifestation of IBD, food or antibiotic responsive diarrhoea, viral enteropathy, GI neoplasia or GI blood loss. cholesterol may be decreased with protein losing enteropathies. globulin may be decreased with PLE. hypocalcaemia can be seen with IBD. Urinalysis rules out kidneys as potential source o protein loss. Fecel floatation for detection of ova of roundworms, hookworms, whipworms, giardia, crypto.
What is masticatory muscle myositis?
An immune idiopathic condition of masticatory muscles which affects mostly middle age dogs. the clinical signs are dysphagia, difficulty in mastication, masticatory muscles may be swollen and painful or atrophied, mouth may be difficult to open. antibody titer to 2m fiber, muscle biopsy of temporalis or masseter muscle can confirm. Immunosuppressive drugs including prednisolone 1-2mg/kg/day, initially daily then every other day. Usually good response to treatment. May need feeding tube.
What is cricopharyngeal achalasia/asynchrony?
Usually congenital. lack of coordination of contraction of pharynx with food bolus and relaation of upper oesophageal sphincter at the cricopharyngeus muscle. with achalasia the cricopharyngeal muscle remains constricted. with asynchrony, relaxation of the cricopharyngeal muscle occurs not concurrently with food bolus propulsion. Signalment: young dogs, genetic in golden retrievers. Clinical signs: dysphagia, exaggerated swallow, pharyngeal regurgitation, aspiration possible, depending upon severity weight loss may occur. Fluoroscopic examination during barium swallow oesophagram is diagnostic. Severeal treatments have been attempted with mixed response. Myotomy of cricopharygeal muscle may be effective in some patients. Injection of botulinum toxin into Cricopharyngeal muscle may also be effective but may need to be repeated. In refractory patients feeding tubes can be placed long term.
What is pharyngeal dysphagia/dysfunction?
Usually acquired disorder that occurs secondary to neuropathy or myopathy of various causes. Includes lesions of cranial nerves required for normal swallowing. Normal food bolus is not propelled by the pharynx caudal into the oesophagus normally. disorders causing this condition may also concurrently cause oesophageal dysmotility. ateiologies: focal myasthenia gravis, botulism toxicity, lead poisoning, acquired neuropathies and myopathies. Usually seen in middle aged to older dogs, occasionally young dogs depending upon etiology. clinical signs are same as cricopharyngeal achalasia. Diagnosis with oesophagram. Treat eatiology. May need feeding tube.
What is congenital megaesophagus?
Seen in young dogs or older patients with mild signs since birth. miniature schauzers, Great Danes, dalmations predisposed. Signs: regurgitation, weight loss, signs of aspiration pneumonia. Thoracic radiographs will show generalised esophageal dilation plus aspiration pneumonia potentially. May be mild to dramatic cranial esophageal dilation.Cisapride may ameliorate signs of concurrent Gastroesoophageal reflux. No definitive treatment for megaeosophagus. More mild cases can be managed by feeding soft food from elevated platform and keep pet upright for 20-30 minutes after each meal.
What is acquired megaoesophagus/eosophageal dysmotility?
Usually due to underlying neuropathy/myopathy/junctionopathy, most commonly associated with myasthenia gravis. other neuromuscular causes include lead toxicity, tetanus, botulism, dermatomyositis in collies, dysautonomia in cats, hypoadrenocorticism. Oesophagitis of any etiology can also lead to esophageal dysmotility. Cough may also occur due to esophageal reflux of gastric contents to larynx/pharynx. thoracic radiographs show generalised or focal esophageal dilation. aspiration pneumonia may be present. Screening for underlying diseases including MG titers, lead levels, baseline cortisol, ACTH stim test.
What is esophagitis?
Inflammation of the esophageal mucosa. can occur secondary to something ingested such as a foreign body, caustic agent or drug also may occur with disease causing Gastroesophageal reflux such as a hiatal hernia or duriing anaeesthesia. also occurs with persistent vomiting or increased gastric acidity. any age breed species. cats more sensitive to doxycycline induced esophagitis so should be administered with food or coated with butter and followed with water. clinical signs: regurgitation, cough, may also see anorexia, increased salivation. Often presumptive based on supportive clinical history. may be subsequent megaoesophagus Treat with depressing acid production with a proton pump inhibitor PPI. Cisapride may decrease reflux events. Sucralfate can protect esophageal mucosa and provide pain relief. surgical treatment of hiatal hernias may be warranted.
What is a hiatal hernia?
Congenital abnormality of the diaphragm that allows prolapse of the cardiac region of the stomach through the diaphragm into the thoracic cavity, leading to eosophageal reflux, may be acquired due to trauma or condition that results in increased abdominal pressure. Young animals, shar peis and bulldogs predisposed. milder cases may appear later. regurgitation, cough, thoracic radiographs may show hernia, especially when pressure on the abdomen is applied. Esophagram or Esophagoscopy may be needed. usually good prognosis with surgery. otherwise treat eosophageal reflux as with eosophagitis - PPI and prokinetics.
What is dysautonomia?
Loss of autonomic nervous function due to unknown etiology. Mostly in cats. clinical signs include regurgitation, dysuria bladder distension, mydriasis, lack of PLR, dry mucous membranes, weight loss, constipation, vomiting, anorexia. Diagnosis with dilation of intestines on radiographs, confirmation of pupil constriction with pilocarpine in one eye or response to b ethanevol. Palliative treatment with bethanecol for urinary signs and prokinetics for GI signs. poor prognosis.
What is vascular ring anomaly
Congenital defect, persistent right aortic arch, regurgitation, possibly aspiration pneumonia. Thoracic radiographs showing cranial esophageal dilation with normal caudal esophagus with focal narrowing at heart base. Barium may be administered to confirm. Esophagoscopy will provide definitive diagnosis.
What is an esophageal foreign body?
Any ingested object that becomes lodged in the esophagus. Clinical signs: regurgitation, anorexia, drooling. If concurrent esophageal perforation may see signs of pneumomediastinum and pneumothorax. May see foreign body on thoracic radiographs if radiopaque, barium swallow may confirm, esophagoscopy may be needed for diagnosis and allows for attempt at non invasive removal of object. Ideally endoscopic removal of object. If foreign body is chronic or esophageal perforation is present, thoracotomy with esophageal resection and anastomosis may be required. after removal of object, treatment with sucralfate and PPIs are recommended to prevent secondary stricture formation. More chronically affected patients or patients with more mucosal damage are more predisposed to complications such as esohageal perforation and strictures.
What is an esophageal stricture?
A stricture in the esophagus is a fibrous band of tissue that causes mild to marked narrowing of the esophagus. there can be one stricture or several. strictures can form secondary to anything that damages the eosophageal mucosa and is most frequently described secondary to reflux under anaesthesia, secondary to foreign bodies or as sequelae to medication (doxycycline and clindamycin). Regurgitation, aspiration pneumonia. Treatment - dilation of the stricture with multiple balloon dilations several days apart until stricture is wide enough that clinical signs are manageable. Gastric feeding tubes may be necessary or liquidized/blenderized diet.
What is acute gastritis?
Acute inflammation of the gastric mucosa, usually due to dietary indiscretion or drug reaction, signs:acute vomiting, anorexia, abdominal pain, usually presumptive diagnosis based on acute presentation, history of dietary indescretion, absence of other causes of vomiting and response to symptomatic care. abdominal radiographs/ultrasound helpful to detect concurrent foreign body. Minimum database can b e used to rule out underlying metabolic distrubances. Discontinue any potentially offending medication, symptomatic care with bland diet, H2 antagonist or PPI, antiemetic such as maropitant, if no response to symptomatic care in a day or two more investigations should be undertaken.
What is haemorrhagic gastroenteritis?
Unknown etiology but likely that more marked inflammation of the gastric and intestinal mucosa results in profuse hematemesis and or hematochezia. Clostridium has been implicated but not proven to be associated. Dogs more than cats, small breeds more commonly affected, Acute vomiting, hematemesis, dehydration. minimum database usually shows hemoconcentration with normal total protein which is highly suggestive in a patient with acute hematemsis. Patients may also exhibit mild to moderate thrombocytopaenia due to blood loss and prerenal azotaemia. renal failure and DIC may be detected in severely Hypovolaemic patients. Fluid resuscitation as appropriate, patients may be Severely hypovolaemic and need aggressive supplementation. Oncotic support may be appropriate. broad spectrum antibiotics usually given for possible bacterial translocation. Good prognosis as long as fluid resuscitation is Sucessful and secondary organ damage from hypoperfusion is avoided.
What is idiopathic inflammatory gastritis?
This form of chronic gastritis includes infiltration of the gastric mucosa with various types of inflammatory cells, most frequently lymphoplasmaytic, lymphocytic, granulomatous or eosinophilic without an obvious underlying cause for inflammation. Chronic vomiting, anorexia, Endoscopic or surgical biopsies required to definitively diagnose. Gastric parasitism should be ruled out. /nat ve responsive to hypoallergenic diet, usually a hydrolyzed protein diet, cases that are refractory to dietary therapy may require immunosuppresive doses of corticosteroid and then tapered to lowest effective dose Acid suppressant medications such as famotidine may help to control clinical signs. Eosinophilic gastritis typically responds best.
Describe a gastric foreign body
Ingestion of foreign object could either cause signs compatible with acute gastritis or gastric outflow obstruction. As with acute gastritis or gastric outflow obstruction. May be acute or chronic. abdomiinal radiographs or ultrasound may demonstrate presence of foreign object. Endoscopy or surgical exploratory or surgical exploratory may be needed to confirm. there may be ulceration or damage to gastric mucosa that may need addressing. Surgical removal of foreign body, endoscopically or surgically. typically excellent, depending upon chronicity and damage to gastric mucosa.
What is gastric dilatation/volvulus?
Unknown what leads to ultimate gastric dilation and volvulus but it is breed related and dependent upon body confirmation. the stomach dilates excessively with gas and may twist on its axis. may also incur splenic torsion. this results in compromised vascular return and can lead to decreased cardiac output, shock and death. additionally, decreased blood supply to the stomach and or spleen may result in gastric wall necrosis and splenic infarction. Most commonly middle aged deep chested dogs. Acute retching, often non productive, abdominal distension, panting, abdominal pain, lethargy, collapse. History and clinical signs typically supportive of diagnosis. a single lateral abdomen may be taken for confirmation. Immediate treatment with aggressive fluid resuscitation is often required. Immediate gastric decompression including passage of a orogastric tube or trocarization of the stomach with a needle. systemic antibiotics should be adminstered. surgery for necrotic gastric mucosa/infarcted spleen or a gastropexy performed
What is gastroduodenal ulceration/erosion?
When there is a breakdown in the normal gastroprotective mechanisms of the mucosal layer, the acid in the gastric lumen can damage the underlying mucosal layer causing erosions and ulcerations. one of the most comon causes is NSAIDs which inhibits gastroprotective prostanoids. Other causes include steroid administration, shock/sepsis, liver disease/portal hypertension, uraemic ulceration and neoplastic diseases such as lymphoma, mast cell disease, gastrinoma and adenocarcinoma. Signs include vomiting, abdominal pain, hematemesis, arnoexia, may be acute or chronic, ulceration can occur with relatively mild signs and persistent use of nsaid in an anorexic patient may lead to gastrointestinal perforation. If suspected dogs are treated symptomatically for presumptive ulceration. Surgical exploration and resection of the ulcer is indicated. Medical management in less severely affected patients includes treating the underlying cause if possible, along with acid suppressing medications. Omeprazole increases gastric ph to allow for healing. Sucralfate binds to exposed ulcer bed and promotes healing
What is helicobacter gastritis?
Helicobacter is is often a normal inhabitant. however in some it triggers chronic gastritis that seems to respond to treatment for helicobacter. symptoms are chronic vomiting, anorexia, nausea, weight loss. Combination therapy with metronidazole amoxicilin bsmuth salicylate or famotidine has been used to ameliorate symptoms.
What is parasitic gastritis?
Physaloptera rara (dogs) and ollulanus tricuspis (cats) cause chronic vomiting. may see worms in vomitus. otherwise may see parasite during endoscopic examination. In suspected cases with exposure, response to empiric traetment may provide presumptive diagnosis. For physaloptera, pyrantel pamoate or ivermectin, for ollulanus, fenbendazole may be effective.
What is pyloric stenosis?
The muscles of the pyloric sphincter become hypertrophied due to an unknown cause but potentially related to gastrin. Most frequently brachycephalic dogs and siamese cats, usually younger animals. vomiting soon after eating, may be projectile. hypochloremic metabolic alkalosis may occur secondary to loss in vomitus of hydrochlorid acid. Gastric outflow obstruction is confirmed using barium contrast abdominal radiographs, abdominal ultrasound or endoscopy. Biopsies should be taken to confirm lack of infiltrative disease. Treat with surgical pyloroplasty.
What is gastric antral mucosal hypertrophy?
Excessive mucosal thickening at the pylorus (versus submucosal/muscular thickening of pyloric hypertrophy). The underlying cause of hypertrophy is unknown. Signalment: small breed dogs. As with pyloric hypertrophy signs consistent with gastric outflow obstruction. Surgical examination of the pylorus, thickened mucosa will be visible. biopsies should be taken to rule out infiltrative disease. surgical pyloroplasty and mucosal resection needed. excellent prognosis with surgical treatment.
What is acute enteritis?
Acute inflammation of the intestinal mucosa, usually due to dietary indiscretion or drug reaction. May also include sudden changes in diet. Acute vommiting/diarrhoea, anorexia, abdominal pain, may be small or large bowel diarrhoea depending on section of intestine affected, may also see hemetochezia, tenesmus or mucous in feces with acute colitis, usually presumptive diagnosis based on acute presentation, absence of other causes of vomiting and response to symptomatic care. rule out foreign body and underlying metabolic disturbances. discontinue any offending medication, feed bland diet, give h2 antagonist or PPI, antiemetic such as maropitant, no response to symptomatic care in a day or two - more investigation, fluid therapy may be needed.
What is dietary responsive diarrhoea?
This is generally considered the mildesst in the inflammatory bowel disease spectrum. most likely related to a food related hyper sensitivity causing inflammation in the intestinal mucosa. usually middle aged to older dogs and cats. chronic vomiting and diarrhoea. could include weight loss and hypoalbuminaemia though patients more mildly affected than with IBD. may be small or large bowel diarrhoea. patients may exhibit signs of atopic dermatitis. Diagnosis of dietary responsive diarrhoea is made presumptively based on a history of chronic GI signs and response to dietary therapy with an elimination diet, typically a hydrolyzed protein diet. Treatment is strict feeding of hydrolyzed protein diet. if these diets are not palatable other novel protein diets may be tried. response typically seen within weeks.
What is antibiotic responsive diarrhoea?
Diarrhoea may be responsive to antibiotics without a confirmed overgrowth of bacteria. Due to various environmental and genetic facotrs, there is a derangement in the normal GI flora , favouring a more pro inflammatory population of bacteria. This results in secondary inflammation in the intestinal mucoa. Presumptive diagnosis made based on response to antibiotic therapy. treatment is with broad spectrum antibiotics with aerobic and anaerobic coverage. treatment with Tylosin or metronidazole is most effective. these antibiotics amy have some immuno modulatory properties as well. there may be better response to one over the other so courses of each should be attempted. Good prognosis for responders.
What is inflammatory bowel disease?
Idiopathic inflammation of the gastrointestinal mucosa that may affect any segment of the intestine. likely a result of a complex series of factors including patient susceptiility, gut microbiome and diet. Lymphocytic plasmacytic infiltration of the intestinal mucosa is most frequently described. eosinophilic infiltration may also be present. chronic vomiting and diarrhoea seen. may also see weight loss, loss of protein into the gut (protein losing enteropathy), if protein loss is severe> may develop ascites or be at risk for thromboembolic disease due to loss of anti coagulant proteins into the gut. Rule out all other causes of inflammation. Confirm infiltrative inflammatory cells by biopsy. Small cell lymphoma appears very similarly. Immunosuppressive doses of prednisolone. Refractory cases may be treated additionally with azathioprine or cyclosporine.
What is intestinal lymphangiectasia?
Obstruction of the lymphatic system of the intestinal mucosa causes lacteal dilation and rupture with secondary inflammation. Subsequent proteins and fats leak into the intestinal submucosa and lumen and may lead to granuloma formation. because lymphocytic plasmacytic inflammation occurs secondary ot IL, and primary inflammatory diseases such as IBD can lead to secondary lacteal obstruction, can be difficult to differentiate from IBD. Presence of diarrhoea is varable but will be small bowel and chronic if present.w eight loss typically occurs. ascites may be present. typically panhypoproteinaemic and hypocholesterolaemic. hypocalcaemia and lymphopenia also fairly common. Faecel a-1 protease inhibitor quantification in the feces may be consistent with intestinal protein loss but is not specific for intestinal llymphangiectasia. abdominal ultrasound may show a thickened mucosal later with hyperechoic mucosal striations. ultimately biopsies are required for diagnosis either via full thickness biopsy by laparotomy or endoscopic biopsies. dilated lacteals may be seen as white dots on the mucosal surface. it is difficult to differentiate between primary intestinal llymphangiectasia and primary IBV. lower fat, hydrolyzed protein diets suc as hills or purina are indicated. if primary lymphangiectasia truly suspected, a non hydrolyzed fat restricted diet may be tried. diets must not be calorie restricted. glucocorticoid therapy also recommended.
What is intestinal foreign body/ obstruction?
Any ingested object that is too large to pass may cause intestinal obstruction. most common area is ileo caecal junction but any small intestinal segment may be affected. linear foreign bodies may also cause obstruction. May include vomiting, diarrhoea, abdominal pain, or may be minimal - anorexia, decreased appetite. signs are usually acute but intermittently obstructive foreign bodies may cause more chronicity to signs. if perforation occurs more severe signs of systemic disease may develop such as shock, collapse, hyptension, distended or plicated loops of owel. Check under tongue in cats. Abdominal radiographs may show two populations of bowel or markedly distended bowel. linear foreign bodies may appearas bunched, plicated bowel. abdominal ultrasound may also show segmental intestinal distension. foreign bodies may also be visualised. exploratory laparotomy may be required for diagnosis, if hypochloremic, metabolic alkalosis is noted on pre anaesthetic bloodwork, this is supportive of gastric outflow obstruction. complete intestinal obstructions typicaly considered surgical emergencies, so relief of obstruction before perforation or devitalization of bowel. IV fluids and stabilisation of patient usually warranted.
What is intussusception?
One segment of bowel telescopes into adjacent section resulting in intestinal obstruction. can be intermittent or persistent. ileocolic intussusceptions are most common. most frequently seen as a complication of acute enteritis. more frequent in young dogs/puppies with acute enteritis of various etiologies. diarrhoea with/without melena or melatochezia, vomiting , abdominal pain, may see Hypoalbuminaemia due to mucosal congestion. elongated tubular structure may be palpable. Abdominal ultrasound more sensitive than radiograph. surgical reduction requited or intestinal resection and anastomosis. sometimes surgical plication performed.
What is canine parvovirus?
Canine parvovirus 1 is relatively non pathogenic, may affect puppies 1-3 weeeks, canine parvovirus 2 causes classic parvovirus, feline parvovirus caused by feline panleukopenia virus (cats can be infected with canine parvovirus) virus attacks crypt cells of intestinal villus causing villus atrophy and collapse. usually puppies and kittens or poorly vaccinated/unvaccinated animals. dobermans, rottweilers, stafs, labs, GSDS. Signs develop 5-12 days after infection, include moderate to severe diarrhoea, inestinal bleeding, vomiting , secondary bacterial translocation, may become severely hypoprotinaemic, neutropenia, fever and septic shosck. In utero infections can cause cerebellar hypoplasia in cats. ELIA for CP2 in feces most sensitive. shedding may be undetectable within 10-14 days of infection. shedding time for feline parvo only a couple of days. Treatment: IV fluids, electrolytes, supportive care, anti emetic therapy, acid suppressant therapy, H2 antagonists or proton pump inhibitors, broad spectrum antibiotic, potentiated amoxicillin or cephalosporin, Plasma indicated in cases of moderate to severe hypoalbuminaemia. Intussusception reported as a sequealae. Recovered patients should be isolated. virus may persist in environment.
What is coronavirus?
Coronavirus infects mature epithelial cells at the villus tip, so signs are less severe than with parvovirus. there is also no effect on bone marrow. as with parvovirus signalment. rarely causes haemorrhagic diarrhoea. similar signs but milder than parvo. signs last 1-2 weeks. usually not definitively diagnosed but treated symptomatically. symptomatic care including IV fluids, anti emetics and nutritional support.
What is campylobacter diarrhoea?
Campylobacter jejuni and upsaliensis are most common. noramally found in intestinal tract of dogs and cats but can also cause typically large bowel diarrhoea. usually animals younger than 6 months in group housing, also seen in dogs with raw food diet or immunosuppressed patients. mucoid diarrhoea, ocasionally haemorrhagic, sometimes also causes arnoexia or fever, usually self limiting but can cause more chronic diarrhoea. May see commas or seagull shaped organisms on direct fecal smear but normal gut inhabitant so not diagnostic for campylobacter. PCR of feces can also be performed in suspect patients where organisms are not visualized. erythromycin is most effective. B lactams are not effective. Treat past resolution of clinical signs but bacteria often not eradicated and signs may recur. good prognosis but may be difficult to clear. humans may be infected so proper disposal of feces essential.
What is salmonellosis?
Salmonella typhimurium most commonly associated with disease. may be from animals shedding or contaminated/underocoked food. Any dog or cat. young a nimals may be more severely affected. Diarrhoea is usually small bowel, may be acute or chronic. more severely affected patients may become septic and neutropenic. vomiting is not common. salmonella may be cultured from feces. (not definitive) culture from blood (sterile) would be definitive for salmonella septicaemia. Can see co infections with parvovirus. Supportive care as indicated - fluids, electrolyte supplementation as indicated, Antibiotics should not be used unless patient is septicaemic because may prolong shedding/induce a carrier state. septicaemic patients should be treated with parenteral antibiotics, ideally based on sensitivity pattern. Fluoroquinolones, potentiated sulfonamides, amoxicillin and chloramphenicol usually effective. patients should be isolated and barrier nursed.
What is clostridial diarrhoea?
Clostridium perfringens and C. difficile most commonly cause diarrhoea but also carried in normal feces of dog. C perfringens diarrhoea requires production of enterotoxin type A. C perfringens with enterotoxin may cause acute Haemorrhagic diarrhoea or chronic small or large bowel diarrhoea (more frequently large). C. difficile is typically large bowel diarrhoea, often after antibiotic therapy. Clostridial organisms can often be found on fecal smear but are not diagnostic for pathogenic infection. clostridial toxin assays are available but enterotoxin may be intermittently shed in chronically affected patients. May resolve spontaneously. Tylosin or metronidazole are usually effective. Some patients may need intravenous fluids.
What is granulomatous colitis?
Also known as histiocytic ulcerative colitis. this syndrome is caused by adherent and invasive E. coli which causes granulomatous inflammation of the colonic mucosa.Most frequently reported in boxers, also in french bulldogs, border colies, any breed. chronic large bowerl diarrhoea which may include hematochezia, tenesmus, mucus. endoscopic biopsies of the colon show granlulomatous /histiocytic inflammation. identification of adherent E. coli requires fluorescent in situ hybridization. Compatible breed, clinical signs and response to therapy adequate for presumptive diagnosis. Fluoroquinolones treatment of choice and usually result in improvement in clinical signs within days. Development of resistant E. coli strains so suspected patients that are non responders should have FISH performed for confirmation of E. coli before immunosuppressive therapy is attempted. culture of mucosal biopsy may be helpful for sensitivity testing.
What is giardiosis?
Ingestion of giardia sp cysts from infected animals, especially in water. Seen in any age dog, especially that drinks water from environmental sources. outdoor cats though more common in dogs. mild to severe diarrhoea, usually small bowel but large bowel signs possible. weight loss possible. co infections may be seen with other parasites. most sensitive technique is ELISA of feces for giardia proteins. Trophozoites may be visible on zinc sulfate flotation. metronidazole is often effective. Fenbendazole and albendazole also effective. resistance and reinfection may occur so environmental decontamination should be performed. Good prognosis but some difficult to resolve due to resistance or reinfection.
What is cryptosporidiosis?
Ingestion of cryptosporidium parvum oocysts which are from other infected animals but may be in contaminated water. affected dogs are usually less than 6 months old. cats of any age may be affected. usually chronic or intermittent small bowel diarrhoea and may include anorexia and weight loss. may be asymptomatic. oocyte may be seen using acid fast stain of direct fecal smear (very small organism), need 1000x power. ELISA is more sensitive. PCR is also available and is the most sensitive test. No reliable treatment. Paromomycin has been used with success but associated with renal failure in cats and may not stop shedding. may be self limiting infection. puppies with infection may be euthanized for lack of response. Puppies with refractory infections carry more guarded prognosis.
What is trichomoniasis?
Tritrichomonas foetus colonizes surface of colonic mucosa. seen in cats, especially young cats in group housing. Large bowel diarrhoea without other systemic signs, may be self limiting after several months. trophozoites may be seen on direct fecal examination (appear similar to giardia trophozoites). Tritrichomonas can be detected with greater sensitivity by fecal culture. Co infections can occur. Ronidazole is effective but can cause neurologic signs. infections may be self limiting though can recur in times of sterss. generally good prognosis but cats can be chronic carriers.
What is coccidiosis?
Isospora are ingested (fecal-oral route) and infective oocysts destroy epithelium. Seen in young dogs and cats especially in group housing. may be asymptomatic in older patients. mild to severe large bowel diarrhoea, occasionally haematochezia. oocysts may be detected via fecal floatation. treat with sulfadimethoxine or trimethoprim sulfa for 10-20 days.
What are whipworms?
Trichuris vulpis is transmitted via fecal oral route. usually dogs, cats are rarely infected and generally more mildly. large bowel diarrhoea, mild to severe, which may be haemorrhagic. may also include hypoproteinaemia, hyponatraemia & hyperkalaemia so can mimic hypoadrenocorticism. Multiple fecal floatations may be needed to detect ova. Multiple anthelmintics are efficacious. fenbendazole may also be used, among others. treatment with fenbendazole is recommended in any patient with chronic large bowel diarrhea.
What are roundworms?
Toxacara canis (dog and cati (cat) and toxacaris leonina (dog and cat ) are infectious via fecal oral route. amy also be transplacental. (t canis) or trans mammary (t Cati). seen in young dogs and cats. small bowel diarrhoea, stunted growth, potbelly appearnce, poor hair coat and lack of weight gain in puppies and kittens. with severe worm burdens, intestinal obstruction may occur. roundworms may occasionally be found in vomitus. ova are generally readily found on fecal floatation though transplacental migration may result in infection prior to shedding of ova. pyrantel is effective and safe in young patients. other anthelmintics also effective – repeated treatment at 2-3 week intervals recomended. Puppies & kittens should be dewormed at 2,3,4,8,12 and 16 weeks of age. Treat pregnant bitches with fenbendazole at day 40 to 2 days post whelping to reduce transmission.
What are hookworms?
Acylostoma caninum is transmitted via fecal oral route or occasionally via skin penetration. adult worms attach to small intestinal mucosa and ingest blood and mucosa. young dogs most frequently are affected. cat infections are uncommon. older dogs are rarely affected. transcolostral infection is possible. Melena,hematochezia, diarrhoea, stunted growht,a naemia. Fecal floatation is usually dianostic. puppies affected via colostrum may suffer severe disease before ova are shed. in these patients strong suspicion of infection can be made via compatible clinical signs and presence of iron deficiency anaemia. multiple anthelmintics may be used, including pyrantel and fenbendazole. blood transfusions may be necessary in severely anaemic patients. moxidectin treatment of bitches at day 55 reduces transcolostral infection. humans may be affected by environmental contamination and may develop visceral larval migrans so environmental contamination and appropriate handling of feces is essential. regular use of dewormer reduces infection rates. good prognosis but more guarding in severely anaemic younger animals.
What are tapeworms?
Dipylidium caninum is most common but taenia spp are also seen with wildlife exposure. mesocestoides spp and echinoccous spp may be infective. fleas and lice are intermediate host for D caninum. Flea infestation must also be treated for control. echinococcus is zoonotic. prognosis excellent.
What is short bowel syndrome?
Occurs with extensive surgical resection of the small intestine. (75-90%). the remaining small intestine is unable to absorb adequate nutrition from a normal diet and may develop small intestiinal bacterial overgrowth. an y patient with extensive intestinal resection and anastomosis prone. history of extensive intestinal resection, along with weight loss and small bowel diarrhoea. appetite is usually increased. signs are most severe after resection, but with time the remaining small bowel may be able to compensate and clinical signs may decrease with time. Treatment is dietary modification with a highly digestible, low fat diet. often homemade diets are initially appropriate such as with cottage cheese and potato. small frequent meals are often better tolerated. antibiotics such as tylosin or metronidazole can decrease small intestinal bacterial overgrowth.
What is constipation/megacolon?
The cause is typically idiopathic and unknown but s suspected to be related to changes in smooth muscle function. additional causes of constipation that may lead to Megacolon include: pelvic canal stenosis, nerve injury or manx sacral spinal cord deformity. Initial stages of idiopathic megacolon are constipation and obstipation, recovery of colonic function at these stages may still be possible. for true dilated megacolon cats, colonic function is usually permanently decreased. most commonly middle aged cats. DSH. siamese may be overrepresented. Reduced, painful or absent defecation. tenesmus may be noted. dilated colon with very firm feces may be palpable on abdominal palpation. cats may also become anorexic and dehydrated, vomit, or develop abdominal pain. Radiographs demonstrate dilation of colon or impaction of feces. pelvic and lumbar spine should be examined for abnormalities causing secondary constipation as well as observation for possible mass lesion causing obstruction. recommended treatment upon first presentation depends on severity of disease. for mild - one or more warm water or lactulose enemas along with oral lactulose or miralax is typically sufficient. Dehydrated patients should be treated with intravenous or subcutaneous fluids, as dehydration exacerbates disease. obstipated cats may need manual de opstipation, sometimes performed in several procedures. After initial treatment and relief of the colonic impaction, medical therapy may be attempted. dietary therapy witha low reside, modified fiber diet is advised, along with oral laxative therapy with lactulose or miralax. cisapride therapy may also benefit mild to moderately affected patients. cats with severe idiopathic megacolon are typically refractory and may require subtotal colectomy for control of disease.
What is a perneal hernia?
Upon weakening of the coccygeus and levator ani muscles, the rectum and other organs ocassionally are pushed externally through the pelvic canal. mostly older intact male dogs (esp boston terriers, boxers, corgis and pekinese) clinical signs:dyschezia and tenesmus which may precede the hernia. constipation and perineal swelling may also be seen. If the bladder has been herniated there may be signs of urinary obstruction. usually can be definitively diagnosed with rectal examination. radiographs can be used to confirm. if bladder is suspected to be herniated a catheter may be passed into the bladder gently and a small amount of contrast injected to confirm bladder herniation. if bladder is involved and urinary obstruction is present the bladder should be emptied and repositioned into the abdomen. IV fluids should be administered for post obstructive diuresis. Surgical reconstruction of the pelvic diaphragm is indicated. neutering is usually recommended at the same time to reduce possible benign prostatic hyperplasia and associated straining.
What is a perineal fistula?
Likely immune mediated and a subset of inflammatory bowel disease, but ultimately etiology is unknown. classically GSDs. hough similar breeds may also be affected. clinical signs - constipation, rectal pain, draining tracts around the anus may be seen. diagnosis is made via physical examination including a gentle rectal examination. sedation may be necessary due to pain associated. granulomas and abscesses may be palpable. treat as for IBD. hypoallergenic hydrolyzed diets beneficial. affected dogs often need immunosuppression, cyclosporine or azathioprine are recommended. tacrolimus topically also has been described. Antibiotics such as metronidazole may also be of benefit. many patients respond well. occasionally patients refractory to treatment and carry a more guarded prognosis. because the disease is primarily immune mediated, surgery is not curative and is not usually recomended.
What are the signs of pancreatic disease?
Anorexia, vomiting, diarrhoea (small or large bowel) abdominal pain, weight loss, lethargy, depression, dehydration, signs of systemic inflammatory response syndrome (abnormal blood pressure, heart rate, respiratory rate, temperature), bleeding with DIC.
What shows up on haematology on pancreatic disease?
Increased RBC count with dehydration, decreased RBC count with anaemia of chronic inflammatory disease (normocytic, normochromic). Stress or inflammatory leukogram causing neutrophilia, sepsis/SIRS causing neutropeina. Platelets - thrombocytopenia with severe pancreatitis/ DIC.
What appears on biochemistry With pancreatitis?
Elevated liver enzymes - primarily hepatocellular with neighbouring inflammation or cholestatic with biliary obstruction or some combination thereof. Azotaemia - pre renal from dehydration, renal with concurrent acute kidney injury from pancreatitis. Bilirubin and bile acids - may be elevated from biliary obstruction from pancreatitis. Amylase/lipase are not helpful in diagnosis.
What is present in urinalysis with pancreatitis?
Concentrated with dehydration, isothenuric with concurrent acute kidney injury. Prteinuria can occur with severe pancreatitis.
What is pancreatic lipase immunoreactivity -
available as canine CPLI or feline FPLI specific quantitive test or SNAP. highly sensitive and specific for pancreatitis - diagnostic of choice.
What is trypsin like immunoreactivity (TLI)
Quantification of trypsinogen and trypsin in systemic circulation - small amount normally leaks from pancreas to blood. Decreased with exocrine pancreatic insufficiency - must be on a fasted sample or may get falsely elevated reading, diagnostic of choice with EPI. May be increased with pancreatitis but less sensitive than PLI.
What is acute pancreatitis?
Inflammation of the pancreas occurs when normal protective mechanisms against premature activation of trypsinogen are overwhelmed. premature activation of trypsinogen within the pancreas results in digestion of pancreatic proteins and activation of more trypsinogen. This results in release of pro inflammatory crytokines with necrosis and in severe cases severe systemic inflammation. Can ultimately lead to multi organ failure and death. certain drugs have been associated with development of pancreatitiis, including potassium bromide, azathioprine, asparaginise. hypthyroidism, obesity, hyperadrenocorticism and diabetes melltius also thought to increase risk of disease. Mostly middle aged. dogs more often get acute. terrier and miniature schnauzers seem to be predisposed.
What are the clinical signs of acute pancreatitis?
There may be a recent history of ingestion of a very high fat meal or dietary indiscretion. clinical signs can vary from very mild to quite severe and can include abdominal pain, pray position, anorexia, dehydration, vomiting, and diarrhoea. more severe cases may have signs of SIRS, DIC or multi organ disease: collapse, shock, tachycardia, pale mucous membranes etc.
How is acute pancreatitis diagnosed?
Minimum database may show hemoconcentration with dehydration,neutrophilia +- left shift or neutropenia with SIRS/sepsis, hyper or hypoglycaemia with altered glucose metabolism, pre renal or renal azotaemia, elevated liver enzymes, hypokalaemia which if present suggests poorer prognosis, concentrated or isothenuric USD, possibly proteinuria. PLI, either SNAP or quantitive should be performed in suspect cases. abdominal radiographs typically unhelpful but may show decreased cranial abdominal detail and an air filled duodenum. Abdominal ultrasound is slightly more sensitive but still not as good as PLI. changes on ultrasound could include thickened hypoechoic pancreas with bright surrounding mesentery.
How is acute pancreatitis treated?
remove any inciting cause if possible/present. remainder of therapy consists of supportive care. IV fluids and electrolyte supplementation often indicated. pain management usually necessary given parenterally usually with an opiod. nutritional support should aso be provided, tube placement mabe necessary. if vomiting is difficult to contorl, trickle feeding of very small amounts continuously via syringe driver or fluid pump is usually slow enough to not stimulate vomiting and provide adequate enteral nutrition. dogs with refractory vomiting may require parenteral nutrition. once patients are eating voluntarily a bland diet easily digestible should be fed. multiple anti emetics may be required o for control of vomiting and gastroprotectants often indicated. antibiotic therapy usually given in severe cases because it is difficult to differentiate between sepsis and SIRS. Plasma transfusions are given to patients in DIC. if pancreatic abscesses are present, surgical debridement can improve outcomes. Mild cases of pancreatitis may be treated supportively as for acute gastroenteritis and self resolves in a couple of days. severe cases may require extensive supportive care and are at high risk for developing severe complications.
What is chronic pancreatitis?
The chronic form of pancreatitis can develop as an extension of acute inflammation that leads to permanent impairment of function or persistent low levels of inflammation. inflammatory infiltrates are usually mononuclear. chronic pancreatitis may occur as a primary autoimmune disease in english cocker spaniels. cats with chronic pancreatitis frequently also have inflammatory bowel disease, Cholangitis or both. More frequently seen in cockers and CKCS though siberian husky, collies and boxers are overrepresented as well. Generally waxing/waning or intermittent. signs can include bouts of anorexia, vomiting and abdominal pain, cats often just anorexic. chronic pancreatitis can lea too enough fibrosis to cause EPI or Dm so patients could present with corresponding clinical signs. inflammation/fibrosis may also induce signs of EHBO.
How is diagnosis of chronic pancreatitis made and how is it treated?
Overall findings with chronic pancreatitis are similar to acute disease, though changes are usually less pronounced so often difficult to diagnose. PLI still test with highest sensitivity but value typically not as high as with acute diseas.e minimum database changes may be consistent with DM or EPI. cobalamin should be measured in all cases. decreased intrinsic factor production with chronic pancreatitis can cause hypocobalaminaemia. biopsy needed for definitive diagnosis ultimately - but usually made with consistent clinical findings. Most with chronic disease will ahve intermittent flare ups or bouts of acute - should be managed as for acute. low fat diet may reduce acute episodes in dogs. cats maintained on highly digestible diet. cobalamin should be supplemented if indicated. periods of anorexia should be managed with feeding tube supplementation if necessary. If DM, EPI, or EHBO are present they should be managed appropriately.
What is exocrine pancreatic insufficiency?
Loss of exocrine pancreatic function may occur secondary to chronic pancreatitis (dogs and cats) or pancreatic acinar atrophy (dogs only). With pancreatitis, chronic inflammation and fibrosis leads eventually to loss of enough exocrine pancreatic tissue that mal digestion occurs. with pancreatic acinar atrophy there is an auto immune reaction against pancreatic acini. EPI from pancreatic acinar atrophy is seen in young GSDS, rough coated collies and chow chows. average age at time of diagnosis is 2-3 years. EPI from chronic pancreatitis can be any age/breed, though middle age to older breeds at risk for pancreatitis (cocker, CKCs) . Most consistent finding is weight loss, which may be severe, diarrhoea is often present and may be small bowel due to maldigestion or large bowel due to bacterial overgrowth. appetite is classically increased but may also be decreased. steatorrhea may be present if over 90% of lipase production is lose. with chronic pancreatitis EPI, DM may also be present. Minimum database is usually unremarkable unless concurrent diseases are present. EPI can cause mild hypoproteinaemia, mildly Increased LE, low cholesterol and triglycerides and mild lymphopaenia.
How is exocrine pancreatic insufficiency diagnosed?
TLI is the diagnostic of choice with high sensitivity and specificity. A fasted sample should be used, however, to reduce liklihood of false negatives. affected patients may ocasionally be in the normal range but are usually on the low end of normal and will be abnormally low if retested with fasted sample. if EPI s diagnosed or suspected, cobalamin should also be measured especially in cats. folate is usually measured at the same time and may be increased with bacterial overgrowth.
What is the treatment of exocrine pancreatic insufficiency?
Medical management consists primarily of pacnreatic enzyme replacement, typically with pancreazyme or something similar. patients should be co administered an H2 antagonist or PPI so that enzymes are not degraaded by gastric acid. over time, pancreatic enzymes may be weaned to lowest effective dose. diet should consist of moderate fat, highly digestible diet that is not high in fibre which can absorb pancreatic enzymes. tylosin or metronidazole can help control bacterial overgrowth. cobalamin should be supplemented in all cats and most dogs depending on serum levels. any concurrent diseases should be managed appropriately. usually excellent with treatment though it may take some time to get clinical signs controlled. pancreatic enzymes are quite expensive, however so owner may elect not to treat. Swine pancreas is an alternative.
What is a pancreatic cyst and a pancreatic pseudocyst?
Pancreatic cysts occur congenitally in some breeds or occasionally in association with neoplastic disease. a pancreatic pseudocyst is a cyst like structure filled with pancreatic enzymes that is seen uncommonly with pancreatitis. they are both important most as a differential for apncreatic abscess, for which surgical debridement may be indicated. usually no clinical signs. occasionaly cysts could cause EHBO and corresponding signs. aspirate of fluid from structure will be modified transudate in a cyst or pseudocyst versus exudate with abscess. no treatment required unless there is biliary tract compression - in this case the cyst/pseudocyst may be drained with ultrasound guidance or surgery.
What is chronic hepatitis?
Underlyng cause usually unidentified but may be infectious or toxic insult that sets up chronic inflammation or in some cases may be primarily autoimmune. inflammation is usually mixed, most often lymphocytic-plasmacytic. Chronic inflammation leads to fibrosis which can cause portal hypertension and lead to the development of acquired portosystemic shunts. Typically occur late in the disease process when there has been over 75% functional liver capacity llost. May include vomiting, diarrhoea, anorexia, weight loss, PU/PD, jaundice, ascites and Hepatic encephalopathy. haematology is often normal but may include anaemia of chronic inflammatory disease and neutrophililc leukocytosis. early on in the disease process, liver enzymes may be mild to moderately elevated. later on with more fibrosis liver enzymes may be normal but indicators of liver function may be abnormal. Liver size may be decreased on abdominal radiographs and abdominal ultrasound, ascites may be present with portal hypertension or hypoalbuminaemia. bile acids tolerance test is abnormal once dysfunction has occured. Manage as with hepatic dysfunction. diet should be moderately restricted, high quality protein easily digestible, cottage cheese, antioxidant therapy including s-adenosylmethionine, vitamin E, milk thisle, ursodeoxycholic acid promotes choleresis and decreases toxic bile salts, antibiotics may be indicated for hepatic encephalopathy, amoxicillin if leptospirosis possible, anti inflammatory doses of gluocorticoids.
What is copper storage hepatitis?
Copper is normally excreted in bile. with defects in copper excretion, copper accumulates leading to secondary inflammation and eventual fibrosis. copper may accumulate also as a secondary process to primary inflammatory hepatitis ( as with chronic hepatitis) but the distribution of copper within the portal triad is typically different. Multiple breeds have been identified to have suspected primary copper accumulation causing hepatitis: bedlington terrier, Labrador retriever, dalmation, doberman, WHWT, skye terrier, a mutation in copper excretion has only been identified in bedlingtons. Signs may be waxing or waning or acute on chronic- vague signs of illness chronically with sudden deteriroation. Clinical signs will be as for chronic hepatitis. susceptible breeds with elevated liver enzymes, even without clinical signs, should be investigated with biopsy because prognosis is significantly better with early intervention. Bloodwork/liver function changes will be identical to chronic hepatitis. biopsy with copper quantification is needed to differentiate. distribution is usually centrilobular, if copper accumulates secondary to chronic hepatitis is it typically milder and periportal. Treatment is general medical management as with chronic hepatitis. specific treatment for copper storage disease includes addition of zinc acetate or zinc gluconate to diet to bind dietary copper. patients that are systemically ill or have a high hepatic copper levels may need copper chelation therapy with D Penicillamine for several months but then can be maintained with hepatic diet and zinc supplementation. prognosis good with early intervention, guarded if fibrosis is present.
What is a congenital portosystemic shunt?
A congenital vascular anomaly remains persistently patent after birth, connecting portal circulation directly to systemic circulation (usually portal-caval or portal-azygous) bypassing the hepatic parenchyma. because the anomalous vessel is a lower pressure system than the hepatic parenchyma, blood shunts past the liver. shunts may be extrahepatic or intrahepatic. Extrahepatic shunts More common in small breed dogs, Yorkshire terriers, WHWT, maltese. Intrahepatic shunts more common in lab, irish wolfhound. typically present under 1 year, some have some normal portal circulation and have milder signs. Signs may be neurologic, gastrointestinal, urinary or general body condition, neurologic signs ay include hepatic encephalopathy, depression, lethargy, circling, blindness, seizures, GI signs include vomiting, diarrhoea, anorexia, urinary signs include PU/PD or presence of urate crystals or cystoliths. Minimum database most often shows a microcytic hypochromic anaemia, normal to mildly elevated liver enzymes, and low urea though may be unremarkable. bile acids tolerance test is extremely sensitive for PSS but not specific. abdominal ultrasound is essentially the opposite, it is specific but not sensitive. if a shunt vessel is seen with ultrasound, it confirms the presence of the anomaly but if one is not seen that does mean it is not present. CT angiography is a more sensitive imaging modality to detect abnormal shunt vessels than ultrasound but also requires GA. Treatment is attenuation of the shunt vessel via surgery (extrahepatic) or transjugular coil embolixation (intrahepatic) usually recomended. cases are usually medically managed for a period of days to weeks prior to definitive treatment to make them more stable.- hepatic diet, oral lactulose and metronidazole or amoxicillin for HE signs, anti epileptics if indicated. prognosis good with definitive treatment.
What is portal vein hypoplasia?
Another congenital vascular anomaly. the portal vasculature within the liver is underdeveloped. also known as microvascular dysplasia. signs are as with extrahepatic PSS, typically slightly older at time of presentation and signs are slightly milder, bile acids tolerance test is usually less elevated than with congenital PSS. diagnostic imaging is used to rule out PSS. hepatic biopsy is used to confirm diagnosis through often medical management. Hepatic biopsy used to confirm diagnosis though medical management is often instituted in suspected patients based on breed, clinical signs and lack of PSS. medical management treatment same as with PSS. dogs may be able to be weaned down to less aggressive medical management over time for instance only on diet or only on diet and lactulose.
What is non cirrhotic portal hypertension?
Similar to portal vein hypoplasia but with secondary portal hypertension, may develop multiple acquired PSS but do not have cirrhosis. Usually presents as young adult 1-4 years more often large than small breed. signs as with PSS but less frequently present with HE signs. often concurrently present with ascites or signs of GI ulceration. diagnosis as with PSS though on ultrasound and CT liver is Typically small. there is usually ascites, portal hypertension and multiple acquired extrahepatic shunts visualized. ultimately liver biopsy needed for definitive diagnosis. Medical management as with PSS - gastroprotectants (H2 antagonists, PPI, sucralfate) may be indicated for increased risk of ulceration and GI signs, drainage of ascitic fluid should be avoided (unless causing resp distress), because it will exacerbate hypoalbuminaemia. generally good prognosis. no definitive treatment available apart from medical management.
What is drug/toxic hepatopathy?
Ingestion of hepatotoxin/treatment with hepatotoxic drug may lead to oxidant injury and subsequent inflammation eventually leading to fibrosis. common offenders include paracetamol, phenobarbital, xylitol, aflatoxin, lomustine. Usually acute signs and may include vomiting, diarrhoea, anorexia, weight loss, PU/PD, HE, jaundice, bleeding from acquired coagulopathy. Presumptive diagnosis made based on history. with acute toxic insults, liver enzyme elevated is usually moderate to severe and is usually primarily hepatocellular or mixed. bile acids and bilirubin may be normal or elevated. hypoglycaemia and hypokalaemia may be present. azotaemia either prerenal or concurrent AKI, may be present. abdomianl ultrasound can occasionally show hyperechoic hepatic parenchyma. coagulopathypotentialy present. Primarily treatment consists of supportive care including IVFT, gastroprotectants, anti oxidants (more specifically indicated for hepatotoxicosis than with other causes of liver diseasE) and vitamin K.
What is vacuolar hepatopathy?
Glycogen accumulates in hepatocytes which leads to cell swelling and cholestasis. it is often secondary to corticosteroid or other drug therapy but is recognised as a primary disorder in some breeds. usually none to minimal clinical signs - differential for elevated cholestatic enzymes. elevation in ALT, GGT, bile acids. abdominal ultrasound usually shows hepatomegaly and diffusely hyperechoic liver. cytology will show vacuolar change though biopsy needed for definitive diagnosis. no definitive treatment. secondary VH usually reversible for withdrawing offending agent. no treatment for scottish terrier VH. excellent prognosis but may be a link between VH and hepatocellular carcinoma in scottish terriers.
What is infectious hepatitis?
Infectious causes of hepatitis are very uncommonly reportedi n the UK. leptospirosis can cause hepatitis. L grippothphosa recognised to cause hepatitis in absence of renal signs. any dog with possible exposure. may be acute or chronic, compatible with effect on liver function and presence of systemic infection. characteristic changes of acute hepatitis. Leptospirosis PCR or serology should be performed. treatment of leptospirosis is amoxicillin.
What is cholecystitis/cholangitis?
Bacterial or unidentified pathogen causes biliary tract inflammation/infection which is usually neutrophilic. there may be a recent history of enteritis or pancreatitis. any age or breed may be affected. signs may include anorexia jaundice, vomiting and pyrexia. Minimum database can show anaemia of chronic inflammation, neutrophilic leukocytosis and cholestatic liver enzyme elevation, including potentially elevated bilirubin and bile acids. abdominal ultrasound indicated to rule out presence of a mucocele and extrahepatic duct obstruction. Bile cytology and culture can confirm presence of neutrophilic inflammation and presence of bacterial infection. Therapy consists of appropriate antibiotics based on culture results. pending results, potentiated amoxicillin would be appropriate. if the dog is anorexic - nutritional support may be required.
What is a gallbladder mucocele?
Mucoid concretions within the gallbladder can result in biliary obstruction. Numerous endocrinopathies, including diabetes mellitus, hyperadrenocorticism, hypothyroidism and pancreatitis can result in changes to biliary secretions increasing risk of mucocele. Usually occurs in middle aged to older dogs, shetland sheepdogs, cocker spaniels, miniature schnauzers seem predisposed. Signs may be absent and mucocele can be diagnosed incidentally on abdominal ultrasound for another reason. Minimum database often shows cholestatic enzyme elevation and elevated bile acids. abdominal ultrasound shows a kiwi gallbladder. clinical sigs include anorexia, lethargy, vomiting and jaundice. Definitive treatment is cholescystectomy. if mucocoele is seen subclinically or surgery is not an option, medical therapy includes Ursodeoxycholic acid and low fat diet as well as management of any concurrent underlying endocrinopathies. guarded prognosis if bile peritonitis is present. subclinical cases can do well with surgery and sometimes with just medical management.
What is hepatic lipidosis? (cats)
A period of anorexia induces a negative energy balances and mobilizes fat stores from peripheral fat to the liver. concurrently, dietary deficiencies of methionine, carnitine and taurine result in an inability to process fats for energy metabolism. hepatocyte swelling leads to cholestasis. Obese cats more predisposed. signs include jaundice, vomiting, diarrhoea, hepatomegaly as well as signs of HE. HE usually includes pytalism and depression in cats. there may be sign sof underlying disease that led to period of anorexia. minimum database can show anaemia of chronic inflammation alkaline phoshatase is clasically elevated, more so than GGT. alanine transferase is usually abnormal. bilirubin may be increased and urea may be decreased with hepatic dysfunction. hypokalaemia, hypophosphtaemia and hypomagnesemia may be present secondary to anorexia and hypokalaemia is associated with a poorer prognosis. coagulation panel can show elevated Pt/PTT with decreased vitamin K recycling. there may be changes indicative of underlying disease that led to anorexia. abdomain radiographs or ultrasound are used to search for concurrent diseases but may show hepatomeagly and hyperechoic hepatic parenchyma. cytology will shw vacuolar change. Most important aspect of treatment is restoration of positive energy balance, which typically requires placement of a feeding tube. if patient is a suitable candidate for anaesthesia, oesophageal feeding tubes are Preffered otherwise nasoesophageal feeding tubes are indicated. Small frequent meals are typically better tolerated. IV fluids and electrolytes appropriate. Vitamin K should be given for coagulopathy. Anti oxidants (SAM-e and vit E) used to replace deficits in glutathione.
What is neutrophilic cholangitis?
Ascending bacterial infections of the biliary tract leads to neutrophilic inflammation of the bile duct an portal tracts, similar to cholangitis in dogs. most frequently isolated bacteria include E. coli, streptococcus, clostridiuum and other enteric bacteria. gallbladder may also be affected. concurrent inflammatory bowel disease/pancreatitis commonly present. Signs may include lethargy, anorexia, pyrexia and jaundice. neutrophilic leukocytosis with possible left shift, alanine transferase and bilirubin most commonly elevated. abdominal radiographs are usually normal and ultrasound may show biliary tract dilation. biliary cytology and culture can isolate infective organism and give sensitivity. Cats should be treated with an extended period of appropriate antibiotics (4-6 weeks) until there is resolution of clinical signs and bloodwork changes. potentiated amoxicilin can be used pending culture results. ursodeoxycholic acid would be appropriate to increase choleresis and reduce cell membrane damange. anorexic patients should be managed appropriately.
What is lymphocytic cholangitis?
lymphocytes infiltrate portal tracts, leading to proliferation of bile ducts and portal fibrosis. it is likely immune mediated and may present similarly to FIP. affects young to middle aged cats. persians overrepresented. chronic waxing and waning illness - jaundice, weight loss, anorexia, lethargy. cats may have high protein ascites. minimum database may show neutrophilic leukocytosis. liver enzymes may be mild to moderately elevated. hyperglobinulinaemia may be present. coagulation times may be prolonged. Ultrasound could show biliary tract dilation that can appear like EHBOO and ascites may be present. Little evidence that immunosuppressives are of benefit. supportive care consists of ursodeoxycholic acid and nutritional support as indicated.
What is extrahepatic bile duct obstruction?
Compression of bile duct can occur secondary to intraluminal or extraluminal causes which can include cholangitis, duodenitis, pancreatitis or some combination thereof. biliary neoplasia can also cause EHBO. choleliths are a rare cause of EHBO. Signs are compatible with cholestasis and may include jaundice, anorexia depression and omiting. hepatomegaly may be present. minimum database is compatible with cholestasis, elevated cholestatic liver enzymes and bilirubin. coagulation panel is often abnormal due to decreased absorption of fat soluble vitamin K without adequate bile mediated fat digestion. abdominal ultrasound demonstrates dilation of gallbladder and bile duct. Underlying cause of EHBO may be visible. Recommended treatment depends on underlying cause. cats usually require vitamin K supplementation, along with UDCA and antioxidants. biliary tract surgery should be avoided - high periooperative morbidiity.
What is a congenital portosystemic shunt (cats)
same etiology as dogs. purebred cats overrepresented. most cats present under 2 years of age. hepatic encephalopathy signs are more consistent in cats than dogs and may be waxing and waning. signs include hypersalivation, beahviour change. head pressing, circling, poor growth. minimum database includes decreased urea and microcytosis, remaining changes on bloodwork are less common in cats than dogs. bile acids tolerance test will be elevated. abdominal ultrasound may show microhepatica and shunt vessel may be visualised. CT angiography can detect or rule out PSS. Medical management typically less effective at controlling clinical signs than in dogs. definitive treatment is with attenuation of shunt vessel, though medical management should be used for stabilisation prior to surgery.
How does emesis ocur?
The process of emesis is complex, a wide number of triggers and pathways being able to induce the vomiting reflex. The main neurotransmitter is acetylcholine but serotonin, dopamine, substance P and histamine are also important. in cats and dogs, stimulation of alpha2 adrenoceptors also induces emesis.The emetic centre is protected by the blood brain barrier. the chemo receptor trigger zone is not so well protected by the BB, which is incomplete in this region.
What are emetics?
Drugs which induce emesis. the main reason for induction of emesis is in the managemtn of poisoning (non corrosive).
Xylazine - is an alpha 2 agonist used as a sedative which induces vomiting in cats especially but also dogs after i/m. if given at lower dose should not cause sedation but may still induce vomiting.
Ipecacuanha - acts as a local irritant, not terribly reliable.
Opiates - apomorphine - emetic action predominant over its other opiod effects (D2 receptors in CRTZ) can be given by any route. subsequent administrations may see reduced efficacy - depression of the emetic centre, respiratory depression with overdose, not suitable for cats.
What is maropitant?
Licensed anti emetic for dogs. its mechanism of action is neurokinin - 1 receptor antagonist, it blocks the effect f substance P (neurotransmitter at these receptors) acts in final common pathway in emetic centre > broad spectrum anti emetic, works for motion sickness, GI irritation, pancreatitis, chemotherapy induced. It is orally bioavailable, given oral and s/c. It has low oral bioavailability - first pass hepatic metabolism, non linear kinetics, hepatic metabolism - 2 isoenzymes, one low capacity, one high capacity, hepatic clearance also, widely distributed, highly bound to plasma protein. There is a wide dose range depending on the cause of vomiting i.e higher dose for motion sickness. once daily dosing schedule. can be given orally or parenterally. oral admin give with small amount of food - for travel sickness.
What is metocopramide?
now licensed for dogs and cats. it is both centrally and peripherally acting. mechanism of action is complex. it centrally inhibits D2 and %Ht2 receptors in the CRTZ. Peripherally inhibits D2 receptors and induces the release of local ACh. Results in increased oesophageal sphincter tone, increased gastric contractions, decreased pyloric sphincter tone, increased peristalsis of the upper intestine.. It has good oral bioavailability, can also be given parenterally, significant first pass metabolism, good distribution, short half life about 90 mins, hepatic and renal elimination. The side affects reported are - behaviour alterations, constipation with long term use, contraindicated in GI obstruction and epilepsy. atropine and the opioid analgesics antagonise the effects.
How do antihistamines work as anti emetics?
Motion sickness (vestibular apparatus). Histamine via h1 receptors is the key neurotransmitter. antihistamines such as cyclizine HCL, meclizine HCL and diphenhydramine Hcl. They may cause drowsiness and xerostoma. oral bioavailability is good, hepatic metabolism and renal elimination.
What are phenothiazines?
Broad spetrum anti emetics. low doses block dopamine and histamine receptors. high doses have antimuscarinic effects also. acepromazine, chlorpromazine and prochlorperazine. sedation and hypotension are also side effects - decrease desirability in older/sck animals..
What are serotonin antagonists?
They block the effect of serotonin on %ht2 receptors. Examples include cyproheptadine and ondansetron. ondansetron used especially for human patients to control vomiting associated with chemotherapy. Ondansetron can be given orally or parenterally. it has a short half life and undergoes hepatic metabolism.
Name the peripherally acting anti emetics?
Protectants, anticholinergics, prokinetics.
What are anti ulcer drugs?
H2 receptor antagonists. examples include cimetidine, ranitidine and famotidine. Cimetidine is orally bioavailable, food decreases boavailability, hepatic metabolism and renal elimination of conjugated and active drug, half like 1 hour, decreases gastric acid and pepsin production. It is an inhibitor of microsomal enzymes and will decrease hepatic blood flow b y about 20% - decrease metabolism of flow dependent on drugs e.g lidocaine and propranolol. May get rebound and hypersecretion on cessation. Famotidine > ranitidine> cimetidine.
Famotidine does not inhibit liver enszymes, can be given IV, longer half life vs cimetidine, SID- BID dosing, dose reduction in renal failure. Basic drug give slowly over 5 mins.
Ranitidine - does not inhibit liver enzymes, can be given i/v, longer half life vs cimetidine, BID dosing, has prokinetic activity, also dose reduction in renal failure.
What is omeprazole?
An anti ulcer drug - proton pump inhibitor. It is a substituted benzimidazole, more potent than the H2 blockers. it irreversibly inhibits the potassium ATPase pump in the luminal surface of the parietal cell. basic drug that requires enteric coated formulation. dissolution and absorption occurs in the small intestine. On absorption the drug is ion trapped in the parietal cells (pH is much lower compared to other cells) absorption improves over first 4-5 days as PH in the GI tract increases. enzyme is permanently inhibited so HCL production only resumes when new enzyme molecule has been formed. high plasma protein binding (about 96%), hepatic metabolism and short half life about 1 hour. safe drug with few side effects.
What is misoprostol?
A synthetic analogue of PGE1. it acts locally - absorbed drug is rapidly metabolised. decreases cAMP in the parietal cell. it increases bicarbonate and mucous production and enhances mucosal blood flow and mucosal epithelialisation. anti ulcer and cytoprotective agent, reduces secretion of histamine from mast cells. Unabsorbed drug in the SI can cause diarrhoea, generally resolves after a few days, used primarily to prevent and treat gastric ulceration caused by NSAIDS.
What are anti ulcer drugs?
Other agents that neutralise gastric acid. examples include sodium bicarbonate and aluminium hydroxide. not especially efficaceous. need to be administered very frequently e.g 6 x daily or with every meal. can get hypersecretion of HCL. AIOH also binds phosphates and used in renal failure to help reduce blood phosphate levels.
What are cytoprotectants?
Misoprostol, antacids and sucralfate.
Antacids e.g aluminium hydroxide - inactivate HCl, binds pepsiin and bile salts also, binds intestinal phosphate (renal disease), a more prolonged antacid effect than some, can cause constipation (mix with magnesium salts), alkalinize urine - ion trapping and increase elimination of acidic drugs. Sucralfate is a dissacharide alminium hydroxide product. in acidic environment acquires negative charge and binds to positively charged elements of exposed epithelial cells at sites of ulceration- seals the ulcer, prevents leakage of protein and electrolyte, binds epidermal growth factor. It requires an acid environment to work, binds to bile acids and pepsin, increases local blood flow perhaps by increasing prostaglandin or NO locally. it acts locally - is not absorbed. binds and inactivates cimetidine and other orally administered drugs.
What are emollient laxatives?
They act locally and are unchanged. they lubricate and soften the faecal mass, include mineral oils and yellow and white soft paraffins , prolonged use may reduce absorption of fat soluble vitamins. local absorption may cause granulomatous lesions, may reduce bowel irritability leading to constipation.
What are bulk laxatives?
These are not absorbed but act locally. they are hydrophilic and absorb water. increasing faecal bulk and water content and stimulating peristaltic movement. examples include sterculia, isphagula and bran. adequate water intake is crucial.
What are osmotic laxatives?
Examples include magnesium sulfate (Epsom salts,) sodium sulfate (Glauber’s salt) and lactulose. these hypertonic solutions draw water into the intestine causing bowel distension and peristalsis. water availability is crucial in the case of lactulose, intestinal ph is reduced, ammonia producing gut flora are reduced. this is useful in the management of hepatic encephalopathy. Phosphates and sodium citrate are also used as osmotic laxatives - they are administered as enema preparations. phosphate enemas should not be given to small dogs and cats as this can induce hyperphosphataemia.
What are stimulant laxatives?
Should never be used if obstruction is suspected. examples include Bisacodyl and phenopthalein. these are diphenylmethane stimulants. precise mechanism of activity is not clear but they appear to stimulate colonic smooth muscle and the myenteric plexus. Phenopthalein undergoes some degree of enterohepatic recycling.
What are modulators of intestinal motility?
Prokinetics and spasmolytics. Some agents used in the management of diarrhoea may increase segmental contractions and decrease peristaltic contractions.
Describe the prokinetics
Metoclopramide - used as an anti emetic, also used to prevent post op ileus in horses.
- Parasympathomimetics such as carbachol - QAC and can cause intestinal rupture.
- Antimicrobial eerythromycin - has prokinetic effects through stimulation of ACh release
- Ranitidine
- Cisapride - acts primarily as an agonist at 5HT4 receptors in the GI tract. Increases lower oesophageal sphincter pressure, gastric emptying, SI motility and colonic motility. More potent than metoclopramide. administered orally - food enhances absorption. withdrawn from marked in the UK and US for human use due to cardiac toxicity associated with concurrent use f Cyp 3A4 inhibiitors. Need an STC.
What are spasmolytics?
Spasmolytics - drugs to treat diarrhoea.
Antimuscarinics;
Atropine sulphate, propantheline and hyoscine (buscopan compositum). Propantheline less lipid soluble than atropine so reduced CNS effects.
Opioids - diphenoxylate HCL, codeine and loperamide. Increase segmental contractions and decrease perisalsis. Diphenoxylate and loperamide are both metabolised in the liver. diphenoxylate is more completely absorbed following oral administration. take care in cats. loperamide may be used in horses. diphenoxylate combined with atropine available. (lomotil)
What are adsorbents?
Thought to adsorb toxins from the GI tract, may also prevent the absorption of other dugs, examples include kaolin, pectin, bismuth salts, activated charcoal, calcium carbonate. Often used in combination in commercial products. Bismuth can come in a variety of forms - bismuth suubnitrate, subcarbinate and subsalicylate. the subsalicylate form is cleaved into bismuth and salicylate. the latter is systemically available and has anti prostaglandin effects - care in cats. has been shown to have antimicrobial and anti secretary effects in some species. Activated charcoal is very effective adsorbent, used in the treatment of ingested toxins pore size is important. powder more efficacious than tablets. forms a stable complex with the substance which is then evacuated from the body.
What is cholesytyramine?
A drug used in human medicine to lower cholesterol. it stays in the GI tract and binds bile acids, preventing their reabsorption. in rabbits it can be used in antibiotic induced diarrhoea as it binds and absorbs clostridia toxiin.
What are appetite sitmulants?
Appetite mainly controlled by the ventral and lateral nuclei of the hypothalamus. neurotransmitters involved - noradrenaline, dopamine and GABA stimulatory, serotonin inhibitory. neuropeptides CCK, CRF and Calcitonin inhibit appetite, while pancreatic polypeptides and opiates stimulate appetite. Benzodiazepines - diazepam most effective, used mainly in cats, inhibits satiety centre and GABAminergic effects, administered IV. Cyproheptadine - anti serotonin effects, good oral bioavailability with a half life about 13 hours. given orally once or twice daiily in cats.
What is ursodeoxycholic acid?
A naturally occuring bile acid. it has less cellular toxicity than many other bile acids (i.e hydrophobiic membranocytolytic BAs). It is preferentially absorbed from the GI tract. it is also acholoretic agent increasing the elimination of toxic bile acids from the liver. it thereby helps protect the diseased liver from toxic bile acids. it is given orally once daily and should be avoided in biliary obstruction.
What is S adenolysl-L-methionine ? (SAMe)
Acts as a methyl donor. it has been shown to improve hepatic parameters in a number of disease conditions . it is important for a large number of processes within the liver including the formation of glutathione. glutathione s important as an antioxidant and for the scavenging of ROS. glutathione often deficient in liver disease. Good oral bioavailability but extensive first pass effect.
What is silibinin/silybin/silybum? (milk thistle)
thought to have an antioxidant anti inflammatory anti fibrotic effect. thought to promote regeneration. experimentally protects dogs from amanita mushroom poisoning. dosing is empirical - clinical efficacy not well established.
What are penicillamine and trientine?
Used in copper hepatotoxicosis. Penicillamine is an anti arthritic drug and also a chelating agent. it binds copper. should be given on an empty stomach. Variable bioavailability, mainly renal elimination but also hepatic, elimination is slow.
Trientine - alternative to penicillamine, has been shown to be associated acute renal failure in dogs.
What are the clinical features associated with GI malignancies?
Oral > ptyalism, dspyhagia, halitosis
Oesophageal > regurgitation, dullness, anorexia
Gastric > dullness, weight loss, vomiting
Small intestine, malaenia, diarrhoea, weight loss,
Colon - diarrhoea, weight loss, tenesmus, haematochezia
Perianal - mass lesion, tenesmus
Describe the key features of oral tumours in dogs and cats
The most common oral tumours in dogs include malignant melanoma, squamous cell carcinoma, fibrosarcoma and the epulides. SCC is the most common feline oral tumour. Fibrosarcoma and melanoma occur but less commonly. Clinical sigs oral tumours include ptyalism, sometimes bloody. inappetance, dysphagia, weight loss, halitosis, exopthalmus, epistaxis and loose teeth. biologic behaviour and prognosis of oral tumours are best predicted by histologic type and tumour location, tumour size and stage of disease.
Describe malignant melanoma
Most common canine oral tumour, golden retrievers, scottish terriers, poodles, and dachshunds over represented. Immunohistochemistry may be necessary to diagnose some melanomas, especially amelanotic tumours. Locally invasive and highly metastatic. true metastatic rate is dependent on size, location and the grade of the tumour. common sites of metastasis: regional lymph nodes and lungs.
What is a squamous cell carcinoma?
second most common canine oral tumour. locally invasive. metastatic rate is variable and dependent on location. Tonsillar SCC has a much higher metastatic rate than more rostral tumours. at diagnosis 10-20% patients of with tonsillar SCC have overt evidence of metastatic disease while 90% have micrometastatic disease, sites of metastasis include tonsils, regional lymph nodes and lungs.
What is a fibrosarcoma?
Occurs less commonly than OMM and SCC. there is a specific variant - histologically low grade, biologically high grade FSA which appears benign histologically but is very locally aggressive and grows rapidly. metastatic rate of FSA is <_20%. Lungs are most common site of metastasis but spread to regional lymph nodes can occur.
