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