13) diseases of the stomach

Question 1

functional anatomy of the stomach

Answer 1

• Lower oesophageal sphincter (LES) and cardia
  • Allows entry of ingesta and prevents reflux of gastric contents
• Fundus
  • Dilates during gastric filling to accommodate a volume of ingesta
• Body
  • Stores ingesta
  • Secretes hydrochloric acid, pepsin and lipase
• Antrum
  • Grinds food into smaller particles
• Pylorus
  • Limits the size of food
  • Prevents reflux of duodenal contents

Question 2

clinical manifestations of gastric diseases

Answer 2

• Vomiting
• Haematemesis
• Melaena
• Anorexia
• Abdominal pain
• Distended abdomen
• Diarrhoea
• Weight loss

Question 3

acute gastritis

Answer 3

• Aetiology
  • Ingestion of spoiled or contaminated food, foreign objects, toxic plants, chemicals, irritating drugs
  • Viral, bacterial, parasitic causes
  • Most common cause for vomiting
• Clinical features
  • Acute onset of vomiting (food, bile, +/- small amount of blood)
  • Loss of appetite
  • Rarely fever or abdominal pain
• Diagnosis of exclusion
  • Good history, physical examination
  • If animal’s condition worsens within 1-3 days → abdominal US, CBC, serum biochemistry
• Treatment
  • Withholding food for 24 hours
  • Antiemetics (maropitant) in persisting/excessive vomiting
  • Fluid therapy/small amounts of cool water
  • Gastrointestinal prescription diet
• Prognosis
  • Self-limiting problem
  • Excellent

Question 4

Gastric erosive ulcerative disease

Answer 4

Gastric mucosal barrier
• Mucus-bicarbonate layer: as a lubricant to prevent mechanical damage
• Underlying glycoprotein gel: traps bicarbonate
• Gastric epithelial cells: low permeability to water and ions and have tight intercellular junctions, ability to continually and rapidly repair injured cells, migrate over the defect within a few hours
• Submucosal capillaries supply oxygen and nutrients
• Prostaglandin E: produced by GI mucosa (mucus ↑, bicarbonate ↑, regulates mucosal blood flow, epithelial cell growth ↑, acid secretion ↓)
- Predisposing factors
• NSAIDs
➢ Direct damage, inhibit synthesis of PGs)
➢ Aspirin, phenylbutazone, ketoprofen, flunixin meglumine, ibuprofen, naproxen, piroxicam, COX-2 inhibitors too, etc.
• Corticosteroids
➢ Mucosal cell growth ↓, mucus production ↓, gastric acid secretion ↑)
➢ High dose, long duration
➢ Associated with other risk factors
➢ Dexamethasone > prednisolone
• Metabolic diseases
➢ Liver failure (gastric mucus production ↓, epithelial cell renewal ↓, blood flow ↓, serum bile acids ↑ → gastrin secretion ↑, gastric acid secretion ↑)
➢ Hypoadrenocorticism (hypotension, loss of vascular tone)
➢ Renal failure (uraemic toxins, gastrin metabolism ↓)
➢ Acute pancreatitis, IBD, neurological disease
• Altered gastric blood flow, stress-related factors
➢ Hypotension, shock, sepsis, surgery, spinal cord disease, GDV
• Increased secretion of gastric acid
➢ Pancreatic gastrin-secreting tumour, mast cell tumour (skin), pyloric outflow obstruction – chronic gastric distension
• Toxic-traumatic agents
➢ Bile salts, pancreatic enzymes, lead, foreign bodies, alcohol
• Gastric neoplasia
➔ - All commonly used NSAIDs
- Corticosteroids alone are not usually ulcerogenic
- Many metabolic diseases predispose to GEU, especially with chronic liver-, renal disease and hypoadrenocorticism
• Radiography
➢ Usually normal, peritonitis or pneumoperitoneum is indicative of perforation
• Endoscopy
➢ Benign ulcers, superficial erosions, malignant ulcers; biopsy is needed!
- Treatment
• Elimination of predisposing causes
• Symptomatic-supportive therapy
➢ Dietary (if vomiting resolves low-fat, single protein-source diet)
➢ Fluid, antiemetics (maropitant)
➢ Antacids: H2-blockers (famotidine), proton-pump inhibitors (omeprazole, pantoprazole)
➢ Protectants (sucralfate, misoprostol)
• Blood transfusion
➢ Severe anaemia, evidence of GI bleeding
• Surgical treatment
➢ If uncontrolled haemorrhage or perforation is suspected
- All critically ill patients (severe trauma, major surgery, organ failure, sepsis) should be considered for development of ulcers
- Diagnostic features
• History
➢ Intermittent vomiting; variable haematemesis or melaena; recent NSAID and/or corticosteroid treatment; acute onset of weakness
• Physical examination
➢ Often normal, anaemia, abdominal pain, melaena
• Laboratory tests
➢ Anaemia regenerative or non-regenerative hypochromic microcytic, renal failure, liver disease, hypoadrenocorticism

Question 5

chronic gastritis

Answer 5

• Clinical occurrence
  • 35% of chronic vomiting, 26-48% of asymptomatic
• Aetiology
  • Lymphocytic-plasmocytic
  ➢ Helicobacter-associated gastritis (especially cats)
  ➢ Physaloptera rara in dogs
  ➢ Immune response to dietary antigens
  ➢ Lymphoma
  ➢ Idiopathic
  • Eosinophilic
  ➢ Allergic reaction to food antigens, immune response to parasites, foreign material, mast cell tumour, idiopathic
  • Atrophic gastritis
  ➢ Maybe the result of chronic gastritis inflammatory disease
  • Hypertrophic gastritis
  ➢ Idiopathic
• Causes
  • Same as acute gastritis
  • Specific causes
  ➢ Helicobacter-associated gastritis
  ➢ Parasitic gastritis
  ➢ Dietary antigens
  ➢ Foreign material (sand contaminated food, trichobezoar)
  ➢ Fungal origin (Pythiosis, Histoplasmosis)
  • Idiopathic
  • Can also be of unknown cause
• Symptoms
  • Intermittent vomiting, no response to symptomatic treatment, anorexia, weight loss, abdominal pain, haematemesis, melaena (if neoplasia or GEU is present)
• Diagnosis
  • Endoscopic or full-thickness biopsy + histopathology
  • Laboratory tests not diagnostic (excluded metabolic causes, anaemia, leucocytosis, eosinophilia, hypoproteinaemia)
  • Radiographs, ultrasonography (foreign bodies, thickened gastric wall, mass lesion, delayed gastric emptying

Question 6

helicobacter gastritis

Answer 6

• In human: H. pylori primary cause of chronic gastritis, gastric and duodenal ulcer disease, gastric cancer
• Dog: H. bizzozeronii, salomonis, heilmannii, felis
➢ Clinically healthy: 67-100%
➢ Vomiting dogs: 74-90%
• Cat: H. heilmannii, bizzozeronii, felis
• Diagnosis
➢ C-13 urea breath test
➢ Endoscopic biopsy
o Rapid urease test
o Histopathologic study: routine haematoxylin-eosin, silver stain, methylene blue stain
o PCR, FISH
• Treatment
➢ First: rule out other causes of chronic vomiting!
➢ Amoxi + metronidazole + bismuth for at least 14 days
➢ + azithromycin or clarithromycin in cats
➢ + famotidine

Question 7

parasitic gastritis

Answer 7

Parasitic gastritis
• Physaloptera rara in dogs
• Ollulanus tricuspis in cats
• Diagnosis
➢ By faecal flotation is difficult
➢ Endoscopy (1-4 cm long nematodes in the fundus)
➢ History of chronic vomiting
• Treatment
➢ Single dose of pyrantel pamoate in dogs
➢ Fenbendazole in cats
➢ Endoscopic removal!

Question 8

treatment of chronic gastritis

Answer 8

• Exclusion of specific causes
➢ Low-fat, low-fibre, elimination diet 2-4 weeks
o Depending on response continue or change to another diet with a different protein source (fish, rabbit, horse, lamb)
➢ Anti-parasitic therapeutic trial
➢ Helicobacter elimination therapy
• If not effective:
➢ Immuno-suppressive therapy
o Dogs: prednisolone or azathioprine (alone or as adjunct to steroids)
o Cats: prednisolone (higher initial dosage) or chlorambucil
➢ Antacids (H2-receptor antagonist or omeprazole), protectants (sucralfate), prokinetics (erythromycin, metoclopramide, cisapride)
➢ Surgical resection of large eosinophilic granulomatous masses

Question 9

delayed gastric emptying

Answer 9

• Gastric outlet obstruction
  • Antral pyloric hypertrophy syndrome / pyloric stenosis
  ➢ Congenital / acquired
  ➢ Young to middle-aged male brachycephalic breeds (Boxers, Boston Terriers, Lhasa apsos, Maltese, Pekingese, Shi-Tzu)
  ➢ Diagnosis
  o Projectile vomiting 6-8 hours after vomiting
  o Radiography: contrast study “beaklike” appearance of pyloric lumen (narrowed lumen), delayed gastric emptying
  o Endoscopy: narrowed pyloric lumen and / or thickened pyloric mucosa sometimes as a protuberant mass
  ➢ Treatment: pyloroplasty
  • Chronic hypertrophic gastritis
  • Gastric ulcer
  • Neoplasia
  • Foreign body
  • Antral polyps
  • Granulomatous gastritis
  • External compression: abdominal mass, pancreatic abscess / tumour

Question 10

gastric motility disorders

Answer 10

• Gastroenteritis
• Pancreatitis / peritonitis
• Abdominal pain / trauma / stress
• Ca2+ ↑↓, K↓
• Drugs: anticholinergics, narcotics, β-adrenergic agonists
• Dysautnomoia
• Post-GDV
• Chronic gastritis, ulcer, neoplasia
• Uraemia, liver failure, DM, IBD
• Hypoadrenocorticism
• Constipation
• Idiopathic (gastric arrhythmia)
➢ Symptoms: postprandial abdominal discomfort, bloating, chronic vomiting
➢ Diagnosis
o Documentation of gastric retention
o Elimination of obstructive and metabolic causes
➢ Treatment
o Diet: frequent feeding, liquid, low-fat, gastro-intestinal diet
o Prokinetics: (cisapride most effective! Metoclopramide, erythromycin, ranitidine)
- Diagnosis
• Vomiting of large amounts of partially digested food and fluid more than 8 hours after eating!
• Physical examination: normal or abdominal tympany
• Laboratory tests: normal, hypochloremic metabolic alkalosis
• Radiography: fluid distended stomach on survey radiographs; most of liquid barium is retained in the stomach after 4 hours, or if liquid barium is present in the stomach longer than 12 hours; narrowed pyloric lumen or obstructive mass
• Endoscopy: confirms of presence of gastric outflow obstruction, no evidence of obstructing lesion → primary / secondary gastric motility disorder

Question 11

gastric neoplasia

Answer 11

• Low incidence in dogs and cats (adenocarcinoma, lymphoma, leiomyoma)
• Symptoms
  • Weight loss
  • Worsening of vomiting
  • Anorexia
  • Melaena
  • Haematemesis
• Adenocarcinoma
  • Most common gastric tumour in dogs
  ➢ Older, male dogs
• Lymphoma
  • Most common gastric tumour of cats
• Others: fibroma, plasmacytoma, squamous cell carcinoma
• Diagnosis
  • Symptoms
  • Ultrasonography
  • Endoscopy
  • Biopsy
• Treatment
  • Surgery (adenocarcinoma)
  • Chemotherapy (lymphosarcoma)
• Prognosis is guarded!