GI1- Gastris Disorders of SA

  1. Describe the poster child for presentation with acute gastritis.
    acute vomiting in an otherwise healthy animal
  2. Describe the poster child for presentation with chronic gastritis.
    chronic vomiting of food or bile, usually otherwise healthy
  3. Describe the poster child for presentation with gastric ulcers or erosions.
    hematemesis, melena, +/- anemia
  4. Describe the poster child for presentation with GDV.
    non-productive retching, abdominal distention, tchycardia
  5. Describe the poster child for presentation with delayed gastric emptying.
    acute or chronic vomiting of food >10hrs after eating
  6. Describe the poster child for presentation with gastric neoplasia.
    chronic vomiting, weight loss, +/- hematemesis, +/- anemia of chronic disease
  7. Describe the Gastric Mucosal Barrier defense mechanisms. (4 components)
    • Pre-epithelial defenses: mucus, bicarb
    • Epithelial defenses: cell membranes and tight junctions, ion pumps (remove H+), rapid epithelial restitution (rather than regeneration)
    • Post- epithelial defenses: mucosal blood flow
    • Prostaglandin E2 and I2:: stimulate mucus and HCO3- secretion, promote epithelial restitution, inhibit acid secretion
  8. Describe how NSAIDs cause gastric mucosal damage.
    NSAIDs block cyclooxygenase enzymes (COX-1 and COX-2), which are critical in the synthesis of protective prostaglandins
  9. Are all NSAIDs equally damaging to the gastric mucosa? Explain.
    COX1- constitutive physiologic functions, COX-2- inducible inflammatory functions; some NSAIDs are COX-1 sparing, and therefore cause less gastric mucosal damage; deracoxib, carprofen, meloxicam, fircoxib
  10. What exogenous factors can cause damage to the GMB? (7)
    drugs, food, chemicals, toxins, foreign bodies, infectious agents, and parasites
  11. What mixture of drugs should NEVER be used because it has a high likelihood of causing gastric ulceration?
    NSAIDs and glucocorticoids
  12. What endogenous factors can cause damage to the GMB? (4)
    hyperacidity, bile, pancreatic enzymes, decreased mucosal blood flow
  13. What are potential causes of gastritis? (11)
    idiopathic***, dietary indiscretion, food sensitivity, foreign body, drugs, parasites, infectious causes, toxins, immune-mediated, motility disorders, secondary to systemic disease
  14. Describe the diagnosis and treatment of acute gastritis.
    • Usually no extensive diagnostics- acute gastritis is a "clinical diagnosis" perhaps better termed "acute self-limiting vomiting"
    • Usually self-limiting and mild and lasts no longer than 24-48 hours
  15. Contrast a food allergy from a food intolerance.
    • Allergy- proven immunologic basis
    • Intolerance- abnormal response to a food additive that is not immunologic
    • We usually just refer to them ll as food sensitivities
  16. Describe the Helicobacter disease-causing capacity in animals and compare it to humans.
    • Microaerophilic, spiral, gram negative, urease-producing bacteria that is present in a LARGE proportion of healthy, asymptomatic animals
    • In animals, if its going to cause any disease at all, it causes chronic gastritis (not ulcers)
    • In humans, it is a major cause of ulcers and even neoplasia
  17. If you opt to treat Helicobacter in dogs and cats, how do you treat?
    amoxicillin, clarithromycin, maybe metronidazole and a PPI (maybe H2 blocker)
  18. What are the stomach worms of dogs and cats, and how do they get them?
    Physaloptera rara; ingestion of beetles, crickets, cockroaches, rodents, or snakes
  19. How do you diagnose and treat Physaloptera?
    endoscopy (fecal not reliable at all); fenbendazole, pyrantel, or ivermectin
  20. What is bilious vomiting syndrome?
    morning vomiting of bile-stained fluid- otherwise healthy; motility disorder in which there is duodenogastric reflux of bile on an empty stomach over night; manage with late night meal and metoclopramide
  21. How do you diagnose chronic gastritis?
    requires and gastric biopsy to demonstrate inflammation
  22. Describe the treatment approach to idiopathic chronic gastritis. (5)
    treat underlying cause if possible, dietary trials (hypoallergenic or hydrolyzed diet), PPI or H2-blocker, prednisolone to decrease inflammation, promotility drugs (inflammation causes secondary decreased motility)
  23. What are gastric ulcers in dogs and cats clinically associated with? (7)
    drugs, increased gastric acid secretion (renal failure, mast cell tumor, liver disease, pyloric obstruction, GDV, gastrinoma), gastric neoplasia, chronic gastritis, "stress conditions" (severe illness, shock/hypotension, trauma, sepsis--> decrease blood flow to mucosa), Addison's disease, lead toxicity
  24. How do you manage GI erosions and ulcers? (4)
    eliminate predisposing factors/cause, fluids, PPI or H2-blocker, sucralfate
  25. What measures can be taken to avoid GI ulceration? (4)
    use COX-1 sparing NSAIDs for orthopedic disease, avoid concurrent use of NSAIDs and steroids, observe a washout period between NSAIDs and steroid use, use concurrent PPI while on NSAIDs
  26. What lab abnormalities often accompany GI bleeding? (5)
    regenerative anemia, iron deficiency (if chronic), hypoproteinemia, evidence of underlying cause, occult blood
  27. How do you get definitive diagnosis of GI bleeding due to ulceration?
    endoscopy or surgery
  28. What does increased eosinophils indicate in a dog or cat with chronic gastritis? How should a case like this be handled?
    parasites or dietary intolerance; empirical txt with panacur and dietary trial
  29. What mechanisms cause clinical signs associated with a gastric foreign body? (3)
    physical presence causing irritation, obstruction, or perforation; outflow obstruction (very severe signs associated with pyloric obstruction); toxins leached from FB
  30. Why are pennies minted after 1983 so dangerous to dogs? How would a patient who has ingested these pennies present?
    • made of zinc--> zinc toxicosis
    • hemolytic anemia, icterus, hemglobinuria, anorexia, vomiting,lethargy
  31. When is it acceptable to induce vomiting as treatment for a gastric foreign body, as opposed to endoscopy or gastrotomy?
    small object, no sharp edges or points, still in stomach
  32. What are complications that can occur with hairballs in cats? (3)
    obstruction, inflammation, vomiting/get trapped in nasopharynx
  33. How can you manage hairballs in cats? (5)
    manage underlying skin and/or GI disorders. hairball control diets, regular grooming, gastric lubricants, +/- promotility drugs
  34. What can cause mechanical gastric outflow obstruction? (7)
    foreign body, pyloric stenosis, mucosal hypertrophy, gastritis/ulcer near pylorus, neoplasia/polyp, GDV, secondary to intestinal obstruction
  35. How do you diagnose a functional disorder as the cause of delayed gastric emptying?
    rule out mechanical obstruction--> diagnosis of exclusion
  36. What functions disorders can cause delayed gastric emptying?
    idiopathic**, drugs, gastric inflammation, acute abdominal inflammation (pancreatitis, peritonitis), GDV, neurogenic
  37. Clinical signs of delayed gastric emptying. (5)
    recognizable food in vomitus >10hrs after eating, projectile vomiting (mechanical obstruction), bloating, belching, metabolic alkalosis
  38. Why does hypochloremic metabolic alkalosis occur with a pyloric obstruction?
    with pyloric obstruction, there is a net loss of HCl through vomiting without concurrent loss of bicarb from the duodenum; this is magnified by the fact that low Cl- prevents the kidneys from excreting bicarb in the urine.
  39. What drugs cause delayed gastric emptying? (4)
    anticholinergic drugs, opioids, beta-adrenergic agonists, vincristine
  40. Describe imaging results for delayed gastric emptying.
    • Survey abdominal radiographs: distended/food-filled stomach> 10hrs after eating; cannot make Dx by this modality unless foreign body.
    • Contrast gastrogram: can identify obstructive lesions, foreign bodies, thickening/mass lesions of pylorus or antrum; barium in stomach after 12-24hr is diagnostic.
    • Ultrasonography: ID gastric wall thickening, masses at outflow tract, external compression by pancreas or liver
  41. Does normal emptying on barium on contrast gastrogram exclude delayed gastric emptying as the diagnosis?
    NO- liquids may empty normally, while solids do not
  42. How does treatment differ for functional versus mechanical delayed gastric emptying?
    • Mechanical: surgical intervention
    • Functional: low fat, high carb diet, soft food, small frequent meals, promotility drugs (CIsapride, Metaclopramide, Eryhtromycin, Ranitidine, Nizatidine)
  43. What kind of fluids are indicated in hypochloremic metabolic alkalosis?
    0.9% saline or Ringer solution (not lactated!!) supplmented with KCl
  44. Describe the clinical presentation of gastric dilation-volvulus. How does this differ from other gastric diseases?
    non-productive retching and salivation, abdominal distention and tympany, tachycardia, pallor, shock; unlike other gastric diseases, there is no vomiting because the vomitus cannot leave the twisted stomach
  45. How do you diagnose GDV?
    readily diagnosed with abdominal radiographs
  46. How is GDV treated? (5)
    fluid therapy and immediate decompression, corticosteroids for shock, antibiotics for endotoxemia, gastropexy
  47. What are the most common malignant gastric neoplasms in dogs? Cats?
    • Dogs- gastric adenocarcinoma
    • Cats- gastric lymphoma
  48. What benign tumor is associated with chronic GI blood loss and iron deficiency anemia in dogs?
    ulcerated leiomyoma
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GI1- Gastris Disorders of SA
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