GI1- Gastris Disorders of SA

acute vomiting in an otherwise healthy animal

chronic vomiting of food or bile, usually otherwise healthy

hematemesis, melena, +/- anemia

non-productive retching, abdominal distention, tchycardia

acute or chronic vomiting of food >10hrs after eating

chronic vomiting, weight loss, +/- hematemesis, +/- anemia of chronic disease

• 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

NSAIDs block cyclooxygenase enzymes (COX-1 and COX-2), which are critical in the synthesis of protective prostaglandins

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

drugs, food, chemicals, toxins, foreign bodies, infectious agents, and parasites

NSAIDs and glucocorticoids

hyperacidity, bile, pancreatic enzymes, decreased mucosal blood flow

idiopathic***, dietary indiscretion, food sensitivity, foreign body, drugs, parasites, infectious causes, toxins, immune-mediated, motility disorders, secondary to systemic disease

• 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

• 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

• 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

amoxicillin, clarithromycin, maybe metronidazole and a PPI (maybe H2 blocker)

Physaloptera rara; ingestion of beetles, crickets, cockroaches, rodents, or snakes

endoscopy (fecal not reliable at all); fenbendazole, pyrantel, or ivermectin

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

requires and gastric biopsy to demonstrate inflammation

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)

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

eliminate predisposing factors/cause, fluids, PPI or H2-blocker, sucralfate

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

regenerative anemia, iron deficiency (if chronic), hypoproteinemia, evidence of underlying cause, occult blood

endoscopy or surgery

parasites or dietary intolerance; empirical txt with panacur and dietary trial

physical presence causing irritation, obstruction, or perforation; outflow obstruction (very severe signs associated with pyloric obstruction); toxins leached from FB

• made of zinc--> zinc toxicosis
• hemolytic anemia, icterus, hemglobinuria, anorexia, vomiting,lethargy

small object, no sharp edges or points, still in stomach

obstruction, inflammation, vomiting/get trapped in nasopharynx

manage underlying skin and/or GI disorders. hairball control diets, regular grooming, gastric lubricants, +/- promotility drugs

foreign body, pyloric stenosis, mucosal hypertrophy, gastritis/ulcer near pylorus, neoplasia/polyp, GDV, secondary to intestinal obstruction

rule out mechanical obstruction--> diagnosis of exclusion

idiopathic**, drugs, gastric inflammation, acute abdominal inflammation (pancreatitis, peritonitis), GDV, neurogenic

recognizable food in vomitus >10hrs after eating, projectile vomiting (mechanical obstruction), bloating, belching, metabolic alkalosis

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.

anticholinergic drugs, opioids, beta-adrenergic agonists, vincristine

• 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

NO- liquids may empty normally, while solids do not

• Mechanical: surgical intervention
• Functional: low fat, high carb diet, soft food, small frequent meals, promotility drugs (CIsapride, Metaclopramide, Eryhtromycin, Ranitidine, Nizatidine)

0.9% saline or Ringer solution (not lactated!!) supplmented with KCl

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

readily diagnosed with abdominal radiographs

fluid therapy and immediate decompression, corticosteroids for shock, antibiotics for endotoxemia, gastropexy

• Dogs- gastric adenocarcinoma
• Cats- gastric lymphoma

ulcerated leiomyoma