Disorders of the stomach and esophagus

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Last updated 6:42 PM on 9/19/26
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23 Terms

1
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How do you clinically differentiate Vomiting from Regurgitation?

  • Vomiting: An active process preceded by nausea (ptyalism, lip licking, anxiety) and accompanied by abdominal contractions/retching. Expels food or bile from the stomach/small intestine.

  • Regurgitation: A passive process without nausea or prodromal abdominal contractions. Expels undigested food or saliva directly from the esophagus. Localizes disease directly to the esophagus.


2
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What are the primary behavioral and physical indicators of Nausea in small animals?

Turning head away from food, excessive salivation (ptyalism), lip licking, pacing, and an anxious facial expression.

3
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What are the primary etiologies of Megaesophagus?

  • Congenital (uncommon): Seen in Irish Setter, Great Dane, German Shepherd, Labrador Retriever, Chinese Shar-Pei, Newfoundland, Miniature Schnauzer, and Fox Terrier.

  • Idiopathic: Most common form in adult dogs.

  • Acquired Secondary: Caused by underlying focal or diffuse neuromuscular diseases (e.g., Myasthenia Gravis, Hypoadrenocorticism, Polyneuropathy).


4
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What is the primary cause of mortality in patients with Megaesophagus?

  • Aspiration Pneumonia resulting from regurgitated esophageal contents.


<ul><li><p><strong>Aspiration Pneumonia</strong> resulting from regurgitated esophageal contents.</p></li></ul><p></p>
5
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What are the most common causes of Esophagitis?

  • Gastroesophageal (GE) Reflux (secondary to general anesthesia, hiatal defects, or malpositioned feeding tubes).

  • Persistent vomiting (gastric acid exposure).

  • Esophageal foreign bodies.

  • Caustic agents (e.g., Paraquat).

  • Retained oral medications/pills (Doxycycline, Tetracycline).


6
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How does Esophagitis exacerbate gastroesophageal reflux?

  • Mucosal inflammation reduces Lower Esophageal Sphincter (LES) tone, which allows progressive, worsening gastric acid reflux in a self-perpetuating cycle.


7
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What is the gold standard diagnostic tool for Esophagitis?

Endoscopy (Esophagoscopy). Radiographs are insensitive unless a hiatal hernia or secondary megaesophagus is present.

8
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What medical therapies are indicated for the management of Esophagitis?

  • Gastric Acid Suppression: Proton Pump Inhibitors (Omeprazole) are superior to H2 receptor antagonists (Famotidine), though Omeprazole takes 2–5 days for maximum efficacy.

  • Prokinetics: Cisapride (more effective) or Metoclopramide to increase LES tone and accelerate gastric emptying.

  • Esophageal Mucosal Protections: Sucralfate suspension.

  • Enteral Support: Gastrotomy feeding tube placement if oral intake is painful.


9
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What are the most common causes of Acute Gastritis?

Ingestion of garbage/contaminated food, foreign objects, toxic plants/chemicals, irritating drugs (NSAIDs), and infectious agents (viral, bacterial).

10
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What differential diagnoses must be ruled out before diagnosing Acute Gastritis?

Gastric/intestinal foreign body or obstruction, Canine Parvovirus, Uremia, Diabetic Ketoacidosis (DKA), Hypoadrenocorticism (Addison's disease), Hepatic disease, Hypercalcemia, and Pancreatitis. (Acute gastritis is a diagnosis of exclusion).

11
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What is the medical management protocol for Acute Gastritis?

  • Fluid Therapy: IV crystalloid rehydration and maintenance.

  • Antiemetics: Maropitant, Ondansetron, Metoclopramide, or Dimenhydrinate.

  • Dietary Management: Withhold food until vomiting is controlled, then introduce a bland diet (e.g., 1 part boiled chicken or cottage cheese to 2 parts boiled rice/potato) and transition to normal food over 1 week.

  • Gastroprotectants/Adsorbents: Sucralfate, Kaolin-pectin, Bismuth subsalicylate, or Activated charcoal.

  • Note: Antibiotics and glucocorticoids are rarely indicated.


12
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What primary diseases and risk factors trigger Gastric Ulceration and Erosion?

  • Drug-Induced: NSAIDs and Glucocorticoids (most common).

  • Metabolic/Endocrine: Hypoadrenocorticism, Uremia, Hepatic Disease, Mastocytosis/Mast Cell Tumor (hypergastrinemia/histamine release), DIC.

  • Neoplastic: Leiomyoma, Adenocarcinoma, Lymphoma, Mast Cell Tumor.

  • Inflammatory: Severe gastritis.

  • Hypotension/Ischemia: Shock, sepsis.

  • Idiopathic/Stress: Extreme exercise (sled dogs), spinal surgery.


<ul><li><p><strong>Drug-Induced:</strong> <strong>NSAIDs</strong> and <strong>Glucocorticoids</strong> (most common).</p></li><li><p><strong>Metabolic/Endocrine:</strong> Hypoadrenocorticism, Uremia, Hepatic Disease, Mastocytosis/Mast Cell Tumor (hypergastrinemia/histamine release), DIC.</p></li><li><p><strong>Neoplastic:</strong> Leiomyoma, Adenocarcinoma, Lymphoma, Mast Cell Tumor.</p></li><li><p><strong>Inflammatory:</strong> Severe gastritis.</p></li><li><p><strong>Hypotension/Ischemia:</strong> Shock, sepsis.</p></li><li><p><strong>Idiopathic/Stress:</strong> Extreme exercise (sled dogs), spinal surgery.<br></p></li></ul><p></p>
13
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What key CBC and Biochemistry abnormalities are characteristic of chronic Gastric Ulceration?

  • CBC: Initially a regenerative anemia that progresses over time to a microcytic, hypochromic, non-regenerative anemia (iron deficiency anemia due to chronic blood loss). Accompanying thrombocytosis and elevated neutrophilia.

  • Biochemistry: Significantly elevated Blood Urea Nitrogen (BUN) with a normal Creatinine (due to digestion and absorption of blood proteins / GI bleeding).


14
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What is the drug of choice for treating or preventing NSAID-induced gastric ulcers?

  • Misoprostol (a synthetic Prostaglandin E1/E2 analogue).


15
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What therapeutic options are indicated for severe, acute, or hypersecretory Gastric Ulceration?

  • Proton Pump Inhibitors: Omeprazole (superior acid suppression).

  • H2-Receptor Antagonists: Famotidine, Ranitidine.

  • Mucosal Coating: Sucralfate (binds to exposed ulcer beds).

  • Somatostatin Analogue: Octreotide (for rapid reduction of gastric acid in hypersecretory states with large ulcers).

  • Analgesia: Opioids or Tramadol.

  • Surgical Resection: Indicated for large, bleeding, or non-healing ulcers.


16
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How is Chronic Gastritis definitively diagnosed and classified?

  • Definitively diagnosed by endoscopic gastric mucosal biopsy. It is classified histopathologically based on the predominant inflammatory cell infiltrate:

    1. Lymphocytic-Plasmacytic

    2. Eosinophilic

    3. Granulomatous

    4. Lymphoid Follicular


17
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What are the main clinical signs of Chronic Gastritis?

  • Intermittent vomiting of food or bile, decreased appetite, weight loss, melena, hematemesis, and potential dermatologic signs (if secondary to food allergy/dietary hypersensitivity).


18
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What step-by-step approach is taken to treat Idiopathic Chronic Gastritis?

  • Dietary Trial: 2-to-3 week trial with a novel or hydrolyzed protein diet.

  • Empirical Deworming: Especially if eosinophilic infiltrate is present.

  • Immunosuppression: Prednisolone if non-responsive to diet.

  • Refractory Cases: Add Azathioprine (dogs) or Chlorambucil (cats).

  • Prokinetics: Metoclopramide, Cisapride, or Erythromycin if delayed gastric emptying is present.


19
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What is the clinical consensus on treating Helicobacter spp. in dogs and cats?

  • Helicobacter has a very high prevalence in normal and sick dogs and cats; its definitive role as a primary pathogen remains debated.

  • Triple therapy (Amoxicillin, Metronidazole, Famotidine + Bismuth) improves vomiting in 90% of cases, but achieves clearance of the organism in only 40% of animals.

  • Treatment decisions are made on an individual basis based on biopsy results and persistent clinical signs.


20
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What physiological process helps localize disease directly to the esophagus?

Regurgitation

21
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What is the primary cause of mortality in megaesophagus?

Aspiration pneumonia

22
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What can be used for gastric acid suppression?

Omeprazole (PPI) is superior to H2-receptor blockers (Famotidine)

23
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What samples are required to definitely classify and treat chronic gastritis?

Gastric mucosal biopsies