GI1- UE Disorders

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  1. What are primary signs of SA UGI disease? (3)
    dysphagia, regurgitation, vomiting
  2. What are secondary signs of SA UGI disease? (9)
    anorexia, polyphagia, hypersalivation, retching, abdominal pain, bloat, weight loss, melena, cough
  3. What is the difference between regurgitation and vomiting?
    regurgitation means the material is coming from the esophagus; vomiting is a reflex initiated in the brain, causing food to be brought back up from the stomach or intestine
  4. Where does the clinical sign of "dysphagia" localize to?
    oral cavity, pharynx, upper esophagus
  5. Where does the clinical sign of "regurgitation" localize to?
    esophagus
  6. Where does the clinical sign of "vomiting" localize to?
    stomach
  7. Describe regurgitating clinically. (5)
    passive event, not a reflex, influence by mechanical events in the esophagus, little/no warning, often associated with eating, undigested food
  8. What are characteristics of dysphagia? (6)
    retching, choking, gagging, repeated swallowing, painful swallowing, difficulty drinking
  9. Give a clinical description of vomiting. (4)
    prodromal signs (drooling, nausea, anxious), retching, abdominal contractions, not releated to eating
  10. If there is bile in the material that has come up, what does that suggest?
    vomit
  11. What are potential complications of vomiting? (3)
    dehydration, electrolyte imbalances, aspiration pneumonia (ess common than with regurg)
  12. What are the clinical signs of GI bleeding? (5)
    hematemesis, melena, pale mm, anemia, iron deficiency (chronic)
  13. What are clinical signs of delayed gastric emptying? (5)
    recognizable food in vomitus >10hrs after eating, projectile vomiting, bloating, belching, metabolic alkalosis
  14. How can you differentiate between upper and lower esophageal causes of regurgitation?
    • Pharynx/ Upper esophagus- choking, gagging, salivation, multiple attempts to swallow, inability to drink
    • Lower esophagus- single attempt to swallow, ability to drink retained
  15. Is aspiration pneumonia more likely to be a complication of regurgitation or vomiting?
    more likely to be associated with regurgitation
  16. What are the most useful imaging methods for GI disease? (4)
    survey radiographs, endoscopy, contrast radiography, fluoroscopy (referral center), ultrasonography
  17. What are the limitations to endoscopy? (3)
    submucosal and muscularis lesions, motility disorders, lesions beyond the reach of the scope (jejunum)
  18. What are indications for endoscopy?(7)
    mucosal biopsy, cytology/microbiology of mucosa, retrieval of gastric or esophageal foreign bodies, balloon dilation of esophageal strictures, placement of gastrotomy tube for nutritional support, polypectamy, monitor therapy
  19. When would surgery be preferred over endoscopy? (5)
    full thickness biopsies, surgical resection of mass lesions, large foreign bodies, evaluation of small intestine (inaccessible to scope), ability to biopsy other organs
  20. What are indications for use of gastroprotectants? (4)
    gastroduodenal erosions or ulcers, reflux esophagitis, gastritis, hypersecretory states (gastrinoma)
  21. What are categories of gastroprotectants? (4)
    histamine-receptor blockers, proton pump inhibitors, sucralfate, prostaglandin analogs
  22. Inhibition of histamine receptors blocks: (3)
    basal acid secretion, nocturnal acid secretion, meal-stimulated acid secretion
  23. Which histamine-receptor blocker has been used for years but recent studies have found that it is not effective in increasing gastric pH?
    Ranitidine
  24. What are some examples of effective (as far as we know) histamine-receptor blockers? (3)
    Cimetidine, Famotidine, Nizatidine
  25. What 2 histamine-receptor blockers also have promotility effects? How do they work?
    Ranitidine and Nizatidine; inhibit acetycholinesterase
  26. How do proton pump inhibitors work?
    inhibit parietal cell ATPase (final phase of H+ secretion)
  27. What are some examples of proton pump inhibitors? (3)
    Omeprazole (prilosec), Iansoprazole (prevacid), Pantoprazole (injectable)
  28. What is the mechanism of action of Famotidine?
    histamine H2 receptor blocker, blocking H2 receptor on gastric parietal cells by competitive inhibition
  29. What is the brand name of Famotidine, and what are its indications? (3)
    Pepsid; gastroduodenal erosions/ulcers, reflux esophagitis, gastritis
  30. What are the contraindications/adverse effects of Famotidine?
    • Contraindications- decrease dose in renal failure
    • Adverse effects- none
  31. What is the mechanism of action of Omeprazole?
    proton pump inhibitor; inhibits H+K+ATPase in parietal cell membrane to inhibit the final step in acid secretion
  32. What is the brand name of Omeprazole, and what are its indications? (4)
    Prilosec; gastroduodenal erosions/ ulcers, reflux esophagitis, gastritis, hypersecretory states (gastrinoma)
  33. What are the contraindications and adverse effects of Omeprazole?
    none- very safe
  34. What is the mechanism of action of Sucralfate?
    aluminum salt of sucrose sulfate that forms a protective barrier, which binds to ulcer crater and inactivates gastric pepsin, adsorbs to bile acids and pancreatic acids, and stimulates protective mucosal prostaglandins
  35. What is the brand name for Sucralfate, and what are is indications? (2)
    Carafate; gastroduodenal erosions/ ulcers, esophagitis (suspension form only)
  36. What are contraindications and adverse effects of Sucralfate?
    no contraindications; adverse effects- constipation
  37. What is the mechanism of action of Metaclopramide?
    • 5HT4 agonist, 5HT3 antagonist- increased release of acetylcholine and sensitization of of muscarinic receptors to increase GES resting tone, increase tone and amplitude of gastric contractions with relaxation of pylorus, and increase peristalsis of proximal small intestine
    • blocks dopamine receptors in the CRTZ to act as antiemetic
  38. What is the brand name of Metaclopramide, and what are its indications? (3)
    Reglan; broad spectrum antiemetic, reflux esophagitis, functional gastric emptying disorder
  39. What are contraindications and adverse effects of Metaclopramide?
    • Contraindications- mechanical gastric outflow obstruction, epilepsy
    • Adverse effects- anxiety, irritability, constipation
  40. What is the mechanism of action of Cisapride?
    5HT4 agonist; serotonergenic effect on cholinergic neurons of GI smooth muscle
  41. What is the brand name of Cisapride, and what are its indications? (4)
    Propulsid; esophageal motility disorders of CATS ONLY, reflux esophagitis, gastric and intestinal hypomotility, colonic hypomotility
  42. What are contraindications and adverse effects of Cisapride?
    • Contraindications- decrease dose with hepatic failure
    • Adverse effects- none reported in dogs and cats; caused fatal arrhythmias in humans
  43. What are the 3 major stimuli for gastric acid secretion by the parietal cell?
    • histamine- stimulates H2 receptors
    • acetylcholine- stimulates M3 muscarinic receptors
    • gastrin- stimulates CCK2 receptors and causes histamine secretion by ECL cells
  44. Why would H2 receptor blockers be effective to treat excess gastric acid secretion caused by increased gastrin release?
    because gastrin is a minor contributor to HCl release; it stimulates release of histamine from local ECL cells, and histamine is the major contributor to HCl release
  45. Are histamine receptors blockers or PPIs more potent in suppressing gastric acid secretion?
    When given BID, PPIs are significantly more effective than H2 blockers at raising gastric pH
  46. What H2 blockers have promotility effects on the GI tract and what is the mechanism?
    Ranitidine and Nizatidine; inhibit acetylcholinesterase
  47. Is Metaclopramide or Cisapride a more effective promotility drug?
    Cisapride
  48. Compare the effects on segments of the GI tract between Metaclopramide and Cisapride.
    • Cisapride affects esophagus (cats), GES, stomach, small intestine, and colon smooth muscle
    • Metaclopramide affects GES, stomach, and proximal small intestine [no effects on distal GI!!!]
  49. Compare the antiemetic effects of Cisapride and Metaclopramide.
    only Metaclopramide has antiemetic effects
  50. Compare the commercial availability of Cisapride and Metaclopramide.
    Cisapride was taken off the market when it caused fatal arrhythmias in humans
  51. What is the mechanism for promotility effects in dogs of the antibiotic Erythromycin? What are indications for its use?
    motilin-like effects on the stomach and small intestine; use when there is no response to Metaclopramide or Cisapride
  52. What is an important factor in using Carafate?
    must be given an hour apart from other oral drugs because it will bind and inactivate them
  53. What is Misoprostal?
    prostaglandin analog, prevents acid secretion
Author:
Mawad
ID:
314899
Card Set:
GI1- UE Disorders
Updated:
2016-02-06 17:50:43
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vetmed GI1
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vetmed GI1
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