EqMed, Q2, II

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  1. what part of the stomach contains stratified squamous epithelium?
    non glandular portion (continuous with esophagus epithelium)
  2. what 3 receptors are required for the secretion of gastric acid? what pump then allows for secretion of HCl? 4
    • histamine 2
    • gastrin
    • acetylcholine
    • H-K-ATPase pump
  3. since the stratified squamous portion of the stomach has no protective layer from HCl, how is it protected from acid injury?
    • highly impermeable until pH <2.5 (then damage would occur)
    • feed bolus in lower portion protects from exposure to HCl/bile acid
  4. what are glandular mucosa defenses against HCl? 4
    • mucus barrier
    • HCO3 secretion
    • rapid regeneration and repair
    • reflux of basic duodenal secretions
  5. how does grain affect pH environment in stomach?
    • less chewing required so less saliva
    • more VFAs produced in gastric fluid
  6. what is legume forage (alfalfa) effect on pH in stomach?
    great buffering effect - protects squamous epithelium from exposure to HCl
  7. How does exercise affect gastric physiology?
    • withholding feed and feeding high concentration diets incr. risk of mucosal injury
    • strenuous exercise decr. pH in upper portion
    • "sloshing effect"
  8. what is role of prostaglandins in gastric physiology?
    • PGI2 - vasodilation so adequate blood flow
    • PGE2 - encourages mucus secretion to protect mucosa
  9. where are erosions/ulcers usually found in the stomach? how does this compare to where foals get ulcers?
    • squamous epithelium along margo plicatus
    • (foals get primary gastric/duodenal ulcer disease)
  10. what are some risk factors associated with adult horses acquiring EGUS? 6
    • housing in stalls, meal feeding
    • stress, show horses
    • high CHO diets
    • incr. exercise intensity; race horses
    • NSAIDs
    • H. pylori
  11. what are some clinical signs associated w/EGUS in adults? 6
    • mild intermittent colic (coincides with meals)
    • decr. appetite; failure to finish grain
    • loss of body condition
    • poor hair coat
    • alterations in attitude
    • (so CS may not be severe or obvious)
  12. how do you definitively diagnose EGUS?
    gastroscopy on fasted patient
  13. what is expected PCV/TS on patient with EGUS? Will there be blood in the feces?
    • normal PCV/TS (no anemia)
    • not even occult blood in feces - microbes break it down
  14. what is the difference between grade 0 and 1 ulcer?
    • 0: WNL
    • 1: mucosa intact, squamous hyperkeratosis
  15. how is grade 2, 3, and 4 ulcer described?
    • 2: small single/multifocal lesions
    • 3: large, superficial
    • 4: extensive lesions/deep ulcerations
  16. what do you do for a suspected EGUS patient if scoping not available?
    • treat anyway - response to tx is considered diagnostic
    • (improved attitude/appetite/coat/resolution of colic)
  17. what is the goal of EGUS treatment?
    • incr. gastric pH and decr. HCl secretion
    • (incr. roughage, decr. grain, meds to alter HCl secretion)
  18. what are some examples of H2 receptor antagonists? 4
    • ranitidine (extended period of therapy required)
    • cimetidine (high doses req)
    • famotidine
    • nizatidine
  19. what are advantages of using Omeprazole (H+pump inhibitor) instead of histamine blockers? 4
    • in addition to decr. HCl, can also promote healing of ulcer
    • low doses can PREVENT ulcer formation
    • only licenced product for tx/prevention
    • single daily dose
  20. what is MOA for sucralfate? what are some disadvantages of this med? 4
    • adheres to ulcerated mucosa
    • stimulates mucus secretion
    • enhances mucosal blood flow and PGE2 synthesis
    • (does NOT promote healing of ulcers and can interfere w/absorption of other meds)
  21. antacids like maalox can coat/soothe stomach but what is problem with using these meds?
    • requires high doses every 2 hours
    • (can be helpful in tx of foals)
  22. how is treatment different with pyloric ulcers?
    may need prolonged therapy; more difficult to resolve
  23. how is gastric impaction treated?
    • gastric lavage via NGT w/warm water
    • DSS detergent to break up impaction
    • bethanecol to encourage emptying
  24. what is a differential cause of gastric impaction if horse lives in UK or South America?
    equine dysautonomia (grass sickness)
  25. In addition to gastric rupture secondary to dilation, what is a reason the stomach would rupture without distention? how is this treated?
    • ischemic infarct of portion of stomach
    • result of gastric ulceration
    • -gastric rupture is a terminal event - no tx -euthanize
  26. what is most common stomach neoplasia in horses?
    • squamous cell carcinoma in teen/geriatrics
    • -can met; no effective therapy
  27. what is the hallmark of malabsorption?
    weight loss
  28. what diagnostic tool is most reliable in evaluating the small intestine?
  29. is small intestine palpable on rectal palpation?
    not in normal/healthy patient but can feel if distended (always an abnormal finding)
  30. Colic signs and copious gastric reflux is a symptom of acute or chronic SI disease? what are expected peritoneal fluid findings? what would US show?
    • acute
    • elevated TP
    • US: dilated loops of SI
  31. what is classic indication of chronic SI disease? how is chronic SI disease demonstrated on US?
    • weight loss (+/- signs of colic)
    • thickened walls (+/- dilation)
    • -chronic patients can have acute episodes
  32. In horses, IBD is typically defined by which cells? how is definitive diagnosis made?
    • granulocytic = eosinophils, lymphocytes, macrophages
    • need histopathology
  33. Which form of IBD is NOT associated with weight loss?
    idiopathic focal eosinophilic enteritis (IFEE - focal and acute)
  34. What is appetite like with IBD? Is there signs of pain? Diarrhea?
    • weight loss despite good appetite
    • intermittent colic
    • diarrhea NOT typical sign of SI disease
  35. Is total protein affected by IBD?
    • yes, PLE
    • hypoalbuminemia w/o liver disease or proteinuria
    • peripheral edema
  36. what would glucose absorption curve look like with IBD? what would abdominocentesis show?
    • flat line, no peak
    • elevated protein but this is not specific
  37. what is treatment for IBD?
    immunosuppressive doses of steroids - largely unsuccessful and can trigger laminitis
  38. what type of surgery can be done for IBD?
    if intramural lesions are present, resection is indicated
  39. what signalment is associated with granulomatous enteritis?
    young standardbred; genetic predisposition
  40. what would histopath show to indicate granulomatous enteritis? what is the cause?
    • macrophages ("granulomatous")
    • unknown cause (may include Mycobacterium avium)
  41. which form of IBD has a dermatitis component? old or young horses?
    • multisystemic eosinophilic epitheliotropic enterocolitis (MEED)
    • young
    • *diarrhea* also component of MEED
  42. what cell is seen on histopath? cause?
    • tissue eosinophilia (also lymphs and macrophages)
    • hypersentitivity? eosinophils in GI but also other tissues/organs
  43. Which form of IBD is rare and histopath shows lymphs and plasma cells in lamina propria w/ villous atrophy?
    lymphocytic-plasmacytic enterocolitis
  44. Which form of IBD will have NO evidence of PLE?
    idiopathic focal eosinophilic enteritis (newly discovered syndrome)
  45. how is IFEE treated that differs from the other form of IBD?
    IFEE usually responds to surgical decompression without required resection (other forms usually require resection of lesions)
  46. does IFEE present with acute signs or persist quietly/chronic?
    acute signs of colic
  47. what obligate intracellular bacterium infects young foals (4-6mo) and is transmitted via fecal-oral route?
    lawsonia intracellularis
  48. what are some risk factors associated with lawsonia problems?
    • overcrowding, diet change, transport, weaning
    • (usu. seen in Fall, Winter)
  49. what is the hallmark sign of lawsonia?
    chronic wasting
  50. is there a PLE associated w/Lawsonia infections? what is appearance of intestines?
    • yes, severe hypoproteinemia (and peripheral edema)
    • corrugated, thickened SI w/mucosal ulceration
  51. What part of the intestine does Lawsonia have an affinity for? what does this cause?
    *crypt cells* - decreased brush border enzyme capacity - can't absorb nutrients - wt. loss +/- malabsorptive diarrhea
  52. what do CBC results show with lawsonia infection? 5
    • mod-severe hypoproteinemia
    • mild anemia
    • hyperfibrinogenemia
    • neutrophilic leukocytosis
    • prerenal azotemia/electrolyte imbalances if diarrhea
  53. what is the gold standard for diagnosing lawsonia? what is prognosis for positive results?
    • isolation/culture from tissue (difficult; Warthin Starry silver stain)
    • good 93% survival (but smaller stature; slower growth)
  54. What sample is needed for PCR of lawsonia?
    • PCR on tissue is sensitive and specific
    • (false pos. if use feces)
  55. what antibiotics are appropriate for tx of lawsonia?
    • Abs that target intracellular organisms
    • -tetracyclines (oxy then doxy up to 17days)
    • -macrolides (erythromycin) + rifampin
  56. what is a characteristic sign of duodenal-proximal jejunal enteritis (DPJ)?
    high volumes of enterogastric reflux (due to excessive fluid/electrolyte secretion into SI)
  57. is DPJ functional or mechanical ileus? is it painful?
    • functional ileus
    • abdominal pain and distention
  58. How would you describe gross lesions of duodenum with DPJ?
    • serositis - bright red to dark ecchymotic hemorrhages
    • fibrinopurulent serosal exudate
    • hyperemia/edema
  59. Is surgery needed for patients with DPJ?
    no, but need to distinguish DPJ from mechanical obstructions that do require sx
  60. Since DPJ is an inflammatory syndrome, what are expected PE findings? 5
    • *fever* (Ddx from mechanical obst.which will not have fever)
    • tachycardia, tachypnea
    • decr. borborygmi; mild/mod/severe colic pain
    • dehydration/volume depletion
    • endotoxemia
  61. how do you distinguish DPJ from mechanically obstructed patient?
    • decompression of reflux in DPJ will lead to relief/depression
    • decompression in obstruction/strangulation will not help pain symptoms
  62. how will US differ in DPJ vs. obstructed/surgery patient?
    • DPJ- thickened walls, fluid filled loop distention, poor motility
    • sx case: dilation, no motility, sediment line
  63. what are peritoneal fluid findings for DPJ?
    • dark yellow/orange (but NOT serosanguinous as will obstruction/deteriorated bowel)
    • high protein (>2.5)
    • normal to slightly elevated WBC (higher WBC with deterioration)
  64. what is treatment for DPJ? 7
    • gastric decompression (indwelling stomach tube)
    • IV fluids to replace losses
    • NSAIDs/lidacain CRI (caution ulcers)
    • prokinetics (metaclopramide, bethanecol, erythromycin)
    • +/- Abs (if WBC very low may need)
    • NPO at least 3 days; TPN
    • laminits prophylaxis (inflammation -endotoxemia)
  65. what are some complications associated with DPJ and treatment? 7
    • laminitis
    • thrombophlebitis
    • adhesions within peritoneum (fibrinous exudates on serosa)
    • peritonitis
    • esophagitis/pharyngitis - rupture
    • cardiac arrythmias (balance electrolytes, acid/base)
    • $$$ - several days in hospital
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EqMed, Q2, II
2013-03-17 15:02:23
EqMed Q2 II

EqMed, Q2, II
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