lecture 9 - digestive ulcer syndrome Flashcards

1
Q

equine stomach is seperated into what 2 regions

A

grandular and non-grandular

- by ‘margo plicatus’

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2
Q

Non-glandular region

A

esophogeal region

- lacks protective mucosal and bicarbonate layers

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3
Q

Glandular region

A

protective mucosal and bicarbonate layers
extensive capillary network
rapid healing

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4
Q

gastric ulcer

A

alteration in gastric mucosa damaging cells of the glandular and non glandular region

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5
Q

erosion

A

not as sever but common precursor for ulcer development

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6
Q

Prevalence of gastric ulcers

A

vigorous race training

  • 70-90% in non glandular region
  • thoroughbred 91% / standardbreds 70-87%

performance horses
- 40-70%

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7
Q

equine gastric ulcer syndrome

A

single or multiple erosions and ulcerations due to lack of protective factors in non-glandular and glandular portions of the stomach, distal esophagus and proximal duodenum

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8
Q

causes of gastric ulcer syndrome

A
diet
feeding schedule
stress
- stall confinement 
- transport
exercise intensity
NSAIDs (advil)
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9
Q

diets effects

A

bad:
high concentrate diets
- increase serum gastrin
- stomach pH < 4

good:
alfalfa hay shown to have protective effects
good quality hay and pasture decreases risk

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10
Q

feeding schedule effects

A

bad:
intermittent feeding
- rapid pH decrease, high acid exposure to non-glandular mucosa

good:
continuous feeding
- continuous flow of saliva and ingesta that buffers stomach pH

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11
Q

stress effects

A

stall confinement
- high grain, intermittently fed, lack exposure to other horses

transport

  • decrease feed and water consumption
  • supresses immune system
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12
Q

effects of high intensity exercise

A
  • increase abdominal pressure
  • decreased stomach volume during exercise
  • increase serum gastrin
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13
Q

NSAIDs

A

non steroidal anti-inflammatory drugs
- phenylbutazone and flunixinmegulamine

increased ulceration of “glandular” muscosa

prostaglandin inhibition

  • decrease muscosal blood flow
  • decrease mucus production
  • increase HCl secretion
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14
Q

Clinical symptoms of gastric ulceration syndrome

A
abdominal discomfort
poor hair coat
loss of appetite
poor body composition
weight loss
diarrhea
decreased performance 
depression
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15
Q

Diagnosis of EGUS

A

no known laboratory markers
- potentially serum gastrin, fecal occult blood, urinary sucrose concentration

gastric endoscopy only reliable method

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16
Q

gastroscopy method

A

flexible endoscope 2m long

fiberoptic endoscope
- glass fibre bundles transmit light to examined area

videoendoscope
- glass fiber bundles transmit light, additional devices transmit image

17
Q

gastroscopy procedure

A
12-16hrs fasted
sedative
flexable endoscope fed into stomach
gastric contents can be flushed
examine different regions of stomach
grading of mucosa
18
Q

grading of ulcers

A
described by
- location, pattern, distribution, depth
graded 0 to 5
multiple scoring developed
- macallister (0 to 5)
- andrews (0 to 4)
- bain (0 to 3)
19
Q

egus treatment

A

hay based diet

proton pump inhibitors

  • omeprazole oral paste 4mg/kg
  • inhibit gastric acid secretion

histamine type-2 receptor antagonist

  • ranitidine
  • inhibits histamine secretion
  • maintains ph of 4.6
20
Q

mycotoxin contamination link to EGUS

- study

A

9 horses, 3 treatments

  • stall confinement with minimal pasture (higher risk)
  • gastrocopy and tissue biopsies
  • normal, contaminated and 2% absorbent

ulcer scores - no effect
gastrin - no effect
correlation analysis - none

hematological and serum biochemical parameters

  • decreased total protein
  • increased free bilirubin

histological evaluation

  • glandular region - increased mononuclear cells
  • microorganisms - present in glandular and non regions

Conclusion

  • fusariummy mycotoxins negative blood parameters
  • no EGUS development, but possible effect on protective factors in glandular region
  • absorbent no effect
  • gastrin no indicator of ulcer development