lecture 9 - digestive ulcer syndrome Flashcards
equine stomach is seperated into what 2 regions
grandular and non-grandular
- by ‘margo plicatus’
Non-glandular region
esophogeal region
- lacks protective mucosal and bicarbonate layers
Glandular region
protective mucosal and bicarbonate layers
extensive capillary network
rapid healing
gastric ulcer
alteration in gastric mucosa damaging cells of the glandular and non glandular region
erosion
not as sever but common precursor for ulcer development
Prevalence of gastric ulcers
vigorous race training
- 70-90% in non glandular region
- thoroughbred 91% / standardbreds 70-87%
performance horses
- 40-70%
equine gastric ulcer syndrome
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
causes of gastric ulcer syndrome
diet feeding schedule stress - stall confinement - transport exercise intensity NSAIDs (advil)
diets effects
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
feeding schedule effects
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
stress effects
stall confinement
- high grain, intermittently fed, lack exposure to other horses
transport
- decrease feed and water consumption
- supresses immune system
effects of high intensity exercise
- increase abdominal pressure
- decreased stomach volume during exercise
- increase serum gastrin
NSAIDs
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
Clinical symptoms of gastric ulceration syndrome
abdominal discomfort poor hair coat loss of appetite poor body composition weight loss diarrhea decreased performance depression
Diagnosis of EGUS
no known laboratory markers
- potentially serum gastrin, fecal occult blood, urinary sucrose concentration
gastric endoscopy only reliable method
gastroscopy method
flexible endoscope 2m long
fiberoptic endoscope
- glass fibre bundles transmit light to examined area
videoendoscope
- glass fiber bundles transmit light, additional devices transmit image
gastroscopy procedure
12-16hrs fasted sedative flexable endoscope fed into stomach gastric contents can be flushed examine different regions of stomach grading of mucosa
grading of ulcers
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)
egus treatment
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
mycotoxin contamination link to EGUS
- study
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
