Gastric Disease Flashcards

1
Q

What are the major intrinsic factors promoting ulcer formation in the stomach?

A
  • hydrochloric acid (predominant factor)
  • bile acids
  • pepsin (pepsinogen secreted by chief cells - converted to pepsin in an acidic environment pH < 3)
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2
Q

What are the intrinsic factors protecting against ulcer formation in the stomach?

A
  • mucus-bicarbonate layer
  • maintenance of adequate mucosal blood flow
  • mucosal prostaglandin E2
  • epidermal growth factor production
  • gastroduodenal motility
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3
Q

What is the normal pH of equine gastric contents?

A
  • variable from < 2 to > 6

- dependent on dietary state (fasted vs fed)

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4
Q

What are the predominant stimuli to hydrochloric acid secretion in the stomach?

A
  • gastrin (released by G cells in antral mucosa; release controlled by gastrin-releasing peptide which is stimulated by gastric distension and increased luminal pH)
  • histamine (released by mast cells and ECL cells in the gastric gland)
  • acetylcholine via the vagus nerve
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5
Q

What are the factors that inhibit gastric acid secretion in the stomach?

A
  • somatostatin (released by fundic and antral D cells)

- epidermal growth factor (EGF), a peptide produced in saliva

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6
Q

What is the predominant mechanism responsible for squamous mucosal ulceration?

A
  • excessive acid exposure
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7
Q

What is the prevalence of ESGD and EGGD?

A
  • prevalence varies with breed, use, level of training as well as between ESGD and EGGD
  • highest prevalence of ESGD occurs in TB racehorses; 37% untrained, increasing to 80-100% within 2-3 months of training
  • prevalence of EGGD less well understood
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8
Q

Where are the majority of EGGD lesions located?

A

pyloric antrum

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9
Q

Are breed, age or sex associated with the presence of ulceration?

A
  • other factors such as intensity or duration of exercise outweigh any potential age or sex effect
  • breed effect may be present with TBs predisposed to ESGD
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10
Q

What are the nutritional risk factors associated with ulceration?

A
  • forage type - increased starch/grain intake
  • increased time between forage feeds (>6h) compared with more frequent forage feeding (<6h) increases the likelihood of ESGD
  • intermittent access to water
  • intermittent starvation causes and increases the severity of ESGD
  • NB. fasting model poorly reflects multifactorial nature of gastric disease
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11
Q

List the main clinical signs associated with EGUS

A
  • colic (postprandial; possibly due to altered GIT motility)
  • reduced appetite (mild to severe)
  • poor body condition
  • behavioural effects (inconsistently reported)
  • poor performance - direct consequence of gastric pain?; other factors need to be considered
  • differences in clinical signs between ESGD and EGGD unknown
  • NB. wide variety of clinical signs may be present but they are nonspecific and poorly associated with presence of EGUS
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12
Q

Which age group is more commonly affected by gastroduodenal ulcer disease (GDUD)

A
  • suckling and early weaning foals
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13
Q

What are the potential complications of GDUD?

A
  • gastric or duodenal rupture
  • pyloric or duodenal stricture
  • ascending cholangitis
  • severe squamous and oesophageal ulceration and aspiration pneumonia can occur secondary to gastro-oesophageal reflux
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14
Q

List the causes of primary gastric dilation

A
  • gastric impaction
  • grain engorgement
  • excessive water intake after exercise
  • aerophagia
  • parastism
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15
Q

List the causes of secondary gastric dilation

A
  • (more common than primary dilation)
  • primary intestinal ileus
    small or large intestinal obstruction
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16
Q

Describe the common location and features of gastric rupture

A
  • usually along greater curvature
  • if resulting from gastric dilation, tears in seromuscular layer frequently larger than corresponding tears in mucosal layer
  • if secondary to gastric ulceration, usually full-thickness tears of equal sizes in all layers