GI Diseases Flashcards

1
Q

What is EGGD thought to result from and what does the mucosal layer consist of?

A

• Breakdown of defense against acid
• reduced blood supply
• altered gastric production

Normal layer: bicarbonate, gastric mucus (glycoproteins, water, electrolyte, antibodies)

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2
Q

Histopathologic features of EGGD

A

Erosive, inflammatory, usually non-ulcerative, nodular, fibrinosuppurative

Mixed cell population: lymphocytes, plasmacytes, neutrophils

Described as glandular gastritis

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3
Q

Risk factors for EGGD

A

• warmbloods
• Trainer
• Training > 4-5 times/week
• less experience in training type
• competition season (decreased in splanchnic blood flow during intense exercise?)
• stress

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4
Q

Sucralfate - mechanism of action

A

• physical barrier against acid diffusion
• stimulates mucus production (mucus blocks acid diffusion)
• inhibits pepsin and bile acid secretion
• promotes epithelialization (prevents fibroblast degradation)
• stimulation is insulin-like growth factors
• increase in mucosal blood flow (increases prostaglandin E production)

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5
Q

Misoprostol - mechanism of action

A

• Prostaglandin E analogue
• increases mucosal blood flow
• suppresses acid production
•inhibitor neutrophilic inflammation

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6
Q

EGGD Management changes

A

• min 2 rest days/week
• stress reduction
• minimal number of carers
• turn out
• 2 L forage 30-60 min before work
• corn oil (decrease gastric acid, increase prostaglandin E)
• pectin-lethicin or sugar beet pulp ( mucosal barrier protectant)

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7
Q

Risk factors for ESGD

A

• Training intensity and duration
• Individual trainers
• Urban area
• Lack of contact with other horses
• solid barriers
• straw feeding
• lack of water access
• > 6 h between meals
• > 2g/kg/day starch (2x increase)
• fasting
• intermittent starvation

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8
Q

Pathophysiology of ESGD

A

• exposure to HCl
• VFA, lactic acid and bile acid synergistic with HCl
• increase intra abdominal pressure during exercise - increased HCl exposure = increased with duration and intensity

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9
Q

How does dysentery happen and what are possible causes?

A

Dysentery = bloody diarrhea

bowel inflammation causing exudation and transudation of : serum proteins, blood, mucus

Causes:

  • salmonellosis
  • clostridium perfringens/difficile
  • lawsownia
  • attaching and effacing e coli
  • campylobacter jejune
  • coccidiosis
  • malignant catarrhal fever
  • arsenic toxicity
  • oak toxicity
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10
Q

Name mechanisms of diarrhea

A
  • Malabsorption (villous atrophy/blunting)
  • Osmotic overload
  • Secretion
  • Abnormal motility
  • Increased blood-lumen hydraulic pressure
  • Inflammation
  • Decreased transit time
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11
Q

How does secretory diarrhea happen and what are possible causes?

A

Enterotoxins:
stimulation of secretion by enterotoxins, e.g. often by stimulation of adenosine monophosphate or other messengers, this promotes Cl and Na (and other e-lyte) secretion and causes an osmotic gradient for water

Examples: enteropathogenic E. coli, Salmonella, C. perfringens

Replacement of damaged mature (absorbing) villous cells for immature (secreting) villous cells (from crypts)

Example: Rotavirus

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12
Q

What are the mechanisms of ascites formation?

A

2 mechanims:
increased pressure in hepatic veins - transudation of fluid (almost pure plasma) lymph and leakage into abdominal cavity through liver capsule
- blockage of portal flow causes high capillary pressure in entire portal system of GI tract - GI edema, fluid transudation

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13
Q

Which clostridium perfringens Toxin is most commonly found in soil and health animals

A

Type A

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14
Q

Which clostridium perfringens toxin usually causes neurological signs?

A

Epsilon Toxin

  • vascular damage, Leads to brain edema and parenchyma necrosis — focal symmetrical encephalomalacia
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