GI Diseases Flashcards
What is EGGD thought to result from and what does the mucosal layer consist of?
• Breakdown of defense against acid
• reduced blood supply
• altered gastric production
Normal layer: bicarbonate, gastric mucus (glycoproteins, water, electrolyte, antibodies)
Histopathologic features of EGGD
Erosive, inflammatory, usually non-ulcerative, nodular, fibrinosuppurative
Mixed cell population: lymphocytes, plasmacytes, neutrophils
Described as glandular gastritis
Risk factors for EGGD
• warmbloods
• Trainer
• Training > 4-5 times/week
• less experience in training type
• competition season (decreased in splanchnic blood flow during intense exercise?)
• stress
Sucralfate - mechanism of action
• 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)
Misoprostol - mechanism of action
• Prostaglandin E analogue
• increases mucosal blood flow
• suppresses acid production
•inhibitor neutrophilic inflammation
EGGD Management changes
• 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)
Risk factors for ESGD
• 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
Pathophysiology of ESGD
• 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
How does dysentery happen and what are possible causes?
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
Name mechanisms of diarrhea
- Malabsorption (villous atrophy/blunting)
- Osmotic overload
- Secretion
- Abnormal motility
- Increased blood-lumen hydraulic pressure
- Inflammation
- Decreased transit time
How does secretory diarrhea happen and what are possible causes?
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
What are the mechanisms of ascites formation?
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
Which clostridium perfringens Toxin is most commonly found in soil and health animals
Type A
Which clostridium perfringens toxin usually causes neurological signs?
Epsilon Toxin
- vascular damage, Leads to brain edema and parenchyma necrosis — focal symmetrical encephalomalacia