Category:Gastric Ulceration

Gastric Ulceration - all species

Gastric Ulceration - Cattle

Gastric Ulceration - Horse

Dog

Gastric Ulceration - all species

• Although ulcers are often secondary to other diseases, primary idiopathic peptic ulcers do occur, due to
  • Hyperacidity
  • Gastric carcinoma in older dog

• Secondary ulcers are often associated with systemic diseases particularly uraemia and mast cell tumours. Gastric ulcer may be the cause of death but is not the primary disease.
  1. Mast cell tumours
     • Boxers and Labradors are predisposed to these.
     • Vomit continually together with abdominal pain.
     • Ulcers are usually near the duodenum.
       • Frequently secondarily infected.
       • Often penetrate deeply.
     • Actively secreting mast cell tumours produce histame, leasing to gastric hyperacidity and therefore secondary peptic ulcers.
  2. Uraemia
     • Gastric lesions usually occur with chronic renal disease.
       • Gastrin is produced by the G cells of the gastric antrum during the gastric phase of digestion .
         • Acts on H2 receptors on parietal cells to increase production of HCl.
         • Increases release of histamine from gastric mucosal mast cells to increase HCl release.
       • Serum levels of gastrin are increased in chronic renal disease in dogs and cats.
     • In acute renal failure death ensues before gastric ulceration develops.
     • Pathogenesis
       • Loss of nephron and medullary concentration gradient in chronic interstitial nephritis mean collecting ducts cannot resorb fluid.
         • A common cause of interstitial nephritis in the dog was leptospirosis.
       • Consequently, the animal drinks and urinates in enormous quantities, and urea is washed out with large quantities of fluid ("compensated renal failure").
       • If fluid is restricted, urea cannot be washed out and the animal becomes uraemic.
         • Urea is excreted into stomach, giving it a horrible ammoniacal smell and filling it with brown smelly liquid.
         • Urea is also excreted into the colon.
       • Urea in the stomach breaks down to ammonia, irritating the mucosa and contributing to gastric ulcer.
       • Uraemia also causes arteriolar degeneration in the submucosa, leading to hypoxic damage to the mucosa. This is another contributing factor to gastric ulcer.
       • Vomiting causes dehydration and further raises blood urea.
         • A vicious circle is produced- ends in death by vomiting, dehydration and shock.
       • Note: If an animal in compensated renal failure is given anaesthetic, it will not drink much. It then may start to vomit and die due to uraemia.

• NSAIDs, Zollinger-Ellison syndrome (due to pancreatic gastrin-secreting tumour), cirrhosis and bile reflux can all also cause gastric ulcers in the dog.

Pig

Gastric Ulceration - all species

• Gastic ulceration is quite common in the pig- May be seen in 50-60% of pigs arriving at slaughterhouses.
• Has serious economic consequences.

• Clinical
  • Occasionally a well-grown pig will drop dead.
    • Deep ulcers have eroded into a blood vessel, causing massive haemorrhage into the stomach from and producing death very rapidly.
  • If long standing ulcers do not result in death, they do produce pain and discomfort.
    • Give low growth rate and poor feed conversion.

• Pathogenesis
  • Gastric ulceration is associated with modern pig rearing, but the exact cause is unknown.
  • Causes are associated with gastric hyperacidity, and gastric ulceration is probably a multifactorial disease.
  • The following are suggested as possible causes:
    • Infection, e.g. Candida albicans, Streptococci, Staphylococci and mixes of these.
    • Copper toxicity- this is probably more significant.
      • Pigs are fed copper as growth promoter; 50 ppm is know to be toxic, and animals are often fed 250 ppm.
    • Vitamin E / Selenium deficiency.
    • Feeding on concrete floors.
      • Sand is licked up whe pigs eat.
    • Feeding finely milled cereal.
    • Stress
    • Possibly genetic factors.

• Pathology
  • Most commonly affects pars oesophagea (squamous or non-glandular portion).
  • Starts with hyperkeratosis in the stratum corneum
    • Appears rough and thickened
    • May stop at this stage.
  • In approximately 30% of animals, the lesion starts to erode and quite deep ulcers may develop.
  • In a significant small number ,very deep ulcers develop and may affect virtually all of pars oesophagea.
  • Histologically, ulcers are large and flask-shaped ulcer with fibrin, necrosis, erosion and fibrosis at base.