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| − | [[Gastric Ulceration - all species]]
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| − | | + | |pagetitle =Gastric Ulceration |
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| − | ====[[Gastric Ulceration - Cattle]]====
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| − | ====[[Gastric Ulceration - Horse]]====
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| − | ====Dog====
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| − | [[Gastric Ulceration - all species]]
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| − | * Although ulcers are often secondary to other diseases, primary idiopathic peptic ulcers do occur, due to
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| − | ** Hyperacidity
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| − | ** Gastric carcinoma in older dog
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| − | * 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.
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| − | *# '''Mast cell tumours'''
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| − | *#*Boxers and Labradors are predisposed to these.
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| − | *#* Vomit continually together with abdominal pain.
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| − | *#* Ulcers are usually near the duodenum.
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| − | *#** Frequently secondarily infected.
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| − | *#** Often penetrate deeply.
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| − | *#* Actively secreting mast cell tumours produce histame, leasing to gastric hyperacidity and therefore secondary peptic ulcers.
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| − | *# '''Uraemia'''
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| − | *#* Gastric lesions usually occur with chronic renal disease.
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| − | *#** Gastrin is produced by the G cells of the gastric antrum during the gastric phase of digestion .
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| − | *#*** Acts on H2 receptors on parietal cells to increase production of HCl.
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| − | *#*** Increases release of histamine from gastric mucosal mast cells to increase HCl release.
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| − | *#** Serum levels of gastrin are increased in chronic renal disease in dogs and cats.
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| − | *#* In acute renal failure death ensues before gastric ulceration develops.
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| − | *#* '''Pathogenesis'''
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| − | *#** Loss of nephron and medullary concentration gradient in chronic interstitial nephritis mean collecting ducts cannot resorb fluid.
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| − | *#*** A common cause of interstitial nephritis in the dog was leptospirosis.
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| − | *#** Consequently, the animal drinks and urinates in enormous quantities, and urea is washed out with large quantities of fluid ("compensated renal failure").
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| − | *#** If fluid is restricted, urea cannot be washed out and the animal becomes uraemic.
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| − | *#*** Urea is excreted into [[Forestomach - Anatomy & Physiology|stomach]], giving it a horrible ammoniacal smell and filling it with brown smelly liquid.
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| − | *#*** Urea is also excreted into the [[Colon - Anatomy & Physiology|colon]].
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| − | *#** Urea in the stomach breaks down to ammonia, irritating the mucosa and contributing to gastric ulcer.
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| − | *#** Uraemia also causes arteriolar degeneration in the submucosa, leading to hypoxic damage to the mucosa. This is another contributing factor to gastric ulcer.
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| − | *#** [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|Vomiting]] causes dehydration and further raises blood urea.
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| − | *#*** A vicious circle is produced- ends in death by [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|vomiting]], dehydration and shock.
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| − | *#** '''Note:''' If an animal in compensated renal failure is given anaesthetic, it will not drink much. It then may start to [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|vomit]] and die due to uraemia.
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| − | * NSAIDs, Zollinger-Ellison syndrome (due to pancreatic gastrin-secreting tumour), cirrhosis and bile reflux can all also cause gastric ulcers in the dog.
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| − | ====Pig====
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| − | [[Gastric Ulceration - all species]]
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| − | * Gastic ulceration is quite common in the pig- May be seen in 50-60% of pigs arriving at slaughterhouses.
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| − | * Has serious economic consequences.
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| − | *'''Clinical'''
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| − | ** Occasionally a well-grown pig will drop dead.
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| − | *** Deep ulcers have eroded into a blood vessel, causing massive haemorrhage into the [[Forestomach - Anatomy & Physiology|stomach]] from and producing death very rapidly.
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| − | ** If long standing ulcers do not result in death, they do produce pain and discomfort.
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| − | *** Give low growth rate and poor feed conversion.
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| − | *'''Pathogenesis'''
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| − | ** Gastric ulceration is associated with modern pig rearing, but the exact cause is unknown.
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| − | ** Causes are associated with gastric hyperacidity, and gastric ulceration is probably a multifactorial disease.
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| − | ** The following are suggested as possible causes:
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| − | *** Infection, e.g. ''Candida albicans'', ''Streptococci'', ''Staphylococci'' and mixes of these.
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| − | *** Copper toxicity- this is probably more significant.
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| − | **** Pigs are fed copper as growth promoter; 50 ppm is know to be toxic, and animals are often fed 250 ppm.
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| − | *** Vitamin E / Selenium deficiency.
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| − | *** Feeding on concrete floors.
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| − | **** Sand is licked up whe pigs eat.
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| − | *** Feeding finely milled cereal.
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| − | *** Stress
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| − | *** Possibly genetic factors.
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| − | *'''Pathology'''
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| − | ** Most commonly affects pars oesophagea (squamous or non-glandular portion).
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| − | ** Starts with hyperkeratosis in the stratum corneum
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| − | *** Appears rough and thickened
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| − | *** May stop at this stage.
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| − | ** In approximately 30% of animals, the lesion starts to erode and quite deep ulcers may develop.
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| − | ** In a significant small number ,very deep ulcers develop and may affect virtually all of pars oesophagea.
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| − | ** Histologically, ulcers are large and flask-shaped ulcer with fibrin, necrosis, erosion and fibrosis at base.
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| | + | <categorytree mode=pages>Gastric Ulceration</categorytree> |
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| | + | </b></big> |
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| | [[Category:Stomach_and_Abomasum_-_Inflammatory_Pathology]] | | [[Category:Stomach_and_Abomasum_-_Inflammatory_Pathology]] |
