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[[Gastric Ulceration - all species]]
====Cattle====
* Management-related in young calves and dairy cows.
* May also be caused by infectious agents, e.g. [[Bovine Viral Diarrhoea Virus|mucosal disease/ bovine viral diarrhoea virus]].
* Ulcers have a tendency to bleed and perforate.
====Horse====
* Affects the pars oesophagea (margo plicatus) in adults and foals.
* Due to '''parasites''' - ''Gasterophilus'' (Bots).
* Bots are not as common as they once were.
* Look like big pink maggots.
* Killed by Ivermectin.
* ''Gasterophilus'' leave large ulcers in glandular regions of the [[Forestomach - Anatomy & Physiology|stomach]].
** Ulcers / erosions are quite deep.
* The parasites are believed to be non-pathogenic, but in large numbers they probably produce some discomfort and poor growth.
* Carcinoma can also produce ulceration in the [[Forestomach - Anatomy & Physiology|stomach]] of the horse as, in other species.
* In foals, the glandular area may sometimes be affected.
** This may be e.g. stress-related, or due to used of NSAIDs.
====Dog====
* 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.
*# '''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.
*# '''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 [[Forestomach - Anatomy & Physiology|stomach]], giving it a horrible ammoniacal smell and filling it with brown smelly liquid.
*#*** Urea is also excreted into the [[Colon - Anatomy & Physiology|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.
*#** [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|Vomiting]] causes dehydration and further raises blood urea.
*#*** A vicious circle is produced- ends in death by [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|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 [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|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====
* 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 [[Forestomach - Anatomy & Physiology|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.
[[Category:Stomach_and_Abomasum_-_Inflammatory_Pathology]]