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|'''Neoplastic'''
 
|'''Neoplastic'''
|Adenocarcinoma, lymphosarcoma, leiomyoma, [[Gastrinoma|gastrinoma]] (Zollinger-Ellison syndrome),  
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|Adenocarcinoma, lymphosarcoma, leiomyoma, [[Gastrinoma|gastrinoma]], (Zollinger-Ellison syndrome), Mast cell Tumours.
 
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|'''Metabolic/endocrine'''
 
|'''Metabolic/endocrine'''
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===Endoscopy and Biopsy===
 
===Endoscopy and Biopsy===
 
Diagnostic test of choice and allows biopsies to be taken. [[NSAIDs|NSAID]] related ulcers are reguarly located in the antrum and there is limited mucosal thickening or irregularity whereas ulcerated [[Gastric Neoplasia|gastric tumours]] will have thickened mucosa and edges. Any biopsies should be taken at the edge of normal and diseased tissue to avoid further deepening or perforation.
 
Diagnostic test of choice and allows biopsies to be taken. [[NSAIDs|NSAID]] related ulcers are reguarly located in the antrum and there is limited mucosal thickening or irregularity whereas ulcerated [[Gastric Neoplasia|gastric tumours]] will have thickened mucosa and edges. Any biopsies should be taken at the edge of normal and diseased tissue to avoid further deepening or perforation.
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==Pathology==
    
==Treatment==
 
==Treatment==
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Omeprazole is the drug of choice to treat ulceration associated with mass cell tumours and gastrinomas. It inhibits the hydrogen-potassium ATPase which prevents hydrogen ion prouction by the parietal cells.
 
Omeprazole is the drug of choice to treat ulceration associated with mass cell tumours and gastrinomas. It inhibits the hydrogen-potassium ATPase which prevents hydrogen ion prouction by the parietal cells.
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===Mucosal protectants===
 
===Mucosal protectants===
 
Such as misoprostol can be given alongside NSAIDs to decrease the risk of ulceration. '''[[Gastroprotective Drugs#Binding Agents|Sucralfate]]''' which is polyaluminium sucrose sulphate, binds to damaged mucosa and assists in the treatment of gastric ulceration. It is best given 2 hours after acid inhibitors to prevent interference.  
 
Such as misoprostol can be given alongside NSAIDs to decrease the risk of ulceration. '''[[Gastroprotective Drugs#Binding Agents|Sucralfate]]''' which is polyaluminium sucrose sulphate, binds to damaged mucosa and assists in the treatment of gastric ulceration. It is best given 2 hours after acid inhibitors to prevent interference.  
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Hall, J.E., Simpson, J.W. and Williams, D.A., (2005) '''BSAVA Manual of Canine and Feline Gastroenterology (2nd Edition)''' ''BSAVA''
 
Hall, J.E., Simpson, J.W. and Williams, D.A., (2005) '''BSAVA Manual of Canine and Feline Gastroenterology (2nd Edition)''' ''BSAVA''
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Ettinger, S.J, Feldman, E.C. (2005)'''Textbook of Veterinary Internal Medicine''' (6th edition, volume 2)W.B. Saunders Company
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Merck & Co (2008) '''The Merck Veterinary Manual'''
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==From Pathology Section==
      
[[Gastric Ulceration - all species]]
 
[[Gastric Ulceration - all species]]
* 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.
   
[[Category:Gastric_Ulceration]][[Category:Dog]]
 
[[Category:Gastric_Ulceration]][[Category:Dog]]
 
[[Category:To_Do_-_Caz]]
 
[[Category:To_Do_-_Caz]]
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