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==Introduction==
 
==Introduction==
 
Uraemia describes the clinical systemic syndrome that occurs in animals suffering from [[:Category:Renal Failure|renal failure]].  Traditionally, uraemia was thought to be caused by [[Azotaemia|azotaemia]], an increase in the blood concentrations of urea and creatinine, but it is now apparent that multiple '''uraemic toxins''' cause derangements in many metabolic processes. Azotaemia is important in the diagnosis of uraemia but it is an insensitive indicator of renal failure, only becoming detectable when more than approximately two thirds of the nephrons are no longer functional.
 
Uraemia describes the clinical systemic syndrome that occurs in animals suffering from [[:Category:Renal Failure|renal failure]].  Traditionally, uraemia was thought to be caused by [[Azotaemia|azotaemia]], an increase in the blood concentrations of urea and creatinine, but it is now apparent that multiple '''uraemic toxins''' cause derangements in many metabolic processes. Azotaemia is important in the diagnosis of uraemia but it is an insensitive indicator of renal failure, only becoming detectable when more than approximately two thirds of the nephrons are no longer functional.
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===Gastro-intestinal Disease===
 
===Gastro-intestinal Disease===
*'''Oral ulceration or uraemic stomatitis''' - This occurs especially at the [[Oral Cavity Overview - Anatomy & Physiology|fauces of the mouth ]]and on the margins of the [[Tongue - Anatomy & Physiology|tongue]]. Uraemic vasculitis and thrombosis lead to necrosis and sloughing of the mucosa. There is irritation of the tissues from the ammonia produced by the bacterial degradation of urea. Halitosis is often a feature of this syndrome as the lesions become secondarily infected with oral bacteria such as ''[[Fusobacterium necrophorum]]''. In severe cases, there may be extensive subepithelial necrosis and sloughing of the tip of the tongue. The lesions are often very painful and contribute to the anorexia often observed in animals with chronic kidney disease. Excessive dental calculus may be evident in animals with chronic kidney disease on oral examination.
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*'''Oral ulceration or uraemic [[stomatitis]]''' - This occurs especially at the [[Oral Cavity Overview - Anatomy & Physiology|fauces of the mouth ]]and on the margins of the [[Tongue - Anatomy & Physiology|tongue]]. Uraemic vasculitis and thrombosis lead to necrosis and sloughing of the mucosa. There is irritation of the tissues from the ammonia produced by the bacterial degradation of urea. Halitosis is often a feature of this syndrome as the lesions become secondarily infected with oral bacteria such as ''[[Fusobacterium necrophorum]]''. In severe cases, there may be extensive subepithelial necrosis and sloughing of the tip of the tongue. The lesions are often very painful and contribute to the anorexia often observed in animals with chronic kidney disease. Excessive dental calculus may be evident in animals with chronic kidney disease on oral examination.
 
*'''[[Gastric Ulceration - all species|Gastric ulceration]]''' - This occurs for three main reasons. First, urea crosses lipid membranes freely and enters the gastro-intestinal lumen of azotaemic animals. The urea is degraded to ammonia by bacterial urease and the ammonia irritates the intestinal mucosa. This is compounded by damage to the blood vessels of the gastric submucosa by the fibrinoid necrosis that is a common feature of uraemia.  Elevated serum concentrations of gastrin (which is normally metabolised in the kidney) also lead to excessive production of gastric acid from parietal cells in the stomach. Animals with gastro-duodenal ulceration may show '''anorexia''', '''[[vomiting]]''', '''haematemesis''' and [[Peritonitis - Cats and Dogs|'''peritonitis''']] and '''haemorrhage''' if the ulcers perforate. Hypergastrinaemia may also cause incompetence of the pyloric sphincter of the stomach, permitting reflux of irritant bile into the stomach. Similar processes result in the development of '''uraemic colitis'''.
 
*'''[[Gastric Ulceration - all species|Gastric ulceration]]''' - This occurs for three main reasons. First, urea crosses lipid membranes freely and enters the gastro-intestinal lumen of azotaemic animals. The urea is degraded to ammonia by bacterial urease and the ammonia irritates the intestinal mucosa. This is compounded by damage to the blood vessels of the gastric submucosa by the fibrinoid necrosis that is a common feature of uraemia.  Elevated serum concentrations of gastrin (which is normally metabolised in the kidney) also lead to excessive production of gastric acid from parietal cells in the stomach. Animals with gastro-duodenal ulceration may show '''anorexia''', '''[[vomiting]]''', '''haematemesis''' and [[Peritonitis - Cats and Dogs|'''peritonitis''']] and '''haemorrhage''' if the ulcers perforate. Hypergastrinaemia may also cause incompetence of the pyloric sphincter of the stomach, permitting reflux of irritant bile into the stomach. Similar processes result in the development of '''uraemic colitis'''.
 
*'''[[Peritonitis - Cats and Dogs|Uraemic peritonitis]]''' - This is a form of chemical peritonitis that results from inflammation of the small mesothelial blood vessels.
 
*'''[[Peritonitis - Cats and Dogs|Uraemic peritonitis]]''' - This is a form of chemical peritonitis that results from inflammation of the small mesothelial blood vessels.
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{{Learning
 
{{Learning
 
|flashcards = [[Veterinary Dentistry Q&A 17]]
 
|flashcards = [[Veterinary Dentistry Q&A 17]]
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|literature search = [http://www.cabdirect.org/search.html?it=any&q2=uremia&q1=uraemia&calendarInput=yyyy-mm-dd&occuring1=title&show=all&rowId=1&rowId=2&rowId=3&options1=AND&options2=OR&options3=AND&occuring3=freetext&occuring2=title&publishedend=yyyy&la=any&publishedstart=yyyy&fq=sc%3A%22ve%22&y=8&x=70 Uraemia publications]
 
}}
 
}}
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==Literature Search==
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[[File:CABI logo.jpg|left|90px]]
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Use these links to find recent scientific publications via CAB Abstracts (log in required unless accessing from a subscribing organisation).
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<br><br><br>
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[http://www.cabdirect.org/search.html?it=any&q2=uremia&q1=uraemia&calendarInput=yyyy-mm-dd&occuring1=title&show=all&rowId=1&rowId=2&rowId=3&options1=AND&options2=OR&options3=AND&occuring3=freetext&occuring2=title&publishedend=yyyy&la=any&publishedstart=yyyy&fq=sc%3A%22ve%22&y=8&x=70 Uraemia publications]
      
==References==
 
==References==
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Ettinger, S.J, Feldman, E.C. (2005) '''Textbook of Veterinary Internal  Medicine (6th edition, volume 2)''' ''Elsevier Saunders''
 
Ettinger, S.J, Feldman, E.C. (2005) '''Textbook of Veterinary Internal  Medicine (6th edition, volume 2)''' ''Elsevier Saunders''
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[[Category:To Do - Helen]]
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{{review}}
 
[[Category:Oral Cavity - Metabolic Pathology]]
 
[[Category:Oral Cavity - Metabolic Pathology]]
 
[[Category:Lungs_-_Pathology]][[Category:Cardiovascular_System_-_Metabolic_Pathology]][[Category:Renal Failure]]
 
[[Category:Lungs_-_Pathology]][[Category:Cardiovascular_System_-_Metabolic_Pathology]][[Category:Renal Failure]]
 
[[Category:Expert_Review]]
 
[[Category:Expert_Review]]
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