Difference between revisions of "Uraemia"

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[[Image:uraemia.gif|right|thumb|125px|<small><center>Lesions due to uraemia associated with pyelonephritis/chronic renal failure (Courtesy of Alun Williams (RVC))</center></small>]]
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*In terminal renal failure animal may present with painful ulcers in mouth, which become secondarily infected with Fusiformis.
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**High concentrations of toxic materials in the blood results in degeneration of small arterioles.
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==Description==
*In the mouth, this damage to the blood supply can cause epithelial necrosis.
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Uraemia describes the clinical syndrome caused by [[Azotaemia|azotaemia]], an increase in the blood concentrations of urea and creatinine.  The major cause of azotaemia is [[Kidney Renal Failure - Pathology|renal failure]] but it is an insensitive indicator of this disease, only becoming detectable when more than approximately two thirds of the nephrons are no longer functional.
*Usually seen as erosions along the ventrolateral borders of the [[Oral Cavity - Tongue - Anatomy & Physiology|tongue]] and on the [[Cheeks - Anatomy & Physiology|cheeks]], especially opposite the [[Oral Cavity - Teeth & Gingiva - Anatomy & Physiology|teeth]].
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*In some cases there may be more extensive necrosis which may involve subepithelial tissue
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Uraemia affects causes pathological changes of arteriolar fibrinoid degeneration and this affects multiple organ systems and produces marked clinical signs.  It may develop acutely or it may develop gradually in animals with chronic kidney disease.
**for example, the tip of the [[Oral Cavity - Tongue - Anatomy & Physiology|tongue]] may slough.  
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*Most commonly seen in dog sometimes in cat.
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==Signalment==
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Uraemia is described almost exclusively in animals with renal failure.
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==Diagnosis==
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===Clinical Signs===
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[[Image:uraemia.gif|right|thumb|125px|<center>Lesions due to uraemia associated with pyelonephritis and chronic kidney disease<br><small>Copyright Alun Williams 2007 (RVC))</center></small>]]
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The most common signs of uraemia are:
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*'''Oral ulceration''', especially at the [[Oral Cavity - Teeth & Gingiva - Anatomy & Physiology|fauces]] of the mouth and on the margins of the [[Oral Cavity - Tongue - Anatomy & Physiology|tongue]].  Halitosis is often a feature of this syndrome as the lesions become secondarily infected oral bacteria such as ''[[Fusobacterium necrophorum]]''. On clinical examination, there may also be excessive dental calculus in animals with chronic kidney disease.  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.
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*'''Gastric ulceration''' occurs for two 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 the manifestations of uraemia.  Animals with gastro-duodenal ulceration may show '''anorexia, vomiting, haematemesis''' and [[Peritonitis - Cats and Dogs|'''peritonitis''']] if the ulcers perforate.
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*Damage to the small vessels of the pulmonary vasculature may result in '''pulmonary oedema''' and '''pleural effusion''' with dyspnoea, tachypnoea and coughing.
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*Electrolyte imbalance.
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*Uraemic peritonitis and colitis.
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*Atrial rupture.
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*Mineralisation.
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*Thrombocytopathia.
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*Arrhthymias.
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*Neurological disease.
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===Laboratory Tests===
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===Other Tests===
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===Diagnostic Imaging===
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==Treatment==
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==Prognosis==
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==References==
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[[Category:Oral Cavity - Metabolic Pathology]]
 
[[Category:Oral Cavity - Metabolic Pathology]]
 
 
[[Category:To_Do_-_James]]
 
[[Category:To_Do_-_James]]
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[[Category:Cat]][[Category:Dog]][[Category:Horse]][[Category:Cattle]][[Category:Sheep]][[Category:Donkey]][[Category:Pig]][[Category:Respiratory_System_-_Pathology]][[Category:Cardiovascular_System_-_Metabolic_Pathology]]

Revision as of 18:22, 22 July 2010



Description

Uraemia describes the clinical syndrome caused by azotaemia, an increase in the blood concentrations of urea and creatinine. The major cause of azotaemia is renal failure but it is an insensitive indicator of this disease, only becoming detectable when more than approximately two thirds of the nephrons are no longer functional.

Uraemia affects causes pathological changes of arteriolar fibrinoid degeneration and this affects multiple organ systems and produces marked clinical signs. It may develop acutely or it may develop gradually in animals with chronic kidney disease.

Signalment

Uraemia is described almost exclusively in animals with renal failure.

Diagnosis

Clinical Signs

Lesions due to uraemia associated with pyelonephritis and chronic kidney disease
Copyright Alun Williams 2007 (RVC))

The most common signs of uraemia are:

  • Oral ulceration, especially at the fauces of the mouth and on the margins of the tongue. Halitosis is often a feature of this syndrome as the lesions become secondarily infected oral bacteria such as Fusobacterium necrophorum. On clinical examination, there may also be excessive dental calculus in animals with chronic kidney disease. 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.
  • Gastric ulceration occurs for two 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 the manifestations of uraemia. Animals with gastro-duodenal ulceration may show anorexia, vomiting, haematemesis and peritonitis if the ulcers perforate.
  • Damage to the small vessels of the pulmonary vasculature may result in pulmonary oedema and pleural effusion with dyspnoea, tachypnoea and coughing.
  • Electrolyte imbalance.
  • Uraemic peritonitis and colitis.
  • Atrial rupture.
  • Mineralisation.
  • Thrombocytopathia.
  • Arrhthymias.
  • Neurological disease.

Laboratory Tests

Other Tests

Diagnostic Imaging

Treatment

Prognosis

References