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Created page with "{{Template:Manson Sparkes}} [[Image:|centre|500px]] <br /> '''A 6-month-old Birman cat presents with poor growth, intermittent ataxia, disorientation, and lethargy. Examine th..."
{{Template:Manson Sparkes}}
[[Image:|centre|500px]]
<br />
'''A 6-month-old Birman cat presents with poor growth, intermittent ataxia, disorientation, and lethargy. Examine the laboratory results.'''
<br />
<FlashCard questions="2">
|q1=What is your assessment of these results?
|a1=
The dramatically elevated postprandial bile acids are suggestive of a hepatopathy. Given the clinical signs and background, the most likely diagnosis is of a congenital portosystemic shunt. The low-normal urea is consistent with this diagnosis. The serum phosphate is mildly elevated; this is normal in a growing young cat.
|l1=Portosystemic Shunt#Diagnosis
|q2=How would you approach treatment of this cat?
|a2=
Initial medical management should be aimed at controlling the hepatic encephalopathy that accounts for the cat’s clinical signs. In cats with congenital portosystemic shunts, an anomalous vessel takes blood from the hepatic portal vein into the systemic circulation without delivering this to the liver first. Feeding a low protein diet limits the amount of protein breakdown products which contribute towards hepatic encephalopathy. Oral dosing of antibiotics (e.g. metronidazole, ampicillin) reduces ammonia absorption by reducing the numbers of ureaseproducing bacteria in the intestine. Oral lactulose produces an acidic environment
which helps to bind ammonia in the bowel, and reduces gastrointestinal transit time. When stable, portovenography and shunt ligation can be attempted.
|l2=Portosystemic Shunt#Treatment
</FlashCard>
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rect 0 0 860 850 [[Feline Medicine Q&A 14|Feline Medicine Q&A 14]]
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[[Category:Feline Medicine Q&A]]
[[Image:|centre|500px]]
<br />
'''A 6-month-old Birman cat presents with poor growth, intermittent ataxia, disorientation, and lethargy. Examine the laboratory results.'''
<br />
<FlashCard questions="2">
|q1=What is your assessment of these results?
|a1=
The dramatically elevated postprandial bile acids are suggestive of a hepatopathy. Given the clinical signs and background, the most likely diagnosis is of a congenital portosystemic shunt. The low-normal urea is consistent with this diagnosis. The serum phosphate is mildly elevated; this is normal in a growing young cat.
|l1=Portosystemic Shunt#Diagnosis
|q2=How would you approach treatment of this cat?
|a2=
Initial medical management should be aimed at controlling the hepatic encephalopathy that accounts for the cat’s clinical signs. In cats with congenital portosystemic shunts, an anomalous vessel takes blood from the hepatic portal vein into the systemic circulation without delivering this to the liver first. Feeding a low protein diet limits the amount of protein breakdown products which contribute towards hepatic encephalopathy. Oral dosing of antibiotics (e.g. metronidazole, ampicillin) reduces ammonia absorption by reducing the numbers of ureaseproducing bacteria in the intestine. Oral lactulose produces an acidic environment
which helps to bind ammonia in the bowel, and reduces gastrointestinal transit time. When stable, portovenography and shunt ligation can be attempted.
|l2=Portosystemic Shunt#Treatment
</FlashCard>
{{#tag:imagemap|Image:Next Question.png{{!}}center{{!}}200px
rect 0 0 860 850 [[Feline Medicine Q&A 14|Feline Medicine Q&A 14]]
desc none}}
[[Category:Feline Medicine Q&A]]