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*Small intrahepatic portal vessels and portal endothelial hyperplasia which allows abnormal communication between portal and systemic circulation.
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*Can develop as a separate entity or in conjunction with a portosystemic shunt.
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*Can cause c/s similar to those of PSS.
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*[[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|Vomiting]], [[Diarrhoea|diarrhoea]], [[Urinary System - Anatomy & Physiology|urinary tract]] changes associated with ammonium biurate urolithiasis, stunted growth, prolonged recovery from anesthesia.
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*Average age of presentation =3yrs.
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*Mainly small dogs, esp. Yorkies
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*Females>males
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===Histology===
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**Arteriolarization of central veins
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==Description==
**smooth muscle proliferation (segmental) within the walls of central veins
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Microvascular dysplasia (MD) is a congenital defect of the hepatic vasculature that results in abnormal communication between the portal and systemic venous circulation.  Unlike [[Portosystemic Shunt|portosystemic shunting]], microvascular dysplasia is not grossly evident and occurs due to vascular connections between microscopic blood vessels.  However, MD may occur in conjunction with a gross shunting vessel and it does cause clinical signs which are very similar to those observed in animals with portosystemic shunts. 
**random distribution of small calibre vessels
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**endothelial hyperplasia within portal triads
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==Signalment==
**dilation of periacinar vascular spaces.
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MD occurs as a congenital disease in several small breeds of dog, particularly the Yorksire terrier and Cairn terrier.  The average age at presentation is 3 years (older than most animals presenting with congenital portosystemic shunts) and the condition is more common in female dogs than males.
**May also see decreased diameter of intrahepatic veins.
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*Can’t be accurately distinguished from PSS alone.
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==Diagnosis==
*Seen in older dogs than PSS
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===Clinical Signs===
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Signs are very similar to those observed in animals with congenital portosystemic shunts, as listed [[Portosystemic Shunt|here]].  Briefly, these include:
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*'''Stunted growth''' compared to littermates.
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*Intermittent '''gastro-intestinal signs''', including vomiting and diarrhoea.
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*'''Urinary tract signs''' resulting from urate urolithiasis.
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*'''Prolonged recovery from sedation or anaesthesia''' due to reduced hepatic metabolism of drugs.
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===Laboratory Tests===
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Diagnosis relies on ruling out the presence of a gross shunting vessel by diagnostic imaging.  A liver biopsy is then performed and histological analysis of the sample will show a pattern identical to that of a congenital portosystemic shunt:
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*'''Arteriolarisation of central veins'''
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*'''Smooth muscle proliferation''' (segmental) within the walls of central veins
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*'''Random distribution of small calibre vessels'''
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*'''Endothelial hyperplasia''' within portal triads
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*'''Dilation of periacinar vascular spaces'''
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*'''Decreased diameter of intrahepatic veins'''
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Blood samples
 
*Higher MCV, serum postprandial bile acid concentrations, serum albumin and cholesterol concentrations when PSS and HMD together, compared to HMD alone.
 
*Higher MCV, serum postprandial bile acid concentrations, serum albumin and cholesterol concentrations when PSS and HMD together, compared to HMD alone.
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==Treatment==
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'''Medical management''' should be implemented, as for [[Portosystemic Shunt|portosystemic shunts]].
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[[Category:Liver_-_Developmental_Pathology]]
 
[[Category:Liver_-_Developmental_Pathology]]
    
[[Category:To_Do_-_James]]
 
[[Category:To_Do_-_James]]
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