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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 | + | ==Description== |
− | **smooth muscle proliferation (segmental) within the walls of central veins | + | 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 | + | |
− | **endothelial hyperplasia within portal triads | + | ==Signalment== |
− | **dilation of periacinar vascular spaces. | + | 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. | + | |
− | *Can’t be accurately distinguished from PSS alone.
| + | ==Diagnosis== |
− | *Seen in older dogs than PSS
| + | ===Clinical Signs=== |
| + | Signs are very similar to those observed in animals with congenital portosystemic shunts, as listed [[Portosystemic Shunt|here]]. Briefly, these include: |
| + | *'''Stunted growth''' compared to littermates. |
| + | *Intermittent '''gastro-intestinal signs''', including vomiting and diarrhoea. |
| + | *'''Urinary tract signs''' resulting from urate urolithiasis. |
| + | *'''Prolonged recovery from sedation or anaesthesia''' due to reduced hepatic metabolism of drugs. |
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| + | ===Laboratory Tests=== |
| + | 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''' |
| + | *'''Smooth muscle proliferation''' (segmental) within the walls of central veins |
| + | *'''Random distribution of small calibre vessels''' |
| + | *'''Endothelial hyperplasia''' within portal triads |
| + | *'''Dilation of periacinar vascular spaces''' |
| + | *'''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== |
| + | '''Medical management''' should be implemented, as for [[Portosystemic Shunt|portosystemic shunts]]. |
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| [[Category:Liver_-_Developmental_Pathology]] | | [[Category:Liver_-_Developmental_Pathology]] |
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| [[Category:To_Do_-_James]] | | [[Category:To_Do_-_James]] |