Difference between revisions of "Category:Liver - Developmental Pathology"

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==[[Liver, Congenital Cysts]]==
 
  
  
 +
== [[Portosystemic Shunt]] ==
  
==[[Liver Displacement]]==
 
 
 
==[[Liver Torsion]] ==
 
 
 
 
 
==[[Liver Rupture]]==
 
 
 
 
==[[Liver Tension Lipidosis]]==
 
 
 
==[[Liver Fibrosis, Capsular]] fibrosis==
 
 
 
== Portosystemic shunt ==
 
*seen in dogs and cats
 
*Inherited in Irish wolfhounds
 
**Not known what mode of inheritance in this breed
 
*these are vessles that allow the blood in the portal vein to bypass the [[Liver - Anatomy & Physiology|liver]] tissue (parenchyma)
 
*congenital
 
**shunting from the portal vein directly into the vena cava, azygos or renal vein
 
**this is the common type seen in small dogs and cats - usually a single communication between the vessels, occasionally multiple
 
**larger breeds tend to have the shunting to the vena cava take place within the [[Liver - Anatomy & Physiology|liver]] itself (persistent ductus venosus)
 
*acquired
 
**due to hepatic fibrosis whcih results in increased resistance of flow of blood into the [[Liver - Anatomy & Physiology|liver]] from the portal vein
 
**produces hypertension in the portal vein and fluid accumulates in the peritoneal cavity - '''ascites'''
 
**several thin-walled tortuous vessels may be seen connecting the mesenteric veins to the vena cava, and the [[Liver - Anatomy & Physiology|liver]] looks atrophic and fibrosed
 
*Bacteraemia is a common finding in severe hepatic disease and PSS in humans
 
**portal or systemic
 
**usually Gram-negatives
 
**also seen in dogs with PSS
 
**presumably due to reduced effectiveness of phagocytic activity in these [[Liver - Anatomy & Physiology|livers]]
 
**or due to shunting of blood around the liver
 
NB: portosystemic shunt is a major cause of hepatic encephalopathy (need link), therefore the affected animals are stunted and seem dull or stupid because of the toxic substances in their systemic circulation
 
  
 
== Hepatic microvascular dysplasia ==
 
== Hepatic microvascular dysplasia ==

Revision as of 12:04, 7 June 2010


Portosystemic Shunt

Hepatic microvascular dysplasia

  • Small intrahepatic portal vessels and portal endothelial hyperplasia which allows abnormal communication between portal and systemic circulation.
  • Can develop as a separate entity or in conjunction with a portosystemic shunt.
  • Can cause c/s similar to those of PSS.
  • Vomiting, diarrhoea, urinary tract changes associated with ammonium biurate urolithiasis, stunted growth, prolonged recovery from anesthesia.
  • Average age of presentation =3yrs.
  • Mainly small dogs, esp. Yorkies
  • Females>males

Histology

    • Arteriolarization 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.
    • May also see decreased diameter of intrahepatic veins.
  • Can’t be accurately distinguished from PSS alone.
  • Seen in older dogs than PSS
  • Higher MCV, serum postprandial bile acid concentrations, serum albumin and cholesterol concentrations when PSS and HMD together, compared to HMD alone.

Idiopathic noncirrhotic portal hypertension

JAVMA paper

  • Portal hypertension
  • Sustained impairment of forward venous flow anywhere along the path from the portal vein to the right side of the heart.
  • Luminal (thrombosis, parasites) or extraluminal obstruction (hepatic fibrosis or nodular regeneration) or relative restriction of flow due to massive portal volume overload (arterioportal fistulas).
  • Hepatomegaly associated with posthepatic obstruction
  • Microhepatica – associated with prehepatic/hepatic causes.
  • Hepatic encephalopathy and GI bleeding not associated with posthepatic causes.
  • Most common causes are RHS heart failure and severe diffuse hepatobiliary disease that results in cirrhosis.

Histology

  • indistinguishable from microvascular dysplasia or surgically created portosystemic shunts
    • Portal triad arteriole proliferation
    • portal veins small to large
    • variable portal triad fibrosis
    • hepatic lobule size variation
    • arterioles scattered throughout hepatic parenchyma
    • portal veins – small
    • expanded perivenular connective tissue by arterioles and distended lymphatics.