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

Liver, Congenital Cysts

Liver Displacement

Torsion

• usually the left lateral lobe
• occurs in rabbits, swine, and dogs (extremely rare in dogs)
• Severe clinical signs, with shock, collapse, etc.

Rupture

• common result of trauma
• often clinically occult (small capsular ruptures may clot and heal) unless larger, severe ruptures cause rapid exsanguination or the biliary tract is involved
• rupture of major bile ducts leads to yellow-stained bile peritonitis
  • may remain sterile and become chronic
  • may be infected by enterohepatic circulation of bacteria such as clostridia followed by rapid death

NB: fatal ruptures can occur in foals during parturition, sometimes concurrent with costal fractures

• predisposition to rupture
  • diffuse hepatic disease causes enlargement and friability of the liver
  • may occur spontaneously
• predisposing lesions include:

1. infectious canine hepatitis

2. amyloidosis

3. severe congestion

4. fatty degeneration

5. secondary neoplasms

Tension lipidosis

• common in cattle and horses
• discrete, pale areas of parenchyma at the liver margins
• affected hepatocytes probably accumulate fat within their cytoplasm (lipidosis) as a consequence of interrupted blood supply and thus hypoxia
• these lesions are of no functional significance to the liver

Capsular fibrosis

• commonly found in older horses
• many fibrous tags or plaques present on the diaphragmatic surface of the liver as well as the adjacent diaphragm
• cause
  • most considered due to migrating parasites
  • some may be focal areas of non-septic peritonitis that have resolved

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 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 itself (persistent ductus venosus)
• acquired
  • due to hepatic fibrosis whcih results in increased resistance of flow of blood into the 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 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 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

• 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.