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

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(Created page with '==Liver, Congenital Cysts== ==Displacement== ===cranial displacement=== *congenital and acquired (trauma) displacement associated with ventral and diaphragmatic hernias *r…')
 
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==Displacement==
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==[[Liver Displacement]]==
===cranial displacement===
 
*congenital and acquired (trauma) displacement associated with ventral and diaphragmatic hernias
 
*results in herniation of the [[Liver - Anatomy & Physiology|liver]] into the thoracic cavity
 
*usually only one lobe enters thorax with other viscera
 
*blood supply may not be interrupted but may be severely congested and rupture
 
*may become hardened over time
 
 
 
===caudal displacement===
 
*more common
 
*[[Liver - Anatomy & Physiology|liver]] will be displaced behind the costal arch
 
*due to organ enlargement or caudal displacement of the diaphragm
 
NB: the diaphragm may be displaced because of pleural effusion or other space occupying lesion in the thorax
 
  
  

Revision as of 11:52, 7 June 2010

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.