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Category:Liver - Developmental Pathology (view source)
Revision as of 11:51, 7 June 2010
, 11:51, 7 June 2010Created page with '==Liver, Congenital Cysts== ==Displacement== ===cranial displacement=== *congenital and acquired (trauma) displacement associated with ventral and diaphragmatic hernias *r…'
==[[Liver, Congenital Cysts]]==
==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
== 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 - Anatomy & Physiology|liver]]
**may occur spontaneously
*predisposing lesions include:
1. [[Liver Inflammatory - Pathology#Infectious Canine Hepatitis|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 - Anatomy & Physiology|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 - Anatomy & Physiology|liver]]
==Capsular fibrosis==
*commonly found in older horses
*many fibrous tags or plaques present on the diaphragmatic surface of the [[Liver - Anatomy & Physiology|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 - 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 ==
*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.
*[[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.
*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.
[[Category:Liver_-_Pathology]]
==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
== 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 - Anatomy & Physiology|liver]]
**may occur spontaneously
*predisposing lesions include:
1. [[Liver Inflammatory - Pathology#Infectious Canine Hepatitis|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 - Anatomy & Physiology|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 - Anatomy & Physiology|liver]]
==Capsular fibrosis==
*commonly found in older horses
*many fibrous tags or plaques present on the diaphragmatic surface of the [[Liver - Anatomy & Physiology|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 - 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 ==
*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.
*[[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.
*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.
[[Category:Liver_-_Pathology]]