|
|
| (6 intermediate revisions by the same user not shown) |
| Line 1: |
Line 1: |
| − | ==[[Liver, Congenital Cysts]]== | + | {{frontpage |
| | + | |pagetitle =Liver - Developmental Pathology |
| | + | |pagebody = |
| | + | |contenttitle =Content |
| | + | |contentbody =<big><b> |
| | | | |
| | + | <categorytree mode=pages>Liver - Developmental Pathology</categorytree> |
| | | | |
| | + | </b></big> |
| | + | |logo =path-logo.png |
| | + | }} |
| | | | |
| − | ==[[Liver Displacement]]==
| |
| | | | |
| | | | |
| − | ==[[Liver Torsion]] ==
| |
| − |
| |
| − |
| |
| − |
| |
| − |
| |
| − | ==[[Liver Rupture]]==
| |
| − |
| |
| − |
| |
| − |
| |
| − | ==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]] | | [[Category:Liver_-_Pathology]] |
