Difference between revisions of "Cirrhosis"

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*a term often used for fibrotic lesions, especially widespread fibrosis
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==Introduction==
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*it is an end stage liver with poor functional ability
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Cirrhosis represents an “end-stage liver” - the final, irreversible result of diffuse hepatic disease, involving architectural disruption of the entire liver. Underlying chronic injury leads to loss of hepatic tissue with replacement [[Liver Fibrosis|fibrosis]]. Nodular regeneration occurs within regions of hepatic tissue in between fibrous tissue bands, giving rise to the characteristic multinodular gross appearance of this condition. Overall, the liver is smaller than normal and firm to cut, firmness is due to the presence of fibrous tissue. It is pale, sometimes yellow in colour.
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*much debate on the definition and classification of cirrhosis
 
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*in any case the following conditions prevail:
 
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1. the whole [[Liver - Anatomy & Physiology|liver]] is involved
 
  
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2.  cellular necrosis occurs at some stage in the disease
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The three characteristic microscopic features of cirrhosis are:
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*Nodular regeneration
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*[[Liver Fibrosis|Fibrosis]]
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*Bile duct hyperplasia
  
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3.  there is nodular regeneration of liver cells
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'''Bile duct hyperplasia''' around portal regions is a non-specific response to a variety of long-standing hepatic insults, but occurs especially in association with diseases that [[Biliary Tract Obstruction|obstruct bile drainage]].
  
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4.  fibrosis occurs and is diffuse
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'''Vascular abnormalities''' are also associated with cirrhosis. Anastomoses occur between the hepatic portal vein and systemic vasculature due to increased portal pressure. Additionally, [[Portosystemic Shunt|vascular shunts]] can result within regenerative nodules, either between central and portal veins, or between hepatic arteries and central veins.
  
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5.  there is disorganisation of the lobular architecture, with fibrous tracts joining portal triads and central veins
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==Causes of Cirrhosis==
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Some of the many possible causes of cirrhosis in animals include:
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*Chronic [[Heart Failure, Right-Sided|right sided heart failure]]
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*[[Hepatitis, Chronic|Chronic hepatitis]]
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**[[Hepatitis, Lobular Dissecting|Lobular dissecting hepatitis in dogs]]
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**Hepatitis due to [[Infectious Canine Hepatitis|infectious canine hepatitis virus]]
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*Chronic [[cholangitis]] or [[Biliary Tract Obstruction|bile duct obstruction]]
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*Chronic toxicity
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**[[Ragwort Toxicity|Pyrrolizidine alkaloid plants]] in herbivores
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**[[Primidone]] anticonvulsants in dogs
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*Inherited diseases of metal metabolism
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**[[Copper]] (Dalmatians, Bedlington terriers, West Highland white terriers)
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**[[Iron]] metabolism
  
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6. clinically it is a chronic disease
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Cirrhosis is usually the end result of multiple pathological processes, in particular cell death and active inflammation with fibrosis. Regardless of the original underlying aetiology, however, the end-stage liver can no longer perform its functions, and is therefore associated with clinical manifestations of [[Liver Failure|hepatic failure]].
  
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7. [[Liver - Anatomy & Physiology|liver]] cell failure always supervenes and portal hypertension is often a feature
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{{Learning
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|Vetstream = [https://www.vetstream.com/canis/search?s=cirrhosis Cirrhosis]
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}}
  
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===Aetiology===
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==References ==
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*precise aetiology is unknown
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Blood, D.C. and Studdert, V.P. (1999)''' Saunders Comprehensive Veterinary Dictionary''' (2nd Edition), ''Elsevier Science''.
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*as in man, may be due to viral hepatitis in Rubarth's disease (ICH)
 
  
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===Gross===
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Ettinger, S.J. and Feldman, E.C. (2000) '''Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat''' Volume 2 (Fifth Edition), ''W.B. Saunders Company''.
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*smaller than normal
 
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*firm to cut
 
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**firmness is due to the presence of fibrous tissue
 
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*pale, sometimes yellow in colour
 
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*regenerating nodule
 
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**can be small and even in size with the [[Liver - Anatomy & Physiology|liver]] having a finely granular appearance
 
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**or much larger, uneven in size, and the [[Liver - Anatomy & Physiology|liver]] surface is deeply fissured and irregular
 
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===Microscopically===
 
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*exhibits all 3 responses to injury
 
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**nodular regeneration of the parenchyma
 
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***haphazard regeneration of liver cells forming islands of new cells surrounded by condensed portal areas
 
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**fibrosis
 
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***early cases show areas of fibrosis connecting two or more portal triads
 
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***later cases have prominent laying down of cartilage
 
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**biliary hyperplasia
 
  
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===Effects of cirrhosis===
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Maxie, M.G. (2007) '''Pathology of Domestic Animals Volume''' 2 (Fifth Edition), ''Elsevier Saunders''.
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due to
 
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*[[Liver - Anatomy & Physiology|liver]] cell failure
 
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*development of portal hypertension
 
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**displacement and compression of efferent veins
 
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***fibrous connective tissue bands enclose veins and constrict them by contraction
 
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***regenerating nodules of [[Liver - Anatomy & Physiology|liver]] cells contribute as well
 
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**abnormal communications open up between arterial and venous branches
 
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**this transmits high arterial pressure directly to the low pressure venous system
 
  
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====Sequelae====
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McGavin, M.D. and Zachary, J.F. (2007) '''Pathologic Basis of Veterinary Disease''' (Fourth Edition),'' Elsevier Mosby.''
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the rise in the venous pressure leads to the development of an accessory portal circulation and contributes to the development of ascites
 
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*prominent collateral pathways form in an attempt to circumvent the portal obstruction
 
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1. via the intercostal veins to the azygous
 
  
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2. via the gastric veins through the oesophageal veins also to the azygous
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Smyth, B (2008) '''Alimentary System Study Guide''''', Royal Veterinary College''.
  
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3.  various venous plexuses, draining back into the renal vein
 
  
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4.  several prominent subcutaneous veins are also seen, running radially from the umbilicus over the abdomen
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{{Nicky Parry
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|date = 22 August 2011
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}}
  
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NB: oesophageal and gastric collaterals in the dog run '''subserosal''', not '''submucosal''' like man, therefore they are not as subject to traumatic rupture
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[[Category:Liver_-_General_Pathology]]
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*ascites
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[[Category:Nicola Parry reviewed]]
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**common finding
 
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**other factors are involved: lowered plasma albumin, causing lowered colloid osmotic pressure[[Category:Liver_-_General_Pathology]]
 
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[[Category:To_Do_-_Clinical]]
 

Latest revision as of 19:25, 25 June 2016

Introduction

Cirrhosis represents an “end-stage liver” - the final, irreversible result of diffuse hepatic disease, involving architectural disruption of the entire liver. Underlying chronic injury leads to loss of hepatic tissue with replacement fibrosis. Nodular regeneration occurs within regions of hepatic tissue in between fibrous tissue bands, giving rise to the characteristic multinodular gross appearance of this condition. Overall, the liver is smaller than normal and firm to cut, firmness is due to the presence of fibrous tissue. It is pale, sometimes yellow in colour.

The three characteristic microscopic features of cirrhosis are:

  • Nodular regeneration
  • Fibrosis
  • Bile duct hyperplasia

Bile duct hyperplasia around portal regions is a non-specific response to a variety of long-standing hepatic insults, but occurs especially in association with diseases that obstruct bile drainage.

Vascular abnormalities are also associated with cirrhosis. Anastomoses occur between the hepatic portal vein and systemic vasculature due to increased portal pressure. Additionally, vascular shunts can result within regenerative nodules, either between central and portal veins, or between hepatic arteries and central veins.

Causes of Cirrhosis

Some of the many possible causes of cirrhosis in animals include:

Cirrhosis is usually the end result of multiple pathological processes, in particular cell death and active inflammation with fibrosis. Regardless of the original underlying aetiology, however, the end-stage liver can no longer perform its functions, and is therefore associated with clinical manifestations of hepatic failure.


Cirrhosis Learning Resources
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References

Blood, D.C. and Studdert, V.P. (1999) Saunders Comprehensive Veterinary Dictionary (2nd Edition), Elsevier Science.

Ettinger, S.J. and Feldman, E.C. (2000) Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat Volume 2 (Fifth Edition), W.B. Saunders Company.

Maxie, M.G. (2007) Pathology of Domestic Animals Volume 2 (Fifth Edition), Elsevier Saunders.

McGavin, M.D. and Zachary, J.F. (2007) Pathologic Basis of Veterinary Disease (Fourth Edition), Elsevier Mosby.

Smyth, B (2008) Alimentary System Study Guide, Royal Veterinary College.


This article has been expert reviewed by Dr. Nicola Parry BVSc, MSc, DipACVP

Date reviewed: 22 August 2011


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