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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]].
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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==Pathology==
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===Gross===
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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 and contains a regenerating nodule that can be small and even in size with the liver having a finely granular appearance, or much larger, uneven in size, and the liver surface is deeply fissured and irregular.
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===Microscopically===
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The liver exhibits all 3 responses to injury:
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:nodular regeneration of the parenchyma - haphazard regeneration of liver cells forming islands of new cells surrounded by condensed portal areas
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:fibrosis - early cases show areas of [[Liver Fibrosis|fibrosis]] connecting two or more portal triads, later cases have prominent laying down of cartilage.
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:biliary hyperplasia
==References ==
==References ==
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*a term often used for fibrotic lesions, especially widespread fibrosis
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*it is an end stage liver with poor functional ability
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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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3. there is nodular regeneration of liver cells
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4. fibrosis occurs and is diffuse
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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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6. clinically it is a chronic disease
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7. [[Liver - Anatomy & Physiology|liver]] cell failure always supervenes and portal hypertension is often a feature
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===Aetiology===
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*precise aetiology is unknown
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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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*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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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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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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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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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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*ascites
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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]]
[[Category:Liver_-_General_Pathology]]
[[Category:Nicola Parry reviewing]]
[[Category:Nicola Parry reviewing]]