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| | [[Biliary Hyperplasia]] | | [[Biliary Hyperplasia]] |
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| | + | [[Cirrhosis]] |
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| − | ==Cirrhosis==
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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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| − |
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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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| − |
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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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| − |
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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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| − |
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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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| − |
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| − | 4. several prominent subcutaneous veins are also seen, running radially from the umbilicus over the abdomen
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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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| − | *ascites
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| − | **common finding
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| − | **other factors are involved: lowered plasma albumin, causing lowered colloid osmotic pressure
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| | [[Molecular pathogenesis of cholestasis]] | | [[Molecular pathogenesis of cholestasis]] |