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Created page with '*a term often used for fibrotic lesions, especially widespread fibrosis *it is an end stage liver with poor functional ability *much debate on the definition and classification o…'
*a term often used for fibrotic lesions, especially widespread fibrosis
*it is an end stage liver with poor functional ability
*much debate on the definition and classification of cirrhosis
*in any case the following conditions prevail:
1. the whole [[Liver - Anatomy & Physiology|liver]] is involved
2. cellular necrosis occurs at some stage in the disease
3. there is nodular regeneration of liver cells
4. fibrosis occurs and is diffuse
5. there is disorganisation of the lobular architecture, with fibrous tracts joining portal triads and central veins
6. clinically it is a chronic disease
7. [[Liver - Anatomy & Physiology|liver]] cell failure always supervenes and portal hypertension is often a feature
===Aetiology===
*precise aetiology is unknown
*as in man, may be due to viral hepatitis in Rubarth's disease (ICH)
===Gross===
*smaller than normal
*firm to cut
**firmness is due to the presence of fibrous tissue
*pale, sometimes yellow in colour
*regenerating nodule
**can be small and even in size with the [[Liver - Anatomy & Physiology|liver]] having a finely granular appearance
**or much larger, uneven in size, and the [[Liver - Anatomy & Physiology|liver]] surface is deeply fissured and irregular
===Microscopically===
*exhibits all 3 responses to injury
**nodular regeneration of the parenchyma
***haphazard regeneration of liver cells forming islands of new cells surrounded by condensed portal areas
**fibrosis
***early cases show areas of fibrosis connecting two or more portal triads
***later cases have prominent laying down of cartilage
**biliary hyperplasia
===Effects of cirrhosis===
due to
*[[Liver - Anatomy & Physiology|liver]] cell failure
*development of portal hypertension
**displacement and compression of efferent veins
***fibrous connective tissue bands enclose veins and constrict them by contraction
***regenerating nodules of [[Liver - Anatomy & Physiology|liver]] cells contribute as well
**abnormal communications open up between arterial and venous branches
**this transmits high arterial pressure directly to the low pressure venous system
====Sequelae====
the rise in the venous pressure leads to the development of an accessory portal circulation and contributes to the development of ascites
*prominent collateral pathways form in an attempt to circumvent the portal obstruction
1. via the intercostal veins to the azygous
2. via the gastric veins through the oesophageal veins also to the azygous
3. various venous plexuses, draining back into the renal vein
4. several prominent subcutaneous veins are also seen, running radially from the umbilicus over the abdomen
NB: oesophageal and gastric collaterals in the dog run '''subserosal''', not '''submucosal''' like man, therefore they are not as subject to traumatic rupture
*ascites
**common finding
**other factors are involved: lowered plasma albumin, causing lowered colloid osmotic pressure[[Category:Liver_-_General_Pathology]]
*it is an end stage liver with poor functional ability
*much debate on the definition and classification of cirrhosis
*in any case the following conditions prevail:
1. the whole [[Liver - Anatomy & Physiology|liver]] is involved
2. cellular necrosis occurs at some stage in the disease
3. there is nodular regeneration of liver cells
4. fibrosis occurs and is diffuse
5. there is disorganisation of the lobular architecture, with fibrous tracts joining portal triads and central veins
6. clinically it is a chronic disease
7. [[Liver - Anatomy & Physiology|liver]] cell failure always supervenes and portal hypertension is often a feature
===Aetiology===
*precise aetiology is unknown
*as in man, may be due to viral hepatitis in Rubarth's disease (ICH)
===Gross===
*smaller than normal
*firm to cut
**firmness is due to the presence of fibrous tissue
*pale, sometimes yellow in colour
*regenerating nodule
**can be small and even in size with the [[Liver - Anatomy & Physiology|liver]] having a finely granular appearance
**or much larger, uneven in size, and the [[Liver - Anatomy & Physiology|liver]] surface is deeply fissured and irregular
===Microscopically===
*exhibits all 3 responses to injury
**nodular regeneration of the parenchyma
***haphazard regeneration of liver cells forming islands of new cells surrounded by condensed portal areas
**fibrosis
***early cases show areas of fibrosis connecting two or more portal triads
***later cases have prominent laying down of cartilage
**biliary hyperplasia
===Effects of cirrhosis===
due to
*[[Liver - Anatomy & Physiology|liver]] cell failure
*development of portal hypertension
**displacement and compression of efferent veins
***fibrous connective tissue bands enclose veins and constrict them by contraction
***regenerating nodules of [[Liver - Anatomy & Physiology|liver]] cells contribute as well
**abnormal communications open up between arterial and venous branches
**this transmits high arterial pressure directly to the low pressure venous system
====Sequelae====
the rise in the venous pressure leads to the development of an accessory portal circulation and contributes to the development of ascites
*prominent collateral pathways form in an attempt to circumvent the portal obstruction
1. via the intercostal veins to the azygous
2. via the gastric veins through the oesophageal veins also to the azygous
3. various venous plexuses, draining back into the renal vein
4. several prominent subcutaneous veins are also seen, running radially from the umbilicus over the abdomen
NB: oesophageal and gastric collaterals in the dog run '''subserosal''', not '''submucosal''' like man, therefore they are not as subject to traumatic rupture
*ascites
**common finding
**other factors are involved: lowered plasma albumin, causing lowered colloid osmotic pressure[[Category:Liver_-_General_Pathology]]