Difference between revisions of "Category:Liver - General Pathology"

Liver response to injury

Liver Necrosis

Regeneration

• occurs quite readily when damaged
• approximately 70% of the liver can be removed surgically without danger to life
  • can reconstitute itself to its former mass in a few weeks
  • may not be its original shape

NB: larger areas of necrosis or continual bouts of necrosis are accompanied by fibrosis and biliary hyperplasia [link to the last two terms]

Fibrosis - Repair

• any hepatic injury of consequence is going to cause a degree of fibrosis when the lesion has resolved
• the fibrosis comes from the proliferation of the supportive connective tissue in the liver
• fibrosis isolates the liver cells by effectively changing the sinusoids into capillaries
• when a certain amount of fibrosis occurs, it can be self-perpetuating
  • the end result is a small scarred liver with functional failure

Histological patterns

Periacinar fibrosis

• the fibrosis surrounds the hepatic venule (centrilobular vein)
• can be seen when there is chronic passive congestion with atrophy of the surrounding periacinar hepatocytes and condensation of the remaining connective tissue

Biliary fibrosis

• accompanying inflammation centered on the portal triads

Post necrotic scarring

• following massive necrosis where the necrotic cells are removed and the defect is reapired by fibrosis
• seen as bands of fibrous tissue

Diffuse fibrosis

• resulting from repeated damage to one or more zones
• the fibrosis generated proliferates throughout to involve all the tissue

Biliary hyperplasia

• bile duct proliferation
• usually in association with portal fibrosis
• reason is unknown

[image - the picture shows fibroplasias invading between hepatocytes - some of the cells are likely to be distorted bile duct profiles]

Cirrhosis

• 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 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 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 having a finely granular appearance
  • or much larger, uneven in size, and the 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 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 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

Molecular pathogenesis of cholestasis

Hepatic Stellate Cells