Week 22 Pathology

Morphologic patterns of hepatic injury.

  • Necrosis
    • Focal – little functional significance
    • Zonal –
      • Centrilobular
      • Mid zonal
      • Portal
      • Bridging necrosis
      • Massive – entire hepatic lobule.
    • Zone 1 rich in O2 – toxins cause damage here
    • Zone 3 poor in O2 – ischaemic injury
  • Balloon degeneration
    • Toxic injury, hepatitis
    • Centrilobular
    • Accumulation of products in cytoplasm, nuclei still in centre but may go onto fade, precursor to cell death.
  • Fatty Change
    • Reversible condition
    • Microvescicular and macrovescicular
    • Alcoholic liver disease, pregnancy, Reyes syn, diabetes, obesity
    • Nuclei are displaced to one side
  • Apoptosis
    • Apoptotic bodies
    • Councilman bodies



Definition / Features. – Implies irreversible liver damage. Histologically there is loss of normal liver architecture, fibrosis with nodular degeneration.

  • Causes
    • Alcohol excess
    • Viral- HBV, HCV
    • Autoimmune
      • Primary biliary cirrhosis- Chronic granulomatous inflam affecting interlobular ducts–> Cholestasis, cirrhosis and PHT.
      • Primary sclerosing cholangitis –
        • Unknown aetiology causing inflammation, fibrosis and strictures of intra and extrahepatic bile ducts.–>cholestasis
        • Associated with: UC, Crohn’s. HIV.
        • Autoantibody- pANCA (anti neutrophil cytoplasmic antibody) in serum 60% of cases.
        • Usually rasied ALP
    • Genetic
      • Alpha 1 antitrypsin deficiency
      • Haemachromatosis
      • Wilson’s Disease.
    • Vascular
      • Budd chiari
    • Drugs
      • Amiodarone
      • Methydopa
      • Methotrexate
  • 5yr survival: 50%
  • Worse if encephalopathy, INR increase a lot, albumin drop a lot or hyponatraemia.
  • Liver transplant is the only definitive treatment raises 5yr survival of end stage disease from 20% to 70%.
  • Otherwise ascites: fluid and salt restriction, spironolactone, frusemide, good nutrition, alcohol abstinence, avoid NSAIDs, opiates and sedatives.


Portal hypertension:

  • Causes.
    • Prehepatic: portal vein thrombosis, splenic vein thrombosis
    • Intrahepatic: cirrhosis, schistosomiasis, sarcoidosis, myeloproliferative disorder, congenital hepatic fibrosis.
    • Posthepatic: Budd-Chiari syndrome, RHF, constrictive pericarditis, veno-occlusive disease
  • Consequences.
    • Ascites
    • Splenomegaly
    • Portosystemic shunting: oesophageal varices, rectal region, umblical
    • Low platelets, low coag factors, high INR, low albumin



  • Overview of bilirubin metabolism.
    • RBC haem bd–> unconjugated bilirubin–> liver glucoridination –> conjugated bilirubin–> secreted in bile–> bowel flora –> urobilinogen–>some reabsorbed and removed in urine and rest secreted in stool.
  • Classification / Causes
    • Unconjugated- haemolytic anaemia
    • Conjugated – hepatic problem, post hepatic eg choledocholithiasis


Hepatic failure:

  • Causes – prehepatic, hepatic, post hepatic
  • Clinical features – encephalopathy, coagulopathy, fetor hepatis, flap,


Viral hepatitis (A, B & C):


  • Hep A – faecal oral route, diarrhoea, hepatitis.
  • Hep B – blood borne Tx, 2-26wks incubation, HepBsAg present, Anti-HepBsAg comes later. Core Ag comes later, e antigen is a marker of infectivity. Chronic in children, transient in adult.
  • Hep C – blood borne Tx, 2-26wks incubation, anti Hep C IgG. Causes chronic infection.


Alcoholic liver disease:

  1. Fatty Liver
  2. Steatohepatitis
  3. Cirrhosis


  • Risk factors. – fat, fourty, female, FHx
  • Pathogenesis / Constituents. – 80% of gall stones are cholesterol (cholesterol saturation, bile factors, gall bladder motility), then rest a pigment stone. Gall stones are very prevalent. Only 20% will give symptoms.
  • Complications – biliary colic, cholelithiasis, cholecystitis, choledocholithiasis, cholangitis, perforation