Morphologic patterns of hepatic injury.
- Focal – little functional significance
- Zonal –
- Mid zonal
- 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
- 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
- Apoptotic bodies
- Councilman bodies
Definition / Features. – Implies irreversible liver damage. Histologically there is loss of normal liver architecture, fibrosis with nodular degeneration.
- Alcohol excess
- Viral- HBV, HCV
- 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
- Alpha 1 antitrypsin deficiency
- Wilson’s Disease.
- Budd chiari
- 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.
- 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
- 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
- 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:
- Fatty Liver
- 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