Jaundice

•    Pre-hepatic: due to haemolysis → ↑ unconjugated bilirubin; normal LFTs

•    Hepatic: impaired conjugation or hepatocyte injury (e.g. hepatitis) → mixed bilirubin pattern, ↑ ALT/AST

•    Post-hepatic: biliary obstruction → ↑ conjugated bilirubin, ↑ ALP; pale stools, dark urine, pruritus

Viral Hepatitis

•    Hepatitis A & E:

o    Faeco-oral transmission

o    Acute, self-limiting hepatitis (no chronic phase)

o    Hepatitis E: high mortality in pregnancy

•    Hepatitis B:

o    Bloodborne, vertical or sexual transmission

o    May become chronic; risk of cirrhosis/HCC

o    HBsAg = active infection, anti-HBs = immunity

•    Hepatitis C:

o    Bloodborne (e.g. IVDU, transfusion pre-1991)

o    High rate of chronicity; may lead to cirrhosis/HCC

o    No vaccine; direct-acting antivirals (DAAs) curative

Drug-Induced Liver Injury (DILI)

•    Common culprits:

o    Paracetamol overdose: centrilobular (zone 3) necrosis

o    Isoniazid, rifampicin

o    Amiodarone, methotrexate, statins

•    Patterns:

o    Hepatocellular: ↑ ALT (e.g. paracetamol)

o    Cholestatic: ↑ ALP (e.g. co-amoxiclav)

o    Mixed

•    Management: stop offending agent ± specific antidote (e.g. NAC for paracetamol)

Autoimmune Hepatitis

•    Features: fatigue, jaundice, young females, other autoimmune diseases

•    Antibodies: ANA, anti-smooth muscle (SMA), ↑ IgG

•    Diagnosis: liver biopsy

•    Treatment: steroids ± azathioprine

•    Risk of progression to cirrhosis if untreated

Alcoholic Liver Disease

•    Spectrum: steatosis → alcoholic hepatitis → cirrhosis

•    Features: hepatomegaly, jaundice, systemic signs

•    Investigations: ↑ GGT, AST > ALT (usually <300)

•    Treatment: alcohol abstinence, nutritional support; steroids if severe hepatitis

Non-Alcoholic Fatty Liver Disease (NAFLD) / NASH

•    Associated with obesity, diabetes, metabolic syndrome

•    NAFLD = fat infiltration only; NASH = + inflammation ± fibrosis

•    Risk of progression to cirrhosis and HCC

•    Diagnosis: elevated LFTs, USS → biopsy to stage

•    Management: weight loss, manage comorbidities

Primary Biliary Cholangitis (PBC)

•    Autoimmune intrahepatic cholestasis, typically in middle-aged women

•    Features: pruritus, fatigue, ↑ ALP, xanthelasma

•    Antibodies: anti-mitochondrial (AMA)

•    Treatment: ursodeoxycholic acid

•    Complications: cirrhosis, osteoporosis, fat-soluble vitamin deficiency

Primary Sclerosing Cholangitis (PSC)

•    Progressive fibrosing cholangitis of intra- and extra-hepatic ducts

•    Associated with ulcerative colitis

•    ↑ ALP, beading of bile ducts on MRCP

•    ↑ Risk of cholangiocarcinoma and colon cancer

•    No effective medical therapy; may require transplant

Cirrhosis

•    Causes: alcohol, viral hepatitis, NAFLD, autoimmune, haemochromatosis, Wilson’s

•    Features: ascites, spider naevi, palmar erythema, gynaecomastia

•    Complications:

o    Portal hypertension

o    Variceal bleeding

o    Ascites, SBP

o    Hepatic encephalopathy

o    Hepatocellular carcinoma (HCC)

•    Diagnosis: LFTs, synthetic function (albumin, INR), imaging ± biopsy

•    Scoring: Child–Pugh, MELD

Portal Hypertension

•    Causes: cirrhosis (most common), schistosomiasis, portal vein thrombosis

•    Features:

o    Splenomegaly

o    Varices (oesophageal, gastric, rectal)

o    Ascites

•    Diagnosis: imaging ± hepatic venous pressure gradient

•    Treatment: non-selective beta-blockers, variceal banding, TIPSS

Ascites

•    Causes: cirrhosis, malignancy, TB, heart failure

•    SAAG >11 g/L = portal hypertension

•    Management:

o    Salt restriction, spironolactone, furosemide

o    Paracentesis ± albumin replacement

o    TIPSS for refractory cases

Spontaneous Bacterial Peritonitis (SBP)

•    Infection of ascitic fluid without identifiable source

•    Diagnosis: neutrophils >250/mm³ in ascitic tap ± positive culture

•    Organism: E. coli most common

•    Treatment: IV cefotaxime; prophylaxis with ciprofloxacin for high-risk patients

Hepatic Encephalopathy

•    Neuropsychiatric dysfunction due to ammonia accumulation

•    Triggers: infection, GI bleed, dehydration, drugs

•    Features: confusion, asterixis, altered sleep–wake cycle

•    Treatment:

o    Lactulose (traps ammonia in gut)

o    Rifaximin (reduces ammonia-producing bacteria)

o    Address precipitating factors

Gallstone Disease

•    RUQ pain, especially postprandial; may radiate to shoulder

•    Types:

o    Cholesterol (most common in West)

o    Pigment (haemolysis)

•    Complications:

o    Cholecystitis: fever, Murphy’s sign → USS, antibiotics, surgery

o    Choledocholithiasis: jaundice, dilated bile duct → ERCP

o    Pancreatitis

Cholangitis

•    Charcot’s triad: RUQ pain, fever, jaundice

•    May progress to Reynolds’ pentad (↓ BP, confusion)

•    Usually due to biliary obstruction (e.g. stone, stricture)

•    Management: IV antibiotics + ERCP for drainage

Liver Tumours

Hepatocellular Carcinoma (HCC)

•    Most common primary liver cancer

•    Risk factors: cirrhosis (any cause), HBV/HCV

•    Marker: ↑ AFP

•    Diagnosis: triple-phase CT/MRI

•    Treatment: resection, transplant, ablation, sorafenib

Cholangiocarcinoma

•    Cancer of biliary epithelium

•    Risk factors: PSC, biliary flukes, congenital ductal anomalies

•    Poor prognosis; often presents late

•    Treatment: surgery ± chemotherapy

Liver Transplantation

•    Indications: end-stage liver disease, HCC within Milan criteria, acute liver failure

•    MELD score used to prioritise transplant listing

•    Post-transplant:

o    Lifelong immunosuppression

o    Monitor for rejection, infection, recurrence of original disease