Hepatology 

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

Functional anatomy and physiology of the GI tract

Oesophageal disorders

Gastric Pathology

Pancreatic disorders

Small intestinal disorders

Nutrition and malabsorption

Large bowel disorders

Gastrointestinal infections

Hepatology