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Largest internal organ (1.2–1.5 kg)

It is functionally divided:

Right lobe (including caudate and quadrate lobes)

Left lobe

The division is marked by the middle hepatic vein.

8 segments

Blood Supply:

Receives 25% of resting cardiac output via:

Hepatic artery (from aorta via celiac trunk)

Portal vein (75% --> drains from GI tract and spleen)

Blood flows from portal tracts → sinusoids → hepatic veins → inferior vena cava.

Ligaments:

Falciform - Connects liver to anterior abdominal wall and diaphragm. remnant of umbilical vein

Round

Coronary -  Attaches liver to the diaphragm

Right triangular

Left triangular

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Acinus:

Smallest functional unit: organised around blood supply

Contains:

Portal vein radicles - highest oxygen supply

Hepatic arterioles

Bile ductules

Zonation of hepatocytes:

Zone 1 - closest to blood supply

Zone 3 - more prone to damage

Hepatic lobules

Structural unit of the liver

Shape: Hexagonal shape

Function

Sinusoids: Capillary-like spaces allowing exchange between blood and hepatocytes

Space of Disse: Separates sinusoids from hepatocytes, site of plasma protein exchange

Blood Flow

portal triad → through sinusoids → to the central vein

Hepatocytes

Main functional cells of the liver (parenchymal)

Functions:

metabolism

bile production

storage (glycogen, vitamins)

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1. Stellate cells

Location: Space of Disse

Resting State - Activated State

Resting State – Store vitamin A and regulate extracellular matrix

Activated State – Transform into myofibroblasts, producing collagen

Functions

Fibrosis and Cirrhosis

excess collagen deposition

Reversal of Fibrosis

Potential for fibrosis reversal if liver injury is resolved

2. Kuppfer cells

Location

sinusoids of the liver

Function

Resident phagocytes of the liver

Protect against infections --> engulf pathogens

Breakdown mature RBC → release bilirubin

Remove debris and foreign bodies from the portal system

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Bile Flow Pathway

1. Bile Canaliculi:

2. Bile Ductules:

3. Bile Ducts:

4. Common Hepatic Duct:

Gallbladder and Cystic Duct

Common Bile Duct

1. Formed by the junction of the:

Cystic duct and Common Hepatic Duct.

2. Ampulla of Vater

3. Sphincter of Oddi

Bile Pathway:

1. Hepatocytes → Bile Canaliculi → Bile Ductules → Bile Ducts → Right and Left Hepatic Ducts → Common Hepatic Duct ↔ Cystic Duct → Common Bile Duct → Ampulla of Vater → Duodenum

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Main site of protein synthesis

Types of proteins produced:

Albumin: Maintains oncotic pressure and transports substances (e.g., hormones, fatty acids)

Transport and Carrier Proteins:  Includes transferrin (iron transport) and ceruloplasmin (copper transport)

Acute Phase Proteins

CRP

Coagulation Factors: Produces most clotting factors (I, II, V, VII, IX, X, XI, XII, protein C, protein S) for blood clotting

does not produce VWF (produced by epithelium)

Complement System Components

Storage

Vitamins: A, D, B12 (large amounts), K and folate (smaller amounts).

Minerals: Iron (stored as ferritin and haemosiderin), copper

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Amino acid breakdown

Urea cycle

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Carbohydrate metabolism

Lipid metabolism

Bilirubin

Angiotensinogen

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4. Formation of Bile and Bile Acid Secretion

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4. Formation of Bile and Bile Acid Secretion

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Source

Process

Conjugation

Conjugation

In the liver, unconjugated bilirubin is conjugated with glucuronic acid by the enzyme UDP-glucuronosyltransferase (UGT).

Conjugated bilirubin is water-soluble and can be excreted in bile.

Excretion

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Hormone inactivation:

Metabolizes and regulates hormones to maintain balance.

Steroid hormones (estrogen, testosterone, cortisol) are inactivated and excreted in bile or urine.

Thyroid hormones (T3 & T4) are deiodinated for excretion.

Insulin & glucagon are broken down to regulate blood sugar levels.

In liver damage in men:

feminisation bcs hormones not metabolised

If liver not working: how give them drugs:

rectally --> bypasses the liver

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Liver Function Tests (LFTs)

Serum albumin

Measures the liver's ability to synthesize albumin.

Low levels indicate liver dysfunction, malnutrition, or chronic liver disease.

Serum Bilirubin

Measures total, direct, and indirect bilirubin.

Elevated levels suggest liver dysfunction or bile duct obstruction.

Prothrombin Time

Assesses liver's ability to produce clotting factors.

Prolonged PT indicates liver damage or vitamin K deficiency.

Liver Biochemistry

Aminotransferases (AST & ALT)

Elevated levels indicate liver cell damage (e.g., hepatitis, fatty liver disease).

Alkaline phosphatase (ALP)

Measures cholestasis or bile duct obstruction.

Elevated levels can also indicate bone disease or liver metastasis.

Gamma-Glutamyl Transpeptidase (γ-GT)

Elevated levels are associated with liver disease, cholestasis, or alcohol-related liver damage.

Total Proteins and Globulin Fraction

Viral Markers and Genetic Tests

Immunological Tests

Serum Immunoglobulins

Autoantibodies

Markers of Liver Fibrosis

APRI (AST to Platelet Ratio Index)

A non-invasive marker of liver fibrosis and cirrhosis based on AST levels and platelet count.

Enhanced Liver Fibrosis (ELF) Test

Transient Elastography (FibroScan)

measures stiffness (fibrosis) of the liver with a tranducer

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Ultrasound Examination

First-line imaging for liver disease.

Uses

Assess liver size, texture, and abnormalities (e.g., fatty liver, tumors, cirrhosis).

Guide biopsy or liver procedure (e.g., drainage).

Colour Doppler Ultrasound

Visualizes blood flow within the liver and surrounding vessels.

Assesses vascular abnormalities, such as portal hypertension or cirrhosis-related changes.

CT

detailed cross-sectional imaging

uses

Characterize liver lesions (e.g., tumors, cysts).

Assess liver vascular anatomy (e.g., portal vein, hepatic artery).

Monitor liver conditions like cirrhosis and liver metastasis.

MRI

Magnetic Resonance Cholangiopancreatography (MRCP)

Radionuclide Imaging (Scintiscanning)

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Endoscopy

Upper GI Endoscopy

Capsule Endoscopy

Endoscopic Retrograde Cholangiopancreatography (ERCP)

Angiography

Hepatic Venous Cannulation:

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Gold standard for histological diagnosis.

Indications:

Techniques:

Complications:

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Caused by hyperbilirubinemia

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1. Hemolytic Jaundice – Increased breakdown of red blood cells.

Cause: Excessive destruction of red blood cells (hemolysis) leads to increased production of unconjugated bilirubin.

Characteristics

Increased unconjugated bilirubin in the blood, no significant liver dysfunction.

Clinical features

Laboratory findings

Increased unconjugated bilirubin.

Normal liver enzymes (AST, ALT).

Decreased haptoglobin (a protein that binds free hemoglobin).

2. Congenital Hyperbilirubinemias –Genetic defects in bilirubin metabolism.

Unconjugated Types

Gilbert's Syndrome

Cause: Mild reduction in UDP-glucuronosyltransferase (UGT) activity.

Clinical Features: Mild jaundice, often triggered by stress or fasting.

Laboratory Findings: Elevated unconjugated bilirubin, normal liver enzymes.

Crigler–Najjar Syndrome

Cause: Severe UGT deficiency.

Clinical Features: Severe jaundice from birth, may lead to kernicterus (brain damage) in Type 1.

Laboratory Findings: Very high unconjugated bilirubin.

Conjugated Types

Dubin–Johnson Syndrome: rare autosomal recessive

Cause: Mutation in ABCC2 transporter responsible for bilirubin excretion.

Clinical Features: Chronic mild jaundice, black liver appearance (melanin deposition) on biopsy.

Laboratory Findings: Elevated conjugated bilirubin.

Rotor's Syndrome

Cause: Defect in hepatic bilirubin storage and transport.

Clinical Features: Mild jaundice, typically with normal liver function.

Laboratory Findings: Elevated conjugated bilirubin, mild elevated liver enzymes.

Benign Recurrent Intrahepatic Cholestasis (BRIC)

Progressive Familial Intrahepatic Cholestasis (PFIC)

3. Cholestatic Jaundice – Impaired bile flow, either within the liver (intrahepatic) or outside the liver (extrahepatic).

Types:

Extrahepatic Cholestasis

Cause: Obstruction of the bile ducts outside the liver (e.g., gallstones, tumors, strictures).

Clinical Features: Jaundice, dark urine, pale stools, itching (pruritus).

Laboratory Findings:

Elevated conjugated bilirubin.

Elevated ALP and GGT.

Intrahepatic Cholestasis

Cause: Obstruction of bile flow within the liver due to liver diseases (e.g., cirrhosis, hepatitis, drug-induced liver injury).

Clinical Features: Jaundice, pruritus, hepatomegaly.

Laboratory Findings:

Elevated conjugated bilirubin.

Elevated ALP and GGT.

Clinical features

Lab findings

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1. Jaundice can present as:

Acute Jaundice

Chronic/Decompensated Jaundice

2. Comprehensive Approach to DD of Jaundice

Demographics and Risk Factors:

Age and Weight Loss

Country of Origin

Occupation and Environment

3. History of Illness and Symptoms:

Duration of Illness:

Abdominal Pain:

Fevers or Rigors:

4. Lifestyle and Exposure History

Intravenous Drug Use, Tattoos, or Recent Injections:

Sexual History:

Men who have sex with men

Female sex workers:

Alcohol Consumption

5. Medical and Surgical History

Medical Treatment in Developing Countries

Recent Surgery

Drug History

Family History

6. Classify jaundice into:

Pre-hepatic (Hemolytic): Increased RBC breakdown.

Hepatic (Hepatocellular): Liver cell dysfunction.

Post-hepatic (Cholestatic): Bile flow obstruction.

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Jaundice is a symptom and not a diagnosis. The underlying cause must always be investigated.

1. Viral markers: for hepatitis

2. Ultrasound imaging: eliminate obstructive casuses

3. Pathological Diagnosis:

4. Liver Biochemistry - confirm jaundice

1. LFTS:

1. Bilirubin (total and conjugated) for jaundice.

2. Aminotransferases (AST, ALT) to detect liver cell injury.

3. Alkaline phosphatase (ALP) and gamma-glutamyl transpeptidase (GGT) to evaluate bile duct issues.

4. Albumin and prothrombin time to assess liver synthetic function.

5. Hematological Tests

Hemolytic Jaundice

Infection Indicators

6. Other Blood Tests

Confirm specific liver diseases

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Sudden onset of liver inflammation.

less than 6 months

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Viruses, drugs, toxins, or autoimmune disorders.

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Histological features --> Degenerative changes in hepatocytes:

Swelling, cytoplasmic granularity, vacuolation.

Necrosis:

Spotty or focal necrosis: Death of single or small groups

of hepatocytes.

Multiacinar necrosis: Involves a substantial part of the

liver → Acute hepatic failure.

Bridging necrosis: Collapse of the reticulin framework

leading to links between:

Central veins.

Central veins and portal tracts.

Portal tracts.

Inflammatory Infiltrate:

Accumulation of immune cells (mainly lymphocytes).

Primarily in portal tracts and lobules.

Other Features:

Cholestasis (particularly in zone 3).

Fatty change:

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More than 6 months

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Chronic liver disease, cirrhosis, and hepatocellular carcinoma.

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Diagnostic Features:

Chronic Inflammatory Cell Infiltrates:

Lymphocytes, plasma cells, and sometimes lymphoid follicles.

Interface Hepatitis:

Loss of definition of the portal/periportal limiting plate.

Damage due to apoptosis (not necrosis).

Lobular Changes:

Focal lytic necrosis, apoptosis, and focal inflammation.

Fibrosis:

Types:

Bridging fibrosis: Across portal tracts.

Cirrhosis

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Epidemiology

Common in developing countries with poor sanitation.

Young children are often asymptomatic carriers, while adults may experience more severe symptoms.

Endemic areas: Southeast Asia, sub-Saharan Africa, and parts of the Middle East.

Global vaccine availability has reduced the incidence in many regions.

Transmission

fecal-oral or poor water sanitation

Clinical features

Prodromal Phase:

Flu-like symptoms: Fatigue, malaise, low-grade fever, anorexia, nausea, vomiting.

Right upper quadrant pain or discomfort from liver inflammation.

Dark urine (due to increased bilirubin levels).

Jaundice may not be present yet.

Icteric Phase:

Jaundice: Yellowing of the skin and sclera due to bilirubin buildup.

Clay-colored stools due to impaired bile secretion.

Pruritus (itching) as a result of bile salt accumulation in the skin.

Hepatic tenderness may be noted.

Biphasic illness

The illness often resolves after the icteric phase, with symptoms improving before the return of normal liver function.

Investigations

Liver biochemistry

Haematological findings

Prognosis

Management

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Epidemiology

Aetiology

Vertical (mother to child) and horizontal transmission

Risk factors: People with multiple sexual partners, intravenous drug users, healthcare workers, tattoos

Pathogenesis

4 phases:

Phase 1: HBeAg-Positive Chronic HBV Infection (High Replication)

Key features:

High levels of HBV DNA and HBeAg in serum.

Active viral replication with minimal immune response.

Elevated liver enzymes (ALT and AST).

no liver damage yet

no treatment yet

Who is affected?

Management

Phase 2: HBeAg-Positive Chronic HBV Infection (Immune Activation)

Key features

Immune system activation leads to hepatitis flares.

Inflammation and liver damage can occur despite viral replication.

Elevated ALT, HBV DNA, and HBeAg.

When does this occur

Often in young adults or those with an acute immune response to HBV.

Risks

Management

Phase 3: HBeAg-Negative Chronic HBV Infection (Inactive Carrier State)

Key features:

HBV DNA levels are low or undetectable.

HBeAg-negative, but anti-HBe positive.

Minimal liver inflammation and stable ALT levels.

Clinical outcomes

Management

Phase 4: HBeAg-Negative Chronic HBV Infection (Reactivation Phase)

Key features:

Increase in HBV replication, with elevated ALT and HBV DNA.

Potential for severe liver damage, including cirrhosis or liver failure.

Challenges

Risks

Cirrhosis, liver failure, and hepatocellular carcinoma.

Management

Clinical Features of Acute Hepatitis B

Investigations

HBsAg: Indicates active infection.

Anti-HBc IgM: Indicates acute infection or recent exposure.

Anti-HBc IgG and Anti-HBs: Indicates prior infection and immunity.

HBeAg and Anti-HBe: Used to monitor viral replication and immune response.

HBV DNA levels: Measure viral replication.

Prevention

Vaccination

Avoid risk factors

Chronic Hepatitis B Virus Infection

Investigations

Management

Indications for therapy

Types of therapy (interferon, oral antivirals, monitoring)

Goals

Prognosis

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What is hepatitis D?

Hepatitis D is a liver disease caused by the hepatitis D virus (HDV).

HDV is a defective RNA virus that requires hepatitis B virus (HBV) to replicate.

HDV infection can only occur in individuals already infected with HBV, making it a co-infection or superinfection.

Transmission and geographic distribution

Bloodborne transmission, through sharing needles, blood transfusions, or unprotected sex.

Vertical transmission from mother to infant is also possible.

Types of infection

Coinfection (HDV + HBV at the same time)

Superinfection

Chronic Hepatitis D:

Overview

Chronic HDV infection can result from superinfection or prolonged coinfection.

It can lead to cirrhosis, liver failure, and hepatocellular carcinoma (HCC).

The course of the disease can be more severe compared to chronic HBV infection alone.

Diagnosis

Management

Prognosis

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Epidemiology

High Risk Populations

Injecting drug users (due to needle sharing).

People receiving blood transfusions or organ transplants prior to screening.

Healthcare workers at risk of exposure to blood (needlestick injuries).

People with HIV, as co-infection can accelerate liver disease.

People with multiple sexual partners or those engaging in unprotected sex.

Transmission

Clinical features

Acute infection:

Often asymptomatic or mild, with some patients experiencing fatigue, fever, anorexia, nausea, and jaundice.

Most people (75-85%) progress to chronic infection without apparent symptoms.

Chronic infection:

Fatigue and mild discomfort are common.

Over time, may lead to cirrhosis, liver failure, and hepatocellular carcinoma (HCC).

Extrahepatic manifestations such as kidney disease, rashes, and joint pain.

Investigations and diagnosis

HCV RNA quantification: Measures the amount of virus present in the blood, used to guide treatment.

Management

no vaccine

Treatment

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Transmission

Fecal-oral transmission is the primary route, typically through contaminated water or food.

High-risk areas: Endemic in parts of Asia, Africa, and Central America.

No carrier state

Diagnosis

Prevention and control

Improved sanitation and access to clean water are key to preventing HEV transmission.

Hepatitis E vaccine is available in some regions but not widely used globally.

Avoiding unclean water and food hygiene can reduce risk in endemic areas.

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Autoimmune Hepatitis (AIH) is a chronic liver disease where the body's immune system attacks the liver cells, leading to inflammation and potential liver damage.

Female predominance: More common in women, with a female-to-male ratio of about 3:1.

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Genetic susceptibility

Molecular mimicry

Impaired immunoregulatory networks

Mechanisms of liver damage

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Two peaks in presentation

Peri and postmenopausal women

Teens and Early Twenties

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Liver biochemistry

Haematology

Autoantibodies

Liver biopsy

Management

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Definition

NAFLD refers to the accumulation of fat in the liver in individuals who consume little to no alcohol. It includes a spectrum of liver conditions, ranging from simple fatty liver to non-alcoholic steatohepatitis (NASH), which can progress to cirrhosis and liver failure.

Risk factors

Obesity, especially central obesity (visceral fat).

Type 2 diabetes and insulin resistance.

Dyslipidemia (high cholesterol and triglycerides).

Hypertension.

Metabolic syndrome (combination of obesity, hypertension, dyslipidemia, and insulin resistance).

Age: More common in middle-aged and older adults.

Genetic factors and family history of liver disease.

Sedentary lifestyle and poor diet.

Clinical features

Pathogenesis

The accumulation of fat in liver cells leads to inflammation and oxidative stress.

Insulin resistance is a key mechanism driving fat deposition in the liver.

In NASH, liver inflammation and damage can progress to fibrosis and eventually cirrhosis.

Diagnosis

Ultrasound: Commonly used to detect fatty liver (hyperechoic liver).

Liver biopsy: Considered the gold standard for diagnosing NASH and assessing the degree of fibrosis.

Elastography (e.g., FibroScan): Non-invasive method to measure liver stiffness, helping assess fibrosis and cirrhosis.

Management

Weight loss (recommended 7-10% weight reduction) through diet and exercise.

Physical activity and healthy eating (low-fat, low-sugar diet).

Lifestyle advice, orlistat, pioglitazone, vitamin E, weight loss following bariatric surgery

Medications:

Orlistat: A weight loss drug that reduces fat absorption.

Pioglitazone: Improves insulin sensitivity and may help with liver inflammation.

Vit a: for steatosis

Vitamin E: Antioxidant therapy, beneficial for NASH, especially in non-diabetic patients.

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Aetiology and epidemiology

Caused by excessive alcohol consumption over time.

Affects 30-50% of heavy drinkers, with a higher incidence in individuals with chronic alcohol use.

35-60yr/old

Clinical features

Often asymptomatic in early stages.

Symptoms may include fatigue, right upper quadrant discomfort, nausea, and mild hepatomegaly.

In advanced stages, may progress to alcoholic hepatitis, leading to jaundice, ascites, confusion (due to hepatic encephalopathy), and portal hypertension.

MDF & MELD scores

Pathophysiology

Alcohol is transported to the liver.

Alcohol is converted to acetaldehyde using 1 out of 3 pathways:

Alcohol Dehydrogenase (ADH)

Peroxisome Pathway.

CYP2E1 Pathway

Consequences of Acetaldehyde formation:

Generation of ROS

Acetaldehyde binds to proteins, forming adducts.

Destruction of hepatocytes

Histological changes:

Fatty liver

Alcoholic hepatitis

Treatment

Management

Glasgow Alcoholic Hepatitis Score:

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Diffuse liver damage that disrupts liver architecture, affecting:

Blood flow within the liver.

Liver function.

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Liver cell necrosis and apoptosis release ROS and cell contents → trigger inflammation → activation of hepatic stellate cells and macrophages → stellate cells transform into myofibroblasts → produce ECM leading to fibrosis --> accumulation of fibrotic tissue replaces normal liver parenchyma, causing liver architecture disruption and impeding liver function.

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Characteristic features

Fibrosis with a distortion of the liver lobules.

Formation of nodules surrounded by fibrous tissue.

Types of cirrhosis (micronodular, macronodular, mixed)

Micronodular cirrhosis: Small, uniform nodules, often seen in alcoholic liver disease and viral hepatitis.

Macronodular cirrhosis: Larger, irregular nodules, often seen in chronic hepatitis or biliary cirrhosis.

Mixed cirrhosis: Combination of both micronodular and macronodular changes.

Complications and Symptoms

Portal hypertension: Due to disrupted blood flow, leading to splenomegaly, ascites, and variceal bleeding.

Liver failure: Progressive dysfunction of liver cells, leading to jaundice, hypoalbuminemia, coagulopathy, and hepatic encephalopathy.

Hepatocellular carcinoma (HCC): Increased risk of liver cancer in cirrhotic patients.

Encephalopathy: Impaired liver function leads to the accumulation of toxic substances (e.g., ammonia) that affect brain function.

Fatigue, weight loss, itching (pruritus), and easy bruising.

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Severity Assessment

Liver function tests:  Assess liver enzyme levels (ALT, AST, ALP, GGT), bilirubin, and albumin to gauge liver performance.

Liver biochemistry

Serum electrolytes

Determining type of cirrhosis

Viral Markers.

Serum Autoantibodies.

Serum Immunoglobulins.

Iron Indices and Ferritin (for haemochromatosis).

Copper and Caeruloplasmin (for Wilson’s disease).

α1-Antitrypsin (for α1-antitrypsin deficiency).

Genetic Markers.

Imaging Techniques

Ultrasound, fibroscan, CT Scan, MRI and MR Angiography

Endoscopy

Liver biopsy

Gold standard

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Monitor + Screen

Regular monitoring for complications such as ascites, variceal bleeding, encephalopathy, and HCC (Hepatocellular carcinoma).

Screening for liver cancer: Routine screening (e.g., ultrasound and alpha-fetoprotein (AFP)) in cirrhosis patients, especially those with hepatitis B or C.

Treat underlying cause

Preventative measure

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5-year survival rate, prognostic indicators, scoring systems (Child-Pugh Score, MELD)

5-year survival depends on the underlying cause, degree of liver damage, and presence of complications (e.g., liver failure, variceal bleeding, HCC).

Early stages of cirrhosis (compensated cirrhosis) have a better prognosis than decompensated cirrhosis.

Child-Pugh Score: A scoring system to assess liver function and prognosis based on factors like bilirubin levels, albumin, encephalopathy, ascites, and prothrombin time.

Child-Pugh A: Mild cirrhosis (best prognosis).

Child-Pugh B: Moderate cirrhosis.

Child-Pugh C: Severe cirrhosis (poor prognosis).

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Primary Sclerosing Cholangitis

Definition: Chronic, progressive disease of the bile ducts leading to fibrosis, strictures, and obstruction. Can result in cirrhosis.

Associations and risk factors

Strongly associated with ulcerative colitis (70-80% of PSC patients).

Increased risk of cholangiocarcinoma and gallbladder cancer.

More men are affected

Clinical features

Can be symptomatic or asymptomatic

Fatigue, pruritus (itching), and jaundice.

Abdominal pain, particularly in the upper right quadrant.

Hepatomegaly and splenomegaly.

Diagnosis

MRCP: shows bile ducts, liver biopsy: bile duct inflammation, fibrosis, and cirrhosis

Primary Biliary Cholangitis: Chronic autoimmune disease characterized by progressive destruction of intrahepatic bile ducts, leading to cholestasis, fibrosis, and cirrhosis.

Definition

90% of patients are women aged 40-50

Aetiology (unknown, AMA)

Clinical features

Investigations

Liver biochem, AMA, Imaging and Biopsy

Management

UDCA: Ursodeoxycholic acid (UDCA): First-line treatment to improve liver function and slow progression.

symptom relief: Antihistamines and cholestyramine for pruritus.

supplements

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Hepatocellular Carcinoma (HCC)

5th most common cancer

Risk factors

Chronic Hepatitis B (HBV) and C (HCV) infections.

Cirrhosis (from any cause), particularly from alcohol and NAFLD.

Males

Diabetes, obesity, and smoking.

Aetiology

Pathology

Clinical Features

Often asymptomatic in early stages.

Abdominal pain, weight loss, jaundice, and ascites (in advanced stages).

Palpable mass in the upper right abdomen.

Hepatic encephalopathy or variceal bleeding due to underlying cirrhosis.

Investigations-

Prevention and Prognosis

HBV vaccination reduce incidence

Poor prognosis - depends on size + spread

HBV vaccination reduces incidence in endemic areas.

Screening for HCC in high-risk groups (e.g., cirrhotic patients, those with chronic hepatitis).

Poor prognosis: Often diagnosed late; depends on tumor size, number of nodules, and extent of spread.

Liver transplantation and resection are potential treatments, but survival rates remain low in advanced stages.

Cholangiocarcinoma

Definition:  Cancer of the bile ducts, either intrahepatic or extrahepatic.

Can be intrahepatic or extrahepatic

Risk factors (IBD, PSC)

Clinical features

Jaundice, pruritus, and weight loss.

Abdominal pain (especially in the right upper quadrant).

Fatigue and anorexia.

Fever in advanced stages or if associated with cholangitis.

Management and Prognosis

surgical resection

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Haemangioma

Epidemiology (5% of general population)

Diagnosis

incidental

Management

conservative

consider resection w/ problematic lesions

Hepatic Adenomas

Aetiology

Contraceptive pill, steroids, obesity

Epidemiology

Diagnosis

MRI

Treatment

Both problematic --> can have bleeding & need to do follow up

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Phases is about the washout of the contrast

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Immunosuppressants