MBBS Year
1st Year
Subject
What Is Usually Asked
Portal vein and portocaval anastomoses
ReferenceAll Years (1st-Final)All UniversitiesLiver Cirrhosis
Liver Cirrhosis: Notes, PPT and PYQs for MBBS
Liver cirrhosis is the end stage of chronic liver injury, in which the normal liver architecture is replaced by fibrosis and regenerative nodules. It leads to liver cell failure and portal hypertension, and is examined in Pathology and Pharmacology in 2nd Year, and in General Medicine and General Surgery in Final Year.
SME-reviewed. Updated 2026.
Open in GeckoMed for PPT slides and notes.Quick Summary: What You Need to Know for University Exams
- Cirrhosis is a diffuse process of fibrosis with regenerative nodules that destroys normal liver architecture.
- Common causes include alcohol, chronic hepatitis B and C, and metabolic dysfunction-associated steatotic liver disease.
- Hepatic stellate cells drive fibrosis by laying down collagen in the space of Disse.
- The two main consequences are liver cell failure and portal hypertension.
- Decompensation is marked by ascites, variceal bleeding, hepatic encephalopathy and jaundice.
- Severity is graded with the Child-Pugh and MELD scores.
- Liver transplantation is the definitive treatment for end-stage disease.
Liver Cirrhosis Across MBBS Subjects
| MBBS Year | Subject | What Is Usually Asked |
|---|---|---|
| 1st Year | Anatomy | Portal vein and portocaval anastomoses |
| 1st Year | Biochemistry | Liver function tests, bilirubin metabolism |
| 2nd Year | Pathology | Definition, classification, pathogenesis, morphology, complications |
| 2nd Year | Pharmacology | Diuretics, lactulose, beta-blockers, vasoactive drugs |
| 2nd Year | Microbiology | Hepatitis B and C viruses |
| Final Year | General Medicine | Clinical features, investigations, complications, management |
| Final Year | General Surgery | Portal hypertension and variceal bleeding |
MBBS Year
1st Year
Subject
What Is Usually Asked
Liver function tests, bilirubin metabolism
MBBS Year
2nd Year
Subject
What Is Usually Asked
Definition, classification, pathogenesis, morphology, complications
MBBS Year
2nd Year
Subject
What Is Usually Asked
Diuretics, lactulose, beta-blockers, vasoactive drugs
MBBS Year
2nd Year
Subject
What Is Usually Asked
Hepatitis B and C viruses
MBBS Year
Final Year
Subject
What Is Usually Asked
Clinical features, investigations, complications, management
MBBS Year
Final Year
Subject
What Is Usually Asked
Portal hypertension and variceal bleeding
Definition and Classification
Definition: Cirrhosis is a diffuse process characterised by fibrosis and conversion of the normal liver architecture into structurally abnormal regenerative nodules.
Classification
| Basis | Types |
|---|---|
| Morphology | Micronodular (nodules smaller than 3 mm; classically alcohol), macronodular (larger than 3 mm; classically viral), mixed |
| Clinical status | Compensated; decompensated (ascites, variceal bleeding, encephalopathy, jaundice) |
| Aetiology | See table below |
Basis
Morphology
Types
Micronodular (nodules smaller than 3 mm; classically alcohol), macronodular (larger than 3 mm; classically viral), mixed
Basis
Clinical status
Types
Compensated; decompensated (ascites, variceal bleeding, encephalopathy, jaundice)
Basis
Aetiology
Types
See table below
Aetiology (Causes)
| Category | Examples |
|---|---|
| Alcohol | Alcohol-related liver disease |
| Viral | Chronic hepatitis B (with or without hepatitis D), chronic hepatitis C |
| Metabolic | Metabolic dysfunction-associated steatotic liver disease (previously non-alcoholic fatty liver disease) |
| Autoimmune | Autoimmune hepatitis |
| Biliary | Primary biliary cholangitis, primary sclerosing cholangitis, long-standing biliary obstruction |
| Genetic and metabolic | Haemochromatosis, Wilson's disease, alpha-1 antitrypsin deficiency |
| Vascular | Budd-Chiari syndrome, long-standing right heart failure (cardiac cirrhosis) |
| Drugs | For example methotrexate |
| Unknown | Cryptogenic cirrhosis |
Category
Alcohol
Examples
Alcohol-related liver disease
Category
Viral
Examples
Chronic hepatitis B (with or without hepatitis D), chronic hepatitis C
Category
Metabolic
Examples
Metabolic dysfunction-associated steatotic liver disease (previously non-alcoholic fatty liver disease)
Category
Autoimmune
Examples
Autoimmune hepatitis
Category
Biliary
Examples
Primary biliary cholangitis, primary sclerosing cholangitis, long-standing biliary obstruction
Category
Genetic and metabolic
Examples
Haemochromatosis, Wilson's disease, alpha-1 antitrypsin deficiency
Category
Vascular
Examples
Budd-Chiari syndrome, long-standing right heart failure (cardiac cirrhosis)
Category
Drugs
Examples
For example methotrexate
Category
Unknown
Examples
Cryptogenic cirrhosis
Pathophysiology
Pathogenesis of Fibrosis (Flowchart)
- Chronic injury (alcohol, virus, fat, autoimmunity) causes repeated hepatocyte death and inflammation
- Cytokines activate hepatic stellate (Ito) cells in the space of Disse
- Activated stellate cells become myofibroblasts and lay down collagen
- Sinusoids lose their fenestrations (capillarisation), reducing exchange between blood and hepatocytes
- Fibrous septa link portal and central areas
- Surviving hepatocytes regenerate as nodules surrounded by scar tissue
Portal Hypertension
Definition: Raised pressure in the portal venous system. A hepatic venous pressure gradient (HVPG) above 5 mmHg indicates portal hypertension; 10 mmHg or more is clinically significant, and a value of 12 mmHg or more is associated with variceal bleeding.
| Site of Obstruction | Examples |
|---|---|
| Prehepatic | Portal vein thrombosis |
| Intrahepatic, presinusoidal | Schistosomiasis, non-cirrhotic portal fibrosis |
| Intrahepatic, sinusoidal | Cirrhosis (most common) |
| Intrahepatic, postsinusoidal | Veno-occlusive disease |
| Posthepatic | Budd-Chiari syndrome, constrictive pericarditis, right heart failure |
Site of Obstruction
Prehepatic
Examples
Portal vein thrombosis
Site of Obstruction
Intrahepatic, presinusoidal
Examples
Schistosomiasis, non-cirrhotic portal fibrosis
Site of Obstruction
Intrahepatic, sinusoidal
Examples
Cirrhosis (most common)
Site of Obstruction
Intrahepatic, postsinusoidal
Examples
Veno-occlusive disease
Site of Obstruction
Posthepatic
Examples
Budd-Chiari syndrome, constrictive pericarditis, right heart failure
Consequences of portal hypertension:
- Portosystemic collaterals (oesophageal and gastric varices, caput medusae, rectal varices)
- Congestive splenomegaly with hypersplenism
- Ascites
(Examiner may ask you to draw the sites of portocaval anastomosis.)
Morphology (Pathology)
| Feature | Description |
|---|---|
| Gross | Liver shrunken (or sometimes enlarged early), firm, nodular surface |
| Microscopy | Regenerative nodules surrounded by fibrous septa; loss of normal lobular architecture |
| Alcohol-related features | Fatty change, Mallory-Denk bodies, neutrophilic infiltrate in alcoholic hepatitis |
Feature
Gross
Description
Liver shrunken (or sometimes enlarged early), firm, nodular surface
Feature
Microscopy
Description
Regenerative nodules surrounded by fibrous septa; loss of normal lobular architecture
Feature
Alcohol-related features
Description
Fatty change, Mallory-Denk bodies, neutrophilic infiltrate in alcoholic hepatitis
Clinical Features
Features of Liver Cell Failure
| System | Signs |
|---|---|
| General | Fatigue, weight loss, muscle wasting |
| Skin | Jaundice, spider naevi, palmar erythema, bruising |
| Hands | Clubbing, leuconychia, Dupuytren's contracture (with alcohol), flapping tremor (asterixis) |
| Endocrine | Gynaecomastia, testicular atrophy, loss of body hair, menstrual irregularity |
| Other | Parotid enlargement (with alcohol), fetor hepaticus |
System
General
Signs
Fatigue, weight loss, muscle wasting
System
Skin
Signs
Jaundice, spider naevi, palmar erythema, bruising
System
Hands
Signs
Clubbing, leuconychia, Dupuytren's contracture (with alcohol), flapping tremor (asterixis)
System
Endocrine
Signs
Gynaecomastia, testicular atrophy, loss of body hair, menstrual irregularity
System
Other
Signs
Parotid enlargement (with alcohol), fetor hepaticus
Features of Portal Hypertension
- Splenomegaly
- Ascites
- Dilated veins on the abdominal wall (caput medusae)
- Haematemesis and melaena from variceal bleeding
Hepatic Encephalopathy (West Haven Grades)
| Grade | Features |
|---|---|
| I | Mild confusion, altered sleep, reduced attention |
| II | Lethargy, disorientation, asterixis |
| III | Somnolence, marked confusion, responsive to stimuli |
| IV | Coma |
Grade
I
Features
Mild confusion, altered sleep, reduced attention
Grade
II
Features
Lethargy, disorientation, asterixis
Grade
III
Features
Somnolence, marked confusion, responsive to stimuli
Grade
IV
Features
Coma
Diagnosis
| Investigation | Findings or Purpose |
|---|---|
| Liver function tests | Low albumin, raised bilirubin; transaminases may be normal or raised; AST:ALT ratio above 2 suggests alcohol |
| Prothrombin time or INR | Prolonged, reflecting reduced synthetic function |
| Complete blood count | Thrombocytopenia and leucopenia from hypersplenism; anaemia |
| Ultrasound with Doppler | Nodular liver, splenomegaly, ascites, portal vein flow |
| Transient elastography (FibroScan) | Non-invasive estimate of liver stiffness |
| Upper GI endoscopy | Detects and grades varices |
| Ascitic fluid analysis | Serum-ascites albumin gradient (SAAG) of 1.1 g/dL or more indicates portal hypertension; neutrophil count for infection |
| Aetiology work-up | HBsAg, anti-HCV, iron studies, ceruloplasmin, autoantibodies |
| Liver biopsy | Confirms the diagnosis and cause when needed |
| Alpha-fetoprotein and ultrasound | Surveillance for hepatocellular carcinoma |
Investigation
Liver function tests
Findings or Purpose
Low albumin, raised bilirubin; transaminases may be normal or raised; AST:ALT ratio above 2 suggests alcohol
Investigation
Prothrombin time or INR
Findings or Purpose
Prolonged, reflecting reduced synthetic function
Investigation
Complete blood count
Findings or Purpose
Thrombocytopenia and leucopenia from hypersplenism; anaemia
Investigation
Ultrasound with Doppler
Findings or Purpose
Nodular liver, splenomegaly, ascites, portal vein flow
Investigation
Transient elastography (FibroScan)
Findings or Purpose
Non-invasive estimate of liver stiffness
Investigation
Upper GI endoscopy
Findings or Purpose
Detects and grades varices
Investigation
Ascitic fluid analysis
Findings or Purpose
Serum-ascites albumin gradient (SAAG) of 1.1 g/dL or more indicates portal hypertension; neutrophil count for infection
Investigation
Aetiology work-up
Findings or Purpose
HBsAg, anti-HCV, iron studies, ceruloplasmin, autoantibodies
Investigation
Liver biopsy
Findings or Purpose
Confirms the diagnosis and cause when needed
Investigation
Alpha-fetoprotein and ultrasound
Findings or Purpose
Surveillance for hepatocellular carcinoma
Child-Pugh Score
| Parameter | Scored From 1 to 3 Points |
|---|---|
| Serum bilirubin | Higher bilirubin scores more |
| Serum albumin | Lower albumin scores more |
| INR (or prothrombin time) | Higher INR scores more |
| Ascites | None, mild, moderate to severe |
| Hepatic encephalopathy | None, grade I to II, grade III to IV |
Parameter
Serum bilirubin
Scored From 1 to 3 Points
Higher bilirubin scores more
Parameter
Serum albumin
Scored From 1 to 3 Points
Lower albumin scores more
Parameter
INR (or prothrombin time)
Scored From 1 to 3 Points
Higher INR scores more
Parameter
Ascites
Scored From 1 to 3 Points
None, mild, moderate to severe
Parameter
Hepatic encephalopathy
Scored From 1 to 3 Points
None, grade I to II, grade III to IV
| Class | Total Score |
|---|---|
| A | 5 to 6 |
| B | 7 to 9 |
| C | 10 to 15 |
Class
A
Total Score
5 to 6
Class
B
Total Score
7 to 9
Class
C
Total Score
10 to 15
MELD score: Uses bilirubin, INR and creatinine (with sodium in the MELD-Na version) and is used to prioritise patients for liver transplantation.
Management
General Measures
- Treat the cause: stop alcohol, antiviral therapy for hepatitis B or C, weight loss in fatty liver disease
- Adequate nutrition with sufficient protein
- Avoid hepatotoxic drugs and sedatives; avoid NSAIDs
- Vaccinate against hepatitis A and B if not immune
- Surveillance for varices and hepatocellular carcinoma
Management of Complications
| Complication | Management Principles |
|---|---|
| Ascites | Sodium restriction; spironolactone with or without furosemide; large-volume paracentesis with albumin for tense ascites |
| Spontaneous bacterial peritonitis | Diagnosed by an ascitic neutrophil count of 250 per mm³ or more; treated with antibiotics such as a third-generation cephalosporin, plus albumin |
| Varices (prevention) | Non-selective beta-blockers (propranolol, carvedilol) or endoscopic variceal ligation |
| Acute variceal bleeding | Resuscitation, vasoactive drugs (terlipressin or octreotide), prophylactic antibiotics, urgent endoscopic band ligation; TIPS in selected cases |
| Hepatic encephalopathy | Identify and treat precipitants; lactulose; rifaximin as an add-on |
| Hepatorenal syndrome | Vasoconstrictors such as terlipressin with albumin |
| End-stage liver disease | Liver transplantation |
Complication
Ascites
Management Principles
Sodium restriction; spironolactone with or without furosemide; large-volume paracentesis with albumin for tense ascites
Complication
Spontaneous bacterial peritonitis
Management Principles
Diagnosed by an ascitic neutrophil count of 250 per mm³ or more; treated with antibiotics such as a third-generation cephalosporin, plus albumin
Complication
Varices (prevention)
Management Principles
Non-selective beta-blockers (propranolol, carvedilol) or endoscopic variceal ligation
Complication
Acute variceal bleeding
Management Principles
Resuscitation, vasoactive drugs (terlipressin or octreotide), prophylactic antibiotics, urgent endoscopic band ligation; TIPS in selected cases
Complication
Hepatic encephalopathy
Management Principles
Identify and treat precipitants; lactulose; rifaximin as an add-on
Complication
Hepatorenal syndrome
Management Principles
Vasoconstrictors such as terlipressin with albumin
Complication
End-stage liver disease
Management Principles
Liver transplantation
Precipitants of Hepatic Encephalopathy
- Gastrointestinal bleeding
- Infection, including spontaneous bacterial peritonitis
- Constipation
- Electrolyte imbalance (such as hypokalaemia) and dehydration
- Sedatives
- Excess dietary protein in some patients
Complications
- Variceal bleeding
- Ascites and spontaneous bacterial peritonitis
- Hepatic encephalopathy
- Hepatorenal syndrome
- Hepatopulmonary syndrome
- Coagulopathy
- Hepatocellular carcinoma
- Malnutrition and sarcopenia
Prognosis
Compensated cirrhosis can remain stable for years, especially if the cause is removed. Once decompensation occurs, survival falls markedly. Child-Pugh class and MELD score help predict outcomes, and transplantation offers the best long-term survival in end-stage disease.
Quick Viva Questions
Q: Which cells are mainly responsible for fibrosis in cirrhosis? A: Hepatic stellate (Ito) cells.
Q: What SAAG value indicates portal hypertension? A: 1.1 g/dL or more.
Q: What ascitic fluid neutrophil count diagnoses spontaneous bacterial peritonitis? A: 250 per mm³ or more.
Q: Name two drugs used in hepatic encephalopathy. A: Lactulose and rifaximin.
Q: What are Mallory-Denk bodies? A: Eosinophilic cytoplasmic inclusions in hepatocytes, seen in alcoholic hepatitis.
How Liver Cirrhosis Appears in MBBS University Exams
Typical question styles (not attributed to specific papers or years):
- "Define cirrhosis. Describe the aetiology, pathogenesis, morphology and complications of cirrhosis." (Long essay, Pathology)
- "Discuss the clinical features, investigations and management of cirrhosis of the liver." (Long essay, Medicine)
- "Discuss the causes and management of portal hypertension." (Long essay, Medicine or Surgery)
- "Write a short note on hepatic encephalopathy." (Short note)
- "Write a short note on the management of acute variceal bleeding." (Short note)
- "Write a short note on spontaneous bacterial peritonitis." (Short note)
Frequently Asked Questions
What is the most important complication of cirrhosis?
Variceal bleeding, ascites, hepatic encephalopathy and hepatocellular carcinoma are all major complications. Variceal bleeding is among the most immediately life-threatening.
What is the difference between compensated and decompensated cirrhosis?
Compensated cirrhosis has no major complications. Decompensated cirrhosis has ascites, variceal bleeding, hepatic encephalopathy or jaundice, and a much poorer prognosis.
Can I download the liver cirrhosis PPT for my presentation?
Yes. Use the Download PPT button at the top of this page. The GeckoMed app also gives offline access to the slides and notes.
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