Introduction
Alcoholic Liver Disease (ALD) is a progressive inflammatory liver condition caused by long-term heavy alcohol intake. Not all heavy drinkers develop ALD, and sometimes even moderate drinkers may be affected. The condition ranges from mild, symptomless liver injury to severe hepatitis and cirrhosis. If alcohol intake continues, liver damage becomes worse. If alcohol is stopped, some improvement may occur, but many individuals are left with permanent scarring (cirrhosis).
Severely affected patients may present with fever, enlarged liver, jaundice, bleeding tendencies, ascites, hepatic encephalopathy and portal hypertension. About 15–20% of chronic heavy drinkers develop alcoholic hepatitis or cirrhosis.
Epidemiology
Alcohol misuse is the most common cause of serious liver disease in Western countries. Mild cases often go unreported because patients do not seek medical care.
Etiology (Causes)
ALD occurs due to chronic alcohol consumption. When the liver breaks down ethanol, toxic chemicals like acetaldehyde are produced, which cause inflammation and kill liver cells. Over time, healthy liver tissue is replaced by fibrous scar tissue, leading to cirrhosis.
Several factors increase the risk of ALD:
- Other hepatitis infections: Alcohol worsens the effect of hepatitis B and C.
- Malnutrition: Heavy drinkers often have poor nutrition or impaired nutrient absorption.
- Sex: Women are more prone to ALD due to differences in alcohol metabolism.
- Genetic factors: Certain genetic mutations affect how alcohol is processed.
- Type of beverage: Beer and spirits are riskier than wine.
- Binge drinking: Sudden heavy drinking episodes can accelerate liver injury.
- Obesity: Alcohol and obesity together produce a stronger damaging effect.
Pathophysiology
Inflammation and Cell Death
- Inflammation begins when hepatocytes are damaged by alcohol and acetaldehyde.
- Inflammatory cytokines (TNF-α, IL-6, IL-8) promote apoptosis and necrosis.
- Increased gut permeability allows endotoxins to enter portal circulation, triggering more liver inflammation.
Mallory Bodies
These are abnormal protein accumulations inside liver cells. Although not exclusive to ALD, they are a characteristic finding.
Ballooning Degeneration
Hepatocytes swell due to accumulation of fat, water and proteins. This swelling can block nearby bile ducts, leading to cholestasis. Ballooning is usually accompanied by necrotic cell death.
Inflammation
Neutrophils enter the liver due to necrotic debris. Kupffer cells may be overloaded, allowing inflammatory cells to spill into liver tissue.
Fibrosis
Chronic inflammation leads to abnormal scar tissue formation. Regenerating liver cells form nodules, making the liver firm and enlarged. Fibrosis reduces the liver’s ability to function normally.
Cirrhosis
Cirrhosis is the final stage of ALD. It involves permanent scarring, liver shrinkage, impaired detoxification and reduced blood flow. Around 10–20% of heavy drinkers eventually develop cirrhosis. Acetaldehyde stimulates collagen production by stellate cells, contributing to fibrosis.
Symptoms
Early stages may show no symptoms. Symptoms worsen after heavy drinking.
Digestive Symptoms
- Abdominal pain and swelling
- Reduced appetite and weight loss
- Nausea and vomiting
- Fatigue
- Dry mouth and excessive thirst
- Bleeding from enlarged esophageal veins
Skin Symptoms
- Jaundice (yellow skin and eyes)
- Spider-like red veins on skin
- Dark or very pale skin
- Redness of hands and feet
- Itching
Most individuals with ALD are malnourished because alcohol suppresses appetite and interferes with nutrient absorption.
Complications
Portal Hypertension
Scar tissue restricts blood flow through the liver, causing increased pressure in the portal vein.
Esophageal and Gastric Varices
Increased portal pressure pushes blood into alternate vessels, causing swollen veins in the stomach and esophagus. These can rupture and cause life-threatening bleeding.
Jaundice
Occurs when liver cannot remove bilirubin from blood, causing yellow discoloration.
Hepatic Encephalopathy
Accumulation of toxins like ammonia affects brain function. Symptoms include confusion, forgetfulness, mood changes and coma in severe cases.
Diagnosis
CBC (Complete Blood Count)
- Neutrophilic leukocytosis (sometimes severe)
- Moderate anemia due to bone marrow suppression
- Increased mean corpuscular volume
- Thrombocytosis due to inflammation or thrombocytopenia due to splenic sequestration
Screening Blood Tests
- HBsAg – screens for hepatitis B
- Anti-HCV – screens for hepatitis C
- Ferritin & transferrin saturation – screens for hemochromatosis
- High ALP with fever – may indicate gallstone-related cholangitis
Liver Function Tests
ALD shows a typical pattern: AST moderately elevated while ALT is normal or mildly elevated (opposite of many other liver diseases).
Ultrasonography
Preferred imaging method. Helps evaluate liver structure and guides biopsy.
Liver Biopsy
Not always required but useful to confirm diagnosis, check for cirrhosis and rule out other liver diseases.
Cirrhosis
Introduction
Cirrhosis is a chronic liver condition where normal tissue is replaced with scar tissue due to years of injury. Most common causes include alcohol abuse, chronic hepatitis B and C, and non-alcoholic steatohepatitis (NASH). Cirrhosis has no cure.
Classification
Compensated Cirrhosis
- Cirrhosis present but liver function is relatively preserved
- No major complications like ascites or encephalopathy
Decompensated Cirrhosis
- Reduced liver function
- Portal hypertension with complications
- Ascites, varices and variceal bleeding
- Hepatic encephalopathy
- Jaundice
Signs & Symptoms of Cirrhosis
- Fatigue
- Jaundice
- Varices
- Ascites
- Edema
- Hepatic encephalopathy
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