Alcohol liver disease Flashcards
What is alcoholic liver disease (ALD)?
Liver disease caused by chronic, heavy alcohol ingestion.
What is the pathophysiology of ALD?
Alcohol is metabolised mainly in the liver through 2 main pathways: alcohol dehydrogenase and cytochrome p450 2E1.
When the alcohol dehydrogenase pathway is over-saturated, the 2nd pathway is used which generated free radicals through the oxidation of NADPH.
Also, alcohol dehydrogenase produces NADH. Excessive NADH inhibits gluconeogenesis and increases fatty acid oxidation, which in turn promotes fatty infiltration in the liver.
What are the key risk factors of alcoholic liver disease?
Key risk factors include:
Prolonged heavy alcohol consumption
Presence of hepatitis C
Female gender
Typical symptoms of ALD
Fatigue Anorexia Weight loss Jaundice Fever Nausea and vomiting Right upper quadrant abdominal discomfort
Typical signs of ALD
No major signs in early-stage ALD but may have: Hepatomegaly Mild jaundice Low-grade fever In advanced ALD, there is: Signs of portal HTN: Ascites, splenomegaly, venous collateral circulations. Confusion Cutaneous Telangiectasias Palmar erythema Finger clubbing Dupuytren's contracture Parotid gland enlargement Feminisation
Initial blood tests in ALD
LFTs FBC Basic metabolic panel (Na+, K+. Cl-, HCO3-, urea, creatinine) Magnesium Phosphorus Coagulation (PT, INR)
Diagnosis of ALD
Exclude alternative causes of liver disease in people with a history of harmful or hazardous drinking who have abnormal liver blood test results.
Refer people to a specialist experienced in the management of alcohol-related liver disease to confirm a clinical diagnosis of alcohol-related liver disease.
Consider liver biopsy for the investigation of alcohol-related liver disease.
Management of ALD
The main goal of treatment in all patients is to reduce liver injury due to excessive alcohol use and prevent progression of liver disease.
1st line:
Alcohol abstinence + Alcohol withdrawal management
Weight reduction + Smoking cessation
Immunisation, nutritional supplementation.
Corticosteroids (patients with an MDF score >32 or hepatic encephalopathy): Prednisolone 40 mg OD
Corticosteroids should be avoided in ALD patients with gastrointestinal bleeding requiring transfusion, in active infection, and in hepatorenal syndrome.
Sodium restriction and diuretics (ascites)
Pentoxifylline (reduces the risk of hepatorenal syndrome)
2nd line:
Liver transplant + alcohol abstinence
Complications of ALD
Hepatic encephalopathy Portal HTN GI bleeding Coagulopathy Renal failure Hepatorenal syndrome Hepatocellular carcinoma
Differentials of ALD
Viral hepatitis Acute liver failure Cholecystitis Hepatic vein thrombosis Wilson's disease Autoimmune hepatitis Wernicke's encephalopathy Biliary obstruction Drug or toxin-induced hepatitis Haemochromatosis
Prognosis of ALD
Alcoholic fatty liver usually reverts to normal with alcohol abstinence.
The acute outlook (< 6 months) is excellent.
Longer follow-up has found that cirrhosis develops more commonly in alcohol abusers with fatty liver changes than in those with normal liver histology.
