Alcoholic Liver disease Flashcards
Aetiology of alcoholic liver disease
- Alcohol overuse (recommended < 14 units a week in M and F)
- alcohol dependence
- genetic component?
Pathophysiology of alcoholic liver disease
There is a stepwise process of progression:
- Alcohol related fatty liver
Drinking leads to a build-up of fat in the liver. If drinking stops this process reverses in around 2 weeks.
- Alcoholic hepatitis
Drinking alcohol over a long period causes inflammation in the liver sites. Binge drinking is associated with the same effect. Mild alcoholic hepatitis is usually reversible with permanent abstinence.
- Cirrhosis (scarring)
This is where the liver is made up of scar tissue rather than healthy liver tissue. This is irreversible. Stopping drinking can prevent further damage. Continued drinking has a very poor prognosis.
Clinical presentation of alcoholic liver disease
signs of liver disesease:
- jaundice
- hepatomegaly
- spider naevi
- palmar erythema
- gynaecomastia
- bruising → due to abnormal clotting
- ascites
- caput medusae → engorged superficial epigastric veins
- Asterixis → “flapping tremor” in decompensated liver disease
Selected investigation findings?
- gamma-GT is characteristically elevated
- the ratio ofAST:ALT is normally > 2, a ratio of > 3 is strongly suggestive of acute alcoholic hepatitis
Blood results in alcoholic liver disease?
FBC – raised MCV (mean corpuscular volume → average size of erythrocytes)
LFTs – elevated ALT and AST (transaminases) and particularly raised gamma-GT. ALP will be elevated later in the disease. Low albumin due to reduced “synthetic function” of the liver. Elevated bilirubin in cirrhosis.
Clotting – elevated prothrombin time due to reduced “synthetic function” of the liver
U+Es may be deranged inhepatorenal syndrome.
Ultrasound in alcoholic liver disease?
- An ultrasound of the liver may show fatty changes early on described as “increased echogenicity”. It can also demonstrate changes related to cirrhosis if present.
- “FibroScan” can be used to check the elasticity of the liver by sending high frequency sound waves into the liver. It helps assess the degree of cirrhosis.
CT and MRI in alcoholic liver disease
CT and MRI can be used to look for fatty infiltration of the liver, hepatocellular carinoma, hepatosplenomegaly, abnormal blood vessel changes and ascites
Liver biopsy in alcoholic liver disease
liver biopsy can be used to confirm the diagnosis of alcohol-relted hepatitis or cirrhosis. NICE recommend considering a liver biopsy in patient where steroid treatment is being considered
Treatment + management of alcoholic liver disease
- Stop drinking alcohol permanently
- Consider a detoxication regime
- Nutritional support with vitamins (particularly thiamine) and a high protein diet
- Steroids improve short term outcomes (over 1 month) in severe alcoholic hepatitis but infection and GI bleeding need to be treated first and do not improve outcomes over the long term
- Treat complications of cirrhosis (portal hypertension, varices, ascites and hepatic encephalopathy)
- Referral for liver transplant in severe disease however they must abstain from alcohol for 3 months prior to referral
Delerium tremens
Symptoms occur at different times after alcohol consumption ceases:
- 6-12 hours: tremor, sweating, headache, craving and anxiety
- 12-24 hours:hallucinations
- 24-48 hours:seizures
- 24-72 hours: “delirium tremens”
medical emergency associated withalcohol withdrawalwith a mortality of 35% if left untreated. Alcohol stimulatesGABA receptors in the brain. GABA receptors have a “relaxing” effect on the rest of the brain. Alcohol also inhibits glutamate receptors (also known as NMDA receptors) having a further inhibitory effect on the electrical activity of the brain.
When alcohol is removed from the system, GABA under-functions and glutamate over-functions causing an extreme excitability of the brain with excessadrenergic activity. This presents as:
- Acute confusion
- Severe agitation
- Delusions and hallucinations
- Tremor
- Tachycardia
- Hypertension
- Hyperthermia
- Ataxia (difficulties with coordinated movements)
- Arrhythmias
Selected management notes for alcoholic hepatitis:
- glucocorticoids(e.g. prednisolone) are often used during acute episodes of alcoholic hepatitis
- Maddrey’s discriminant function (DF)is often used during acute episodes to determine who would benefit from glucocorticoid therapy
- it is calculated by a formula usingprothrombin time and bilirubinconcentration
- pentoxyphylline is also sometimes used
- the STOPAH study (see reference) compared the two common treatments for alcoholic hepatitis, pentoxyphylline and prednisolone. It showed that prednisolone improved survival at 28 days and that pentoxyphylline did not improve outcomes
