We have a guest author this week, a Mr Philip Nelson from the University of Glasgow who has been working with the medical education department for the past 5 weeks.
Scots have an unenviable reputation for alcohol consumption. Unfortunately this means that there are a lot of admissions to hospital due to alcohol abuse. It seems as though it is going to be a big problem in the future as compared with 30 years ago there are 4 times as many people dying of alcoholic liver disease(ALD) now.
The liver is a complicated organ, so it's helpful to simplify its functions into three main groups:
- Storage - glycogen, vitamins A, D, B12, K, iron, copper
- Metabolism - drugs, carbohydrates (gluconeogenesis, glycogenolysis), lipids, proteins
- Production - bile, albumin, clotting factors, hormones (inslulin like growth factor 1, thrombopoeitin)
With that in mind we will focus on how alcohol effects the liver. In chronic alcohol abuse the liver is damaged and some of these functions become impaired. There are three main pathologies that constitute ALD:
- Steatosis: Fatty liver is a reversible condition that occurs in nearly all people who are chronic alcohol abusers. Excess fatty acids accumulate in hepatocytes. Ususally asymptomatic.
- Hepatitis: Again reversible, affecting about 1 in 4 alcoholics. Hepatocyte inflammation and necrosis. Signs and symptoms include jaundice, weight loss, tender hepatomegaly, fevers.
- Cirrhosis: Usually irreversible, affecting 10-20% of alcoholics. The liver becomes inflamed, fibrosed and undergoes micronodular regeneration.
Patients who have cirrhosis will exhibit some of the signs of chronic liver disease, including:
- Hepatomegaly +/- Splenomegaly
- Gynaecomastia
- Spider naevi
- Palmar erythema
- Finger Clubbing
- Dupytrens contracture
- Asterixis
- Ascites
- Encephalopathy
When you're assessing a patient with ALD, its important to take a thorough history and examination to get an idea of the effects of the disease on the individual. Blood tests are also an important part of the assessment. The main ones to look in ALD at are:
- Albumin, INR - Synthetic function of the liver. Albumin decreases and INR increases in cirrhosis.
- AST/ALT - Hepatic enzymes. Both raised, if ratio AST:ALT = >2:1 it is due to alcohol
- ALP, GGT - Cholestatic enzymes. ALP mildly raised, GGT significantly raised.
- Bilirubin - Conjugated by liver. Raised in cirrhosis, higher in acute hepatitis.
Three complications of ALD that patients may present with are ascites, encephalopathy and varices. We talked about these in the presentation and the links provide another good introduction to each topic.These complications all have an effect on the prognosis of the disease, which can be estimated using the Child-Pugh score.
Here are some sample LFTs for you to think about. Try to come up with differential diagnoses for each. The information on the slides might give you some help.
Measure | 1 point | 2 points | 3 points |
---|---|---|---|
Total bilirubin, μmol/l | <34 | 34-50 | >50 |
Serum albumin, g/l | >35 | 28-35 | <28 |
PT INR | <1.7 | 1.71-2.30 | > 2.30 |
Ascites | None | Mild | Moderate to Severe |
Hepatic encephalopathy | None | Grade I-II (or suppressed with medication) | Grade III-IV (or refractory) |
Points | Class | One year survival | Two year survival |
5-6 | A | 100% | 85% |
7-9 | B | 81% | 57% |
10-15 | C | 45% | 35% |
Here are some sample LFTs for you to think about. Try to come up with differential diagnoses for each. The information on the slides might give you some help.