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KS5 Biology
Lesson Plan 6 – Alcoholic Liver Disease
Science at Work in Healthcare
Post – 16 Science Education Pack
Resource Sheet 6.2 – Alcoholic Liver Disease
Alcoholic liver disease is caused by the excessive consumption of alcohol and is the
major cause of liver disease in western countries.
Because the liver is the main organ involved in breaking alcohol down into water and
carbon dioxide it is most prone to developing alcohol related problems.
The Stages of Liver Disease
Alcoholic liver disease is a broad term that actually refers to a number of more
specific conditions.
Steatosis, otherwise known as fatty liver, is the first stage of liver disease and is
basically the accumulation of fat in the liver cells. These appear under a microscope
as large fatty globules and can also be caused by diabetes, obesity and starvation.
Steatosis caused by alcohol intake can usually be reversed by reducing or
completely stopping alcohol consumption. However, 20 to 30 percent of people
developing steatosis and continuing to drink excessively will go on to develop the
next stage of liver disease; alcoholic hepatitis. At this stage liver function tests such
as those for bilirubin and albumin are usually normal, tests for aspartate aminotransferase (AST) and alkaline phosphatase (ALP) may show slight increases and γglutamyl transferase (GGT) levels will invariably be elevated.
Alcoholic hepatitis can occur when those cells affected by steatosis suffer an acute
inflammatory reaction. This reaction is not directly related to the quantity of alcohol
being consumed and some people seem more prone to it than others. The
inflammation is called alcoholic steatonecrosis and is thought to predispose sufferers
to develop liver fibrosis. As with steatosis, this condition can usually be reversed by
reducing or completely stopping alcohol consumption. However, even with complete
abstinence the condition can take up to six months to resolve.
At this stage bilirubin levels can reach between 300 and 500 μmol/L and GGT levels
can rise substantially. The levels of albumin in the blood serum will fall.
Alcoholic hepatitis will progress to liver fibrosis and cirrhosis in 25 to 30 per cent of
cases.
KS5 Biology
Lesson Plan 6 – Alcoholic Liver Disease
Science at Work in Healthcare
Post – 16 Science Education Pack
Cirrhosis is a late stage of liver disease characterised by fibrosis and alterations to
the structure of the liver.
Biochemical abnormalities include a low serum albumin and elevated levels of
bilirubin and AST. AST levels may reach up to 300 IU/L (International Units per litre).
Alcoholic cirrhosis is often progressive and can lead to total liver failure. The later
stages of cirrhosis are irreversible but can usually be managed with the appropriate
treatments for long periods of time.
Patients who manage to abstain from alcohol at this stage have a five year survival
rate of between 60 and 70 per cent, which falls to 40 per cent for those who continue
to drink.
Hepatocellular carcinoma (malignant liver cancer) occurs in 10 per cent of stable
cirrhotics and is usually fatal within six months.
Managing Liver Disease
Recognising alcoholic liver disease in its early stages is very important. Patients
presenting with anorexia, nausea, diarrhoea, tenderness in the area of the right lower
chest below the diaphragm and elevated levels of GGT are prime candidates for
alcoholic liver disease. The most important therapy in the early stages of alcoholic
liver disease is simply abstinence from alcohol and a nutritious diet. Drugs such as
diazepam and chlordiazepoxide can be used to treat withdrawal symptoms.
The different stages of alcoholic liver disease will lead to a variety of different
symptoms. For example, patients with chronic liver disease will often become
hyperglycemic due to insulin resistance. Patients suffering liver failure, on the other
hand, will become hypoglycemic as the liver loses its ability to make glucose
(gluconeogenesis) and depletes its glycogen stores.
Patients with severe alcoholic hepatitis will need hospital treatment as they will
usually have some significant metabolic abnormalities. These can include:

Hypomagnesemia - low levels of magnesium in the blood

Hypokalemia - low levels of potassium in the blood

Metabolic acidosis - a blood pH of less than 7.35
KS5 Biology
Lesson Plan 6 – Alcoholic Liver Disease

Science at Work in Healthcare
Post – 16 Science Education Pack
Ketoacidosis - a life-threatening condition in which ketones, which result from
the breakdown of fat for energy, accumulate in the bloodstream and the pH of
the blood decreases.
Alcoholic hepatitis can be treated with corticosteroids and amino acid supplements
can be given intravenously to treat protein malnourishment.
Cirrhosis itself is irreversible so therapy is directed at relieving the complications of
liver failure and in particular high blood pressure in the portal vein (portal
hypertension).
Portal hypertension can cause stretching of
the veins at the base of the oesophagus.
These are called oesophageal varices and if
they burst the bleeding can be fatal. To
treat this condition a portacaval shunt is
created surgically between the portal vein
and the inferior vena cava to allow blood
from the abdominal organs to bypass the
liver.
A liver transplant, however, remains the only
Diagram 1. A portacaval shunt
option for those patients with end stage alcoholic cirrhosis. The ethical issues
around using such a scarce resource as a healthy transplant-ready liver for a disease
which is widely considered to be self-inflicted are still hotly debated.
KS5 Biology
Lesson Plan 6 – Alcoholic Liver Disease
Science at Work in Healthcare
Post – 16 Science Education Pack
Liver Function Tests
There are a range of blood tests that can be carried out on patients with suspected
liver disease. Here are some of them:
o ALB – Albumin. Normal range 35 – 48 IU/L (International Units per Litre)
Albumin is synthesised by the liver and will decrease if the liver is damaged.
o AST – Aspartate Amino-Transferase. Normal range 12 – 40 IU/L
This enzyme is produced by hepatocytes, leaking out if the cells are damaged. Therefore
the level will rise in a damaged liver. High levels of AST can also be present due to
myocardial infarct (heart attack).
o ALP – Alkaline Phosphatase. Normal range 30 – 95 IU/L
This enzyme is produced by the biliary ducts of the liver and will leak into the blood if the
cells are damaged. However it is also present in bone and placenta and renal and
intestinal damage can also result in elevated levels in the blood.
o GGT – γ-Glutamyl Transferase. Normal range 3- 28 IU/L
This enzyme is specific to liver cells and production rises due to alcohol toxicity. It can be
elevated by even very minor liver dysfunction.
o ALT – Alanine Transaminase. Normal range 10 – 40 IU/L (male), 7 – 35 IU/L (female)
This enzyme is involved in the metabolism of the amino acid alanine in the liver. Injury to
the liver results in ALT leaking out into the blood. ALT is the most sensitive marker for
liver cell damage. When making a diagnosis the ratio of AST to ALT can be useful to
investigate as a ratio of AST:ALT higher than 2:1 is usually a sure sign of advanced
alcoholic liver disease.
o Tbil – Total Bilirubin. Normal range 3 - 20 μmol/L
Bilirubin is a product of the breakdown of haemoglobin from red blood cells. The liver is
responsible for clearing the blood of bilirubin so elevated levels of bilirubin are a sign that
the liver may not be functioning as it should.