Alcoholic hepatitis is a very common cause of liver injury. It is caused by excessive alcohol consumption.Typically there will be steatosis of the liver.In Steatosis pathological fat globules begin to accumulate in the cytoplasm of liver cells.Sometimes this can be pretty harmless, and as a result, steatosis is not very specific for predicting if the liver will develop cirrhosis.
Mallory’s hyalin is an aggregate of filament found in the hepatocytes.If present it indicate a risk of irreversible changes in hepatocytes(livercell).It may ultimately lead to cirrhosis. Mallory’s hyalin is not specific for alcoholic liver disease.
Ethanol(alcohol)after consumption is oxidised to acetaldehyde. Acetaldehyde is then converted to acetate by the mitochondria of liver cells.90% of this conversion is seen in liver.Acetate is then released into the bloodstream and it is taken up by peripheral tissues.In the peripheral tissue acetate is metabolised to carbon dioxide, fatty acids and water
Epedemiology of alcoholic hepatitis
10-30% of heavy drinkers will ultimately develop cirrhosis and 50% of alcoholic will have fatty liver.
Role of nutritional factors are controversial, although it is possible that obesity and malnutrition both contribute to liver damage.
The risk of hepatitis is increased by high alcohol consumption combined with hepatitis C infection.
In males with alcoholic hepatitis, average alcohol consumption was about 16 units/day over a period of 8 years. However,the amount is highly variable.In females,the corresponding dose was 11 units/day.
Why alcohol is is toxic to liver cells?
The first sign of alcoholic hepatitis is fatty liver.This can occurs in most heavy drinkers at some time, but it is completely reversible upon cessation of alcohol consumption.
1.The hepatocytes have to metabolise the alcohol which is done at the expense of metabolising fats.As a result, fat metabolism is altered which results in fat deposits inside the cells.More fat is released into the blood stream (fatty acids) as well as within the hepatocytes.Due to the elevated levels of fatty acids there is increased synthesis of triglycerides and fatty acids.
2.The product of alcohol metabolism ,Acetaldehyde binds to liver cell proteins, and causes hepatocytes injury, leading to inflammation.This inflammation may be a causatory factor in liver cirrhosis.
3.Alcohol stimulates collagen synthesis by fibroblasts and also fibroblast proliferation.Finally, the fibrosing process will end up linking hepatic veins to portal veins, cell regeneration occur at these areas resulting in nodules formation – this is the start of the process of cirrhosis.
What are the clinical sign of chronic liver disease
Malnutrition
1.Very thin arms and legs(due to muscle wasting)
2.Swollen abdomen
3.Red tongue (iron-deficiency anaemia)
4.Dry scaly cracked skin (due to zinc /fatty acid deficiency)
Endocrine manifestation of chronic liver disease
1.Gynaecomastia
2.Testicular atrophy
3.Loss of body hair
4.Signs of 'pseudo-Cushings’ (red face, hump, striae)
Face /skin manifestations of chronic liver disease
1.Parotid enlargement
2.Spider naevi
3.Easy bruising
4.Dupuytren’s contracture
Neuromuscular manifestations
1.Tremor
2.Memory loss / cognitive impairment
3.Peripheral myopathy- degradation of muscle
4.Epilepsy
5.Wernicke-Korskoff syndrome
Cardiovascular manifestations
1.Hypertension
2.Cardiomyopathy
3.Hyperdynamic circulation
Bone
1.Rib fractures on CXR
2.Spinal osteoporosis (particularly in men)
Generally, patients with fatty liver are asymptomatic or have few symptoms, however they may notice nausea and malaise. Mild alteration in LFT’s
Mild alcoholic hepatitis is indistinguishable from fatty liver disease- and the two may co-exist. The symptoms of mild alcoholic hepatitis are more severe include Anorexia,Nausea ,Abdominal pain Weight loss
