Good day everyone, Today we are going to discuss fully on diseases of the liver;
Learning outcomes
After studying this section, you should be able to:
- compare and contrast the causes, am and effects of chronic and acute hepatitis
- describe the main non-viral inflammatory conditions of the liver
- discuss the causes and consequences of liver failure
- describe the main liver tumours.
Liver tissue has a remarkable capacity for regeneration and therefore damage is usually extensive before it is evident. The effects of disease or toxic agents are seen when:
- regeneration of hepatocytes (liver cells) does not keep pace with damage, leading to hepatocellular failure
- there is a gradual replacement of damaged cells by fibrous tissue, leading to portal hypertension.
In most liver disease both conditions are present.
Also read: axial skeleton
Acute hepatitis
Areas of necrosis develop as groups of hepatocytes die and the eventual outcome depends on the size and number of these areas. Causes of the damage may be a variety of conditions, including:
- viral infections
- toxic substances
- circulatory disturbances.
Viral hepatitis
Viral infections are the commonest cause of acute liver injury and different types are recognised. The types are distinguished serologically, i.e. by the antibodies produced to combat the infection. The severity of the ensuing disease caused by the different virus types varies considerably, but the pattern is similar. The viruses enter the liver cells, causing degenerative changes. An inflammatory reaction ensues, accompanied by production of an exudate containing lymphocytes, plasma cells and granulocytes. There is reactive hyperplasia of the hepatic macrophages (Kupffer cells) in the walls of the sinusoids.
Also read: obstructive lung disorder
As groups of cells die, necrotic areas of varying sizes develop, phagocytes remove the necrotic material and the lobules collapse. The basic lobule framework becomes distorted and blood vessels develop kinks. These changes interfere with the circulation of blood to the remaining hepatocytes and the resultant hypoxia causes further damage locally. Fibrous tissue develops in the damaged area and adjacent hepatocytes proliferate. The effect of these changes on the overall functioning of the liver depends on the size of the necrotic areas, the amount of fibrous tissue formed and the extent to which the blood and bile channels are distorted.
Hepatitis A
Previously known as ‘infectious hepatitis’, this type often occurs as epidemics in all parts of the world. It affects mainly children, causing a mild illness although it is often asymptomatic. Infection is spread by the faecaloral route, e.g. via contaminated hands, food, water and fomites. Viruses are excreted in the tances for 7-14 days before clinical symptoms appear nd for about 7 days after. Symptoms may include general malaise followed by a period of jaundice that is accompanied by passing of dark urine and pale faeces. Antibodies develop and confer lifelong immunity after recovery Subclinical disease may occur but not carriers.
Hepatitis B
Previously known as ‘serum hepatitis’, infection occurs at any age, but mostly in adults. The incubation period is from 50 to 180 days. The virus enters the blood and is spread by contaminated blood and blood products. People at greatest risk of infection are those who come in contact with blood and blood products in the course of their work, e.g. health-care workers. The virus is also spread by body fluids, i.e. saliva, semen, vaginal secretions, and from mother to fetus (vertical transmission). Others at risk include intravenous drug users and men who have sex with men. Antibodies are formed and immunity persists after recovery. Infection usually leads to severe illness lasting from 2 to 6 weeks, often followed by a protracted convalescence. Carriers may, or may not, have had clinical disease. Hepatitis B virus may cause massive liver necrosis and death. In less severe cases recovery may be complete. In others chronic hepatitis may develop; live viruses continue to circulate in the blood and other body fluids.
Hepatitis D. This virus contains no RNA and can only replicate in the presence of hepatitis B virus. It most ofter infects intravenous drug users who already have hepatitis B but also affects others with hepatitis B.
Hepatitis C
This virus is spread by blood and blood products, which accounts for the infection of many people with haemophilia. In countries, including the UK, where blood donors are now screened for the virus this route of transmission is now rare although it is prevalent in intravenous drug users. The infection is very frequently asymptomatic although a carrier state occurs. Infection is usually diagnosed later in life when cirrhosis or chronic liver failure becomes evident.
Toxic substances
Many drugs undergo chemical change in the liver before excretion in bile or by other organs. They may damage the liver cells in their original form or while in various intermediate stages. Some substances always cause liver damage (predictably toxic) while others only do so when hypersensitivity to normal doses develops (unpredictably toxic). In both types the extent of the damage depends on the size of the dose and/or the duration of exposure.
Circulatory disturbances
The intensely active hepatocytes are particularly vulnerable to damage by hypoxia, which is usually due to impaired blood supply caused by:
- fibrosis in the liver following inflammation
- compression of the portal vein, hepatic artery or vein by a tumour
- acute general circulatory failure and shock
- venous congestion caused by acute or chronic right-sided heart failure.
Chronic hepatitis
This is defined as any form of hepatitis which persists for more than 6 months. It may be caused by viruses, alcohol or drugs, but sometimes the cause is unknown.
Mild, persistent inflammation may follow acute viral hepatitis. There is usually little or no fibrosis.
