Ross & Wilson Anatomy and Physiology in Health and Illness (153 page)

Protein material secreted by the acinar cells blocks the tiny acinar ducts. This eventually leads to the formation of encapsulated cysts which are a feature of acute and chronic pancreatitis.

The most common cause in the Western world is excessive chronic alcohol consumption. In developing countries dietary factors and malnutrition have been implicated. It is also associated with cystic fibrosis.

Cystic fibrosis (see
p. 258
)

Tumours of the pancreas

Benign tumours are very rare.

Malignant tumours

These are relatively common and affect up to twice as many men as women. They occur most frequently in the head of the pancreas, obstructing the flow of bile and pancreatic juice into the duodenum. Jaundice, sometimes accompanied by itching, develops. Weight loss is the result of impaired digestion and absorption of fat, although anorexia and metabolic effects of the tumour may also play a role. Tumours in the body and tail of the gland rarely cause symptoms until the disease is advanced. Irrespective of the site, metastases are often recognised before the primary tumour and the prognosis is generally poor. There is an association with cigarette smoking, diabetes mellitus and possibly chronic pancreatitis.

Diseases of the liver

Learning outcomes

After studying this section, you should be able to:

compare and contrast the causes, forms 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.

New liver cells develop only when needed to replace damaged cells. Capacity for regeneration is considerable and 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.

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.

As groups of cells die, necrotic areas of varying sizes develop, phagocytes remove the necrotic material and the lobules collapse. The basic lobule framework (
Fig. 12.35
) 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. 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 affects mainly children, causing a mild illness. Infection is spread by hands, food, water and fomites contaminated by infected faeces. The incubation period is 15 to 40 days and the viruses are excreted in the faeces for 7 to 14 days before clinical symptoms appear and for about 7 days after. Symptoms may include general malaise followed by a period of jaundice (
p. 327
) 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 50 to 180 days. The virus enters the blood and is spread by 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 IV drug users and men who have sex with men. Antibodies are formed and immunity persists after recovery. Infection usually leads to severe illness lasting 2 to 6 weeks, often followed by a protracted convalescence. Carriers may, or may not, have had clinical disease. Type B virus may cause massive liver necrosis and death. In less severe cases recovery may be complete. In chronic hepatitis (see opposite) that may develop, live viruses continue to circulate in the blood and other body fluids. The condition is thought to predispose to liver cancer.

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. It is prevalent in IV drug users. The infection is very frequently asymptomatic as a carrier state occurs. Infection is usually diagnosed later in life when cirrhosis (see opposite) 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 (
Box 12.1
).

Box 12.1
Some hepatotoxic substances