Diseases of Liver: 2 Diseases

The following points highlight the two major diseases of liver. The diseases are: 1. Liver Damage 2. Jaundice.

Disease # 1. Liver Damage:

i. Hepatitis:

(a) The liver becomes tender and enlarged fol­lowing continued excessive intake of al­cohol. The patient may become jaundiced.

(b) If alcohol intake is continued, acute liver failure may arise with deep jaundice and several cerebral symptoms.

(c) The patients may complain of general ma­laise, anorexia and a variety of digestive disturbances and become progressively undernourished.

(d) During the course of chronic hepatitis there is slow progressive fibrosis leading to major disturbances of liver structure and function.

ii. Cirrhosis of the Liver:

(a) It is now referred to any diffuse chronic disease of the liver.

(b) Venous congestion leads to enlargement of the spleen which is detected by palpa­tion. It leads to varicosities which may bleed.

(c) Oesophageal bleeding is a common and serious consequence of cirrhosis of the liver.

(d) Damage to liver cells leads to jaundice that may be severe. The clinical features and disordered sleep rhythm, restlessness or drowsiness, impaired intellectual func­tion with confusion and, in severe cases, stupor and coma. The onset may be sud­den.

Sometimes these features are the first manifestations of liver failure to appear and then they may be mistaken for a psy­chiatric disorder. The condition is due to unidentified toxic substances reaching the brain in the systemic circulation. These may arise from disturbances of intermedi­ary metabolism or to substances absorbed from the gut that the damaged hepatocytes are unable to detoxify.

Disease # 2. Jaundice:

(a) This is caused by the increase in the bi­lirubin in the blood. The skin and sclera of the eyes appear yellow and the urine is usually dark yellow or brown. It is not detectable until the plasma bilirubin rises above 8 mg/I.

(b) There are three types of jaundice. Hepato­cellular jaundice is due to damage to hepatocytes by toxic or infectious agents interfering with the uptake and conjuga­tion of bilirubin by the cells or to block­ing of the bile eanalieuli (cholestatic jaun­dice).

Pre-hepatic (hemolytic) jaundice is due to increased bilirubin from excessive de­struction of R.B.C. It may arise from congential defects causing the erythro­cytes to be unduly fragile (spherocytosis, sickle cell anemia, thalassemia or from some drugs, incompatible blood transfu­sions).

Post-hepatic jaundice is due to an obstruc­tion of bile flow between the liver and duo­denum. Common causes are impacted gall­stones and cancer of the head of the pan­creas. The excess of bilirubin in the plasma is then in the conjugated form, whereas in pre-hepatic jaundice it is unconjugated.

(c) Jaundice is sometimes accompanied by itching (pruritus) and this may be severe. The cause is retention of bile salts in the blood and it may be relieved by cholestyramine. This is an anion exchange resin which binds bile salts in the gut and so interrupts the enterohepatic circulation and increases fecal excretion of bile salts.

Agent Damaging the Bile Salts:

i. Dietary Deficiency:

Low protein intake causes the fatty changes in the liver in kwashiorkor and there is evidence of re­duced capacity to secrete β-lipoproteins but not of choline deficiency in man. Choline deficiency is not at all responsible for liver damage in man. Fatty changes in the liver are common when­ever there is a high proportion of fat in the meta­bolic mixture, e.g., in uncontrolled diabetes, in star­vation, in some cases of obesity.

ii. Infective Agents:

Hepatitis A virus is excreted in the stools and spreads by the fecal oral route. Children or adoles­cents are affected by this infection where hygienic condition is low. The initial symptoms are loss of appetite, nausea and malaise and usually mild fe­ver. Jaundice appears after 4 to 7 days and the liver is enlarged and tender. The symptoms usually last from 2 to 6 weeks but complete recovery may take many months.

Very rarely there is fulminant hepatitis with symptoms of acute liver failure and the death usu­ally occurs within 10 days. Some healthy people, who have no clinical history of the attack of the disease, excrete the vi­rus in their feces. Such carriers may cause epidemic. Some of the cases of cirrhosis in which no cause can be found may be due to long continuing expo­sure of the liver to the virus.

Hepatitis B virus produces a disease known as homologous serum jaundice because it arises after transfusion of blood. It can also be spread by the use of one needle to give injections to a series of patients without effective sterilisation.

The virus is never spread by the fecal-oral route and the infec­tion arises from close personal contact, as between sexual partners. They cause similar type of illness as that in Hepatitis A virus. A carrier can be de­tected by the presence of the antigen of the virus (HBeAG) in the serum.

Yellow fever virus has a specific affinity for hepatocytes. It is much more virulent. More than 20 per cent of patients died of acute liver failure. Yellow fever is now very rare, as the mosquito re­sponsible for its transmission is a domestic species and easily controlled.

iii. Other Infective Agents:

In three diseases the liver is especially involved. In Weil’s disease leptospira invade all organs and tis­sues but markedly the liver and jaundice is the com­mon feature. Amoebiasis is primarily a disease of the large intestine but protozoa may migrate up the portal vein and cause amoebic hepatitis and liver ab­scesses.

In schistosomiasis with infection of the large intestine by Schistosoma mansoni, ova frequently move up the portal vein and cause multiple granulomata in the liver; these become fibrosed and are a common cause of cirrhosis of the liver.

iv. Toxic Agents:

(a) Alcohol, other undetected toxic chemicals and infective agents may act synergistically to produce progressive liver dam­age.

(b) Foods may be contaminated by moulds that produce toxin. Aflatoxins are known to cause liver disease.

(c) Many drugs can damage the liver in sus­ceptible individuals and produce a clini­cal and biochemical picture similar to acute viral hepatitis. Examples are para­cetamol, a much used analgesic, some­times used in the treatment of depression. Cholestatic jaundice may follow the use of methyl testosterone and very rarely oral contraceptives.

(d) Workers in the chemical industry may be exposed to many chemicals that damage the liver and produce jaundice. Examples are hydrocarbons, carbon tetrachloride, ar­senic, trinitrotoluene, etc.

(e) Excess stores of iron, copper, galactose and glycogen may accumulate in the liver and in time lead to cirrhosis. These conditions are usually due to hereditary defects. He­reditary defects in the transport and con­jugation of bilirubin may lead to jaundice.

People suffering from Gilbert’s disease have no symptoms but jaundice, anorexia, nausea and abdominal pain may arise dur­ing a period of stress, such as an infection, fasting or strenuous exercise.

Dietetic Management and Treatment:

i. Acute Hepatitis:

(a) There is no antiviral agent for use against the hepatitis virus but metronidazole is very effective in amoebic hepatitis. Pa­tients with viral hepatitis do well with rest.

(b) No specific dietary treatment is needed but as patients lack appetite and suffer from nausea, meals should be well-cooked and attractively served. Several small meals may be better tolerated than three large ones.

(c) Fat intake should be restricted. Carbohy­drate and protein diet should be taken. Vi­tamins and minerals should be given through fruits and vegetables.

ii. Hepatic Failure:

(a) Hemorrhages as a result of lack of clotting factors synthesized by the liver lead to shock and renal failure. Profound hypoglycemia and potassium depletion occur.

(b) Intravenous infusion of hypertonic glu­cose and electrolytes is required with re­peated monitoring of blood level.

(c) Sedatives may be needed for delirium but are potentially dangerous due to the state of the liver.

(d) Despite all treatment majority of the pa­tients die.

iii. Chronic Hepatitis:

This is common in alcoholics and occasionally fol­lows viral hepatitis. When it is due to alcoholics, most patients do well when alcohol intake is stopped.

Some chronic alcoholics are malnourished because they eat irregularly and seldom take proper meal. They need to change dietary habits and re­quire professional advice.

iv. Cirrhosis:

(a) Many patients with cirrhosis are seriously malnourished, especially those who are alcoholic and require nutritional rehabili­tation with a high energy, high protein diet. This may be difficult to achieve on account of poor appetite, and admission to hospital is necessary.

(b) The fat-soluble vitamins are poorly ab­sorbed because of the poor absorption of fat owing to the absence of bile salts. Therefore, supplements may be needed. A monthly intramuscular injection of Vita­min K (10 mg), of Vitamin A (30 mg) and of Vitamin D (25 mg) provides for mainte­nance. As bleeding is common and often severe, Vitamin K should be given at once and continued.

(c) Osteomalacia is a well-known complica­tion of chronic liver disease and also re­serves of Vitamin A in the liver is low. Vitamins A and D should be given in proper doses and should not be given more which may cause toxic effect.

v. Ascites:

(a) Fluid accumulates in the peritoneal cav­ity because of increased capillary pressure in the portal vessels and decreased oncotic pressure owing to a failure of the liver to synthesize plasma albumin. Sodium is re­tained in the fluid.

(b) The ascitic fluid often amounts to 10 li­tres and contains protein in concentrations of 10 to 20 g/I.

(c) It depletes plasma proteins and carries a risk of introducing infection.

(d) Treatment consists of a diet rich in pro­tein and low in sodium, and also diuretics to increase urinary output of sodium and fluid. With all of them there is a danger of electrolyte imbalance. Over-dosage may lead to sodium deficiency and also to po­tassium depletion.

(e) The patient should avoid salt-rich foods.

vi. Portal Hypertension:

Bleeding from oesophageal and gastric varices is common and often serious and a cause of death. The anemia is treated with iron and repeated blood transfusion are often necessary. Pressure in the veins can be relieved by a surgical operation but such operations are dangerous and increase the risk of death from liver failure.

vii. Biliary Cirrhosis:

Stagnation of bile in the canaliculi of the liver may lead to hepatitis and subsequently to cirrhosis. This may be a consequence of unrelieved obstruction of the bile duct and then secondary bacterial infec­tion is often an additional factor.

This disease oc­curs most commonly in middle-aged women. Prompt surgical treatment prevents any dam­age to the liver from progressing jaundice fluctu­ates in intensity as does pruritis which is often seri­ous and then may be relieved by cholestyramine.