Liver Cirrhosis

Heavy consumers of alcohol should be aware of the adverse effects it can have on the liver. Cirrhosis of the liver is caused by the accumulation of fat and protein in the liver. It can be reversible with abstinence in early stages, but can become irreversible with scarring of the liver parenchyma if left untreated. This is seen in 10 to 15% of alcoholics. In patients exhibiting cirrhosis, coagulation factors are affected due to the effects of altered liver production on the production of factors II, V, VII, X and XIII.

It is estimated that 10% of patients who consume 80g of alcohol daily for 10 years will develop cirrhosis of the liver. readers should know that a typical beer, wine, or shot has approximately 14 grams of alcohol. 80 grams is about 5-6 drinks per day. Patients with cirrhosis develop hepatomegaly, weight loss, accumulation of ascitic fluid and splenomagally. In addition, in such patients Palmar erythema appears and spider angiomas are common over the face, back, chest and arms. Vitamin deficiencies and decreased coagulation result in subcutaneous bleeding. Portal hypertension results in esophageal varices. Further, aminotransferases are increased, prothrombin time is prolonged and plasma albumin concentration decreases.

Cardiovascular function in cirrhosis is characterized by hyperdynamic circulation. Arteriovenous fistulas exist in numerous sites, including the liver and lungs. Patients with cirrhosis commonly have arterial hypoxemia due to intrapulmonary shunting and the mechanical effects of ascites. Anemia, thrombocytopenia, prolonged prothrombin time and partial thromboplastin time, along with decreased albumin production are seen in these patients.

Encephalopathy may manifest itself due to insufficient hepatic elimination of nitrogenous compounds, especially ammonia. Further, renal dysfunction is also seen in patients with cirrhosis of the liver, characterized by decreased urinary excretion of Na+. This results in increased extracellular fluid volume and causes ascites and edema.

Effects of Alcohol on the Liver:
Ethanol absorbed from the small bowel is carried to the liver where it becomes the preferred fuel. This results in the accumulation of NADH and, in turn, oxygen use escalates. Gluconeogenesis is then impaired, resulting in a fall in the amount of glucose produced from glycogen in the liver. Lactate production increases and there is a decrease in the oxidation of fatty acids in the citric cycle. This results in an increase in fat accumulation within liver cells. With repeated exposure to ethanol, severe changes in liver function will likely occur. These include fat accumulation, alcohol induced hepatitis, sclerosis and cirrhosis.

Alcohol causes mobilization of fat from peripheral tissues and increased hepatic production of fat. In fact, fat accumulates in the liver after ingestion of even small amounts of alcohol.

Alcohol also inhibits the secretion of protein from hepatic cells and, with chronic use, results in the accumulation of protein. Acetaldehyde, a product of alcohol metabolism, binds to proteins and inhibits their enzymatic function. With high alcohol intake, acetaldehyde accumulates and causes hepatocyte engorgement with proteins and fat, and, eventually leads to necrosis and fibrosis. Alcoholic hepatitis usually develops only after many years of heavy ethanol abuse. It has a mortality rate of 10 to 30% and presents similarly to viral hepatitis.

Chronic alcohol use is associated with enhanced toxicity to certain drugs. A significant incidence of such increased toxicity occurs with acetaminophen. The induction of microsomal oxidases from ethanol, coupled with depletion of glutathione enhances acetaminophen toxicity. In addition, liver pathology may depress the metabolism and slow the clearance of drugs from in the liver, thus increasing the half life of any drugs administered to the patient.