Cirrhosis of the Liver The accumulation of fat and protein in the liver are reversible with abstinence in early stages, but
can become irreversible and proceed to liver cirrhosis, which is characterized by scarring of the liver parenchyma. 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.
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.