Chronic liver disease and cirrhosis have a number of etiologies that are treatable
Madan Dharmar MD
What to Do – Gather Appropriate Data, Interpret the Data, Make a Decision
They present with a similar complex of symptoms including hepatosplenomegaly, nevi, varices, or hemorrhoids. The treatment principles need to be known and followed.
Injury to the liver results in alterations in hepatic structure and function due to cell (hepatocytes) injury. This results in inflammation or cell death, which leads to scar formation (fibrosis), and potentially nodule formation (regeneration). Chronic hepatitis is defined as a persistent inflammatory condition of the liver in which the biochemical and histopathological abnormalities are present for >6 months. Cirrhosis is the end result of virtually any progressive liver disease.
Chronic liver disease can be caused by a wide spectrum of etiologies including infectious, metabolic, genetic, drug-induced, idiopathic, structural, and autoimmune diseases. Many of these diseases have similar presentations and initial laboratory findings that definitive diagnosis can be made only by specialized laboratory tests and the histological examination of the liver tissue. Most acute hepatitis, if lasting >3 months, needs to be aggressively investigated to determine the etiology of the disease, because most of these diseases lead to chronic hepatitis, which may respond to specific medical therapy. Patients with chronic liver disease present with clubbing, spider telangiectasia, and hepatosplenomegaly (stigmata of chronic liver disease); and/or with evidence of severe liver disease (hepatic failure).
Based on the location of the inflammatory lesion on histopathology, chronic hepatitis can be chronic persistent hepatitis (CPH) or chronic active hepatitis (CAH). In CPH the inflammatory cells are limited to the portal triad preserving the lobular architecture, whereas in CAH, they are not restricted to the portal triad and enter the lobule thereby disturbing the lobular architecture. CPH is typically due to a slow resolving viral hepatitis, α1-antitrypsin deficiency or Wilson disease. CPH is insidious in its presentation, with the patients being asymptomatic or with mild symptoms, whereas CAH presents with prominent clinical manifestations of liver disease.
Cirrhosis is considered to be a clinical-pathologic state that represents the end stage of any chronic liver disease. Histologically, the liver shows scarring and regeneration nodules devoid of central veins, surrounded by bands of fibrous tissues which distorts the lobular architecture. The progressive scarring of the tissue in the liver leads to altered hepatic flow and increased resistance to portal blood flow, causing portal hypertension and loss of he- patic function. Patients with cirrhosis may be either in a compensated or decompensated state. In the compensated state, the patient is asymptomatic with physical findings of enlarged liver, spleen, or both; whereas in a decompensated state, patients present with symptoms of hepatic dysfunction, portal hypertension, or both.
Presentation and Diagnostic Workup.
Chronic liver disease causes profound cholestasis, which can lead to nonspecific symptoms of liver disease such as fatigue, anorexia, abdominal pain, malnutrition and growth failure, and bleeding. These symptoms precede signs of jaundice, dark urine, and light-colored stools. The presence of physical signs of liver disease such as palmar erythema, spider angiomas, xanthomas, ascites, muscle wasting, and an enlarged firm liver and spleen indicates the chronic nature of the disease. Patients with cirrhosis present with splenomegaly, ascites, and gastroesophageal varices, which are indicative of portal hypertension. Hepatorenal syndrome is a functional renal failure in patients with end-stage liver disease. Hepa- topulmonary syndrome is characterized by the triad of hypoxemia, intrapulmonary vascular dilations, and liver disease. Variceal bleeding and ascites are lethal complications of chronic liver disease and cirrhosis.
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