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Chapter: Medical Surgical Nursing: Assessment and Management of Patients With Hepatic Disorders

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Hepatic Dysfunction

Hepatic dysfunction results from damage to the liver’s parenchymal cells, either directly from primary liver diseases or indirectly from obstruction of bile flow or derangements of hepatic circulation.

Hepatic Dysfunction

Hepatic dysfunction results from damage to the liver’s parenchymal cells, either directly from primary liver diseases or indirectly from obstruction of bile flow or derangements of hepatic circulation. Liver dysfunction may be acute or chronic; chronic dys-function is far more common than acute.

 

Chronic liver disease, including cirrhosis, is the seventh most common cause of death in the United States among young and middle-aged adults. More than 40% of those deaths are associated with alcohol. The rate of chronic liver disease for men is twice that for women, and chronic liver disease is more common among African Americans than Caucasians.

 

Disease processes that lead to hepatocellular dysfunction may be caused by infectious agents such as bacteria and viruses and by anoxia, metabolic disorders, toxins and medications, nutritional deficiencies, and hypersensitivity states. The most common cause of parenchymal damage is malnutrition, especially that related to alcoholism.

 

The parenchymal cells respond to most noxious agents by re-placing glycogen with lipids, producing fatty infiltration with or without cell death or necrosis. This is commonly associated with inflammatory cell infiltration and growth of fibrous tissue. Cell regeneration can occur if the disease process is not too toxic to the cells. The result of chronic parenchymal disease is the shrunken, fibrotic liver seen in cirrhosis.

 

The consequences of liver disease are numerous and varied. Their ultimate effects are often incapacitating or life-threatening, and their presence is ominous. Treatment often is difficult. Among the most common and significant symptoms of liver dis-ease are the following:

 

        Jaundice, resulting from increased bilirubin concentration in the blood

 

        Portal hypertension, ascites, and varices, resulting from circu-latory changes within the diseased liver and producing severe GI hemorrhages and marked sodium and fluid retention

 

        Nutritional deficiencies, which result from the inability of the damaged liver cells to metabolize certain vitamins; responsi-ble for impaired functioning of the central and peripheral nervous systems and for abnormal bleeding tendencies

 

        Hepatic encephalopathy or coma, reflecting accumulation of ammonia in the serum due to impaired protein metabolism by the diseased liver

 

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