Liver Failure

Paper Summary:

This paper takes a look at liver disease, the liver transplant operation, patients awaiting liver transplants and post transplant patients. This paper specifically focuses on the surgical intensive care unit Mayo Clinic at St. Luke's Hospital, Jacksonville USA, and studies a patient referred to as F.M, a 58 year old white male from Boston, MA.

From the Paper:

"F.M. had a history of ETOH abuse. It is reported that he had a history of 42 beers/wk for thirty years. This amounts to a six pack a day for thirty years. F.M. reports quitting in March of 2003. Alcohol can induce alcoholic cirrhosis. Alcohol is converted to acetaldehyde that causes the alteration of hepatocyte function. It impairs mitochondrial function that decreases oxidation of fatty acid. Enzyme and protein synthesis is altered leading to diminished degradation of hormones and ammonia. When inhibition of export of protein from the liver occurs alteration in metabolism of vitamins and minerals induce malnutrition. The alteration of hepatocyte function is what ultimately triggers the cellular damage to the liver which initiates the inflammatory response. The damage caused from this process is slowly progressive and thought to be reversible depending on extent of damage (Dirksen, Heitkemper, & Lewis 2004).
The major risk factor that F.M. has contributing to his current condition is Hepatitis C Virus (HCV). HCV is an RNA virus that is mainly transmitted percutaneously. This virus causes direct cellular damage to the liver initiating the inflammatory response. The course of this virus varies with extensive damage not showing up until 25-30 years later. A reliable antibody test was not widely available before 1992. So many patients given blood or blood products before then are at risk for infection (Dirksen, Heitkemper, & Lewis 2004). F.M was a veteran of the Vietnam War in the 1960s and received a blood transfusion at that time. "

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