IPLab:Lab 2:Fatty Change and Cirrhosis: Difference between revisions

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In this case, alcohol abuse (toxin) is the most likely etiologic agent.
In this case, alcohol abuse (toxin) is the most likely etiologic agent.
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* <spoiler text="What causes hepatocellular steatosis in an alcoholic?">Alcohol induces hepatic steatosis primarily by:
 
* the shunting of normal substrates away from catabolism and toward biosynthesis due to generation of excess NADH by alcohol dehydrogenase,
* impaired assembly and secretions of lipoproteins,
* and increased peripheral catabolism of fat.
 
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Revision as of 10:11, 21 August 2013

Clinical Summary

This 54-year-old man with a long history of alcohol abuse had been admitted to the hospital numerous times for abdominal pain thought to be due to gastritis or a peptic ulcer. On several occasions his serum amylase level was elevated into the range of 300-500 u/L indicating relapsing or recurrent pancreatitis. Three weeks prior to his demise, the patient began an alcoholic binge. The binge continued until three days prior to the patient's death at which time he developed fever and malaise, prompting him to cease drinking. He was brought to the hospital semi-comatose and with a fever of 105.4°F. Shortly after arriving at the hospital, the patient died from massive pneumonia.

Autopsy Findings

At autopsy, a necrotizing lobar pneumonia was present which contained organisms consistent with Klebsiella pneumoniae. The liver was enlarged--weighing 2700 grams--and had a yellow-orange color. The liver was firm to palpation and the cut surface had a slightly granular appearance suggestive of early cirrhosis. The pancreas showed multiple areas of fibrosis.

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Study Questions