IPLab:Lab 2:Fatty Change and Cirrhosis
This 54A normal PaCO2 is 35 to 45 mmHg.-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 gastritisGastritis is inflammation of the stomach. or a peptic ulcer. On several occasions his serum amylase level was elevated into the range of 300-500 u/LA normal serum amylase level is 30 to 110 u/L. indicating relapsing or recurrent pancreatitisChronic inflammation of the pancreas (pancreatitis) is most often caused by alcoholism or biliary tract calculi.. 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 pneumoniaIn alcoholics, aspiration pneumonia is common--bacteria enter the lung via aspiration of gastric contents..
At autopsy, a necrotizing lobar pneumoniaNecrotizing lobar pneumonia is a severe acute pneumonia caused by virulent organisms and aspirated of gastric contents. was present which contained organisms consistent with Klebsiella pneumoniae. The liver was enlarged--weighing 2700 gramsA normal liver weighs 1650 grams (range: 1500 to 1800 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 cirrhosisCirrhosis is a liver disease characterized by necrosis, fibrosis, loss of normal liver architecture, and hyperplastic nodules.. The pancreas showed multiple areas of fibrosis.
A high-power photomicrograph of the liver parenchyma shows that each individual liver cell is filled with a large, clear droplet which represents the space remaining after lipid was dissolved by the dehydration procedure used to embed the tissue. Note that each empty space is surrounded by a thin rim of eosinophilic cytoplasm; in many instances, the hepatocyte nucleus can be seen as well. The red body (arrow) seen within a cell in the center of the slide is an acidophilic body associated with alcoholic hepatitis.
An oil red O stain for fat was performed on a frozen section of this liver tissue. The red droplets represent fat in the tissue which is typical of fatty degeneration in the liver. By using frozen sections the tissues do not have to be dehydrated through alcohol solutions and thus the fat does not get washed out.
This photomicrograph of the liver is from another patient with a history of alcohol use. There are some clear vacuoles indicating fat droplets (1) and there are numerous red-staining granular deposits within the cytoplasm of hepatocytes (3)this is alcoholic hyalin. Alcoholic hyalin is easily distinguished from red blood cells (2) that are also present in this section.
This is a low-power photomicrograph of liver stained with a trichrome stain. In this section, connective tissue stains green (arrows) and hepatic parenchymal cells are red. Note that many of the parenchymal cells have clear spaces indicating fatty degeneration. The proliferation of scar tissue between the liver lobules is the result of cirrhosis.
Liver: Fatty Change and Cirrhosis
- What are possible causes of steatosis and which of these may have produced the fatty liver seen in this case?
Steatosis can be caused by:
- protein malnutrition
- diabetes mellitus
In this case, alcohol abuse (toxin) is the most likely etiologic agent.
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.
Many other factors also come into play.
- eMedicine Medical Library: Cirrhosis
- eMedicine Medical Library: Alcoholic Hepatitis
- Merck Manual: Alcoholic Liver Disease
- Merck Manual: Cirrhosis
- Satapathy SK, Narayan S, Varma N, Dhiman RK, Varma S, Chawla Y. Hyposplenism in alcoholic cirrhosis, facts or artifacts? A comparative analysis with non-alcoholic cirrhosis and extrahepatic portal venous obstruction. J Gastroenterol Hepatol 2001 Sep;16(9):1038-43.
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