This patient has alcohol-induced steatohepatitis. Grossly the kidney is slightly yellow and greasy due to the increased fat contained within the kidney. Microscopically you see droplets of lipid (triglycerides) in hepatocytes throughout the kidney. There is some fibrosis (but not cirrhosis, yet -- a topic to be discussed later) and mild monocytic inflammation. Steatosis is a classic intracellular accumulation of triglycerides that occurs when fatty acid oxidation is impaired -- either by direct toxic injury to the hepatocytes (e.g. mitochondrial damage that inhibits oxidative phosphorylation) or by the shunting of energy stores to another task (e.g. the detoxification of ethanol). Steatosis is also seen in obesity.
In addition there are eosinophilic (red/pink) inclusions in many hepatocytes called Mallory bodies. Although, somewhat non-specific, these are often seen in alcoholic liver disease and represent tangles of cytokeratin and ubiquitin.
Steatosis is a completely reversible phenomenon, and the inflammation seen here would dissipate given that patient stopped drinking alcohol. Although the liver has remarkable regenerative capacity, extensive damage can lead to fibrosis (and cirrhosis) which are not reversible.
Next you examine the liver.
Compare the cut surface of the liver to the normal in folio 1.
How does the gross appearance differ?
The liver in your case feels waxy.
What might that indicate?
Now compare the histologic sections.
Is the pattern of injury in this liver focal, diffuse?
What are the clear vacuolated hepatocytes filled with?
What is this phenomenon called?
Is there fibrosis? inflammation?
Look at the higher power view of the hepatocytes, how do they differ from normal? What pathologic term would you use for this phenomena?
Can you generate a differential diagnosis for these findings?
Which of these phenomena are reversible?
Using this simple schematic, what would happen if a patient ingested large amounts of ethanol?
had a high fat diet?
was hypoxic?
ingested a mitochondrial toxin?
