What histologic features are typical of alcoholic hepatitis?

Prepare for the CVP and GI Pathology Exam 2 with detailed questions and comprehensive explanations. Enhance your understanding of key topics to increase your chances of passing with confidence and excel in your exams!

Multiple Choice

What histologic features are typical of alcoholic hepatitis?

Explanation:
The pattern of alcoholic hepatitis is defined by fat accumulation in the liver cells along with specific injuries to the hepatocytes and a distinctive inflammatory response. In this setting you see macrovesicular steatosis (fatty change) with hepatocellular ballooning degeneration, where swollen, damaged hepatocytes appear pale and enlarged. A hallmark feature is Mallory-Denk bodies, which are eosinophilic, filamentous intracytoplasmic inclusions formed from damaged cytokeratin intermediate filaments. Accompanying these changes is a neutrophil-rich inflammatory infiltrate, typically surrounding damaged hepatocytes and contributing to lobular inflammation. Together—steatosis, ballooning degeneration, Mallory-Denk bodies, and neutrophilic inflammation—these elements characterize alcoholic hepatitis. Granulomatous inflammation with eosinophils is not typical for alcoholic hepatitis. Necrosis with lymphocytic infiltration suggests other etiologies such as viral or autoimmune hepatitis, and fatty infiltration without inflammation points to simple steatosis rather than alcoholic hepatitis.

The pattern of alcoholic hepatitis is defined by fat accumulation in the liver cells along with specific injuries to the hepatocytes and a distinctive inflammatory response. In this setting you see macrovesicular steatosis (fatty change) with hepatocellular ballooning degeneration, where swollen, damaged hepatocytes appear pale and enlarged. A hallmark feature is Mallory-Denk bodies, which are eosinophilic, filamentous intracytoplasmic inclusions formed from damaged cytokeratin intermediate filaments. Accompanying these changes is a neutrophil-rich inflammatory infiltrate, typically surrounding damaged hepatocytes and contributing to lobular inflammation. Together—steatosis, ballooning degeneration, Mallory-Denk bodies, and neutrophilic inflammation—these elements characterize alcoholic hepatitis.

Granulomatous inflammation with eosinophils is not typical for alcoholic hepatitis. Necrosis with lymphocytic infiltration suggests other etiologies such as viral or autoimmune hepatitis, and fatty infiltration without inflammation points to simple steatosis rather than alcoholic hepatitis.

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