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Category Archives: Liver
Alcoholic cirrhosis
Alcoholic Cirrhosis
This is the final and irreversible stage of alcoholic liver diseases, starting from hepatic steatosis, then alcoholic hepatitis which then leads to alcoholic cirrhosis.
Cirrhosis can develop more rapidly in the presence of steatohepatitis (1-2 years).
Liver Appearance
Initially large, tan, fatty liver, very heavy >2 kg
After years of chronic alcohol intake the liver becomes brown, shrunken, and non-fatty. With fibrosis the liver is light and does not weight much, <1 kg.
Microscopic Appearance
Three features are important to see in liver cirrhosis. These are:
Fibrosis
Hepatocytes regeneration
Architectural distortion
Delicate fibrous bands run within the lobules, sinusoidal and central veins
Portal to portal fibrosis
Entrapped hepatocytes degenerate and try to regenerate forming micronodules
Nodularity becomes more prominent with formation of thick fibrous septa and macronodular formation
Ischemic necrosis and extensive fibrosis lead to tough scar formation and subsequent Laënnec cirrhosis
Bile stasis and rare mallory bodies may be present.
Remember that common end stage cirrhosis is independent to the cause (ALD, viral hepatitis, PBC, others)
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Alcoholic hepatitis
Alcoholic hepatitis
The liver appears mottled and red with bile stained areas
Normal or slight increase in size.
Nodular formation and fibrosis demonstrates evolution of cirrhosis
Microscopic Appearance:
Single hepatocyte swelling (ballooning) and necrosis
Steatosis- fat within cells
Mallory bodies
Mallory bodies have eosinophilic cytoplasmic inclusions in degenerative hepatocytes, which is characteristic but not specific to alcoholic hepatitis (can be seen in other diseases like PBC, Wilson disease, hepatocelluler tumors)
Intermediate cytokeratins and proteins
Neutrophilic reaction
Fibrosis
Fibrosis is almost always present. Can be sinusoidal and perivenular and periportal fibrosis.
Hemosiderin
Microscopic features
- Hepatocyte swelling and necrosis
- Mallory bodies
- Neutrophilic reaction
- Fibrosis
Clinical complications
- Cirrhosis
- Hepatocellular carcinoma
- Bleeding from esophageal varices
- Hepatic coma
- Infection
- Hepatorenal syndrome
Main findings in cirrhosis
- Fibrosis extending from central veins to portal tracts and from portal tracts to portal tracts
- Hepatocellular regeneration leading to the formation of micronodules and macronodules
Besides alcohol, most common causes of cirrhosis in North America
- Viral hepatitis (HBV, HCV)
- Non-alcoholic steatohepatitis
- Autoimmune hepatitis
References: Robbins & Cotran Pathologic Basis of Disease, Seventh Edition
by: Vinay Kumar, Nelso Fausto, Abul Abbas
Posted in Liver
Tagged , Alcohol, Alcoholic hepatitis, cirrhosis, Esophageal varices, Fibrosis, Hepatic coma, hepatitis, hepatocellular carcinoma, Hepatocyte necrosis, Hepatocyte swelling, Hepatorenal syndrome, liver cancer, liver cirrhosis, Liver fibrosis, Mallory bodies
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Hepatic steatosis
Hepatic steatosis
The liver is large, soft, yellow and greasy.
Microscopic features
Microscopic features depend on the amount of alcohol intake:
Microvesicular formation: small lipid droplets in hepatocytes
Macrovesicular formation: larger clear globules compressing and displacing hepatocytes’ nuclei to one end
Centralobular – entire lobule
No or minimal fibrosis around central vein
Reversible if the patient stops drinking
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Hepatitis C
Hepatitis C
What happens with untreated Hepatitis C?
Natural history of Hepatitis C.
Incubation period ranges from 2-26 weeks (mean 6-12 weeks). In symptomatic acute HCV infection, antibodies to HCV only detected in 50-70% of patients; otherwise antibodies seen in 3-6 weeks. Clinical course is milder than HBV infection; rare cases are severe. Patients with chronic hepatitis C have characteristic episodic elevations of serum aminotransferases with intervening normal or near-normal periods. 15% of acute cases resolve; 85% become chronic hepatitis (rare cases of fulminant hepatitis exist). Of the 85% of cases of chronic hepatitis, 80% are stable; 20% progress to cirrhosis and eventually hepatocellular carcinoma (approximately 10 years later). 50% of the cirrhotic cases remain stable, the other 50% of cases are fatal.
Microscopic features
- Lymphoid aggregates within portal tracts
- Focal sublobular regions of macrovesicular steatosis
- Bile duct epithelial cell proliferation
- Interface hepatitis
- Bridging inflammation and necrosis
- Fibrosis and cirrhosis
Most common mode of transmission of Hepatitis C in North America
- Intravenous drug use (60%)
- Sexual transmission (15%)
- Transfusions prior to 1991 (10%)
- Hemodialysis patients and healthcare workers (5%)
- Perinatal transmission (6% of infected mothers)
References:
Robbins Basic Pathology 7th ed, edited by Vinay Kumar, Ramzi S. Cotran, and Stanley J. Robbins, 873 pp, Philadelphia, Pa, Sounders, 2003.
Posted in Liver
Tagged , cirrhosis, hepatitis, hepatitis c, hepatocellular carcinoma, intravenous drug use, liver cancer, serum aminotransferase, sexual transmission
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