Examqo

Examqo › Examqo library › Pathology › Systemic pathology · IMLE

Patterns of injury on liver biopsy and hepatocellular tumours

A liver biopsy is read by pattern — hepatitic, cholestatic, steatotic, vascular or granulomatous — and by location in the lobule (periportal versus around the central vein), then activity is graded and fibrosis staged; in a liver mass, adenoma, FNH and hepatocellular carcinoma are distinguished by architecture and markers.

Why it matters in the exam

The bank asks where alcoholic injury begins, what characterises large bile duct obstruction and how tumours are distinguished. In hepatitis there is portal and lobular inflammation and "interface" hepatitis; in autoimmune hepatitis plasma cells are prominent, and in hepatitis C there are sometimes lymphoid follicles and fat. In fatty liver of metabolic or alcoholic origin, changes begin around the central vein (zone 3): large-droplet fat, "ballooned" hepatocytes, Mallory-Denk bodies and pericellular fibrosis. Fibrosis is produced by activated Ito (stellate) cells.

In large bile duct obstruction there is portal oedema, proliferation of bile ductules at the edge of the portal tract (ductular reaction) with neutrophils, bile plugs and finally "bile lakes" and bile infarcts. In primary biliary cholangitis there is destructive injury of small ducts with granulomas and antimitochondrial antibodies; in primary sclerosing cholangitis — "onion-skin" layered fibrosis around ducts, with an association with inflammatory bowel disease. In South-East Asia liver flukes such as Clonorchis are linked to cholangiocarcinoma.

In a liver mass in a non-cirrhotic liver: FNH shows a central scar and "map-like" glutamine synthetase staining; hepatocellular adenoma is classified into subtypes — HNF1A-inactivated (fatty, without significant malignant risk), inflammatory (bleeding risk), and β-catenin-activated (diffuse glutamine synthetase and nuclear β-catenin), which has the highest risk of malignant transformation. Hepatocellular carcinoma is characterised by trabeculae thicker than 3 cells, loss of the reticulin network and glypican-3 staining, and arises mainly in a cirrhotic liver.

Key points

Summary table

Pattern or lesionSite or featureKey findingExample
HepatitisPortal and lobular, interfacePlasma cells in autoimmuneViral, autoimmune
SteatoticZone 3 around the central veinFat, ballooning, Mallory-DenkAlcohol, metabolic
Large bile duct obstructionPortal tractOedema, ductular proliferation, neutrophils, bile lakesStone, tumour
β-catenin-activated adenomaMass in non-cirrhotic liverDiffuse glutamine synthetaseHighest malignant risk
Hepatocellular carcinomaMostly in cirrhotic liverThick trabeculae, reticulin loss, glypican-3—

Free exam questions

למטופל בן 67 בוצעה האבחנה ההיסטולוגית, בביופסיית מחט, של of angiosarcoma the liver . חשיפה לאיזה מבין החומרים הבאים מהווה גורם סיכון להתפתחות גידול זה? (the question as examined, in Hebrew)

  1. א. Vinyl chloride
  2. ב. Aflatoxin
  3. ג. Aldehydes
  4. ד. Naphthalene

See the answer and explanation

מוטציות בגנים 1 JAG או 2 NOTCH , הגורמות לתסמונת ,Alagille קשורות לאיזו מהאנומליות הלבביות הבאות? (the question as examined, in Hebrew)

  1. א. טטרלוגיה על שם פאלו
  2. ב. פגם במחיצה הבין- .חדרית
  3. ג. צינור עורקי פתוח
  4. ד. לב שמאלי היפופלסטי

See the answer and explanation

In the full version for subscribers

The full version is open to subscribers of: Diagnostic pathology, Internal medicine, Medical licensing exam (IMLE).

Subscriber? Read the full topic Plans and prices 25 free questions

Sources

Sources are given for further reading; the text is written afresh and not copied from them.

Reviewed by the Examqo AI Professor · 2026-11-06. The text may contain errors; when in doubt, check the source.