A 30-year-old woman is incidentally found to have a 4 cm liver lesion on ultrasound performed for non-specific abdominal pain. She denies oral contraceptive use and has normal liver function tests and AFP. Ultrasound reveals a slightly hypoechoic, well-circumscribed lesion with a stellate hypoechoic area at its centre (marked **A**). Colour Doppler demonstrates a central feeding artery with radial branching (spoke-wheel pattern). Multiphase CT shows homogeneous arterial enhancement becoming iso-dense in the portal venous phase, with the central area marked **A** remaining non-enhancing. Hepatobiliary phase MRI with gadoxetate shows the lesion as isointense to hyperintense. Based on these imaging findings, what is the pathological significance of the structure marked **A**?
A. Contains the large feeding artery and abnormal vessels within fibrous septa, representing a hyperplastic response to a pre-existing arteriovenous malformation
B. Represents a region of fibrosis with bile duct proliferation and inflammatory infiltrate, but lacks functional hepatocytes and Kupffer cells
C. Indicates a hemorrhagic focus within an adenoma, necessitating cessation of oral contraceptives and close surveillance
D. Is a focus of fatty infiltration with malignant potential, requiring urgent resection to prevent hepatocellular carcinoma
Explanation
Why option 1 is correct
The structure marked A — the central stellate hypoechoic scar in focal nodular hyperplasia (FNH) — is pathologically a zone containing the large feeding artery and abnormal vessels within radiating fibrous septa. This scar represents the structural hallmark of FNH: a hyperplastic, non-neoplastic response of normal hepatocytes to a pre-existing arteriovenous malformation. Microscopically, the scar contains abnormal arteries, bile ductular proliferation, and inflammatory infiltrate. The key discriminator is that FNH contains functional hepatocytes and Kupffer cells throughout the lesion (including around the scar), which explains the isointense-to-hyperintense appearance on hepatobiliary phase MRI with gadoxetate — a feature that definitively distinguishes FNH from hepatic adenoma. The spoke-wheel arterial pattern and non-enhancing scar on delayed phase are classic imaging signatures of this pathology (EASL Guidelines on Benign Liver Tumors; AASLD).
Why each distractor is wrong
Option 2: While the scar does contain bile duct proliferation and inflammatory infiltrate, this option incorrectly states that it lacks functional hepatocytes and Kupffer cells. FNH is defined by the presence of functional hepatocytes and Kupffer cells throughout, which is why it shows uptake on gadoxetate and sulphur colloid scintigraphy — this is the critical feature that confirms the diagnosis.
Option 3: Fatty infiltration with malignant potential is characteristic of hepatic adenoma, not FNH. FNH has no malignant potential and is not associated with fat content. The patient's lack of OCP use and normal AFP further argue against adenoma.
Option 4: Hemorrhage within an adenoma is a recognized complication, but this patient's imaging shows a non-enhancing central scar (not hemorrhage), and the spoke-wheel arterial pattern is specific to FNH, not adenoma. Additionally, FNH is not causally related to OCPs and does not require cessation of oral contraceptives.
High-YieldNEET PG
FNH = hyperplastic response to AVM + central scar with feeding artery + functional Kupffer cells (gadoxetate uptake) = benign, no treatment needed, no malignant potential.
EASL Guidelines on Benign Liver Tumors; AASLD
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