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17 Cards in this Set
- Front
- Back
Focal Lesions in the Cirrhotic Liver
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- Regenerative nodules (RN)
- Dysplastic nodules - Hepatocellular carcinoma (HCC) |
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Regenerating Nodules
Usually too small to detect by imaging |
- May be surrounded by fibrotic septa
- May contain iron, copper Siderotic nodules - Hyperdense on NCCT, disappear on HAP & PVP - Hypointense on T2 MR, “bloom” on GRE Larger or vascular/enhancing RN - Can not be distinguished from dysplastic nodule or HCC |
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Dysplastic Nodules
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- “Adenomatous hyperplasia” (old term)
- Are premalignant (larger, high-grade DNs) - Rarely diagnosed by US or CT |
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Dysplastic Nodules
Small, low-grade DNs are often indistinguishable from regenerative nodules (by imaging + histology) |
- Usually <1.5 cm diameter, minimal vascularity
- Usually hypointense on T2WI Larger, high grade DNs are often indistinguishable from HCC - Usually >2cm, moderate vascularity - May be hyperintense on T2WI |
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Primary Criteria for Dx of HCC
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- Mass-like arterial phase hyperenhancement with “washout” (becomes hypodense to liver)
- Tumor within the portal (or hepatic) vein - Increase in size by > 10 mm within one year |
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HCC - Helical CT Pitfalls
THAD (transient hep. attenuation differences) |
- Small peripheral wedge-shaped
- Ignore, usually due to AP shunt or aberrant veins Larger segmental or lobar - Often due to tumor occlusion of portal vein Arterioportal shunt - Common in cirrhosis - Usually benign if small, peripheral, non-spherical, isodense on PVP, visible vessels into + out |
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Screening Recommendation for Known Cirrhosis
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1. AFP and PIVKA II – every 3 months
2. Ultrasonography – every 3 or 4 months - Most useful in less advanced cirrhosis - Very nodular/coarse liver is difficult 3. CT or MR ~ every 12 months - (For chronic hepatitis without cirrhosis, extend intervals) 4. For high clinical suspicion or indeterminate lesion, shorten intervals |
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Steatosis (Fatty Infiltration of the Liver)
CT Findings |
- Decreased density (less than spleen on NC, 25 HU less on CECT)
- Vessels course through undisturbed - Geographic areas --Can be rounded (esp ~ ligaments + vessels), resemble metastases |
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Nonalcoholic Fatty Liver Disease
Common cause of chronic liver disease |
- Usually asymptomatic, mild elevation of aminotransferase levels
- Common in diabetics, obese (metabolic syndrome) - Affects 15-25% of American adults (10% of kids) |
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Nonalcoholic steatohepatitis (NASH)
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- Subtype of NAFLD (25% of those w steatosis)
- Carries risk of progressive liver disease, cirrhosis - May soon be #1 cause of cirrhosis + HCC in USA - Can only be diagnosed by Bx, not imaging - (can’t distinguish NAFLD from NASH) |
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“CASH”: ChemoRx-associated steatohepatitis
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- Common cause of liver dysfunction in cancer patients
- Associated with various agents - May mask liver mets on CT - Liver injury may limit other Rx options (e.g., partial resection, ablation) |
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Diffuse Disease that May Simulate Fatty Liver
Diffuse tumor |
- Lymphoma > mets > diffuse HCC
Diffuse infection - Especially in AIDS (viral, mycobacterial, fungal, etc) Diffuse acute liver injury - Severe hepatitis - Tylenol OD, mushroom poisoning - Radiation hepatitis |
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Iron Deposition in the Liver
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Hemochromatosis:
- Common autosom recess disorder, absorption of iron - Deposited in hepatocytes, pancreas, heart, etc - Leads to cirrhosis, HCC, “bronze” diabetes - “Primary” = pancreatic involvement Hemosiderosis: - Due to hemolysis, transfusions - Iron deposition in liver (RES), spleen - “Secondary” = spleen |
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Iron Deposition
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CT:
- Liver much denser than spleen, muscle - DDx: amiodarone Rx, glycogen storage disease, (Wilson’s disease – not!) MR: - Marked downward signal on T2 + T1WI - T1WI: liver + spleen much darker than muscle - Signal “drop-out” on in-phase GRE (opposite of steatosis) |
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Sarcoidosis of the Liver
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- Periportal involvement
- Can simulate or lead to cirrhosis - Hepatomegaly, splenomegaly, periportal SI on T2WI - Multifocal liver/splenic nodules - Lung disease +/ or nodes (chest + abdomen) |
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Focal Lesions in the Cirrhotic Liver
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Cysts, hemangiomas, focal fat, confluent fibrosis
- Can usually be diagnosed accurately Hemangiomas shrink and become sclerosed in cirrhotic liver - Often not identified in advanced cirrhosis Focal fat - Key is out-of-phase MR (focal sign dropout) Brancatelli et al. Radiology 2001; 219: 69-74 |
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Confluent Hepatic Fibrosis
(Focal Confluent Fibrosis) |
Present in ~ 30% of advanced cirrhosis
- > 50% of PSC Most common in anterior + medial segments - Usually wedge-shaped lesion 80% have focal volume loss - Capsular retraction, crowded vessels Low density on NCCT - Delayed persistent enhancement - Can simulate tumor |