Liver Flashcards
(24 cards)
Hypoattenuating liver
Amyloid, Steatosis
Hyperattenuating liver
Iron, Meds (Amio, gold, MTX), Copper (Wilsons), Glycogen (Von Gierke)
Types of hepatic iron overload and key difference
- Hemochromatosis: Defective storage, Cannot store in RES (Spleen,. BM not affected). Need phlebotomy
- Hemosiderosis: Excess in RES. Need chelators
Cirrhosis types
Micronodular- metabolic case
Macronodular: Infectious (HepB/C)
Caudate lobe in cirrhosis
C: RHL= 0.65 is specific
Caudate drains directly to IVC
Other signs of cirrhosis
-Empty gall bladder fossa sign->parenchyma replaced wih periportal fat
Secondary signsL
PHTN-Splenomegaly, portosystemic collatrals,v arices
Gallbladder wall thickenng
Gamna-Gandy bodies : splenic microhemorrhage (HYPOINTENSE ON GRE)
Multiple hypoattenuating lesions
- Candidiasis
- Mets
- Lymphoma
- Biliary hamartoma
- Caroli disease
Hepatic abscess appearance, causes
- Diverticulitis, Appendicitis, Crohns, Bowel surgery, hepatobilioary infx (ascending cholangitis)
- Ring-enhancing CT. MRI central hypperintensitiy on T2 weighted , irregular wall with late enhancement
Fluid attenuating cysic mass with undulating membrane or complex hypoechoic on US with hyperechoic undulating membrane
Hepatic echinococcosis (eggs ingestion of Echinococcus granulosus, associated with sheep-raising). Eggs–>hydatid cyst, usually associated dausghter cyst. !peripheral calcification
Regenerative versus dysplastic nodules CT/MRI
Regenerative: Portal vein supplied. Not premalignant. NO ENHANCEMENT IN ARTERIAL PHase
-low signal on T2 weighted
-Variable on T1 (only hyperintense 2/2 glycogen deposits).
-With contrast: hypo to isointense
Dysplastic: Premalignant. Only enhance in arterial phase if high grade as portal vein supplied
-Hypointense on T2, hyperintense if high drade
-Variable T1
-With contrast: Iso-enhancing (if high grade, enhance, cannot distinguish from HCC)
Siderotic nodule
- Iron rich or dysplastic
- Hyperattenuating CT
- T1 and T2* hypoaintense
- Not premalignant
HCC
- Imaging
- Labs
- Other imaging findings
- T2 only: Slightly hyperintense
- T2 + contrast: hyperintense late arerial phase, wash out portal venous
- Unenhanced CT: isoattenuting
- Can have nodule in nodule appearance (enhancing nodule in dysplastic)
- locally invasive (portal system, ducts)
- AFP elevated
Fibrolamellar HCC imaging
- Large heterogenous with fibrotic central scar thats hypointense on T1 and T2. Capsular retraction. No capsule
- compare to FNH
FNH
T2 hypertense scar with late enhancement
Hypervascular mets (best seen on arterial phase)
- Neuroendocrine (pancreatic, carcinoid)
- RCC/thyroid
- Melanoma/Sarcoma
Capsular retraction masses
Met (post tx) Fibrolamellar hCC (10%) HCC Epitheloid hemangioendothelioma Intrahepatic cholangio Confluent hepatic fibrosis
Hypovascular mets
Colorectal
Pancreatic adenocaricoma
(Portal Venous)
Calcifications mets
Mucinous colorectal
Ovarian Serous
Mets MRI
-T1 hypointense
-T2 hyperintense
-If blood products and melanin(melanoma), T1 hyperintense
NOTE: Heapatic arteries!
Epitheloid hemangioendothelioma
Multiple subcapsular masses which become confluent
“halo, target”
Pseudocirrbosis
Macronodular liver contour 2/2 scirrhous met, mimics cirrhosis. e.g. treated breast ca. Capsular retraction can be seen
FNH (demographics, imaging findings)
- Women, NOT associated with OCP
- disorganized liver tissue, nomalignant potetial
- Central sccar (non-fioibrotic): T2 hyperintense ductules and venules with delayed enhancement. No capsule
- ON CT, arterial enhancement, wash out quick!
- Hase kupffer and bile duct epithelium. Confirm kupffer with sulfur colloid study, bile duct cells on HIDA
Hemangioma
T1 contrast enhancement (discontinuous) which increases towards the center. Peripheral enhancement is like the aorta. On delayed, areas of non enhancement (cystic degeenration)
On T2 it is hyperinteense with areas of higher intensity (cystic degeneration)
Adenoma
CT: Portal venous phase enhancing hypoattenuation
MRI:
