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CORE: GI > Liver > Flashcards

Liver Flashcards

(59 cards)

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1
Q

Couinaud classification

A

8 segments
portal veins divide the superior from inferior segments

hepatic veins segments in axial planes; middle hepatic vein divides right and left lobes

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2
Q

caudate lobe drains into

A

IVC

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3
Q

compensatory hypertrophy of caudate lobe

A

morphological change of early cirrhosis; direct drainage into IVC spares caudate from increased venous pressures due to portal hypertension

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4
Q

portal venous phase, timing

A

routine CT abd/pelvis; 70 sec

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5
Q

arterial phase, timing

A

20-25 s after IV injection

however, optimal conspicuity in the late arterial phase ~35 sec

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6
Q

hepatic steatosis imaging

A

noncontrast CT: hyperattenuating to spleen; 10 HU greater than spleen

contrast enhanced CT: liver attenuates <25 HU than spleen

in and out of phase MRI: signal loss in liver on out of phase imaging

liver biopsy

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7
Q

liver decreased signal on in-phase images

A

hepatic iron overload due to longer TE; allows a longer dephasing time, exaggeration of T2*, and loss of signal

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8
Q

geographic regions of focal hepatic fat

A

gallbladder fossa, subcapsular (along falciform ligament), periportal, nodular throughout the liver

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9
Q

amyloid deposition in the liver

A

focal/diffuse areas of decreased attenuation on CT

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10
Q

wilson disease in the liver

A

high levels of copper (basal ganglia, cornea, liver)

hyperattenuating multiple nodules –> hepatomegaly/cirrhosis

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11
Q

pathways for hepatic iron accumulation

A

hemochromatosis and hemosiderosis

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12
Q

hemochromatosis, treatment

A

most common; genetic defect causing increased iron absorption; excess iron cannot be stored in the RES so deposited in hepatocytes, pancreas, myocardium, skin/joints

spleen/bone marrow normal

treatment phlebotomy

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13
Q

MR imaging of iron overload

A

hypointense liver

spleen/bone marrow hypointense in hemosiderosis

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14
Q

hemosiderosis, treatment

A

excess iron in the RES due to frequent blood transfusions or defective erythrocytosis

treatment: iron chelators

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15
Q

Ddx hypoattenuating liver (less than spleen)

A

fatty liver, hepatic amyloid

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16
Q

Ddx hyperattenuating

A

iron overload, medication (amiodarone, gold, methotrexate), copper overload, glycogen excess

<75 HU

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17
Q

viral hepatitis findings

A

nonspecific, gallbladder wall thickening or periportal edema

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18
Q

candidiasis

A

multiple tny hypoattenuating microabscesses in liver/spleen; may be rim enhancing

typically immunocompromised

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19
Q

Ddx for multiple tiny hypoattenuating hepatic lesions

A

metastases, lymphoma, biliary hamartomas, caroli disease, candidiasis

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20
Q

hepatic abscess cause, organism

A

typically bowel process (diverticulitis, appendicitis, Crohn disease, bowel surgery, ascending cholangitis) > nidus > portal system

E. coli

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21
Q

hepatic abscess imaging feature

A

rim enhancing mass
MRI: central hyperintensity on T2 with irregular wall that may enhance late

may mimic mets

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22
Q

echinococcal disease

A

ingestion of Echinococcus granulosus (Mediterranean basin) and associated with sheep-raising

echinococcal eggs –> hydatid cysts

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23
Q

imaging of echinococcis

A

well defined hypoattenuating mass featuring a floating membrane or an associated daughter cyst; peripheral calcifications may be present

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24
Q

Cirrhosis causes, types

Study These Flashcards
A

repeated cycles of injury/repair –> fibrosis and attempted, disorganized regeneration

micronodular: metabolic causes (alcohol, steatohepatitis, hemochromatosis, Wilsons disease)
macronodular: postviral (hep B/C)

also inflammatory (PBC/PSC) and infectious

25
Signs of early cirrhosis on imaging
expansion of preportal space; atrophy of medial segment of L hepatic lobe, enlargement of the caudate lobe, empthy gallbladder fossa sign
26
secondary manifestations of cirrhosis
portal hypertension (splenomegaly, portosystemic collaterals/varices) gallbladder wall thickening (hypoalbuminemia/edema) Gamma Gandy bodies (splenic microhemorrhages), which appear hypointense on GRE
27
how is HCC formed
regenerative nodule > dysplastic nodule > HCC regenerative nodule: supplied by portal vein, not premalignant, does not enhance dysplastic nodule: premalignant, do not demonstrate arterial phase enhancement
28
MRI findings of regenerative and dysplastic nodules
regenerative: low T2, variable T1; enhance to the level of parenchyma or slight less dysplastic: variable T1, hypointense T2 (high grade nodules will be T2 hyperintense); isoenhancing relative to liver
29
HCC tumor markers
AFP elevated in 75% of cases
30
imaging findings of HCC
hypervascular mass with cirrhosis arterial phase enhancement, encapsulated, washes out on portal venous phase T2 hyperintense on liver locally invasive, can invade into portal veins, IVC, bile ducts
31
HCC treatments
partial hepatectomy, orthotopic liver translantation, percutaneous ablation, transcatheter embolization
32
fibrolamellar HCC
subtype that occurs in young patients without cirrhosis AFP is not elevated
33
fibrolamellar HCC imaging findings
large heterogenous mass with a fibrotic central scar; capsular retraction possible, no capsule (unlike HCC) T1/T2 hypointense scar
34
hepatic metastases enhancement
most mets (colorectal, pancreatic adenocarcinoma) are hypovascular best seen on portal venous phase HCC is hypervascular, visualized on late arterial phase
35
hypervascular hepatic mets
neuroendocrine (pancreatic, carcinoid), RCC, thyroid, melanoma, sarcoma
36
calcifications with mets
seen with mucinous colorectal or ovarian serous tumors imply better prognosis
37
T1 hyperintense lesions
blood products and melanin
38
metastatic lesions on MRI
hypointense T1, hyperintense T2
39
peudocirrhosis
macronodular liver contour from multiple scirrhous hepatic mets, mimics cirrhosis; will have capsular retraction commonly breast cancer will do this
40
hepatic lymphoma
usually presents with splenomegaly and LAD
41
epithelioid hemangioendothelioma
multiple confluent spherical subcapsular masses; vascular malinancy halo or target appearance cause of capsular retraction
42
ddx capsular retraction
mets (mostly post treatment), fibrolamellar HCC, HCC (uncommon), epithelioid hemangioendothelioma, intrahepatic cholangiocarcinoma, confluent hepatic fibrosis
43
FNH associations, imaging
disorganized lvier tissue with no malignant potential asymptomatic women , not associated with OCP ``` central scar (does not contain fibrotic tissue); no capsule T2 hyperintese area; avidly enhances during arterial phase and washes out quickly ```
44
sulfur colloid and HIDA visualizes?
sulfur colloid >> Kupffer cells | HIDA >> bile duct cells
45
hemangioma
benign mass of disorganized endothelial-lined pockets of blood vessels; more common in females peripheral, discontinuous, progressive nodular enhancement; nonspecific hypoattenuating lesion on noncontrast CT
46
hepatic adenoma pathology
benign neoplasm: hepatocystes, scattered kupffer cells, no bile ducts (can differentiate on HIDA for FNH which has bile ducts)
47
hepatic adenoma
more common in females, prolonged OCPs or associated with anabolic steroids in men; high risk of hemorrhage
48
multiple hematic adenoma
von Gierke disease (type I glycogen storage disease)
49
adenoma on imaging
hypervascular on arterial phase; microscopic fat may be seen on in/out of phase MRI intralesional hemorrhage will look like T1 hyperintensity
50
budd chiari pathology, causes
hepatic venous outflow obstruction hypercoagulative states, hematolgic disorders, pregnancy, OCP, malignancy, infection, trauma
51
clinical triad of acute Budd Chiari
hepatomegaly, ascites, abdominal pain
52
budd chiari findings
edematous peripheral liver | progressive liver --> atrophy with caudate hypertrophy ;caudate spared as it drains directly into the IVC
53
veno-occlusive disease
destruction of post-sinusoidal venules with patent hepatic veins; seen in bone marrow transplate patients
54
cardiac hepatopathy
passive hepatic congestion from HF, constrictive pericarditis, right sided valvular disease --> cirrhosis enlarged hepatic veins/IVC; reflux of contrast from right atrium liver is enlarged with mottled enhancement; ascites present
55
congenital cystic liver disease
biliary hamartoma (von Meyenburg complex) and ADPLD
56
biliary hamartoma
incidental small cystic hepatic lesion; irregularly shaped simple cysts
57
autosomal dominant polycystic liver disease
40% of ADPKD have similar disease in the liver, called ADPLD hepatic failure remains rare
58
most common organ injured in trauma? second most common?
spleen > liver
59
MDCT grading of hepatic injury
Grade I: Superficial laceration or subcapsular hematoma <1 cm in size. • Grade II: Laceration or subcapsular/intraparenchymal hematoma >1 and <3 cm in size. • Grade III: Laceration or subcapsular/intraparenchymal hematoma >3 cm in diameter. • Grade IV: Massive hematoma >10 cm, or destruction/devascularization of one hepatic lobe. • Grade V: Destruction or devascularization of both hepatic lobes.

CORE: GI (9 decks)

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