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CORE: GI > Liver > Flashcards

Liver Flashcards

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

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
Q

Signs of early cirrhosis on imaging

A

expansion of preportal space; atrophy of medial segment of L hepatic lobe, enlargement of the caudate lobe, empthy gallbladder fossa sign

26
Q

secondary manifestations of cirrhosis

A

portal hypertension (splenomegaly, portosystemic collaterals/varices)

gallbladder wall thickening (hypoalbuminemia/edema)

Gamma Gandy bodies (splenic microhemorrhages), which appear hypointense on GRE

27
Q

how is HCC formed

A

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
Q

MRI findings of regenerative and dysplastic nodules

A

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
Q

HCC tumor markers

A

AFP elevated in 75% of cases

30
Q

imaging findings of HCC

A

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
Q

HCC treatments

A

partial hepatectomy, orthotopic liver translantation, percutaneous ablation, transcatheter embolization

32
Q

fibrolamellar HCC

A

subtype that occurs in young patients without cirrhosis

AFP is not elevated

33
Q

fibrolamellar HCC imaging findings

A

large heterogenous mass with a fibrotic central scar; capsular retraction possible, no capsule (unlike HCC)

T1/T2 hypointense scar

34
Q

hepatic metastases enhancement

A

most mets (colorectal, pancreatic adenocarcinoma) are hypovascular best seen on portal venous phase

HCC is hypervascular, visualized on late arterial phase

35
Q

hypervascular hepatic mets

A

neuroendocrine (pancreatic, carcinoid), RCC, thyroid, melanoma, sarcoma

36
Q

calcifications with mets

A

seen with mucinous colorectal or ovarian serous tumors

imply better prognosis

37
Q

T1 hyperintense lesions

A

blood products and melanin

38
Q

metastatic lesions on MRI

A

hypointense T1, hyperintense T2

39
Q

peudocirrhosis

A

macronodular liver contour from multiple scirrhous hepatic mets, mimics cirrhosis; will have capsular retraction

commonly breast cancer will do this

40
Q

hepatic lymphoma

A

usually presents with splenomegaly and LAD

41
Q

epithelioid hemangioendothelioma

A

multiple confluent spherical subcapsular masses; vascular malinancy

halo or target appearance

cause of capsular retraction

42
Q

ddx capsular retraction

A

mets (mostly post treatment), fibrolamellar HCC, HCC (uncommon), epithelioid hemangioendothelioma, intrahepatic cholangiocarcinoma, confluent hepatic fibrosis

43
Q

FNH associations, imaging

A

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
Q

sulfur colloid and HIDA visualizes?

A

sulfur colloid&raquo_space; Kupffer cells

HIDA&raquo_space; bile duct cells

45
Q

hemangioma

A

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
Q

hepatic adenoma pathology

A

benign neoplasm: hepatocystes, scattered kupffer cells, no bile ducts (can differentiate on HIDA for FNH which has bile ducts)

47
Q

hepatic adenoma

A

more common in females, prolonged OCPs or associated with anabolic steroids in men; high risk of hemorrhage

48
Q

multiple hematic adenoma

A

von Gierke disease (type I glycogen storage disease)

49
Q

adenoma on imaging

A

hypervascular on arterial phase; microscopic fat may be seen on in/out of phase MRI

intralesional hemorrhage will look like T1 hyperintensity

50
Q

budd chiari pathology, causes

A

hepatic venous outflow obstruction

hypercoagulative states, hematolgic disorders, pregnancy, OCP, malignancy, infection, trauma

51
Q

clinical triad of acute Budd Chiari

A

hepatomegaly, ascites, abdominal pain

52
Q

budd chiari findings

A

edematous peripheral liver

progressive liver –> atrophy with caudate hypertrophy ;caudate spared as it drains directly into the IVC

53
Q

veno-occlusive disease

A

destruction of post-sinusoidal venules with patent hepatic veins; seen in bone marrow transplate patients

54
Q

cardiac hepatopathy

A

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
Q

congenital cystic liver disease

A

biliary hamartoma (von Meyenburg complex) and ADPLD

56
Q

biliary hamartoma

A

incidental small cystic hepatic lesion; irregularly shaped simple cysts

57
Q

autosomal dominant polycystic liver disease

A

40% of ADPKD have similar disease in the liver, called ADPLD

hepatic failure remains rare

58
Q

most common organ injured in trauma? second most common?

A

spleen > liver

59
Q

MDCT grading of hepatic injury

A

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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