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AA Sal Abdominal Radiology > Liver > Flashcards

Liver Flashcards

1
Q

What is T1 and T2 relatinship b/w liver and spleen?

A

Liver is brighter on T1 (because of enzymes). Spleen is brighter on T2 (because spleen is a bag of water)

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2
Q

2 fat related artifacts on MRI

A

Type 1; “chemical shift” Type 2; “india ink”

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3
Q

In abdominal imaging, Which direction is frequency encoding. Which is phase encoding

A

Frequency is transverse direction (long direction, long word). Phase encoding is AP (short direction, short word)

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4
Q

How does field strength effect chemical shift artifact (frequeny)

How does receiver bandwith effect Chemical shift (frequency)

A

Higher field strength (1.5 T to 3T) makes artifact worse

Differences in frequency are LESS noticiable at a high receiver band with.

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5
Q

How does receiver bandwith effect Chemical shift (frequency)

A

Differences in frequency are LESS noticiable at a high receiver band with.

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6
Q

Type 1 artifact

A

Due to Gradient. Difference in fat and water causing localization problems. Occurs in Frequency encoding direction

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7
Q

Type 1 artifact is worse with __ and more noticiceable with ___

A

Higher field strength. Narrower receiver bandwith.

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8
Q

Type 1 artifact occurs with __, and __ echos

A

Spin echo and gradient echo

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9
Q

Type 2 artifact; dropout occurs on ___ phase. And occurs only w/ __ echo

A

Opposed phase

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10
Q

In/out of phase runner analogy

A

there is a slow and fast runner on a track. On out of phase they are at opposite sides. The in Phase, they are at the same spot.

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11
Q

On in/out phase which phase comes first?

A

Opposed phase is first (2.2 seconds) in pahse is 2nd (4.4 seconds)

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12
Q

What happens if you obtain the out of phase image late

A

You will have more T2 star effect on outer phase. So the liver artificially loses signal on out of phase. You would notbe able to tell difference b/w fatty liver and iron-rich liver.

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13
Q

Blooming artifact gets __ as time goes on when doing in/out phase

A

Blooming signal gets worse as time goes on. So the more blooming with air and metal, the more later the acquisition was.

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14
Q

Liver segment I? (What seperates it from liver)

A

Caudate lobe, Ligamentum venosum and IVC separate it from liver

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15
Q

Liver segments II and III?

A

Lateral division of left lobe. II-superior. III-inferior.

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16
Q

Liver segments IV?

A

Medial division of left lobe. IVa-superior. IVb-inferior.

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17
Q

Liver segments V and VIII?

A

Anterior segments of right lobe. VIII-superior. V-inferior.

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18
Q

which Right lobe Liver segments are Anterior? Which are posterior?

A

Anterior: 5, 8

Posterior segments of right lobe. VII-superior. VI-inferior.

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19
Q

Third inflow?

A

Areas of liver supplied by aberrant systemic veins. Porta hepatis, adjacent to gallbladder, adjacent to fissure of ligamentum teres.

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20
Q

The caudate lobe is spared (and may have compensatory hypertrophy) in early cirrhosis because?

A

It is drained by IVC, which is spared from increased venous pressures.

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21
Q

DDx Hepatic metabolic liver disease (4)

A

Hepatosteatosis, amyloid, Wilson’s, hemochromatosis

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22
Q

Hepatic steatosis, focal fat patterns

A

GB fossa, Subcapsular (along falciform), periportal, nodular. (focal fat should not have any mass effect).

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23
Q

Fatty infiltration CT attenuation

A

On unenhanced: 10 HU less than spleen or under 40HU. On PV; 25 less than spleen.

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24
Q

Wilson’s disease. Where does copper accumilate. Genetic inheritance

A

Basal ganglia, cornea, liver. Will lead to hepatomegaly/cirrhosis. Autosomal recessive genetic defect.

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25
Q

Which disease has Liver signal dropping out on In-phase

A

Hemochromatosis

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26
Q

PPPPrimary hemochromatosis. Which organs does it effect? Demographics

A

Liver and PPPancreas (also myocardium, skin, and joints). In hepatocytes. Mostly white. It will effect women later in life (because they menstrate early in life)

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27
Q

SSSecondary hemochromatosis Which organs does it effect

A

Liver and SSSpleen. Due to hemosiderosis from frequent transfusions or thallasemia, and depositions in RES (Kupffer cells).

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28
Q

Where does hemochromatosis effect the hand in arthritis?

A

2nd, 3rd MCP, TFCC. Hook osteophytes (similar to CPPD)

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29
Q

Ddx Hypoattenuating liver (2)

A

Amyloid. Hepatosteatosis.

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30
Q

Ddx Dense liver (5)

A

Drugs (*Amiodarone*). Wilson’s. Hemochromatosis. Glycogen storage disease. Thorotrast

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31
Q

Amiodarone effect on liver (and lungs)

A

Liver Is dense. Lungs have chronic interstitial pneumonia (peripheral areas of dense airspace disease)

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32
Q

Ddx Hepatic infection (4)

A

Viral hepatitis, candidiasis, pyogenic, echinococcal cyst

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33
Q

HIV manifestations in the liver

A

Peliosis hepatis (bartonella infection), candidiasis, kaposi sarcoma, PCP, AIDS related lymphoma

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34
Q

Hepatitis findings in liver

A

Periportal edema, GB edema, Enlarged liver

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35
Q

Candidiasis in liver

A

Systemic infection seeding to liver (and spleen) on PV drainage. Tiny hypoatenuating microabscesses, immunocompromised patients.

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36
Q

Ddx Multiple tiny hypoattenuating liver lesions (5)

A

Candidiasis, lymphoma, mets, Caroli disease, Biliary hamartomas (von-Meyerburg)

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37
Q

Hepatic abscess (common causes, common bug, appearance)

A

caused by bowel process (diverticulitis, appendicitis, crohn’s, bowel surgery. Ascending cholangitis less common). E. Coli. Ring enhancing on CT and MR. Center is T2 bright.

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38
Q

Echinococcal disease (cause). Develops into ___ cyst

A

ingestion of eggs (echinococcus granulosus, endemic in Mediterrian a/w Sheep raising). Develop into hydatid cysts. hypoattenuating mass with floating membrane or associated daughter cysts. Peripheral calcifications may be present.

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39
Q

Imaging of Hydatid cyst

A

hypoattenuating mass with floating membrane or associated daughter cysts. Peripheral calcifications may be present.

40
Q

Early signs of cirrhosis

A

Expansion of preportal space, atrophy of medial left hepatic lobe. Enlargement of caudate (if caudate >0.65). Empty gallbladder fossa sign

41
Q

Empty gallbladder fossa sign (cirrhosis)

A

Hepatic parenchyma surrounding the gallbladder is replaced w/ periportal fat

42
Q

Secondary manifestations of cirrhosis

A

Portal HTN, splenomegaly, collaterals, varices. GB wall thickening

43
Q

Gamna-Gandy bodies

A

Due to cirrhosis. Splenic microhemorrhages. Hypointense on GRE

44
Q

Micronodular vs. macronodular cirrhosis

A

Micro; metabolic causes. Macro; post-viral

45
Q

Liver nodules in cirrhosis?

A

Regenerative nodules Dysplastic nodules Small HCC nodules Metastatic disease Hemangiomas

46
Q

CT features of portal hypertension?

A

Portosystemic collateral vessels Enlarged portal vein, > 13 mm. Splenomegaly Ascites

47
Q

Calcifications in liver ddx

A

Most likely Mets (adenocarcinoma/colorectal). Fibrolamellar and HCC are less common. Fibrolamellar has calcification more often than HCC.

48
Q

Ddx Malignant hepatic lesions (5)

A

Epithelioid hemangioendothelioma, HCC, Fibrolamellar carcinoma, Lymphoma, mets,

49
Q

What liver malignancies may calcify?

A

Fibrolamellar HCC. Hepatoblastoma. Intrahepatic cholangiocarcinoma. Metastases.

50
Q

Pathway to HCC

A

Regenerative nodule –>dysplastic nodule–>HCC

51
Q

Regenerative nodule

A

supplied by PV, not premalignant. Low T2, no enhancement

52
Q

Dysplastic nodule

A

premalignant. Blood supply still from PV. Variable T1/T2, but the worse it is, the more T2 hyperintense. High grade dysplastic nodules may enhance

53
Q

Siderotic nodule

A

Iron-rich regenerative/dysplastic nodule. Hypointense on T1/T2* and hyperatteunating on CT. Not malignant.

54
Q

HCC features? (size, MRI, biomarker)

A

Small tumors(< 3cm). Arterial enhancement, PV washout. T2 hyperintense on MR. Elevated AFP. Locally invasive (PV, IVC, bile ducts).

55
Q

How can you get HCC in a non-cirrhotic adult?

A

Acute HBV

56
Q

What does HCC look like on PET

A

It will not light up.

57
Q

Fibrolammelar Carcinoma CT features?

A

Large mass in healthy liver heterogenous enhancement Central scar Difficult to distinguish from FNH. No capsule (unlike HCC)

58
Q

Central scar features of Fibrolamellar HCC vs. FNH

A

Fibrolamellar HCC: T1/T2 hypointense.

FNH is T2 hyperintense and enhances late. Its also “wispy”

59
Q

Metastases to liver features on CT?

A

Most common liver malignancy. Usually hypovascular. Most commonly from colon. Target appearance. Some cystic/nectrotic, calcification

60
Q

Ddx Hyperenchancing (vascular) liver mets (5) (‘neuroendocrine mets shine right through)

A

Neuroendocrine, melanoma, Sarcoma, RCC, thyroid (also Pheo, choriocarcinoma)

61
Q

Ddx Hypovascular liver mets (2)

A

Colorectal, pancreatic adenocarcinoma

62
Q

Liver mets w/ calcifications

A

Mucinous colorectal, ovarian serous tumors (think adenomas)

63
Q

Liver mets on MRI (melanoma exception)

A

T1 hypo, T2 hyper. Melanoma will be T1 hyper.

64
Q

what is “pseudocirrhosis”

A

macrondular liver contour due to multiple scirrhous heptic mets. May mimic cirrhosis. Can be seen w/ treated breast cancer.

65
Q

Liver lymphoma CT features?

A

Diffuse infiltration, Well-defined, homogeneous low-density nodules, Numerous small nodules resembling microabscesses

66
Q

Epithelioid hemangioendothelioma

A

Multiple spherical subcapsular masses. Halo or target appearance. Capsular retraction

67
Q

Ddx for capsular retraction of liver (6)

A

Mets, epitheliod hemangioendothelioma, Fibrolamellar, HCC, intrahepatic cholangiocarcinoma, confluent hepatic fibrosis.

68
Q

Ddx Benign liver masses (3)

A

FNH, Hemangioma, hepatic adenoma

69
Q

FNH CT features?

A

Mini liver central scar with T2 hyperintense ductules and venules w/ arterial enhancement.

Unenhanced, isodense to liver. Arterial phase, immediate intense homogeneous enhancement. May have delayed enhancement of scar. Positive sulfur colloid uptake

70
Q

Nuc medicine study to cofirm FNH from HCC?

A

Sulfur colloid scan (FNH has kupffer cells and will light up)

71
Q

FNH (central scar enhancement pattern). MRI contrast agent.

A

T2 bright (FL HCC is T2 dark), T1 dark, Enhances arterially and persists longer. Will retain eovist.

72
Q

Explain Eovist

A

It is transported into bile duct by OATP transporter. Therefore with FNH, lesion retains OATP tranpoter, but with HCC, the OATP transpoter is gone. Well differentiated HCC is the exception to the rule.

73
Q

Cavernous Hemangioma CT features?

A

Disorganized blood vessels supplied by hepatic artery. Unenhanced, hypodense mass. Arterial phase, periphera, dicontinious, progressive nodular enhancement.

74
Q

Hemangioma enhancement patterns

A

Classic pattern w/ peripheral discontinous nodular filling. Flash filling. Delayed fill with a central star type of look (can do a late delay for confirmation)

75
Q

Giant hemangioma features

A

May not have enhancing center

76
Q

Nuclear medicine test to confirm hemangioma

A

Tagged RBC scan

77
Q

Hepatic adenoma CT features?

A

Hepatocytes, scattered kupffer cells. No bile ducts. OCPs/anabolic steroids. Surgical removal for fear of rupture or malignant transformatoin. Unenhanced, isodense to liver. Arterial phase, early homogeneous enhancement. Few Kupffer cells, no sulfur colloid uptake

78
Q

Adenoma MRI

A

Microscopic fat (drop in in/out), Internal hemorrhage may cause T1 hyperintensity.

79
Q

Hepatic adenoma types

A
  1. Ones w/ fat (HNF Alpha), 2. ones that bleed (inflammatory)
80
Q

Heptic adenoma (classic location, history, what if they are multiple)

A
  1. Right subcapsular region, 2. OCP/steroids, 3. Glycogen storage disease
81
Q

Ddx Vascular liver disease (3)

A

Budd-chiari, veno-occlusive disease, cardiac hepatopathy.

82
Q

CT features of Budd-Chiari syndrome?

A

Enlarged caudate lobe. Central liver enhances early and peripheral liver enhances late. Lack of venous flow. Collaterals. Edematous peripheral liver.

83
Q

3 ways to show Budd Chiari

A

Hypertrophy of caudate. Central liver enhances first (opposte of normal), Budd Chiari nodules.

84
Q

Budd Chiari clinical triad

A

Ascites, abdominal pain, hepatomegaly

85
Q

Hot Quadrate sign

A

Caudate lobe enhancement. A sign of SVC obstruction. Complex collateral pathway.

86
Q

Veno-occlusive disease (explain entity. Imaging findings.

A

destruction of post-sinusoidal venules, patent hepatic veins. Seen in BMT pts. Imaging findings nonspecific, including periportal edema, narrowing of hepatic veins.

87
Q

Cardiac heptatopathy

A

Passive hepatic congestion from CHF, constrictive pericarditis, valve disease. Can lead to cirrhosis.

88
Q

Cardiac hepatopathy imaging clues

A

Enlarged hepatic veins and IVC. Reflux of contrast. Enlarged/mottled liver.

89
Q

Numerous liver cysts, differential and how do you differentiate them.

A

Biliary hamartomas (von-Meyenburg complex) vs. Caroli’s disease. Determine if they communicate w/ biliary system vs. PCKD

90
Q

Biliary hamartomas - name of disease, cause

A

Von Meyenburg complexes. Small cystic hepatic lesions that do not communicate w/ biiary tree. Caused by embryologic failure of normal bile duct formation.

91
Q

MDCT grading of hepatic injury (grades I-V)

A

I: superficial laceration or subcapsular hematoma <1cm. II, lac or hematoma 1-3cm. III lac or hematoma >3cm. IV; massive hematoma >10cm or destruction/devascularization of a hepatic lobe. V; destruction or devascularization of both hepatic lobes.

92
Q

Liver transplant: Elevated diastolic flow in HA

A

Sensitive for severe stenosis (may be post-op due to edema)

93
Q

Liver transplant: elevated diastolic flow and Tardua Parvus in HA

A

Specific for severe proximal stenosis.

94
Q

HHT findings

A

AVMs in skin (nose), Lungs (shunt to brain, stroke, abscess), liver, Bowel (GI bleed)

95
Q

Subcapsular hematoma in a pregnant patient

A

HELLP syndrome (young, first pregnancy, 3rd trimester, eclampsia, DIC

AA Sal Abdominal Radiology (6 decks)

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