GI Section III: Liver Masses Flashcards

1
Q

The most common benign liver neoplasm

A

Hemangioma

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2
Q

Hemangioma facts

A

Favors women 5:!
Enlarge with pregnancy.

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3
Q
A

Hemangioma

Hyperechoic (dark in fatty liver)
Vessels adjacent to the lesion, NOT in the lesion

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4
Q
A

Hemangioma

tends to match the aorta in signal and have

“peripheral nodular discontinuous enhancement”.

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5
Q

can be used to diagnose hemangiomas - bigger than 2 cms

A

Tc-99m-labeled RBCs

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6
Q

Typical Hemangioma

A
  • Classically Hyperechoic (bright) on ultrasound
  • Enhanced thru transmission is common
  • NO Doppler flow inside the lesion itself
  • Calcifications are extremely rare
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7
Q

Giant Hemangioma

A

> 5 cm

Similar CT findings to regular hemangioma

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8
Q

Potential complication complication of Hemangioma

A

Kasabach-Merritt syndrome - consumptive coagulopathy

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9
Q

Flasii Filling
Hemagioma

A

< 2 cm

Technically not a hemangioma, but historically referred to as one. - Rapid flash filling

They otherwise retain contrast and remain isodense to blood pool. They do not washout the way an HCC would.

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10
Q

The second most common benign liver neoplasm.

A

Focal nodule hyperplasia

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11
Q

FNH start in utero as an?

A

AVM

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12
Q

FNH composistion

A

Normal hepatocytes abdnomally arranged ducts and Kupffer cells (reticuloendothelial cells)

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13
Q
A

FNH

“spoke wheel” US Doppler

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14
Q
A

FNH

“Homogeneous” on arterial phase - Same to the IVC (not aorta)

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15
Q
A

FNH

Can be a “Stealth” lesion on MRI - T1 and T2 isointense. Can have acentralscar.

Scar will demonstrate delayed enhancement (like scars do).

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16
Q

FNH biopsy rule

A

You have to hit the scar, otherwise path results will say normal hepatocytes.

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17
Q

Can develop after chemotherapy treatment with oxaliplatin (chemo for bowel cancer)

A

FNH

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18
Q

What other test is used to confirm FNH

A

Sulfur Colloid - Hot

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19
Q

Usually a solitary lesion seen in a female on OCPs

A

Adenomas

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20
Q

Alternatively could be seen in a man on anabolic steroids.

A

Adenomas

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21
Q

Associated with glycogen storage disease (von Gierke) or liver adenomatosis

A

Adenomas

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22
Q

Big fat diabetic girl named Von Gierke + hepatic mass?

A

Adenomas

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23
Q

What imaging methods can reliably differentiate hepatic adenoma from hepatocellular carcinoma?

A

NONE

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24
Q
A

Adenomas

Chemical-shift imaging showing loss of signal on out-of-phase images can confirm the presence of fat.

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25
Q

Most common location for hepatic adenoma (75%)

A

Right Lobe liver

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26
Q

Adenoma Managment

A
  • Stop the OCPs and re-image, they should get smaller.
  • Smaller than 5cm, watch them.
  • Larger than 5cm they often resect because
    (1) they can bleed and
    (2) they can rarely turn into cancer.
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27
Q

What are teh adenoma subtypes?

A

Inflammatory
* Most common
* Highest bleed rate

HNF-1 alpha mutated
* Second most common
* Multiple masses

Beta catenin mutated
* Least common
* Anabolic steroids
* Glycogen storage disease
* Familial adenomatous polyposis

28
Q

HCC occurs typically in what setting?

A

Cirrhosis and chronic liver disease; Hep B, Hep C, hemachomatosis, glycogen storage disease, Alpha 1 antitrypsisn

29
Q

What is elevated in HCC

A

AFP (80-95%)

30
Q

HCC invades what vessles?

A

Portal vein

Hepatic vein invation - more specific finding

31
Q

What is the average doubling time of HCC?

A

3 - 4.5 months

32
Q
A

Early HCC

You will only see them in the arterial phase

Sometimes there is rim enhancement - mistaken for hemangioma

RIM enhancement is NEVER hemangioma

33
Q
A

Large HCC with mozaic pattern in a non cirrhotic patient. - LATE appearance

PVP: Hypodense - due to fast washout
Delayed: Prolonge capsule and septal enhancement

very large with a mozaic pattern, a capsule, hemorrhage, necrosis and fat evolution.

HCC is a silent tumor, so if patients do not have cirrhosis or hepatitis C, you will discover them in a late stage.

34
Q
A

LEFT: Diffusely enhancing tumor thrombus in HCC with portal vein invasion.

RIGHT: Tumor thrombus with vessels within the thrombus.

35
Q

Classic HCC vs FL HCC

A

Fibrolamellar HCC

36
Q

Classic HCC vs FL HCC

A

Classic HCC

37
Q

Central Scars of FNH and Fibrolamellar HCC

A

Focal Nodular Hyperplasia

38
Q

Central Scars of FNH and Fibrolamellar HCC

A

FL HCC

39
Q

NECT, arterial and portal venous phase in a patient with Hepatitis C with two lesions in the liver (arrows).

A

Hypervascular lesions in the right and left lobe

Upper images
NECT: isodense
AP: enhancement (not as dense as the bloodpool)
PVP: Isodense

Lower Images
NECT/AP/PVP: as dense as the blood pool

UPPER: Right lobe HCC
LOWER: Hemangioma

40
Q

cancer of the bile duct

A

Cholangiocarcinoma

Cholangiocarcinoma believes in nothing Lebowski. It flicks you up, it takes the money (prognosis is poor).

41
Q

Cholangiocarcinoma.

Who gets it?

A

Classic:

80 y.o. man + Primary sclerosis cholangitis (PSC, main risk factor in the west) + recurrent pyogenic “oriental” cholangitis (main risk factor in the east)
+ Caroli disease (Type V)
+ Hepatitis
+ HIV
+ Hx of cholangitis
+ Liver worms (clonorchis)

42
Q

Non enhanced, arterial, portal venous and equilibrium phase.

A

Cholangiocarcinoma.

AP: Hypodense
PVP: Hypodense + peripheral enhancement
Equilibirum phase: Hyperdense

+ Liver capsule retraction

infiltrating mass with capsular retraction and delayed persistent enhancement is very typical for

43
Q

What does cholangiocarcinoma look like?

A

Scar generating cancer
+ Delayed enhancement
+ desmoplastic pulling of the scar (capsular retration and ductal dilatation)

44
Q
A

Cholangiocarcinoma

Only on the delayed images at 8-10 minutes after contrast injection a relative hyperdense lesion is seen. This is the fibrous component of the tumor.

45
Q

“Painless jaundice”

A

CholangioCA (Just like pancreatic head CA)

46
Q

Invades the Portal Vein

A

HCC

47
Q

Encases the Portal Vein

A

CholangioCA

48
Q

Cholangiocarcinoma that occurs at the bifurcation of the right and left hepatic ducts

A

Klatskin tumor

49
Q
A

Klatskin tumor

Mass at the bifurcation fo the right and left hepatic ducts

50
Q
A

Klatskin Tumor

small mass causing biliary obstruction
“Shoulder/abrupt tapering”

51
Q

Delayed Enhancement
Peripheral Biliary Dilation
Liver
Capsular Retraction
NO tumor capsule

A

Cholangiocarcinoma

52
Q

key factor for surgical candidacy for cholangioCA

A

Proximal extent of involvement

53
Q

Implies biliary +/- vascular involvment of the hepatic lobe in Cholangiocarcinoma?

A

Atrophy of a lobe

54
Q

Tumor markers:

A. Increased CEA and CA19-9
B. Normal CEA INC CA19-9
C. INC CEA Normal CA19-9

A

A. CholangioCA
B. Pancreatic CA
C. Colon CA

55
Q

the most common primary sarcoma o f the liver

A

Angiosarcoma

Very rare

56
Q

Associated with Toxic exposure -

Aresnic
Plyvinyl Cl
Radiation
Thorotrast

A

Hepatic Angiosarcoma

57
Q

Assoc with Hemochomatosis and NF1 patients

A

Hepatic Angiosarcoma

58
Q

Uncommon benign cystic neoplasm of the liver
+ middle aged women + Pain + jaundice

Solid + Nodular enhancing + capsule

A

Biliary Cystadenoma

59
Q

This is way more common than a primary liver cancer

A

Hepatic metastasis (20-40x)

60
Q

If you see mets in the liver, first think:

A

Colon

61
Q

Calcified mets are usually the result of what mucinous neoplasms?

A

Colon
Ovary
Pancreas

62
Q
A

Hepatic metastasis

Calcified metastasis in a patient with colon cancer.

Hyperechoic + hypervascular (renal, melanoma, carcinoid, choriocarcinoma, thyroid, islet cell)

63
Q

Hypoechoic mets on usd =

A

Hypoechoic mets are often hypovascular -> more common look

Colon
Lung
Pancrease

64
Q
A

Hepatic metastasis

Hypoechoic halo (target) - classic description

65
Q

Mass on CT scan

A

low density masses with a continuous rim of enhancement

discontinueous = hemangioma

A background fatty liver may result in the lesions looking bright (higher density).

66
Q

What type of lymphoma involves the liver 60% of the time

A

HL

67
Q
A

Kaposi sarcoma

Causes diffuse periportal hypoechoic infiltration.

Similar to biliary duct dilatation