Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Core > Gastrointestinal: Liver/Biliary > Flashcards

Gastrointestinal: Liver/Biliary Flashcards

1
Q

What is the hepatic bare area?

A

An area of the liver surface abutting the diaphragm that is not covered by visceral peritoneum

Note: An injury to the bare area can result in a retroperitoneal bleed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What parts of the liver are not covered by visceral peritoneum?

A
  • Bare area
  • Porta hepatis
  • Gallbladder fossa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What separates hepatic segments 7 and 8?

A

The right hepatic vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What separates hepatic segments 5 and 6?

A

The right hepatic vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What separates hepatic segments 4a and 8?

A

The middle hepatic vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What separates hepatic segments 4b and 5?

A

The middle hepatic vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What separates hepatic segments 2 and 4a?

A

The left hepatic vein/fissure for the ligamentum teres (falciform)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What separates hepatic segments 3 and 4b?

A

The left hepatic vein/fissure for the ligamentum teres (falciform)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What separates hepatic segments 2, 4a, 7, and 8 from segments 3, 4b, 5, and 6?

A

The portal vein separates the upper segments from the lower segments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Why is hepatic segment 1 unique?

A

It is the caudate lobe and drains directly into the IVC (rather than into a hepatic vein)

Note: It also received blood supply from both the left and right portal veins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Cantlie’s line

A

Runs from the IVC to the middle of the gallbladder fossa (divides the liver into functional left and functional right hepatic lobes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What separates the liver into functional left and right hepatic lobes?

A

Cantlie’s line (running from the IVC to the middle of the gallbladder fossa)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Why is the caudate lobe usually spared in Budd Chiari?

A

It receives blood from both the right and left portal veins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Name the hepatic segments

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Why does the right hepatic lobe shrink and left hepatic lobe grow in cirrhosis?

A

The intrahepatic course of the right portal vein is longer and more susceptible to fibrosis, leading to right lobe atrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the most common variant of the hepatic blood vessels?

A

Replaced right hepatic artery (originating from the SMA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the most common biliary variant?

A

Right posterior segmental duct draining to the left hepatic duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the normal MRI characteristics of the liver, spleen, and pancreas?

A
  • Liver (T1 bright and T2 dark)
  • Spleen (think water: T1 dark and T2 bright)
  • Pancreas (T1 brightest and T2 dark)

Note: The pancreas is the brightest organ on T1 (think about all the pancreatic enzymes; the liver has enzymes also but not as many and isn’t as T1 bright).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What fetal structure allows blood to bypass the liver in utero?

A

Ductus venosus

Note: This becomes the ligamentum venosum.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How does blood get from the placenta to the heart in utero?

A

Placenta -> umbilical vein -> ductus venosus -> IVC -> right atrium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q
A

Splenic vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q
A

SMA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q
A

Pancreatic head

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q
A

Left renal vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q
A

Aorta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q
A

IVC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How can you tell whether the pancreas is more hypoechoic that it should be?

A

If it is hypoechoic relative to the liver parenchyma it may be edematous

Note: The pancreas should be more echogenic than the liver.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q
A

Common bile duct

Note: “Mickey Mouse” sign.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q
A

Hepatic artery

Note: “Mickey Mouse” sign.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q
A

Portal vein

Note: “Mickey Mouse” sign.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

A?

A

Left renal vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

C?

A

Pancreas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

E?

A

Splenic vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

F?

A

SMA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q
A

Falciform ligament (ligamentum teres)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q
A

Common bile duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q
A

Right hepatic artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q
A

Portal vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Why do hepatic abscesses almost always involve the right hepatic lobe?

A

The right portal vein has a longer intrahepatic course than the left (most pathogens spread through the portal vein to cause hepatic abscesses)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What common measurement is most specific for hepatic cirrhosis?

A

Caudate to right hepatic lobe ratio

Note: C/RL ratio > 0.75 is 99% specific for cirrhosis).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Which parts of the liver atrophy/hypertrophy in cirrhosis?

A
  • Right lobe atrophies
  • Left lobe and caudate hypertrophy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is the most common cause of hepatic cirrhosis?

A
  • Schistosomiasis (globally)
  • EtOH cirrhosis (in US)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are the common causes of portal hypertension?

A
  • Pre-hepatic (portal vein thrombosis, tumor compression)
  • Hepatic (cirrhosis, schistosomiasis)
  • Post-hepatic (Budd-Chiari)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

As fibrosis causes portal hypertension, what happens to velocities in the hepatic artery?

A

Velocities increase in the hepatic artery (to compensate for the reduced blood supply from the portal vein)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Transient hepatic attenuation differences

A

Areas of hepatic parenchymal hyperenhancement that are only visible during the arterial phase and then go away by the equilibrium/delayed phases

Note: This is due to the dual blood supply to the liver. Those areas of hyperenhancement are receiving a greater percentage of their blood supply from the hepatic artery rather than the portal vein.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What causes the regions of hyperenhancement in transient hepatic attenuation differences?

A

The hyperenhancing regions aren’t getting enough portal venous flow so respond by increasing hepatic arterial flow (leading to hyperenhancement on arterial phases)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are the most common causes of transient hepatic attenuation differences?

A
  • Cirrhosis (usually subcapsular hyperenhancement)
  • Portal vein branch thrombosis (usually larger wedge-shaped hyperenhancement)
  • Mass (mass effect compressing the veins and/or tumor upregulating arterial flow)
  • Abscess/infection (hyperemia of the arteries and/or edema compressing veins)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Why does there tend to be peripheral hyperenhancement and relative central hypoenhancement in cirrhotic livers?

A

The fibrosis that occurs in cirrhosis progresses from the periphery inward, reduced portal veinous flow to the periphery causes upregulation of hepatic arterial flow in the periphery (leading to relative hyperenhancement)

Note: This is the “central-peripheral” phenomenon.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is the normal direction of flow in the portal veinous system?

A

Hepatopetal (towards the liver)

Note: Hepatofugal (Fugal means Flee away from the liver) flow is abnormal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Why does flow sometimes reverse in the portal veins in cirrhosis rather than just clot off?

A

When pressures get too high in the liver, the portal veinous system can decompress through the creation of collaterals. The hepatic artery can’t do this and instead decompresses by creating shunts to the portal veinous system. The shunting of blood from the hepatic artery to the portal vein is what causes portal veinous flow reversal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Portal hypertensive colopathy

A

Edematous colon due to backup of pressure from the portal veinous system. This is usually worse on the right-sided colon because the left is more easily decompressed through the creation of collaterals (e.g. splenorenal shunt, short gastrics, esophageal varices, etc.)

Note: Portal hypertensive colopathy can resolve after a liver transplant.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Portal hypertensive gastropathy

A

Thickened gastric wall due to backup of pressure from the portal veinous system that can also cause GI bleeding

Note: This can happen even in the absence of gastric varices.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

How do regenerative liver nodules appear on MRI as they progress to dysplastic nodules and HCC?

A

Regenerative nodules (T2 dark)
Dysplastic nodules (T2 isointense to dark)
HCC (T2 bright, enhancing)

Note: The “nodule within a nodule” (where there is a T2 bright spot within a T2 dark nodule) is concerning for transformation to HCC.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Why does hepatocellular carcinoma usually appear dark on delayed phase imaging with biliary contrast agents (e.g. Eovist)?

A

As hepatocytes become cancerous they usually lose the OATP bile uptake transporter which prevents those cells from taking up biliary contrast agents.

Note: A notable exception is well differentiated HCC, which maintains its OATP transporters, which is why this subtype actually appears bright on delayed imaging with biliary contrast agents.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Why are all lesions considered more suspicious in hepatic cirrhosis?

A
  • Cirrhosis is a significant risk factor for HCC
  • The squeezing process in cirrhosis that leads to portal hypertension also squeezes out most benign liver lesions (e.g. cysts and hemangiomas)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

At what timepoinnt does the hepatic arterial phase occur?

A

25-30 seconds after injection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

At what timepoints does the portal venous phase occur?

A

70 seconds after injection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is the liver window?

A

Center: 100
Width: 200

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

How does gadolinium work as a contrast agent?

A

Gadolinium is paramagnetic, which causes T1 shortening (appearing bright on T1 images)

Note: Gadolinium is highly toxic and so is bound to a chelation agent to prevent it from killing the pt.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What are the major types of MRI contrast agents used in liver imaging?

A
  • Extracellular (blood flow dependent: work just like iodine contrast agents in CT)
  • Hepatocyte specific (taken up by hepatocytes and excreted into the bile)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What is the classic example of an extracellular MRI contrast agent?

A

Gd-DTPA (Magnavist)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What is the classic example of a hepatocyte specific MRI contrast agent?

A

Gd-EOB-DTPA (Eovist)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What are the main indications for using Gd-EOB-DTPA (Eovist)?

A
  • Proving an FNH is an FNH
  • Looking for bile leaks
  • Looking for new metastases (once a baseline MRI has characterized any benign cysts/lesions present)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Is eovist a pure hepatocyte specific agent?

A

No, it also acts like a non-specific extracellular agent early on (55% ends up excreted into the bile)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What is the most common benign liver neoplasm?

A

Hemangioma (followed by FNH)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Are hemangiomas more common in men or women?

A

Women (5:1)

Note: They may also enlarge in pregnancy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Classic ultrasound appearance of a hepatic hemangioma

A
  • Hyperechoic (unless in a fatty liver)
  • No internal flow on color Doppler (may have peripheral vascularity)
  • Posterior acoustic enhancement is common
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Classic CT/MRI appearance of a hepatic hemangioma

A
  • Discontinuous peripheral nodular enhancement
  • Isodense/isointense to aorta on all phases/sequences
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

If you were to biopsy a hepatic hemangioma, what type of biopsy would you need?

A

Core biopsy

Note: FNA will only show blood, not enough tissue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Hepatic lesion that changes appearance during the course of a single ultrasound exam…

A

Think hemangioma (no other hepatic lesion does this)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What imaging study can be used to diagnose hepatic hemangiomas larger than 2 cm?

A

Tc-99m labeled RBCs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What is a giant hepatic hemangioma?

A

A hepatic hemangioma over 5 cm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Kasabach-Merritt syndrome

A

Consumptive coagulopathy due to a growing vascular tumor (e.g. giant hepatic hemangioma)

Note: This increases bleeding risk.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Flash filling hemangioma

A

Smaller (<2 cm) hemangiomas that homogeneously enhance “flash-filling” on arterial phase, but still remain isodense to blood pool on all phases

Note: They do not washout on delayed images the way HCC would.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

If you were to biopsy focal nodular hyperplasia, where should you biopsy?

A

Through the central scar (if present)

Note: If you don’t get the scar, the biopsy will just say normal hepatocytes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Which hepatic lesion is classically seen in females on oral contraceptives?

A

Hepatic adenoma

Note: These are also often seen in men on anabolic steroids.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Focal nodular hyperplasia can develop after treatment with what chemotherapy agent?

A

Oxaliplatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Classic appearance of focal nodular hyperplasia on MRI

A

Stealth lesion (isointense to liver on both T1 and T2)

Note: If there is a central scar, you may see that (which should show delayed enhancement).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

How does FNH enhance on CT?

A

Homogenous enhancement on arterial phase (delayed enhancement of a central scar, if present)

Note: FNH should be isodense to the IVC, hemangiomas are isodense to the aorta.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What nuclear imaging study can be used to differentiate FNH from malignancy?

A

Sulfur colloid (FNH should have normal or increased uptake, since it contains normal liver cellularity)

Note: FNH also shows up on HIDA scintigraphy due to the normal liver cellularity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Multiple hepatic adenomas…

A
  • Glycogen storage disease (von Gierke)
  • Liver adenomatosis

Note: Usually hepatic adenomas are solitary.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Why are hepatic adenomas sometimes surgically excised?

A
  • Propensity to bleed
  • Risk of degeneration into HCC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What is the most common location for a hepatic adenoma?

A

Right liver lobe (75%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

First line treatment for hepatic adenoma

A

Stop oral contraceptives (if taking) and repeat imaging

Note: Many hepatic adenomas regress after OCPs are stopped.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Which adenomas are often surgically resected?

A

Persistent adenomas that are >5 cm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What are the major subtypes of hepatic adenoma?

A
  • Inflammatory (most common)
  • HNF-1 alpha mutated
  • Beta-catenin mutated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Which hepatic adenoma subtype has the highest rate of bleeding?

A

Inflammatory (also the most common subtype)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Which hepatic adenoma subtype is associated with having multiple hepatic adenomas?

A

HNF-1 alpha mutated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Which hepatic adenoma subtype is associated with anabolic steroids, glycogen storage disease, and familial adenomatous polyposis?

A

Beta catenin mutated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Is AFP elevated in HCC?

A

Almost always (80-95%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Hepatic mass infiltrating the hepatic vein…

A

Think HCC

Note: HCC also invades the portal vein, but invasion of the hepatic vein is more specific.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Major risk factors for HCC

A
  • Cirrhosis
  • Hep B/C
  • Hemochromatosis
  • Glycogen storage disease
  • Alpha 1 antitrypsin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What is a standard doubling time for HCC?

A

150-300 days

Note: There are 3 described growth patterns for HCC: slow (>300 days), medium (150-300 days), and fast (<150 days).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What is an appropriate follow up time for repeat imaging if you are not sure whether a lesion is HCC (despite exhausting all available imaging)?

A

3-4.5 months

95
Q

What HCC subtype is more common in younger pts without cirrhosis and usually has a normal AFP?

A

Fibrolamellar HCC

Note: These often have a central scar and can be mistaken for FNH.

96
Q

Does HCC tend to calcify?

A

Rarely

Note: The fibrolamellar HCC subtype does sometimes calcify (more often than classic HCC).

97
Q

Which HCC subtype classically has a central scar?

A

Fibrolamellar subtype

Note: Don’t confuse with FNH.

98
Q

How can you differentiate FNH from fibrolamellar HCC?

A

Both usually have central scars, but the central scar in fibrolamellar HCC does NOT enhance and is usually T2 dark

Note: The central scar in FNH does enhance and is T2 bright.

99
Q

Hepatic mass with a non enhancing, T2 dark central scar…

A

Think fibrolamellar HCC

100
Q

Hepatic mass with an enhancing, T2 bright central scar…

A

Think FNH

101
Q

Which HCC subtype is gallium avid on nuclear imaging?

A

Fibrolamellar HCC

102
Q

Which HCC subtype is usually associated with a normal AFP level?

A

Fibrolamellar HCC

103
Q

How can nuclear imaging studies help differentiate FNH from fibrolamellar HCC?

A

If the mass is sulfur colloid avid, it is likely FNH

If the mass is gallium avid, it is likely Fibrolamellar HCC

104
Q

Risk factors for cholangiocarcinoma

A
  • Primary sclerosis cholangitis (main risk factor in the western world)
  • Recurrent pyogenic cholangitis (main risk factor in the eastern world)
  • Caroli disease
  • Hepatitis
  • HIV
  • History of cholangitis
  • Liver worms (Clonorchis)
105
Q

Why might a history of ulcerative colitis make you worry more about cholangiocarcinoma?

A

Ulcerative colitis is highly associated with primary sclerosis cholangitis (the major risk factor for cholangiocarcinoma in the western world)

106
Q

Classic imaging appearance of cholangiocarcinoma

A
  • Mass with delayed enhancement (due to fibrosis)
  • Hepatic capsular retraction (due to fibrosis)
  • Peripheral bile duct dilatation (due to fibrosis)

Note: Think of cholangiocarcinoma as a fibrotic scar tissue mass.

107
Q

Classic clinical presentation of cholangiocarcinoma

A

Painless jaundice

108
Q

Large hepatic mass that encases (not invades) the portal vein…

A

Think cholangiocarcinoma

Note: HCC is more likely to invade the portal vein.

109
Q

Does cholangiocarcinoma have a tumor capsule?

A

No

110
Q

Klatskin tumor

A

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

Note: These can cause biliary obstruction even when very small.

111
Q

What staging system is used to classify Klatskin tumors?

A

Bismuth-Corlette system

112
Q

What does atrophy of a hepatic lobe suggest in the setting of cholangiocarcioma?

A

Biliary and/or vascular involvement of that lobe

Note: Imaging often underestimates disease burden. Look for these secondary signs of involvement.

113
Q

What factors make a klatskin tumor less likely to be resectable?

A
  • Proximal extent (extending deeper into the peripheral liver)
  • Bilateral involvement (involving both the left and right hepatic ducts)
114
Q

Elevated CEA and CA 19-9…

A

Think cholagniocarcinoma

115
Q

Elevated CA 19-9 with normal CEA…

A

Think pancreatic cancer

116
Q

Elevated CEA with normal CA 19-9…

A

Think colon cancer

117
Q

Risk factor for hepatic angiosarcoma

A
  • Arsenic exposure
  • Polyvinyl chloride exposure
  • Radiation
  • Thorotrast exposure (history of time spent in Nazi Germany)
  • Hemochromatosis
  • NF1
118
Q

What is the most common hepatic sarcoma?

A

Hepatic angiosarcoma (still extremely rare)

119
Q

Imaging appearance of hepatic angiosarcoma

A
  • Usually multifocal
  • Propensity to bleed
120
Q

Differential for a hepatic mass with hemorrhage

A
  • Hepatic adenoma
  • Hepatocellular carcinoma
  • Hepatic angiosarcoma (rare)
121
Q
A

Multilocular cystic lesion in the liver, possible biliary cystadenoma

Note: No reliable method to distinguish from biliary cystadenocarcinoma.

122
Q

Multilocular cyst in the liver with a nodular enhancing solid component…

A

Think biliary cystadenocarcinoma

Note: An enhancing nodular solid component is the best way to distinguish this from a regular biliary cystadenoma.

123
Q

Most common primary cancer to result in liver metastases

A

Colon cancer

124
Q

Most common malignant mass in the liver

A

Metastasis (20-40x more common than a primary liver cancer)

125
Q

What primaries are most common if you see calcified liver metastases?

A

Mucinous neoplasms:

  • Colon
  • Ovary
  • Pancreas
126
Q

What primaries are likely if you see hyperechoic liver metastases?

A

Think hypervacsular metastases:

  • Renal
  • Melanoma
  • Carcinoid
  • Choriocarcinoma
  • Thyroid
  • Islet cell
127
Q

What primaries are likely if you see hypoechoic liver metastases?

A

Think hypovascular metastases:

  • Colon
  • Lung
  • Pancreas

Note: Liver mets are more commonly hypoechoic than hyperechoic.

128
Q

Multiple hyperechoic hepatic masses with hypoechoic halos…

A

Think hepatic metastases (with halos of fat-spared liver)

129
Q

Hypotenuse liver masses with a continuous rim of enhancement…

A

Think liver metastases

Note: Hematic hemangiomas usually have a discontinuous rim on enhancement.

130
Q

Why might hepatic metastases appear hyperdense on CT?

A

Hepatic metastases are usually hypodense, but can appear hyperdense if there is a background of fatty liver (hypodense liver parenchyma)

131
Q

Pt has breast cancer and multiple hepatic hypodensities that are too small to further characterize…

A

Hepatic lesions that are too small to further characterize are still likely to be benign (90-95%) even in the setting of known malignancy (without definite hepatic mets)

132
Q

Can lymphoma involve the liver?

A

Yes, Hodgkins lymphoma involves the liver 60% of the time and non-Hodgkins involves the liver 50% of the time

133
Q

Imaging appearance of hepatic Kaposi sarcoma

A

AIDS pt with diffuse periportal hypoechoic infiltration (appears similar to biliary duct dilatation)

134
Q

What ultrasound features suggest that a hepatic cyst might be something else (e.g. hydatid cyst)?

A
  • Cyst larger than 2 cm
  • Presence of membranes
  • Abundant sediment in the cyst
135
Q

What ultrasound features suggest that what looks like a hepatic hemangioma might be something else?

A

Internal flow on color Doppler

Note: Hemangiomas can have peripheral flow, but should now have internal flow.

136
Q

Liver ultrasound

A

Think FNH

Note: This is the “spoke wheel” appearance of vascularity on Doppler.

137
Q

Ultrasound features of FNH

A
  • Difficult to see (isoechoic to liver)
  • Look for bulging of the liver
  • Central scar
  • Spoke wheel appearance on doppler (vessels radiating out from a central point)
138
Q

Classic ultrasound appearance of hepatic adenomas

A
  • Round mass with well-defined borders and a hypoechoic halo of fatty sparing
  • Peripheral flow on color Doppler (sometimes)

Note: Ultrasound appearance is highly variable due to the possibility of hemorrhage, fat, calcification, necrosis, etc.

139
Q

Classic ultrasound appearance of HCC

A
  • Cirrhotic liver contour (huge hint)
  • Lots of internal and/or peripheral vascularity (not in the spoke wheel configuration seen in FNH)
  • Thin peripheral hypoechoic halo (due to a fibrous capsule)
140
Q

How does FNH appear on delayed eovist MRI sequence?

A

Bright

Note: HCC (other than well-differentiated HCC) will appear dark on this sequence due to loss of functional contrast uptake.

141
Q

Which benign hepatic lesion classically contains microscopic fat (signal drop on in/out of phase imaging)

A

Hepatic adenoma

Note: Hepatic angiomyolipomas also usually contain microscopic fat, but usually have macroscopic fat also.

142
Q

Hepatic mass with macroscopic fat on CT…

A

Think hepatic angiomyolipoma

Note: 50% of hepatic angiomyolipomas do not have macroscopic fat.

143
Q

Hepatic angiomyolipomas are associated with…

A

Tuberous sclerosis

Note: This association isn’t as strong as it is for renal angiomyolipomas.

144
Q

Follow up for an incidental liver mass that homogeneously enhances on arterial or portal phase imaging

A

MRI (if >1.5 cm OR high risk pt: alcohol use, sex work, IV drug user, known cancer)

No follow up (if <1.5 cm AND low risk pt)

145
Q

Which cystic kidney disease is also associated with hepatic cysts?

A

Autosomal dominant polycystic kidney disease

Note: Autosomal recessive polycystic kidney disease is more often associated with hepatic fibrosis.

146
Q

Multiple AVMs in the liver and lungs with cirrhosis and a massively dilated hepatic artery…

A

Think hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu)

147
Q
A

Think hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu)

Note: Multiple liver and lung AVMs.

148
Q

Multiple hepatic AVMs in a pt with a brain abscess…

A

Think hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu)

Note: The pulmonary AVMs also seen in this condition predispose to brain abscesses.

149
Q
A

Think liver edema (e.g. hepatitis)

Note: This is the “starry sky” appearance due to prominence of the periportal fat against a background of hypoechoic liver.

150
Q

Hepatic cyst containing gas…

A

Hepatic abscess

151
Q

Classic cause of a single hepatic pyogenic abscess

A

Klebsiella

152
Q

Classic cause of multiple hepatic pyogenic abscesses

A

E. coli

153
Q

Classic ultrasound appearance of viral hepatitis

A

Starry sky (hypoechoic liver edema with bright spots of periportal fat)

154
Q
A

Hepatic abscess

Note: This is the “double target” sign with central pus, peripheral hyperdense capsule, and surrounding hypodense edema.

155
Q

What is the most common location for a hydatid cyst?

A

Liver (76%)

Note: Lung is the second most common (15%) followed by spleen (5%).

156
Q
A

Hydatid cyst (Echinococcus infection)

Note: This is the “water Lilly” sign.

157
Q
A

Hydatid cyst (Echinococcus infection)

Note: Daughter cysts within the cyst.

158
Q

Treatment of hydatid cyst

A

Surgical resection (usually)

159
Q

Treatment for amebic abscess in the left hepatic lobe

A

Emergent drainage (these can rupture into the pericardium)

160
Q
A

Hepatic Schistosomiasis infection

Note: This is the “tortoise shell” appearance of the liver.

161
Q

RUQ pain with history of pelvic inflammatory disease…

A

Fitz-Hugh-Curtis syndrome

Note: PID and right upper quadrant pain with enhancement of the liver capsule.

162
Q

Focal fatty liver is most common in what locations?

A
  • Next to the gallbladder
  • Next to ligamentum theres (falciform ligament)
163
Q

CT criteria for hepatic steatosis

A
  • 40 HU or less
  • More than 10 HU less than the spleen (on contrast enhanced CT)
164
Q

US criteria for hepatic steatosis

A

Liver is hyperechoic to kidney

165
Q

MRI criteria for hepatic steatosis

A

Signal dropout on out of phase imaging (by 2 standard deviations)

Note: Signal dropout will be maximal if there is 50% fat infiltration, if there is more infiltration than 50% the signal dropout will actually be less.

166
Q
A

Hemochromatosis

Note: Liver is T2 hypointense relative to muscle. Normally liver should always be T2 hyperintense relative to muscle.

167
Q

Which MRI sequence has the India ink artifact?

A

Out of phase imaging

168
Q
A

Hemochromatosis

Note: Liver appears more hypointense on in phase imaging than out of phase imaging (this is the opposite of the signal dropout seen with microscopic fat).

169
Q

Liver is T2 hypointense relative to muscle and the spleen is absent…

A

Think secondary hemochromatosis secondary to chronic hemolytic anemia

Note: The spleen is often surgically removed in the setting of chronic hemolytic anemia.

170
Q

How can you differentiate primary vs secondary hemochromatosis on imaging?

A

Primary hemochromatosis tends to involve the pancreas and spare the spleen

Secondary hemochromatosis tends to involve the spleen and spare the pancreas

Note: Pancreas = primary and spleen = secondary.

171
Q

What are the major causes of hemochromatosis?

A
  • Primary (genetically inherited)
  • Secondary (acquired due to chronic illness and/or multiple transfusions)
172
Q

Budd-Chiari syndrome

A

Abdominal pain, ascites, and hepatomegaly secondary to hepatic vein thrombosis (more acute) or hepatic vein fibrosis (more chronic)

173
Q

Risk factors for Budd-Chiari syndrome

A

Any hyper coagulable state (classically pregnancy)

174
Q

Classic imaging findings of Budd-Chiari syndrome

A
  • Thrombosed hepatic veins
  • “flip-flop” pattern of enhancement in acute phase (delayed peripheral enhancement and central hepatic hypodensity)
  • Nutmeg liver (inhomogenous mottled appearance)
  • Hypertrophy of the caudate lobe (which has its own veinous drainage to the IVC)
175
Q

What part of the liver hypertrophies in the setting of Budd-Chiari syndrome

A

The caudate lobe

Note: This is because it has its own veinous drainage to the IVC that wouldn’t be affected by hepatic vein thrombosis.

176
Q

“flip-flop” appearance of liver enhancement

A

Delayed enhancement of the peripheral liver resulting in peripheral enhancement with central hypodensity due to washout on portal veinous images. On arterial images this will be flip-flopped (central enhancement with peripheral hypodensity).

Note: This is classically seen in Budd-Chiari syndrome (hepatic vein thrombosis).

177
Q
A

Nutmeg liver

Note: This is a perfusion abnormality, usually due to hepatic venous congestion (e.g. Budd-Chiari).

178
Q

Differential for nutmeg liver

A
  • Budd-Chiari (hepatic vein thrombosis)
  • Hepatic veno-occlusive disease
  • Hepatic congestion secondary to right heart failure
  • Hepatic congestion secondary to constrictive pericarditis
179
Q

How can you differentiate regenerative hyper plastic liver nodules from multifocal HCC?

A

T2 imaging (regenerative nodules are usually T2 dark/iso and HCC is usually T2 bright)

180
Q

Classic clinical presentation of acute Budd-Chiari due to hepatic vein or IVC thrombus

A

Rapid-onset ascites

181
Q

Differential for massive caudate lobe hypertrophy

A
  • Budd-chiari Syndrome (hepatic vein thrombosis)
  • Primar sclerosing cholangitis
  • Primary biliary cirrhosis
182
Q

Hepatic veno-occlusive disease

A

A form of Budd-Chiari that occurs due to occlusion of small hepatic venules

Note: The main hepatic veins and IVC will be patent, but portal waveforms will be abnormal (slow, reversed, to to-and-fro).

183
Q

Common causes of hepatic veno-occlusive disease

A
  • Alkaloid bush tea (common in Jamaica)
  • Radiation/chemotherapy
184
Q

Nutmeg liver, contrast reflux into hepatic veins, and increased portal veinous pulsatility…

A

Think passive hepatic congestions secondary to right heart failure or constrictive pericarditis

185
Q

Portal vein thrombosis with cavernous transformation…

A

Cavernous transformation (many serpiginous vessels in the porta hepatis) indicates that the portal vein thrombosis is chronic (at least 12 months old)

186
Q

History of metastatic breast cancer s/p treatment

A

Hepatic pseudocirrhosis

Note: Treated breast cancer metastases to the liver can give a cirrhotic appearance (multifocal liver retraction, caudate lobe hypertrophy).

187
Q

Cryptogenic cirrhosis

A

Cirrhosis without a known cause (most are thought to be due to nonalcoholic fatty liver disease)

188
Q

What is the most common disease requiring liver transplant?

A

Hepatitis C (followed by EtOH liver disease and cryptogenic cirrhosis)

189
Q

Which vessels are anastomosed during liver transplant?

A
  • IVC
  • Hepatic artery
  • Portal vein
  • CBD
190
Q

Which segments of the liver are most commonly transplanted?

A

Right lobe (segments 5-8) in adults

Note: In pediatric pts, segments 2-3 are usually transplanted.

191
Q

Common contraindications to liver transplant

A
  • Extrahepatic malignancy
  • Advanced cardiac disease
  • Advanced pulmonary disease
  • Active substance abuse

Note: Portal hypertension is not a true contraindication, but does increase surgery difficulty and postoperative mortality.

192
Q

What are the normal ultrasound findings for a liver transplant?

A
  • Rapid systolic upstroke (diastolic to systolic in less than 80 msec)
  • Resistive index 0.5-0.7
  • Hepatic artery peak velocity < 200 cm/sec
193
Q

What should the hepatic artery peak velocity be in healthy liver transplants?

A

<200 cm/sec

194
Q

What should the resistive index be in healthy liver transplants?

A

0.5-0.7

195
Q

How fast should the systolic upstroke be in healthy liver transplants?

A

Rapid (diastolic to systolic in less than 80 msec/0.08 sec)

196
Q

What is the ultrasound sequence in the syndrome of impending thrombosis for liver transplants?

A

Over the 3-10 days post transplant:

  1. Initial normal waveform
  2. No diastolic flow
  3. Dampening of systolic flow (trades parvus, resistive index < 0.5)
  4. Loss of hepatic waveform
197
Q

What percentage of hepatic blood flow comes from the portal vein?

A

70%

198
Q

What is the most important vessel in liver transplants?

A

The hepatic artery (primary source of blood flow to the bile ducts)

Note: This is counterintuitive because normally the liver gets 70% of its blood flow from the portal vein.

199
Q

When does ehpatic artery thrombosis tend to occur s/o liver transplant?

A
  • Early (<15 days post op)
  • Late (years later, usually due to chronic rejection or sepsis)
200
Q

Is trades parvus of a transplanted hepatic artery more likely to be secondary to stenosis or thrombosis?

A

Tardus parvus is more likely secondary to stenosis

201
Q
A

Think pneumobilia when gas is more central in the liver

Note: Bile ducts drain towards the porta hepatis.

202
Q
A

Think portal venous gas when gas is more peripheral in the liver (within 2 cm of the liver capsule)

Note: Portal veins drain towards the periphery.

203
Q

When should you consider branching air in the liver to be portal venous gas?

A

When it is peripheral (within 2cm of the liver capsule)

204
Q

Common causes of pneumobilia

A
  • Recent biliary instrumentation
  • Anything that messes up the sphincter of Oddi (e.g. sphincterotomy)
205
Q

Common causes of portal venous gas

A
  • Bowel necrosis (look for pneumatosis)
  • COPD
206
Q

Jaundice, fever, and right upper quadrant pain…

A

Think bacterial cholangitis

207
Q

Does primary sclerosis cholagnitis recur in pts s/o liver transplant?

A

Sometimes (20% of cases)

208
Q

Cirrhotic liver with dilated intrahepatic bile ducts…

A

Think primary sclerosing cholangitis

Note: Intrahepatic bile duct dilatation is rare in other forms of cirrhosis due to the squeezing pathophysiology.

209
Q

MRCP

A

Think primary sclerosing cholangitis

Note: This is the “withered tree” appearance due to multifocal intrahepatic strictures.

210
Q

MRCP

A

Think primary sclerosis cholangitis

Note: This is the “beaded” appearance of intrahepatic bile ducts due to multifocal strictures and dilated segments.

211
Q

Primary sclerosing cholangitis

A

Idiopathic disease characterized by progressive inflammation leading to multifocal strictures of the intrahepatic and/or extra hepatic bile ducts

Note: These pts are at high risk for cholangiocarcinoma.

212
Q

AIDS pt

A

AIDS cholangiopathy

Note: This is an infection of the biliary epithelium (classically Cryptosporidium) that leads to multifocal bile duct strictures similar to primary sclerosis cholagnitis.

213
Q

Differential for multifocal bile duct strictures

A
  • Primary sclerosing cholangitis
  • AIDS cholangiopathy
  • Chemotherapy-induced cholangitis
  • Recurrent pyogenic cholangitis (look for multiple pigmented stones)
214
Q

Multifocal bile duct strictures and papillary stenosis…

A

Think AIDS cholangiopathy

Note: Papillary stenosis = sphincter of Odd dysfunction.

215
Q

How do bile duct strictures differ in primary sclerosing cholangitis and AIDS cholangiopathy?

A

Extra hepatic bile duct strictures are rarely >5 mm in PSC, but often >2 cm in AIDS

Saccular deformities of the ducts are common in PSB but rare in AIDS

216
Q

Where is recurrent pyogenic cholangitis common?

A

Southeast Asia

217
Q

Multifocal intrahepatic bile duct dilatation containing multiple pigmented stones…

A

Think recurrent pyogenic cholangitis

218
Q

Which hepatic lobe is more often involved in recurrent pyogenic cholangitis?

A

Left hepatic lobe

Note: This is because the biliary system is longer and flatter on the left (opposite of hematogenous processes, which prefer the right lobe).

219
Q

Primary biliary cirrhosis

A

An autoimmune disease that results in destruction of the small and medium bile ducts resulting in progressive irregular dilatation of the intrahepatic bile ducts with normal extrahepatic bile ducts

Note: Early on, the bile ducts are normal.

220
Q

Pt is positive for antimitochondrial antibodies…

A

Primary biliary cirrhosis

221
Q

Pts with primary biliary cirrhosis are at an increased risk for…

A

HCC

222
Q

Treatment for primary biliary cirrhosis

A

Ursodeoxycholic acid

223
Q

Primary biliary sclerosis is most common in what pt population?

A

Middle-aged women

224
Q

Long common channel

A

An anatomic variant in which the CBD and pancreatic duct fuse prematurely (at the level of the pancreatic head rather that at the normal location, just proximal to the sphincter of Oddi)

225
Q

Pts with a long common channel are at increased risk for…

A

Pancreatitis

Note: A long common channel is premature fusion of the CBD and pancreatic duct.

226
Q

Long common channel is associated with…

A

Type 1 choledochal cysts (focal dilatation of the CBD)

227
Q

Todani classification of choledochal cysts

A
  • 1 (focal CBD dilatation)
  • 2 (CBD diverticulum)
  • 3 (choledochocele)
  • 4 (both intra and extra hepatic dilatation)
  • 5 (intrahepatic only, AKA Caroli’s)
228
Q
A

Caroli’s disease

Note: Large, saccular intrahepatic bile duct dilatation WITH “central dot sign” (portal vein surrounded by dilated bile ducts).

229
Q

What does the “central dot sign” represent in Caroli’s disease?

A

Portal veins (surrounded by dilated bile ducts)

230
Q

Inheritence pattern of Caroli’s disease

A

Autosomal recessive

231
Q

Caroli’s disease is associated with…

A
  • Polycystic kidney disease
  • Medullary sponge kidney
232
Q

Complications of Caroli’s disease

A

Cholestasis:

  • Cholangiocarcinoma
  • Cirrhosis
  • Cholangitis
  • Intraductal stones
233
Q

Primary sclerosing cholangitis is associated with…

A
  • Ulcerative colitis (80%)
  • Crohns (20%)
234
Q

How can you tell the difference between bile duct strictures due to cholagniocarcinoma vs benign causes (e.g. sclerosing cholangitis)?

A

Cholangiocarcinoma tends to produce long strictures with shouldering

Benign strictures tend to be abrupt and short

Core (98 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions