Hepatobiliary Flashcards

1
Q

Name of system that divides liver into multiple functional segments

A

Couinaud System

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

Cantile’s Line

A

Divides liver into functional left and right lobes. From IVC to middle of gallbladder fossa

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

MC vascular variant in the liver

A

Replaced right hepatic artery (from SMA)

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

MC biliary variant

A

Right posterior segmental into left hepatic duct

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

Bare areas of liver

A

1) bare area-superopst
2) gb fossa
3) porta hepatitis

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

What is result of injury to bare area

A

RP bleed

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

Light bulb sign

A

hemangioma

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

target sign

A

echogenic center surrounded by hypoechoic rim

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

reverse target sign

A

hypoechoic core with hyperechoic rim

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

double target sign

A

hypo center with surrounding vascular rim following by surrounding edema

  • which is silly bc a “target’ sign is hyperecho center with hypo ring.
  • aka abscess (pyogenic or amebic)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

organism of amebiasis

A

entamoeba histolytica

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

ddx amebic abscess

A
  • post treatment met
  • pyogenic abscess
  • infarct
  • hydatid cyst
  • biliary cystadenocarcindoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

organism of hydatid cysts

A

Echinococcus granulosus=MC. Echinogoccus multilocularis (alveolar)-less common but aggressive, tumor-like form.
-definitive host=dog/feox. Intermediate host=human, sheep or wild rodents.

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

MC causes pyogenic abscess

A

Klebsiella, E. Coli (multiple), SA

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

MC causes fungal abscess

A

Candida (MC), cyrptococcus, aspergillus

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

Amebiasis-mc locations

A

99% GI tract. Liver 2nd MC. Then peritoneum, pleural space, lung, pericardium, skin, brain.

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

When do you get maximum signal drop out on chemical shift?

A

50% fat, 50% water

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

Spared organs 1˚ vs 2˚ hemochromatosis

A

Primary-involves Pancreas, spleen spared (vice versa 2˚)

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

Von Meyenburg complex

A

numerous biliary hamartomas, uniform size (<15 mm)

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

flip flop pattern

A

classic acute BC imaging finding on PV phase: low attenuation centrally, high peripherally

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

Who gets nutmeg liver

A
  • budd chiari
  • hepatic veno-occlusive disease
  • right hear failure
  • constrictive pericarditis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Who gets massive caudate lobe hypertrophy?

A
  • budd chiari
  • primary sclerosis cholangitis
  • primary biliary cirrhosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

cryptogenic cirrhosis

A

unknown cause of cirrhosis. MC nonEtOH fatty liver disease

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

MC reasons for liver tx

A
  • hep C (MC)
  • EtOH liver disease
  • cryptogenic cirrhosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Difference in liver transplant btw adults and kids

A
  • adults-right lobe implanted

- kids-left lobe (little=left)

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

Liver transplant contraindications

A
  • extrahepatic malignancy
  • advanced cardiopulmonary disease
  • active substance abuse
  • PVT not a true CI but makes sx more difficult
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

MCC cirrhosis world-wide

A

Schistosomiasis

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

organism of schistosomiasis

A

Schisotoma (parasite)

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

“tortus shell/turtle back”

A

periportal fibrosis with septal and capsular calcification pathognomonic for schistosomiasis fibrosis

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

right posterior hepatic notch sign

A

focal indentation of the posteroinferior surface of the right lobe of the liver at the level of the right kidney secondary to enlargement of caudate lobe and atrophy of right lobe

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

caudate/right hepatic lobe ratio

A

> 0.75

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

Which lobe is more common in hepatic abscesses and why?

A

Right (75%) via longer right power vein (ascending hematogenous sources)

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

Definition of cirrhosis by pressure. When does variceal bleeding & ascites occur?

A

PV > HV by 6-8 mmHg. Varices + ascites at >12mmHg

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

What’s particular about collateral formation in pre-hepatic cirrhosis?

A

ABOVE diaphragm and in hepatogastric lig (to bypass obstruction)

35
Q

What happens to hepatic artery in cirrhosis?

A

Increased velocity

36
Q

Causes of THAD

A

-cirrhosis (pressure on vein first), clot, mass (dir ME or recruitment), abscess/infection (cholecystitis) (ME or “siphon effect”-hyperemia)

37
Q

“central peripheral” phenomenon

A

-increased arterial response at periphery/subcapsular liver due to (portal?) venous fibrosis/decrease bf

38
Q

why does PV reverse flow in cirrhosis (Rather than just clotting off?)

A

hepatic artery “parasitizing portosystemic decompression apparatus”

39
Q

Portal hypertensive colopathy-why more common on right?

A

Colonic venous backup/stasis. More shunts on left. Resolves after tx

40
Q

portal hypertensive gastropathy

A

-thickened wall AND UGI bleed IN ABSENCE OF VARICES

41
Q

“nodule within nodule”

A

central bright T2 nodule has T2 dark border, concerning for transformation of regenerative nodule –> HCC

42
Q

OATP-changes in HCC and exception?

A

Bile uptake transporter that decreases in HCC -HCC is hypoenhancing on delayed sequences.
*exception: well differentiated HCC retains OATP function

43
Q

liver phase timing and window

A
  • LATE arterial (20-30 s)
  • PV (60-80s)
  • hepatic venous-90 s if extra cell agent. 20 mins if biliary (45-3 hrs if Gd-BOPTA/multihance)
  • window: C= 100, W=200
44
Q

What is unique about hemangioma during US scanning?

A

Can change sonographic appearance during course of sing exam

45
Q

Caveat of biopsying hemangioma?

A

must core (FNA doesn’t get enough tissue, only blood)

46
Q

biopsy trivia for FNH

A

must hit scar (otherwise, results as normal hepatocytes)

47
Q

multiple adenomas

A
  • glycogen storage diseases (von Gierke)

- adenomatosis

48
Q

FNH vs FL HCC CENTRAL SCARS

A
  • FL HCC- T2 dark, central scar doesn’t enhance, gallium avid
  • FNH- T2 iso-hyper, central scar enhances on delays, sulfur colloid avid
49
Q

what chemotherapy agent can cause FNH

A

oxaliplatin (cry for bowel cancer)

50
Q

Portal v involvement of HCC vs CholangioCA

A
  • HCC invades

- Cholangio encases

51
Q

RFs cholangioCA

A
  • PSC-MC in West
  • recurrent pyogenic oriental cholangitis-MC in East
  • Caroli
  • hepatitis, HIV, cholangitis, Clonorchis
  • Thorotrast
52
Q

THIS vs THAT- HCC vs cholangioCA

A

-cholangioCA-encases PV, delayed enhancement, no capsule, capsular retraction, biliary dil

53
Q

surgical candidacy for cholangioCA

A

-worse if: proximal, vascular (atrophied lobe), bilateral

54
Q

RFs hepatic angiosarcoma

A

-arsenic ~25 yrs latency
-thorotrast
-polyvinyl chloride
radiation
-hemochromatosis
-NF1

55
Q

imaging of angiosarcoma

A

aggressive vascular malignancy, most often MF + splenic involvement

56
Q

Hepatic lymphoma

A

hypoechoic masses

57
Q

ultrasound of hepatic metastases

A
  • hypervasc=hyperechoic (renal, melanoma, carcinoid, chorioCA
  • hypovasc= hypoechoic (colo, lung, pancreas). MC.
  • “target sign”-echogenic center with hypo echo rim
58
Q

Hepatic kapose sarcoma

A

AIDS. periportal hypoechoic infiltration that looks similar to bd dil.

59
Q

Hemangioma at US

A
  • no doppler (slow flow)
  • can change throughout course of exam
  • hyperechoic. Atypically, “reverse target”
60
Q

incidental liver lesions-size cut off for determine next step

A

1 cm

61
Q

distance cut-off for portal venous gas

A

within 2 cm liver capsule

62
Q

MCC jaundice

A

benign stricter

63
Q

buzzword: central regenerative hypertrophy

A

cirrhotic pattern of PSC

64
Q

buzzword: withered tree

A

PSC appearance on MRI with abrupt narrowing of branches

65
Q

buzzword: beaded appearance

A

PSC strictures & focal dilations

66
Q

aids cholangiopathy-what is it, classic orgm and classic association/finding?

A
  • infection of biliary epithelium, ID app to PSC
  • Cryptosporidium
  • papillary stenosis
67
Q

this vs that: aids cholangiopathy vs PSC

A

AIDs: long segment extra hepatic strictures >2cm, no saccular deformities, papillary stenosis

68
Q

“straight rigid intrahepatic ducts”

A

recurrent pyogenic cholangitis, aka oriental cholangitis

69
Q

Recurrent pyogenic cholangitis

A
  • recurrent pyogenic choangitis MC in SE asia
  • imaging-dilated ducts (central predominant) full of pigmented stones
  • L > R (via longer flatter left biliary system.)
70
Q

Which side is “recurrent pyogenic cholangitis” dominant and why?

A

Left, long/flatter biliary system

71
Q

post transplant recurrence of PSC

A

20%

72
Q

antimitochondiral ab’s (AMA)

A

primary biliary cirrhosis

73
Q

Long common channel. Associated with which type of choledococyst?

A
  • CBD and PD unite prematurely prior to sphincter of Oddi.
  • Incr risk pancreatitis.
  • associated with type I choledococysts
74
Q

MC type of choledococyst?

A

Type 1

75
Q

What is Caroli dx associated with?

A

PKD, medullary sponge kidney, cholangioCA, recurrent cholangitis (2/2 stones), cirrhosis

76
Q

central dot sign

A

PV sure by dilated duct

77
Q

duct of luschka

A

accessory cystic duct

78
Q

mirizzi syndrome

A

duct in CD obstruction CHD

  • co-incidence of GB CA 5x incr
  • occ more commonly in people with low cystic duct insertion (normal variant)-more parallel course and pros to chd
79
Q

> 50% stenosis of renal artery- acceleration time and index cutoffs

A
  • > 0.07 s

- 3 m/s

80
Q

direct and indirect signs stenosis

A
  • direct: (+) PSV, spectral broadening

- indirect: tardes parvus, with time to peak (systolic acceleration) > 70ms. RI <0.5 (orgn starved for blood)

81
Q

gallbladder polyp mx

A

< 6 mm: No follow-up
7-9 mm: Yearly US follow-up to monitor size
> 10 mm: Surgical consult

82
Q

causes of hepatic retraction

A
  • hepatic epithelioid hemangioendothelioma
  • mets
  • intrahepatic cholangioCA
83
Q

ct evaluation of cirrhosis

A
  • widened hepatic fissures
  • segmental atrophy/HTr
  • sg’s of portal HTN
  • hepatic surface nodularity (least reliable)