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KB-GI radiology > Biliary > Flashcards

Biliary Flashcards

1
Q

56yo male has an abnormal GB identified on a CT scan. What is the approx. likelihood that he will develop GB carcinoma?

A
  • <20%.
  • Porcelain GB, w/o soft tissue thickening.
  • Low risk of GB carcinoma unless there are other associated findings, e.g., a soft tissue density mass.
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2
Q

This patient had abdominal pain + fever & a gallstone that was seen on US.

What is the name of this sign?

Dx?

A
  • Rim sign: hyperenhancement of the liver adjacent to a thickened, inflamed GB wall (transmural GB inflammation).
  • Dx: acute chole.
  • This attenuation difference is different from THAD:
    • THAD is usually small, wedge-shaped and subcapsular.
    • In this case, the hyperperfused area abuts the GB only.
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3
Q

34yo female w/abdo pain + fever, but negative Murphy.

A

Dx: gangrenous chole.

  • Laminated, discontinuous, markedly thickened GB wall.
  • Adjacent ascites, extensive inflammation & absent Murphy add weight to the Dx.
  • RUQ tenderness is absent due to destruction of the nerves in the GB wall by the transmural severe inflammation.
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4
Q

This gallstone is in the duodenum.

  1. What is the name of this syndrome?
  2. If the gallstone travels through the small bowel, what can occur?
A
  1. Bouveret syndrome.
  2. Gallstone ileus.
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5
Q

Dx?

A

Caroli syndrome.

  • At least one “central dot” sign & dysmorphic/fibrotic liver from repeated cycles of inflammation/infection.
  • Caroli syndrome = Caroli disease + hepatic fibrosis.
  • This pt had a RLQ renal xplant b/c they had ARPCKD, which gives a spectrum of abnormalities resulting in variable degrees of fibrosis & cystic anomalies of the liver & kidney.
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6
Q

Dilated ducts Dx

Dx?

  1. How to differentiate b/w choledocholithiasis and an ampullary mass (cholangio)?
A
  • Dx: extrahepatic, ampullary cholangio.
  • For a mass: enhancing, eccentric.
    • More often will have marked duct dilation (like this) and jaundice.
    • Will not obstruct the pancreatic duct.
  • For a stone: not enhancing, shadowing, central.
    • May have any attenuation on CT.
    • Will have signal voids on MRCP.
    • Most will show GB stones.
    • Less common to have marked duct dilation or jaundice.
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7
Q

Biliary MR

  • Sequence type normally used for MRCP.
  • Optimal T2 time for MRCP.
  • Advantages over ERCP-3.
  • Disadvantages compared to ERCP-3
  • Effect of Eovist (gadoxetic acid disodium)
A
  • Fast spin echo
  • TE 80-100ms
  • Advantages of MRCP:
    • See extra-luminal findings.
    • Can see obstructed ducts.
    • Non-invasive.
  • Advantages of ERCP:
    • Intervention if required.
    • Can actively distend biliary system w/contrast.
    • Better spatial resolution.
  • Eovist:
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8
Q

DDx cystic hepatic lesion

A
  • Benign:
    • Simple cyst
    • von Meyenberg
    • biliary cystadenoma
    • Caroli
  • Neoplastic:
    • biliary cystadenocarcinoma
    • cystic, necrotic met
  • Infectious:
    • abscess
    • echinococcal cyst
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9
Q

Choledochal cysts

  • List the different types.
  • When are most diagnosed?
  • Typical Tx & rationale.
  • Most common type & prevalence.
  • Association w/type V/Caroli.
    • Defn Caroli syndrome.
    • What forms the central dot of the central dot sign?
A
  • See types below.
  • Most diagnosed in childhood.
  • Tx: resection or choledochoenteric drainage & surveillance for cholangioca; 25% increased risk of cholangioca.
  • Most common type = type 1 (common = fusiform common bile duct dilation); prevalence = 50% of all Todanis.
  • Caroli: assoc w/polycystic kidneys.
    • Syndrome = Caroli + hepatic fibrosis.
    • Central dot = portal vein + hepatic artery, i.e., the other 2 components of the portal triad, as the biliary duct is dilated.
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10
Q

Biliary anatomical variants

  • What is the standard anatomy & prevalence.
  • Next most common variant & prevalence.
  • Problem w/low insertion of cystic duct.
  • Aberrant R posterior duct:
    • To where can this drain & prevalences?
    • Issue w/aberrant R posterior duct.
A
  • Standard anatomy: 63%
    • LHD: branches into segs 2 & 3.
    • RHD: branches into anterior & posterior.
  • Next most common variants = RP into LHD (11%) & triple confluence (RAD, RPD, LHD).
  • Low insertion: surgeon may misidentify cyst duct as common duct & ligate the CBD.
  • Aberrant R:
    • 3 anomalous connections: to LHD (11%); CHD (6%); cystic duct (2%).
    • Issue: surgeons must anastomose 2 ducts if using a R lobe liver xplant.
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11
Q

Bile duct infection/inflammation:

  • What symptom is common to the -itis conditions and not PBC?
A
  • Ascending cholangitis & PSC present w/fever, as they are inflammatory conditions, PBC does not.
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12
Q

Bile duct infection/inflammation: ascending cholangitis

Px: general cause, most common cause.

  • Other causes-3

Sx: clinical triad. Clinical pentad.

US-2

CT-2

Tx-3; prognosis.

A

Px: general = biliary tree blockage; most common cause = choledocholithiasis.

  • Others: 20% malignancy; PSC; ERCP.

Sx: Charcot’s triad (Charco = yello): jaundice, RUQ pain, fever.

  • Reynold pentad: Charcot’s triad + shock + delirium.

US: thickened bile duct walls +/- debris w/in the biliary system may be present.

CT: hyperenhancement & thickening of bile duct walls often w/a CBD stone.

Tx: initially w/Abx & fluids, & if refractory, ERCP: stone removal & sphincterotomy.

  • Prognosis: 50-90% mortality if severe, acute.
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13
Q

Bile duct infection/inflammation: PSC

Px: 1

Ex: IBD assocn; sex;

ERCP/MRCP: app; which parts of the biliary tree most affected?

How differs from HIV cholangiopathy?

Long-term complications-3

A
  • Px: idiopathic inflammation
  • Ex: assoc w/UC (the two -itis-es are together, Crohn’s doesn’t have an -itis).
    • 75% of pts w/PSC have UC.
    • Only 4-5% of UC pts have PSC.
    • More common in males.
  • ERCP/MRCP: beaded, irregular appearance of the CBD & central intrahepatic ducts.
    • Mnemonic: it’s more common in males, who are larger than females; likewise, PSC affects the larger ducts.
  • HIV cholangio: similar app, but HIV more commonly associated w/papillary stenosis.
  • Complications: cholangio, recurrent biliary infections.
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14
Q

Bile duct infection/inflammation: PBC (primary biliary cholangitis, but used to be cirrhosis)

Px: which ducts affected?

Ex: who?

Sx: common initial presentation?

Sequela?

A

Px: unlike PSC, this affects smaller ducts (women are smaller).

Ex: middle-aged women; (mnemonic: PBC; B stands for “broads”).

Sx: pruritis, but also fatigue.

Sequela: cirrhosis.

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15
Q

Bile duct infection/inflammation: AIDS cholangitis/cholangiopathy

​Px: 2 bugs involved.

Ix: common feature & unique; % of cases w/the unique feature.

A
  • Px: Cryptosporidium & CMV.
  • Ix: similar appearance to PSC, but w/papillary stenosis & upstream CBD dilation.
    • Only 50% of cases have papillary stenosis.
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16
Q

Bile duct infection/inflammation: chemoTx-induced cholangiopathy/cholangitis

Px: cause.

Ix: ducts affected/spared.

A
  • Px: caused by intra-arterial chemotherapy to treat liver mets.
  • Ix:
    • Affects: central ducts, i.e., CHD & R/L main duct.
    • Spares: the bookending ducts, i.e., CBD & peripheral intrahepatic ducts.
17
Q

Bile duct infection/inflammation: recurrent pyogenic cholangitis (Oriental cholangiohepatitis)

Px: bug involved; what does this lead to?

Ex: where?

Ix: triad.

Sequela-1

A
  • Px: Clonorchis sinensis.
    • These form pigment stones, then biliary stasis, then cholangitis.
    • The fluke acts as a nidus for stone formation.
  • Southeast Asia.
  • Ix: pneumobilia, lamellated bile duct filling defects (hyperdense to liver parenchyma), intra- & extrahepatic bile duct dilation & strictures.
    • GB calculi are usually not present.
    • Lateral L lobe often affected, & may see atrophy.
  • At risk for cholangiocarcinoma.
18
Q

Biliary neoplasia: biliary cystadenoma

Px: cell type; does it communicate w/the biliary tree?

Ex: sex?

Ix: general appearance; how to differentiate from other similar entities.

Tx:

Sequela.

A
  • Px; cystic structure lined by columnar or cuboidal cells found in biliary ducts; NO communication w/ the tree (like von Meyenburgs).
  • Like PBC, in middle-aged women.
  • Ix: large, unilocular or multilocular mass.
    • Septations may mimic an echinococcal cyst.
    • A thick, enhancing wall is not present, unlike abscess or necrotic mets.
    • If a thick calc or solid component is present, think biliary cystadenocarcinoma.
  • Tx: although benign, if resected, they can recur.
19
Q

Biliary neoplasia: cholangiocarcinoma

  • Most common type? Rarest?
    • From where in the biliary tree do these not arise?
  • What does this tumour tend to do? …and cause what 2 things?
  • RFs-7.
A
  • Most common: Klatskin; rarest: peripheral.
    • Will not arise from the GB or ampulla.
  • Tends to obstruct bile ducts, then cause ductal dilation and lobar atrophy.
  • RFs:
    • Caroli/choledochal cyst
    • choledocholithiasis more than cholelithiasis
    • cirrhosis
    • PSC
    • infections: Clonorchis sinensis; HIV, hep B/C
    • toxins: thorium dioxide: not used since the 1950s; polyvinylchloride; heavy EtOH.
    • FAP syndrome (familial adenomatous polyposis)
20
Q

Thorium dioxide:

  • This is associated w/cholangioca, but what other 2 entities as well?
A
  • HCC
  • angiosarcoma
21
Q

Biliary neoplasia: GB carcinoma

  • Px-1; major cell type.
  • Ex-1, sex.
  • Ix: 3 Ix presentations
  • 3 types of tumour spread.
  • Prognosis-2.
A
  • Due to GB inflammation–any kind.
    • 90% adenocarcinomas, 10% squams.
  • RARE! Elderly women (4:1, F:M).
  • 3 Ix appearances:
    • Common: scirrhous infiltrating mass that invades through the GB wall into the liver.
    • Uncommon: polypoid mass.
    • Rare: mural thickening.
  • Tumour spread: directly into the liver; lymphatic; hematogenous.
  • Prognosis: often poor, but small polypoid lesions may undergo curative resection.
    • 5-year survival 1-5%.
22
Q

Biliary neoplasia: GB mets

  • Ex: how common?
  • Most common met.
  • 2nd most common.
  • Ix: US, CT, MR
A
  • Rare: <5% of all GB cancers.
  • 1st: melanoma (50-70% of cases).
  • 2nd: gastric carcinoma (in Asians).
  • US: hyperechoic masses w/broad base & flow.
  • CT: enhancing polypoid masses (one or more), often w/associated mural thickening; enhancement will vary w/hypervascular vs. non-mets.
  • MR: T1 often hyper b/c of melanoma & T2 hypo.
23
Q
  • Which syndrome has a higher incidence of ampullary carcinoma?
  • Typical clinical presentation?
A
  • Gardner syndrome.
  • Painless jaundice.
24
Q

Dx?

A

Dx: type 4A choledochal cyst.

25
Q

58yo male w/several weeks of RUQ pain, clay-coloured stools & jaundice. Dx?

  • Most common presenting symptom?
  • Standard Tx?
A

Dx: ampullary carcinoma

  • Obstructive jaundice.
  • Whipple procedure: pancreaticoduodenectomy.
26
Q

Name the components of the ampulla of Vater.

A
  • The confluence of the distal CBD & main pancreatic duct.
  • Sphincter of Oddi muscle.
  • Papilla of Vater
27
Q
  1. 38yo male w/abdo pain, otherwise in good health? Dx?
  2. Mgt?
A
  1. “Balls on the wall” sign of cholesterolosis/cholesterol GB polyps.
  2. No further workup necessary; this finding is almost certainly benign.
  • Immobile & non-shadowing.
  • No assocn w/GB cancer.
28
Q
A
29
Q

What other organ may be affected in this pt?

A
  • Kidneys.
    • Can get, ADPCKD, ARPCKD, medullary sponge kidney, medullary cystic kidney.
  • Dx: Caroli disease.
    • AR
    • If large bile ducts affected then Caroli disease results.
    • If small ducts, then congenital hepatic fibrosis.
    • If both, then Caroli + congenital hepatic fibrosis = Caroli syndrome.
30
Q
A

KB-GI radiology (11 decks)

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