3. GI (Biliary)

Question 1

Commonest cause of jaundice

Answer 1

Benign stricture (post traumatic from surgery or biliary intervention)

Question 2

Bacterial cholangitis (2)

Answer 2

Hepatic abscess can develop due to cholangitis, usually due to stasis (stones).
Triad of Jaundice, Fever, RUQ pain.

Question 3

Primary sclerosing cholangitis (7)

Answer 3

Chronic cholestatic liver disease of unknown aetiology.
Characterised by progressive inflammation, leading to multifocal strictures of the intra-and extrahepatic ducts.
Often results in cirrhosis.
Strongly associated with cholangiocarcinoma.
Buzzword for cirrhotic pattern is “central regenerative hypertrophy”.
Associated with inflammatoy bowel disease (UC 80%).
Indication for transplant, with post transplant recurrence of 20%.

Question 4

AIDS cholangiopathy

Answer 4

Infection of the biliary epithelium (classically cryptosporidium) can cause distal disease in AIDS patients.
Mimics PSC with intra and extrahepatic multifocal strictures.
Associated with papillary stenosis in 60%

Question 5

AIDS cholangiopathy vs PSC (3)

Answer 5

Focal strictures of the extra-hepatic duct >2cm vs extrahepatic strictures rarely >5mm
Absent saccular deformities of the ducts vs Saccular deformities of the ducts.
Associated papillary stenosis.

Question 6

Oriental cholangitis (5)

Answer 6

aka recurrent pyogenic cholangitis.
Common in southeast asia (hence the name).
Dilated ducts, full of pigmented stones.
“Straight rigid intrahepatic ducts”
Cause unknown, may be associated with clonorchiasis, ascariasis and nutritional deficiency.
Don’t do well with endoscopic decompression, often need surgical decompression.

Question 7

PBC (6)

Answer 7

Autoimmune disease resulting in destruction of small and medium intrahepatic ducts.
Mainly affects middle aged women, often asymptomatic.
Early stages, normal bile ducts help distinguish it from PSC.
Later stages, irregular dilatation of the intrahepatic ducts, with normal extrahepatic ducts.
Increased risk of HCC.
Excellent prognosis if caught early, responds to medical therapy with ursodeoxycholic acid.
Antimitochondrial antibodies positive in 95%.

Question 8

Choledochal cysts/Caroli’s (7)

Answer 8

Congenital dilatation of bile ducts.
Type 1 is focal dilatation of CBD, by far most common (4 other types).
Type 2 is diverticulum of bile duct.
Type 3 is a choledococele.
Type 4 is both intra and extra.
Type 5 is Caroli’s and is intrahepatic only.
- AR disease, associated with polycystic kidney disease and medullary sponge kidney
- Intrahepatic duct dilatation, large and saccular.
- Central dot sign - portal vein surrounded by bile ducts.
Dilated bile ducts and hx of repeated cholangitis, think choledocal cyst.

Question 9

Complication of Choledochal cysts (4)

Answer 9

Cholangiocarcinoma
Cirrhosis
Cholangitis
Intraductal stones

Question 10

Normal gallbladder (4)

Answer 10

Inferior to interlobar fissure, between right and left lobe.
Size depends on recent eating, but should be <4x10cm.
Wall thickness should be <3mm.
Lumen should be anechoic

Question 11

Phyringian cap

Answer 11

GB folds on itself. No clinical significance (anatomic variant).

Question 12

Intrahepatic gallbladder.

Answer 12

Most found right above the interlobar fissure

Question 13

Duplicated gallbladder

Answer 13

Can happen, not much clinical significance

Question 14

Duct of Luschka (3)

Answer 14

Accessory cystic duct.
Can cause big problem (persistent bile leak) after cholecystectomy.
Several subtypes, not likely to be tested

Question 15

Wall thickening (2)

Answer 15

Non-specific, can be due to biliary (cholecystitis, AIDS or PSC) or non-biliary (hepatitis, heart failure, cirrhosis)

Question 16

Gallstones (3)

Answer 16

Found in 10% of asymptomatic patients.
Most (75%) cholesterol, other 25% are pigmented.
They cast shadows, unless <3mm in size

Question 17

Wall Echo Shadow GB (3)

Answer 17

Can occur for 3 reasons.
1) GB full of stones (clean shadowing)
2) Porcelain gallbladder (variable shadowing)
3) Emphysematous cholecystitis (dirty shadowing)

Question 18

Porcelain gallbladder (3)

Answer 18

Extensive wall calcification.
Increased risk of GB cancer.
Surgically removed.

Question 19

GB polyps (6)

Answer 19

Cholesterol (most common) or non-cholesterol (adenomas/papillomas).
Cholesterol ones aren’t real polyps, but essentially enlarged papillary fronds full of lipid filled macrophages, attached to wall by stalk.
Non-cholesterol polyps are almost always solitary and usually larger.
Larger ones may have doppler flow. NOT mobile and NO shadow.
Surgically removed if >1cm.

Question 20

Adenomyomatosis (6)

Answer 20

Due to hyperplasia of wall with formation of intramural diverticula (Rokitansky-Aschoff sinuses), which penetrate into the wall of the gallbladder.
These become filled with cholesterol crystals, which show as “comet tail artefact” - highly specific for adenomyomatosis.
3 types
- Generalised (diffuse)
- Segmental (annular)
- Fundal (localized or adenomyoma), cannot be differentiated from GB cancer.

Question 21

GB adenomyomatosis vs cholesterolosis (4)

Answer 21

Both benign.
Gallbladder adenomyomatosis - hypertrophied mucosal and muscularis propria, with cholesterol crystals deposited in an intraluminal location (within Rokitansky-Aschoff sinuses)
Cholesterolosis - Cholesterol and triglyceride deposition within the substance of the lamina propria, associated with formation of cholesterol polyps

Question 22

Gallbladder cancer (2)

Answer 22

Most GB cancers are associated with gallstones.
80% have direct tumour invasion of the liver or portal nodes at time of diagnosis.

Question 23

Mirizzi syndrome (5)

Answer 23

Occurs when common hepatic duct is obstructed due to impacted cystic duct stone.
Stone can eventially erode into CHD ot GI tract.
Increased co-incidence of gallbladder Ca (5x risk) with Mirizzi.
Mirizzi occurs more in people with low cystic duct insertion (normal variant), allowing for more parallel course and closer proximity to the CHD.

Question 24

Liver Doppler - terminology (2)

Answer 24

Duplex means colour
Spectral means colour with a waveform

Question 25

Arterial resistance (4)

Answer 25

Some organs require continuous flow (brain), whereas others don’t (muscles).
The body alters flow to organs accordingly to save energy.
When an organ needs to be “on”, the arteriolar bed dilates, waveform becomes low resistance.
Opposite happens to become high resistance at other times.
Resistive Index (peak velocity minus trough velocity divided by peak velocity) is used to quantify this.

Question 26

Resistive index for liver doppler (6)

Answer 26

Normal RI for liver is 0.5-0.7
If RI >0.7 is non-specific in itself, can be due to postprandial state, advanced age or diffuse distal microvascular disease.
If RI <0.5, due to proximal stenosis or distal vascular shunting.
Commonest cause of shunting is arteriovenous or arterioportal fistulas in severe cirrhosis.
Other causes include trauma (iatrogenic injury from biopsy) or Osler-Weber-Rendu syndrome.

Question 26

Tardus parvus (5)

Answer 26

Tardus - slowed systolic upstroke
- Can be measured by accelleration time, the time from end diastole to first systolic peak
- Acceleration time >0.07 seconds correlates with >50% stenosis of renal artery.
Parvus
- Decreased systolic velocity
- Measured by calculating accelleration index, change in velocity from end diastole to first systolic peak
- Acceleration index <3m/s correlates with >50% stenosis of renal artery.

Question 27

Causes of low RI (6)

Answer 27

Proximal arterial narrowing
- Atherosclerosis (Coeliac or Hepatic)
- Stenosis at an anastomosis (transplant)
- Median arcuate ligament compression (severe)
Peripheral vascular shunts
- Shunting in cirrhosis
- Post traumatic (liver biopsy)
- Osler-Weber-Rendu

Question 28

Causes of high RI (5)

Answer 28

Post prandial
Age
Cirrhosis
Hepatic congestion (acute or chronic)
Transplant rejection

Question 29

Cirrhosis and RI (3)

Answer 29

Shints that develop decrease RI
However, the fibrosis that develops increases RI.
As a result, RI is useless to diagnose or assess severity of cirrhosis.

Question 30

Stenosis terminology (2)

Answer 30

Upstream: Blood not yet passed through the stenosis
Downstream: Blood that has passed stenosis.

Question 31

Signs of stenosis (5)

Answer 31

Direct
- Found at the stenosis itself
- Include elevated peak systolic velocity and spectral broadening (immediately post stenosis)
Indirect
- Tardus parvus (downstream), time to peak <70ms.
- RI downstream will be low (<0.5) because liver is starved for blood.
- RI upstream will be elevated (>0.7) because blood needs to overcome area of stenosis.

Question 32

Hepatic veins - doppler (6)

Answer 32

Flow in hepatic veins is complex, alternating forward and backward flow.
Bulk of flow should be antegrade (liver to heart).
Things that alter waveform include:
- Pressure changes in the right heart (transmitted to hepatic veins) e.g. CHF, tricuspid regurg
- Compression of veins directly (cirrhosis).
Anything increasing right atrial pressure (atrial contraction) will cause the wave to slope upward.
Anything that decreases right atrial pressure will cause the wave to slope downward.

Question 33

Abnormal hepatic vein waveforms (5)

Answer 33

1) More pulsatile
- Tricuspid regurg
- Right sided CHF
2) Less pulsatile
- Cirrhosis
- Hepatic venous outflow obstruction (any cause)
3) Absent
- Budd Chiari

Question 34

Tricuspid regurg vs right sided CHF (2)

Answer 34

Tricuspid regurg has deeper D wave than S
Right heart failure has S deeper than D

Question 35

Portal vein doppler (4)

Answer 35

Flow should always be antegrade (towards liver).
Some normal cardiac variability from hepatic venous pulsatility transmitted through the hepatic sinusoids.
Velocity in the normal portal vein is between 20-40cm/s.
Waveform should be gentle undulation, always remaining above baseline.

Question 36

Patterns of portal vein doppler (3)

Answer 36

Normal (always positive).
Pulsatile (still always positive)
Reversed (always negative)

Question 37

Causes of portal vein pulsatility (3)

Answer 37

Right CHF
Tricuspid regurg
Cirrhosis with vascular AP shunting

Question 38

Causes of portal vein reversed flow

Answer 38

Portal HTN (any cause)

Question 39

Causes of absent flow in portal vein (2)

Answer 39

Can be considered a 4th pattern.
Seen in thrombosis, tumour invasion and stagnant flow from terrible portal HTN

Question 40

Slow flow in portal vein - causes (5)

Answer 40

Velocity <15 cm/s.
Portal HTN is commonest.
Others include
Pre-hepatic - portal vein thrombosis
Intrahepatic - cirrhosis (any cause)
Post hepatic - Right CHF, tricuspid regurg, Budd-chiari

Question 41

Doppler trivia

Answer 41

Angle should be less than 60 degrees.