GI Section III: HCC progression

Question 1

How does multi-focal HCC start?

Answer 1

Hepatocyte injury = regenerative nodules = dystplastic nodules (increased size and cellularity = HCC

Question 2

How does dysplastic nodule change?

Answer 2

the nodule changes from drinking PORTAL blood to ONLY wanting ARTERIAL blood.

HCC has arterial enhancement and rapid washout

Question 3

dysplastic to HCC transformation in MRI

Answer 3

From T2 dark (regenerative) to T2 bright (HCC)

Question 4

Explain the “Nodule within nodule” in MRI

Answer 4

Central bright T2 with Dark border

– transformation to HCC

Question 5

What happens with heptatocarcinogenesis?

Answer 5

Decrease in OATP bile uptake transporter

Question 6

What is OATP bile uptake transporter?

Answer 6

moves contrast agents to the cells

Its the reason why normal liver cells look brigh ton the delayed phase when using hepatocyte specific agen..

Question 7

Whay does FNH look super bright on the delayed phase?

Answer 7

Because basically they are hypertrophied hepatocytes.

Question 8

As hepatocytes become cancer they lose function in the bile uptake transporter (moves biliary contrast agents into cells) =

Answer 8

become dark on the delayed phase.

The exception is the well differntiated HCC wich retains OATP (organic anion-tranporting polypeptides) function and is bright on the 20 minute delayed sequence.

Question 9

Answer 9

Dysplastic

Question 10

Answer 10

Regenerative

Question 11

T2 Bright with enhancement

Answer 11

HCC

Question 12

The squeezing that causes portal hypertension also squeezes out most benign liver lesions (cysts, hemangiomas), SO?

Answer 12

lesions in a cirrhotic liver should be treated with more suspicion.

Question 13

Hepatic Contrast Timing and Window

Arterial phase

PVP

Liver window:

Answer 13

Question 14

What is the moset critical phase for HCC evaluation?

Answer 14

“Late arterial phase”

Contrast = hepatic artery and portal vein

NO Contrast = hepatic veins