GI Section III: Dialogue of the Liver

Question 1

Hepatocyte injury can occur from a variety of causes including

Answer 1

Viruses
Alcohol
Toxins (alfatoxins - peanut fungus)
Non alcoholic fatty liver disease

Question 2

Hepatocyte injury = increased __?

Answer 2

Liver cell turnover = regenerative nodules

Question 3

In addition to activation of hepatocytes, what becomes active after hepatocyte injury?

Answer 3

Stellate cells living in the space of Disse become active and proliferate

Question 4

Stellate cells can change into a what type of cell after activation of hepatocyte?

Answer 4

Myofibroblast like cell that produces collagen

Question 5

myofribroblast-like cell produces collagen

collagen deposition causes?

Answer 5

fibrosis

Question 6

what does fibrosis do on the right portal vein?

Answer 6

Squeezes it (which usually has a longer intrahepatic course)

Causes atrophy of S6/7 and hypertrophy of the S1 S2 and S3.

Question 7

What is the caudate/right lobe ratio?

Answer 7

C/RL > 0.75 is 99% specific to call cirrhosis

Question 8

Whats the consequence of the Long right portal vein course?

Answer 8

Hepatic Abscess (often from ascening hematogeneous sourse) nearly always (75%) involves teh right hepatic lobe

Question 9

Morphologic changes of cirrhosis

Answer 9

Question 10

Hepatocyte turnover = Myofibroblast like cell producing collagen = fibrosis = squeezes the portal vein = ?

Answer 10

Portal hypertension

Question 11

the result of increased hepatic resistance

Answer 11

Portal hypertension

Question 12

Portal hypertension causes

Answer 12

1. Prehepatic (PV thrombosis, tumor compression)
2. Hepatic (cirrhosis, schistosomiasis)
3. Port hepatic (Budd-chiari - obstruction of the normal venous flow)

Question 13

What happens when portal venous pressure exceeds hepatic venous pressure?

Answer 13

When it exceeds by 6-8 mmHG = portal hypertension (variceal bleeding + ascites around > 12)

Question 14

What happens with portal hypertension? and why?

Answer 14

collaterals form to decompress the liver from carrying blood away from it = ESOPHAGEAL and GASTRIC VARICES

Question 15

Why do collaterals form above the diaphragm and in teh hepatogastric ligaments in PRE-hepatic portal hypertension?

Answer 15

to bypass the obstruction?

Question 16

Blood supply of the liver. What is the significance?

Answer 16

70% portal vein - 30% hepatic artery

with compensatory relationships between the two inflows.

Question 17

What happends in Doppler US in fibrosis?

Answer 17

As fibrosis leads to portal hypertension, velocity of the hepatic artery increass

(Arterial flow increases as portal flow decreases)

“Hepatic arterial buffer response”

Question 18

What is THAD?

Answer 18

Transient Hepatic Attenuation Differences
seen in the arterial/early portal phase (not on the equilibrium/delayed phases

FOCAL “arterial buffer responses”

In other words, in that tiny little spot right there the liver feels like there isn’t enough portal flow, so it responses by increasing the arterial flow

Question 19

If the liver feel like there isn’t enough portal flow, it respones by increaseing the arterial flow, This can happen for severel reasons:

Answer 19

Cirrhosis - fibrosis = deforms sinusoids = tiny portal veins compressed (shunting), most in the subcapsular region
Clot = clot in PV = venous flow compormiesed (wedge shaped, extends towards the periphery
Mass = 1) direct mass effect smashing the veins 2) recruitment/up regular arterial flow (VEGF)
Abscess/Infection - mass effect/hyperemia = siphon effect

Question 20

Where does fibrosis blocked occur?

Answer 20

Central lobular vein (into sinusoids), flow remains adequate in the central zone, but not for the peripheral zones

arteriel response = enhancment of the peripheral subcapsulare hepatic parenchymal (Central-peripheral phenomennon on CT)

Question 21

Why does the portal vein reverseflow instead of just clotting offin the setting of high resistance to inflow?

Answer 21

unique dual hepatic blood supply (70% P / 30% A)

obstruction in the outlfow vessels (hepatic venules and distal sinusoids) including the hepatic artery = increased resistance

Question 22

So why doesn’t the artery clot or reverse in the setting of outflow obstruction?

Answer 22

Portal system = decompress through collaterals

Artery = CANNOT decompress, so it opens little connections to the portal system.

Question 23

What do you call the enlargement of the arterial CONNECTION to the portal system?

Answer 23

“Parasitizing the portosystemic decompressive apparatus”

If the resistance is high enough, hepatic artery inflow will be shunted into - and can precipitate hepatofugal flow in the portal vein.

Question 24

Reversal of flow =

Answer 24

Hepatofugal flow

Question 25

Why does cirrhotic changes lead to THADs and why these cirrhosis related THAD’s tend to be subcapsular?

Answer 25

in patients with hepatofugal flow in the main portal vein or intrahepatic portal vein branches, the shunted blood comes from the hepatic artery.

Question 26

What will you have if you with increased resistance in the liver to the portal circulation that can be worse on the right?

Answer 26

Colonic venous stasis = Portal Hypertensity Colopathy = edematous bowel (mimics colitis)

Colonic venous stasis = Portal Hypertensity Gastropathy = thickened gastric wall = UGIB in the abscence of varices

worse on the right = collateral pathways develop more on the left (Splenorenal shunt, short gastrics, esophageal varices, and decompress that side.