3. GI (Liver) Flashcards
Biliary anatomy (6)
Liver is covered by visceral peritoneum, except at porta hepatis, bare area and gallbladder fossa.
Injury to bare area can cause retroperitoneal bleed.
Division of the liver into segments is done by Couinaud system.
Caudate lobe (segment 1) has direct connection to IVC through it’s own hepatic veins (don’t communicate through primary hepatic veins).
Caudate is supplied by branches of both right and left portal veins (therefore spared of hypertrophy by various pathologes such as Budd Chiari.)
Intrahepatic course of right portal vein is longer than left, hence more susceptible to fibrosis (right liver shrinks and left grows in cirrhosis).
Biliary anatomy - trivia (2)
Most common vascular variant = replaced right hepatic (origin from SMA).
Most common biliary variant = right posterior segmental branch emptying into left hepatic duct.
Normal MRI characteristics (3)
Spleen is T2 birght, T1 dark.
Pancreas is brightest T1 structure in the body, due to enzymes.
Liver also has enzymes, not as much as pancreas, so also T1 bright and T2 darker.
Fetal circulation anatomy (4)
Placenta –> Umbilical vein –> Both Liver and Ductus Venosus –> Both return to IVC
Ultrasound anatomy - vascular (3)
Aorta sits anterior to vertebral body.
IVC to the right of aorta, Left renal vein coming off draping over aorta.
Left renal vein runs between aorta and SMA.
Splenic vein drapes over SMA.
CBD/portal vein anatomy US
RIght hepatic artery sits between portal vein (posterior) and CBD anteriorly
Mickey mouse sign (3)
Ears are Bile Duct and Hepatic artery.
Face is portal vein.
Liver fibrosis - pathophysiology (5)
Hepatocyte injury can be due to viruses, alcohol, toxins (e.g. aflatoxin) or NAFLD.
Injury results in increased hepatocyte turnver, to which the body reacts by forming regenerative nodules.
Regenerative nodules are an attempt to replace damaged hepatocytes, but also compensate for lost hepatic function.
In addition to activation of hepatocytes, stellate cells living in space of Disse become active and proliferate, changing into myofibroblast-like cells, producing collagen.
This collagen deposition causes fibrosis.
Fibrosis to Portal Hypertension - pathophysiology (4)
Fibrosis first squeezes the right portal vein (longer intrahepatic course).
This causes atrophy of segments 6&7, and compensatory hypertrophy of caudate lobe and segments 2 and 3.
Some people use caudate/right lobe ratio to diagnose cirrhosis (>75% is 99% specific).
Such squeezing leads to portal hypertension.
Portal hypertension - causes (3)
Due to increased hepatic resistance from pre-hepatic (portal vein thrombosis, tumour compression), hepatic (cirrhosis, schistosomiasis) and post hepatic (Budd-Chiari) causes.
Most cases are hepatic, schistosomiasis is commonest cause worldwide, alcoholic cirrhosis commonest in USA.
Portal hypertension - features (4)
Once portal venous pressure exceeds hepatic venous pressure by 8mmHg, portal HTN has occurred.
In reaction, collaterals will form to decompress the liver by carrying blood away.
Tends to be oesophageal and gastric varices.
In pre-hepatic portal HTN, collaterals will form above the diaphragm and in hepatogastric ligaments to bypass obstruction.
Hepatic blood supply
Dual blood supply, 70% portal, 30% hepatic artery.
Compensatory relationship between the 2 inflows, as one increases, the other decreases.
As fibrosis leads to portal HTN, velocity in the hepatic artery increases.
Fibrotic hepatic blood flow (4)
Fibrosis causes blockade at the level of central lobular vein (into sinusoids).
Flow is therefore adequate for central zones of liver, but not for peripheral zones.
Arterial response produces enhancement of the peripheral subcapsular hepatic parenchyma with relative hypodensity of the central perihilar area.
Consequent CT pattern referred to as “Central-peripheral” phenomenon.
Hepatofugal flow in cirrhosis (5)
Sometimes, you get reversal of flow (hepatofugal, away from the liver). Reversal in portal system is seen in cirrhosis in 5-25%.
Why reversal of flow instead of clotting?
In cirrhosis, principal area of obstruction to blood flow is at the outflow vessels (hepatic venules and distal sinusoids).
Outflow obstruction also affects hepatic artery, causing increased resistance also.
However, the portal veinous system can decompress, through creation of collaterals, the artery cannot.
The artery instead opens up connections to the portal system. These enlarge, called “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.
Portal hypertensive Colopathy (5)
Increased resistance in the liver to portal circulation can cause colonic venous stasis, worse on right, leading to portal hypertensive colopathy.
Oedematous bowel that mimics colitis.
Colateral pathways develop more on the left (splenorenal shunt, short gastrics, oesophageal veins), decompressing that side, hence worse on right.
It resolves after liver transplant.
Same process can affect the stomach “portal hypertensive gastropathy” - causing thickened gastric wall on CT and upper GI bleed in abscence of varices.
Multifocal HCC pathophysiology (6)
Regenerative nodules –> dysplastic nodules (increased size and cellularity) –> HCC.
As this happens, nodules start to be mainly supplied by arterial blood rather than portal.
This explains why HCC has arterial enhancement with rapid washout.
This transformation follows a progression from T2 dark (regenerative) to T2 bright (HCC).
Buzzword “nodule within a nodule”, central bright T2 nodule has dark T2 border. Concerning for transformation to HCC.
Regenerative nodule vs Dysplastic nodule vs HCC (8)
Regenerative
- Contains iron
- T1 and T2 dark
- Doesn’t enhance
Dysplastic
- Contains fat, glycoprotein
- T1 bright, T2 dark
- Usually doesn’t enhance
HCC
- T2 bright
- Enhances
HCC delayed imaging (7)
Hepatocarcinogenesis causes decrease in OATP bile uptake transporter.
This moves biliary contrast agents into cells.
This is why normal liver looks bright on delayed phase when using hepatocyte specific agent.
Also why FNHs look super bright on delayed images, they’re basically hypertrophied hepatocytes.
Has hepatocytes become cancerous, they lose function in this transported, and become dark on delayed phase.
The exception is well differentiated HCC, which retains OATP function and is therefore bright on 20 min delayed sequence.
Other lesions in cirrhotic liver (2)
The squeezing that causes portal hypertension also squeezes out most benign liver lesions (cysts, haemangiomas).
Lesions in a cirrhotic lover should be treated with more suspicion.
Polycystic kidney disease (liver) (2)
Patients with AD polycystic kidney disease will also have cysts in the liver.
AR form tends to get liver fibrosis.
Hereditary Haemorrhagic Telangiectasia (Osler-Weber-Rendu) (3)
AD, characterised by multiple AVMs in the liver and lungs.
Leads to cirrhosis and massively dilated hepatic artery.
Lung AVMs can lead to brain abscesses.
Viral infection (4)
Hepatitis is chronic with B and C, acute in the others.
HCC in the setting of hepatitis is due to acute form of Hep B, can also happen due to chronic.
Hep C increases risk of HCC.
USS: Starry sky appearance is non-specific, due to liver oedema making fat look even brighter.
Pyogenic liver infection (5)
Can mimic cysts.
Single abscess usually Klebsiella.
Multiple abscesses usually E.Coli.
Presence of gas is highly suggestive of pyogenic abscess.
“Double target” sign, with central low density, rim enhancement, surrounded by more low density on CT.
Left lobe abscess need emergency drainage, can rupture into pericardium.
Haemangioma (liver) (7)
Most common benign liver neoplasm.
Favours women 5:1.
Can enlarge with pregnancy.
USS: Bright relative to normal liver, flow can be seen in vessels adjacent to the lesion but not in the lesion.
CT/MRI: Signal matches aorta, has “peripheral nodular discontinuous enhancement”.
Should totally fill in by 15 mins.
Atypical haemangiomas can have reverse target sign
Haemangioma (liver) - USS (7)
Ultrasound
- Haemangiomas can change their sonographic appearance during a single examination.
- Needs core biopsy, FNA will only get blood.
- Hyperechoic (65%)
- Enhanced through transmission is common.
- No doppler flow in lesion itself.
- Atypical appearance - hyperechoic periphery, with hypoechoic center (inverse target)
- Calcifications are extremely rare.
