GI - Liver Flashcards
What causes changes in cirrhosis?
Damage to hepatocytes leads to then turning into regenerative nodules which activate collagen to repair
Collagen over time causes contraction and fibrosis of the liver.
Right portal vein longer than left and most contraction/fibrosis occurs in right lobe of liver. Compensatory hypertrophy of left lobe and caudate
Prinicpal areas of obstruction to blood flow tends to occur in outflow e.g. hepatic venules and sinusoids
This causes increases pressure in the portal vein
Reverse flow can be seen in cirrhosis if there is a collateral shunt between hepatic artery and portal venous system
Complications to increased portal vein resistant include portal gastropathy and portal colopathy (right side of colon affected the worst as left side can be decompressed by collaterals from spleen and gastric vessels)
What are the features of a regenerative liver nodules?
Nodules contain iron. Often <3mm
Dark T1 and Dark T2
(also called siderotic nodules - siderotic = iron)
How does dysplastic liver nodule appear?
Nodules containing FAT and PROTEIN
Bright T1. Dark T2
Sometimes arterially enhance but don’t wash out
How does HCC nodule appear on MRI?
Does it washout?
How to differentiate from dysplastic nodule?
Arterially enhancing WITH washout
Washout is how you differentiate with low grade dysplastic nodule which doesn’t washout
-however as dysplastic nodule becomes more high grade it will begin to washout
What are features of focal nodular hyperplasia?
Believed to be due to arise from areas of congential vascular formation (AVM) resulting in increased blood supply and hypertrophy of liver tissue
ART/PV/DELAYED
HIGH/ISO/HIGH
-High T2 (can be iso T1 and T2 called a ‘Stealth lesion’)
-Can cause mass effect
-Arterial enhancment
-Enhancement of central scar on delayed phase
On the delayed hepatobiliary phases the lesions are shown to have retained contrast while the adjacent normal liver parenchyma will gradually wash out. They are the ‘only’ hepatic lesions to do this (haemangiomas are composed of large vascular channels and usually match the enhancement of hepatic blood vessels.
- -Not related to use of OCP (however they can promote growth)*
- -Can appear bright on Sulphur colloid scan*
- Need to biopsy Central scar to get path
What are the 3 different ways haemangiomas can enhance?
Solid benign liver lesions
Made up of large vascular channels (usually supplied from hepatic artery) with SLOW FLOWING BLOOD
1. Flash filling - immediate and uniform enhancement which persists on delayed sequences
2. Peripheral nodular enhancement - fills peripherally from outside in. Complete filling on delayed sequences
3. Peripheral nodular enhancement with INCOMPLETE FILLING IN - usually in giant >5cm haemangioma where central portion is thrombosed
Haemangiomas will have VERY HIGH T2 signal (higher than spleen) and possibly cause T2 shine through on DWI
Mets will also demonstrate high T2 but wont outshine the spleen
Hepatic veno occlusive disease vs graft v host disease post stem cell transplant
What are time frames for each
Hepatic veno-occlusive = 20-30 days post transplant
Graft v host = 3-12 months
Hepatic veno-occlusive disease – fibrosis of the tiny venules can develop following a stem-cell transplant, and by pyrrolizidine alkaloids found in Jamaican bush teas. Clinically patients present with weight gain due to fluid retention, hepatomegaly and jaundice.
How to diagnose bile leak on MRI?
Use Primovist (hepatocyte specific - excreted by hepatocytes into biliary system) or Multihance
Perform delayed scan at 20 mins post Primovist
or
100 minutes post Multihance
What are features of cholangiocarcinoma?
Where is most common site?
What is appearance on CT?
Cancer of bile ducts (excluding ampulla)
Any disease which causes chronic biliary inflammation puts patient at risk of cholangio
PC: Abdo pain/weight loss/painless jaundice
Types
Can be intrahepatic or extrahepatic (most common)
Tumours proximal to cystic duct and at confuence of right and left hepatic ducts are most common (70%)
Distal to cystic duct - less common
Klatskin Tumour - when tumour occurs at bifurcation of right and left hepatic ducts. Causes biliary obstruction
- a mass is not always visible
- look for change in calibre of the ducts
Apperances on imaging
CT - hypodense mass with peripheral rim enhancement followed by filling in
Any disease which causes chronic biliary inflammation puts patient at risk of cholangio
Pearls
CEA and CA 19-9 both elevated
Combination of bilateral vein or duct involvement confers bad prognosis
What are appearances of hepatic adenoma on US and MRI?
Women on OCP or men on steroids typical presentation
Benign lesions usually caused by hormone use (anabolic steroids in men, OCP in women) but can occur spontaneously
- Have central scar
- Fibrous pseudocapsule (hypoechoic rim on US)
- Can spontaneously haemorrhage (may be subcapsular haematoma on CT)
T1 - Isointense
Post contrast - NO enhancement on MRI (will enhance on CT though arterially)
- Will appear hypointense on delayed hepatobiliary imaging (therefore differentiating from FNH which will be bright)*
- Note have a high suspicion for any lesion seen in cirrhotic liver. Contraction of the liver during development of cirrhosis tends to squeeze out haemangiomas and cysts in the process****
- Stopping OCP and repeating imaging can be an option as the get smaller*
- <5cm watch*
- >5cm resect*
Changes that lead to HCC
Liver damage
-
Regenerative nodules (Dark T2)
-
Dysplastic nodules
-
HCC (Bright T2)
Over time nodules go from preferring portal vein blood to arterial blood like in HCC
Blood supply to the liver is 70% portal, 30% arterial
Haemangioma features on US/MRI
More common in women
Bright on ultrasound unless in a fatty liver where it can appear dark
Will have vessels adjacent to it but NOT in it
- Peripheral nodular discontinuous enhancent on CT/MR*
- Will fill in after 15mins*
Features of HCC on MRI
HCCs occure typically in setting of cirrhosis and chronic liver disease such as Hep B/C, haemochromatosis alpha 1 antitrypsin.
Types
- Focal (massive)
- Multifocal (nodular)
- Diffuse (infiltrative)
* AFP elevated in 80-95%*
* Often invades portal vein and/or hepatic veins*
* Can cause spontaneous hepatic bleeds (so can hepatic adenomas)*
Doubling time is around 300 days (not a definite number)
- Arterial blood supply*
- Can have central scar (differentiate from FNH as it wont enhance on delayed)*
- Rim enhancement on delayed can be specific sign*
(If younger patient <40 years with liver lesion and central scar that doesnt enhance WITHOUT cirrhosis think Fibrolamellar HCC)
Fibrolamellar HCC
How to differentiate from classic HCC?
Typically younger patient
No cirrhosis
Normal AFP
Most common cause of liver mets?
Colon cancer most common cause
Hypervascular Mets
Will appear HYPERechoic on ultrasound
- Renal*
- Melanoma*
- Carcinoid*
- Choriocarcinoma*
- Thyroid*
- Pancreatic*
Hypovascular Mets
Will appear HYPOechoic on US
- Colon*
- Lung*
Pancreas
Calcified Mets
Colon
Ovary pancreas
Benign liver masses summary
Osler weber rendu features?
Pulmonary and liver AVMS
Tends to cause cirrhosis of the liver
Pulmonary AVMS cause brain abscesses
Liver abcesses
What are common causes?
Name 3
Single abscess = Klebsiella
Multiple abscesses = E coli
Amoebic abscess in left lobe of liver = Needs urgent drainage as can rupture into pericardium
Hydatid Disease = Water lily sign
Fitz hugh curtis syndrome
What is it?
Seen in loose women
May have PID
- -Enhancement of anterior liver capsule*
- -Perihepatic fluid*
- -Peritoneal septations*
What are features of haemochromatosis on MRI?
Difference between primary and secondary?
Liver and spleen T1 and T2 Dark
Primary = in Pancreas (and liver)
Secondary = Spleen (and liver)
Trick
In/out of phase imaging
-Drop out on IN phase imaging due to iron in haemochromatosis
-Drop out on OUT of phase imaging due to fat in fatty liver
What is most common scenario for Budd chiarai syndrome?
Idiopathic is most common, however:
Pregnant women in multiple choice Q
Nutmeg liver
Perfusional abnormality of the liver due to hepatic venous congestion
Prevents normal diffusion of blood through the liver
-Reduced peripheral enhancement compared to the centre
Causes
- Budd chiari (regenerative nodules can appear)
- Hepatic veno-occlusive disease
- Right heart failure
- Constrictive pericarditis
- In the acute phase periphery can appear bright and central low*
Carolis disease
What is most common type?
Carolis disease is characterised by choledochal cysts
- Associated with ADPKD and medullary sponge kidney*
- ‘Central dot sign’*
- This is the apperance of the portal vein branch within dilated intrahepatic duct*
There are different types
Type 1 is most common - focal dilatation of the CBD
Complications
- Cholangiocarcinoma*
- Cirrhosis*
- Cholangitis*
- Intraductal stones*
Adenomyomatosis
What is it?
What are US features?
Benign
Hyperplasia of the gallbladder wall mucosa and muscularis causing small intramural diverticula
Has epithelial invaginations causing cystic pockets
Presentation in a 50 year old with RUQ pain and diffuse or annular thickening of gallbladder
Comet tail artefact is typical on ultrasound
Significant of gallbladder polyps
When do you followup?
Can be:
- Cholesterol
- Non-cholesterol (adenoma, papilloma)
Unless large - they are asymptommatic
Larger ones can have doppler flow
NON MOBILE
NO SHADOWING
- Followup if >5mm*
- Malignant if >1cm*
Portal vein blood flow
What is normal?
What side of graph should wave be on?
Should be towards liver (hepatopetal flow)
Normal velocity is 20-40cm per second
Waveform should be always ABOVE the baseline
What is pancreatic divisum?
Where main duct of the pancreas is drained by minor papilla rather than major papilla more inferiorly
Minor papilla sits above major papilla (Wirsung duct)
Santorini drains Superior which is Smaller
Significance is there is an increased risk of pancreatitis
Turtoise shell appearance to the liver in what conition?
Schistosomiasis
Due to thic
Choledochal cyst types
-
type I: most common, accounting for 80-90% 1 (this type can present in utero)
- Ia: dilatation of extrahepatic bile duct (entire)
- Ib: dilatation of extrahepatic bile duct (focal segment)
- Ic: dilatation of the common bile duct portion of extrahepatic bile duct
- type II: true diverticulum from extrahepatic bile duct
- type III: dilatation of extrahepatic bile duct within the duodenal wall (choledochocele)
-
type IV: next most common
- IVa: cysts involving both intra and extrahepatic ducts
- IVb: multiple dilatations/cysts of extrahepatic ducts only
- type V: multiple dilatations/cysts of intrahepatic ducts only (Caroli disease)
- type VI: dilatation of cystic duct
Pancreatic injury
Grade 1: Min Bruise
Grade 2: Maj Bruise
Grade 3: Tail with duct
Grade 4: Head and body with duct inj
Grade 5: Completely destroyed
Choledochal Cyst summary
What type is Carolis?
What are the features of Gauchers disease?
- Hepatosplenomegaly
- Thrombocytopenia
- Anaemia
Flask deformities of the bones are characteristic (flared metaphysis and diaphyseal thinning)
