Gastroenterology Flashcards

(361 cards)

1
Q

two types of hiatus hernia?

A

Sliding

Rolling

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2
Q

Most common type of hiatus hernia

A

sliding

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3
Q

what ligament normally attached the oesophagus to the hiatus?

A

phrenico-oesophageal ligament

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4
Q

Define a rolling hiatus hernia

A

The stomach herniates above but the GOJ remains in the same position

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5
Q

what happens to GOJ during REM sleep?

A

Lower oesophageal sphincter relaxation - can cause reflex which is normal

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6
Q

The length of the LOS and the pressure required to maintain competence are related. The ??????? the sphincter, the lower the pressure needed to maintain competence.

A

longer

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7
Q

what happens to the length of the LOS after overeating?

A

It shortens, therefore higher pressures are required to keep it working.

reflux is normal if overeating in people

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8
Q

How much GORD is not detected at endoscopy?

A

40%
symptomatic but without oesophagitis

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9
Q

what does a fatty diet cause in the stomach motility?

A

delayed gastric emptying

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10
Q

Overeating and delayed gastric emptying (fat in diet) cause:

A

Prolonged fundal distension
Sphincter shortening
Repetitive transient LOS pressure collapse

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11
Q

How bad is GORD to be seen on barium?

A

Very bad
less than 2cm
less than 1cm intrabdominally

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12
Q

What are the three groups of patients who get GORD and develop symptoms/side effects?

A

One group of patients develop gastric metaplasia (Barrett’s) and become at increased risk of adenocarcinoma formation.

Another group develop visible oesophagitis which may progress to ulceration and stricture formation.

A third group appear to have little visible response (endoscopic negative GORD) but can be quite symptomatic.

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13
Q

features of reflux oesophagitis - motility issues

A

Abnormal motility (up to 50%): impaired primary peristalsis, proximal escape of barium (i.e. barium left behind during the peristaltic wave indicative of reduced amplitude), tertiary contractions

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14
Q

features of reflux oesophagitis

A

nodularity
ulceration

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15
Q

IN barium studies what is the difference between an A ring and a B ring?

A

An A ring is due to muscular contraction of the oesophagus at the junction of the tubular oesophagus and the vestibule. By its nature, an A ring is transient and not a fixed stricture.

B ring -An A ring is due to muscular contraction of the oesophagus at the junction of the tubular oesophagus and the vestibule. By its nature, an A ring is transient and not a fixed stricture.

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16
Q

What cancer devlops in Barretts oesophagus

A

adenocarcinoma

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17
Q

What are the symtpoms of post parandial choking attacks

A

choking
asthma - try PPI if high gord suspicion, otherwise 24 hr pH moniotr.
cough
chronic laryngitis

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18
Q

Raised upper oesophageal pressure on barium study might show?

A

Premature closure or non relaxing cricopharyngeus

Zenkers pouch formation

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19
Q

Raised upper oesophageal pressure findings on endoscopy

A

laryingyitis
airway (upper) inflammation

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20
Q

reporting on a patient with suspected reflux disease:
headings

A

Indication
Technique
Findings:

Structure
Motility assessment
Reflux assessment
Marshmallow test

Conclusion:
No evidence of GORD
Early GORD
Advanced GORD

Recommendations:
Endoscopy
Consideration of surgical opinion

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21
Q

The mucosal pattern is the ‘feline’ oesophagus or the ‘oesophageal shiver’. what does this indicate?

A

contraction of muscularis mucosae response to acid reflux

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22
Q

GOJ star pattern view is associated with what?

A

The star pattern with a mound suggests a tightly closed sphincter which is bulging into the fundus. This indicates a competent sphincter and whilst intermittent reflux due to transient relaxations may occur, volume reflux is less likely.

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23
Q

Oesophageal intramural pseudodiverticulosis can lead to what complication

A

Squamous carcinoma

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24
Q

What are the most common oesophageal tumours>

A

adenocarcinoma and SCC

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25
1-year-survival for metastatic oesophageal cancer
20%
26
UPPER GI imaging is mostly for what purpose?
staging and response to treatment. Endoscopy and biopsy are done for the symptoms
27
what are the oesophagus landmarks for the three parts
oharynx to aortic arch aortic arch to inferior pulmonary vein inferior pulmonary vein to GOJ
28
risk factors for oesophgeal SCC
smoking and alcohol age - over 40 afrocaribbean radiotherapy hot drinks
29
Oesophageal SCC is associated with what other cancers?
Head and neck SCC - staging often includes the neck
30
Oesophageal SCC is most common in which part of the oesophagus?
middle - 50%
31
What is Barretts
rrett's oesophagus: This is a condition where oesophageal stratified squamous cell epithelium undergoes metaplasia to columnar epithelium.
32
Patients with high grade dysplasia are given what options?
Surgey - oesophagectomy - are considered - 30% will develop cancer.
33
Once oesophageal tumour is confirmed, further investigations can be considered to aid staging:
Positron emission tomography (PET)/CT Endoscopic ultrasound
34
Oesophageal CT tumours
Oesophageal tumours usually show as thickening of the oesophageal wall. The oesophagus proximal to the tumour may be dilated and contain food residue.
35
what is diagnostic for achalasia? physiology teting
high pressure scphincter that doesn't relax.
36
biochemical indicators of iron deficiency anaemia
Low ferritin <12-15 μg/l Microcytosis Hypochromia B12 and/or folate deficiency may mask hypochromia and microcytosis: look for increased red cell distribution width (RDW)
37
The serum ferritin correlates well with iron stores, but it can also be elevated with.... ?
liver disease, inflammatory conditions, and malignant neoplasms.
38
Common causes of occult GI blood loss
Aspirin NSAID 10-15% Colonic carcinoma 5-10% Gastric carcinoma 5% Benign gastric ulceration 5% Angiodysplasia 5%
39
Risk factors of colon cancer
Genetic - FAP IBD - UC and diet
40
How is colon cancer staged?
TNM
41
Colon cancer - 80%of all colon cancers are what stage at presentation?
T3 - Tumour extends beyond the muscle layer into pericolic or perirectal tissue
42
Fro colon staging scan what parameters should be used?
Oral contrast. IV contrast with delay of 25s thorax and 60 s for abdo pelvis
43
Colon cancer when can MRI be used?
distal sigmoid and upper rectum
44
Colon cancer when can PET CT be used?
recurrence if markers going back up. Detectin of extrahepatic disease if undergoing hepatic recetion for metastasis
45
Colorectal TNM - what is the N staging
N0 - none N1 three or less N2 - four or mroe
46
streaky change in the fat surrounding the sigmoid colon, which may be a result of ???
peritumoural inflammation or infiltration of tumour into the surrounding fat.
47
Colorectal cancer staging - lymph node size cut offs?
if >1cm likely malignanct involvement. If under then likely inflammatory.
48
Colon cancer relationship of lung and liver mets?
If lung mets then normally there will be liver mets first
49
Colorectal cancerr - why do MRI?
Determining the size, location and extent of primary tumour Evaluating the relationship to adjacent structures, particularly the mesorectal envelope, the prostate/seminal vesicles or uterus/vagina Establishing the presence and extent of LN involvement
50
Low rectal tumours an achieve wider dissemination - why?
bypoass the liver capillary netowrk that captures other cells or lymphatic spread
51
Colorectal cancer - R2 meaning
there is macroscopic involvement of tumour resection margin.
52
Colorectal cancer - R1 meaning
indicates that there is microscopic involvement of the resection margin or that the tumour comes within 1 mm of the margin.
53
Colorectal cancer - R0 meaning
R0 indicates that there was a margin of at least 1 mm of normal tissue between the tumour and the resection margin.
54
Path report - V1
Vascular invasion.
55
Vascular invasion of colon cancer seen on what modality?
MRI - if greater than 3mm
56
Patients with lymph node involvement at surgery are usually offered are usually offered what?
adjuvant chemotherapy to reduce the risk of recurrent disease.
57
Colon cancer - metastatic locations
27% of patients develop liver metastases, approximately two thirds are identified at presentation and the other third present in next 3 years.
58
Colon liver mets appear as what on CT? and why?
hypovascular and so best seen as hypodense on portal venous phase study.
59
Colon liver mets appear as what on MRI? and why?
MR metastases are typically intermediate low signal on T1 and intermediate high signal on T2, and are hypovascular with the thin rim of peripheral enhancement seen almost invariably on an arterial phase acquisition post-gadolinium
60
Do mets take up MR contrast?
no
61
Colon cancer - Right-sided tumours recur within .....
para-aortic nodes adjacent to the superior mesenteric artery (SMA),
62
Colon cnacer - left-sided tumours metastasis
to the para-aortic nodes adjacent to the origin of the inferior mesenteric artery (IMA).
63
why are liver and lung mets excised?
cascade of colon mets shows that once embedded in liver and lung it then goes all throughout the body. Attmepts to stop the cascade at the liver and lung have been successful in patiens.
64
How is MRI used to differnetiate recurrence at an anastomosis?
Magnetic resonance imaging is better at differentiating between malignant and benign disease. Fibrosis is usually dense dark material on T2 with angular margins whereas tumour is of intermediate signal with rounded margins and rim enhancement
65
Hydronephrosis post colon cancer surgery?
Sinister sign for recurrence
66
IN colon cancer when is MR used?
if there is a known liver met and no extra hepatic mets then can be used to aid surgical approach
67
Chemo in the use of cancer treatment - 3 types what are they>
As a treatment therapy in its own right, as in this situation where there is identifiable recurrent disease As an adjuvant therapy when the primary therapy has been completed (usually surgery) with no residual macroscopic disease but the histological features of the tumour put the patient at high risk of recurrence (e.g. a T3 N1 V1 colonic tumour), chemotherapy being used to reduce the risk of recurrence As a neoadjuvant therapy where chemotherapy is used (often in combination with radiotherapy) prior to what is considered the definitive treatment (surgery) to improve the likelihood of a favourable outcome e.g. converting a rectal cancer which is deemed as likely to have a R1 resection on the basis of a staging MR to an R0 resection after chemoradiotherapy and thus reducing the risk of local and distant recurrence
67
what are diverticula?
herniations of mucosa and submucosa through the colonic wall.
68
which points are suscepitble to divertiucla?
Where the vasa recta penetrate
69
two types of diverticlosis
The first one is mainly left-sided, discernible by muscle thickening (acquired, low-residue diet and physical inactivity implicated, prevalence rises with age) The other is due to diffuse connective tissue abnormality, resulting in pancolonic disease
70
Diverticulitis CT features
Diverticula Fat stranding Centipede sign (hyperaemic engorged vasa recta) Arrow head sign Wall thickening >4 mm
71
How to diverticula bleeds occur?
They occur through arterial blood supply - thinnning of the vasa recta
72
External anal sphincter is made of what muscle?
Striated muscle Squeezed to withold defecation
73
internal anal sphincter is made of what@
smooth muscle 85% of resting anal pressure
74
What muscle lies between the EAS and IAS ?
interspincteric plane - longitudinal muscle
75
On US - smooth muscle is generally what kind of pattern?>
hyporeflective
76
what are the two causes of incontinence>
1. Disruption of the sphincter muscles childbirth but can also occur secondary to surgical procedures, trauma, etc. 2. Atrophy of the sphincter muscles This may be due to ageing or the effect of pudendal nerve stretching during pregnancy and childbirth.
77
what are the two syndromes of anal spinchter atrophy?
IAS atrophy or ‘degeneration’ where the IAS is thinned and difficult to visualise EAS atrophy where the EAS is thinned and replaced by fat
78
Fistula in ano is believed to arise from ??????
chronic infection of the anal glands.
79
'Parks classification of sphincters is what?
Intersphincteric Transsphincteric Suprasphincteric Extrasphincteric
80
How to treat fistulas in anus?
lay - open can be tricky based on type of fistula and not causing further damage. Imaging therefore is to evaluate surgical approach and also review for extensions
81
Anal fistula A certain fistula cannot be an intersphincteric fistula because these never have tracks in the ischioanal fossa, but it could be one of the following:
Transsphincteric Supralevator Extrasphincteric
82
Supralevator sepsis in anal fistulas is important to note - why?
difficult to treat surgically and is very important to detect pre- or peri-operatively. infection above the pelvic floor - best seen on coronal views on MR
83
T or F MR imaging is as accurate as clinical examination for classification of fistula in ano
F MR imaging is far superior.
84
T or F The main role of MR imaging is the pre-operative detection of areas of sepsis
T It has been shown that MR imaging can detect sepsis that would otherwise be missed.
85
T or F Sphincter division is greater for a transsphincteric fistula than intersphincteric fistula
T When laying open an intersphincteric fistula the EAS is not divided.
86
T or F The internal opening of a suprasphincteric fistula is higher than an extrasphincteric fistula
F The internal opening of extrasphincteric fistulas are, by definition, above the anal canal whereas suprasphincteric fistulas open into the anus, usually at the dentate line.
87
T or F It has been shown that pre-operative MR imaging can reduce subsequent fistula disease
T By up to 75% in complex cases.
88
Liver is created in which mesentry?
ventral
89
falciform ligament become what?
ligamentem teres
90
Special blood supply of caudate lobe?
frm left and right hepatic arteries. Venous drainage straight to IVC
91
Oesophageal staging type
TNM
92
Oesophagus lymph node drainage?
nodes near the primary are involved and from there, drainage may take place superiorly through the para-oesophageal lymphatics to the paratracheal, mediastinal, hilar, para-aortic, cervical and internal jugular nodes. Inferior drainage takes place through the para-oesophageal nodes to para-cardial, left gastric and beyond to celiac axis, and abdominal para-aortic nodes.
93
Location of Oesophageal mets?
liver and lung being the most common sites. Other sites include brain, bone, and intra-abdominal organs.
94
When is PET /CT FDG used in oesophageal cancer?
Proximal to GOJ if no mets found on CT then PET is done with diangostic laparoscopy and endoscopic ulrasoun
95
normal oesophageal wall thickness
is less than 3 mm thick
96
How to tell T staging?
Very difficult if outer edge against fat is irregular assume T3.
97
Oesophageal cancer lymph node size cut off?
10mm though some groups are 6mm like supraclavicular
98
Features of a benign node
Benign nodes tend to be oval, triangular, flat or kidney shaped
99
features of malignant node
fatty core replaced by malignant tissue, spherical, hypoechoic, well defined
100
Oesphageal T staging
T1 Tumour invades lamina propria, muscularis mucosae, or submucosa EUS T1a Tumour invades lamina propria or muscularis mucosae T1b Tumour invades submucosa T2 Tumour invades muscularis propria EUS T3 Tumour invades adventitia EUS, CT T4 Tumour invades adjacent structures EUS, CT T4a Resectable tumour invading pleura, pericardium, or diaphragm Positron emission tomography (PET), CT/EUS T4b Unresectable tumour invading other adjacent structures, such as the aorta, vertebral body, and trachea PET, CT/
101
Fluorouracil (5 FU)) can produce what side effect
coronary spasm
102
reasons for neo adjuvant therapy
sterilise lymph nodes down stage the disease reduce chance of spread
103
post chemo CT reviews what?
Size of primary size of lymphadenopathy any mets / response
104
Gastric cancer risk factors
low fruit and veg smoked food, salted foods
105
Gastric cancer signs and symptoms
Indigestion nausea and vomitting dysphagia postprandial fullness
106
Gastric cancer late complicaitons
pathologic perotneal and pleural effusions GOT obstruction bleeding
107
Duodenal cancer - risk facotrs
coeliac disease crohns colonic polyps
108
Duodenal cancers are mostly
Adenocarcinomas others are carcinoid and sarcomas
109
how does H Pylori cause gastric cancer
Atrophic gastritis leads to atrophy, metaplasia, dysplasia and then malignancy.
110
Pernicious anaemia gives a higher risk of what
gastric malignancy
111
Relationship of mgastric polyps to gastric malignancy
gastric polyps are less common than malignancy. x30 cancer is more common than polyps Most polyps are inflammatory.
112
duodenum - where is most common for adneocarcinoma?
third part
113
mets to duodenum are from what cancers?
melanoma, breast and lung
114
most common benign tumour f the stomach
leiomyomas
115
less common benign cancers of the stomach
Neurilemmomas Neurofibromas Vascular tumours (glomus tumours, lymphangiomas, haemangiopericytomas) Lipomas (these show typical features on cross-sectional imaging of consisting of almost entirely fat) Carcinoid Fibromas Amyloidoma
116
Hamartomas occur in patients with
Peutz-Jegher's syndrome (muco-cutaneous pigmentation, increased risk of cancer) Cowden's syndrome (multiple hamartomas of the skin and internal organs, fibromas of the skin and particular malignant potential in the thyroid and breast)
117
Adenomatous polyps occur in patients with:
Familial polyposis coli (the majority of these patients have gastric polyps) Gardner's syndrome (osteomas, soft tissue tumours, dental anomalies)
118
what are the three types of gastric volvulus?
Mesentero-axial organo-axial vertical most common - organo axial. axis from cardia to pylorus
119
what are the three types of gastric volvulus?
Mesentero-axial organo-axial vertical most common - organo axial. axis from cardia to pylorus
120
Duodenum divertiucla are assocaited with what?
small bowel overgrwoth and malabsorption
121
oesophagus - what level does striated uscle turn into smoth muslce?
around aortic arch - xzone of transition
122
Achalasia is characterised as.....
aperistalsis of the oesophagus with associated lower oesophageal dysfunction. reduced ganglionic cells in myenteric plexus.
123
radiographic appearance of oesophagus onf nutcracker syndrome
normal
124
myenteric plexus can also become damaged simulating achalasia in
chronic Chagas’s disease
125
Chagas’s disease is by
Trypanosome cruzi and is endemic in Central and South America. Reduvid bug.
126
How does scleraderma affect the bowel?
Scleroderma is an autoimmune condition that leads to the atrophy and fibrosis of the smooth muscle layer of the bowel dilates the oesohpagus
127
Technetium-99m (99mTc) as pertechnetate is cleared from the circulation into the
thyroid, the choroid plexus of the brain, the salivary glands and the normal gastric mucosa.
128
How is octreotide used for neuro endocrine tumours
Octreotide is a synthetic octapeptide analogue of somatostatin which can be chelated using diethylenetriaminepentacetic acid (DPTA) and labelled with 111In to provide a sensitive technique for localisation of neuro-endocrine tumours and their functioning metastases.
129
FDG is labelled with what for the Nuc med scans
Flu 18
130
Simple cysts and peoples age
become more frequent in lder age
131
Simple cysts are associated with other diseases
Tuberous sclerosis Polycystic kidney disease (approximately 30% of patients also have liver cysts) Polycystic liver disease (auto-dominant) Von Hippel-Lindau (VHL) syndrome
132
Can you list three sonographic criteria that allow this lesion to be called a simple cyst?
Anechoic/water echogenicity Posterior acoustic transmission A well-defined or imperceptible wall
133
Simple cyst on CT - HU should be
10 or less
134
Simple cyst on MRI
low signal on T1W spin-echo (SE) images, and very high signal on T2W images, as shown in Fig 1.
135
US appearance of complex cysts
A thick wall Internal septa Haemorrhage Debris Calcification
136
Name the types of benign liver cystic lesions?
Biliary cystadenoma Hydatid Multiple biliary hamartomas
137
Where to biliary cystadenomas arise from?
Bile ducts, occur often in the right lobe
138
Symptoms of biliary cystadenomas?
abdominal pain
139
Characteristics of biliary cystadenomas?
They are often multilocular and contain internal septa and mural papillary projections, the latter feature of which is highly characteristic. CT these lesions, which are classically cystic and well defined with internal septa, the septa, cyst walls, and solid components may enhance helping differentiate them from simple cysts.
140
Risk of biliary cystadenomas?
can have malignant transformation
141
What is hydatid disease?
Hydatid disease is a multi-system condition effecting the bowel, liver, lungs, spleen, kidney, bone and central nervous system (CNS).
142
Complications of hydatid?
Jaundice. Other complications include rupture, infection and anaphylaxis.
143
How does hydatid appear on imaging?
classical appearance is of a large enhancing cyst with calcification and smaller daughter cysts within. Other signs are the water-lily appearance of a collapsed membrane within a larger cyst
144
What treatment is used ofr hydatid cysts ahead of srgery?
albendazole
145
Multiple biliary hamartomas, also known as
von Meyenburg complexes,
146
what are multiple biliary hamartomas
Lesions comprise small groups of dilated bile ducts.
147
US appearances of multiple biliary hamartomas
appear as multiple rounded cystic lesions throughout the liver (Fig 1). Smaller lesions are usually hyperechoic with larger hamartomas often appearing hypoechoic. They may have ring-down comet tail artefact associated with them and can mimic metastases.
148
What is most common benign focal liver lesion?
haemangioma
149
Two types of haemangioma?
typical and giant
150
features of typical haemangiomas
the smaller, typical type are more common and are normally asymptomatic (Fig 1). Haemangiomas may increase in size, particularly during pregnancy or oestrogen administration and are multiple in 10% of patients
151
features of giant haemangioma
these are uncommon, >5 cm in size and may be symptomatic with risk of haemorrhage and thrombosis
152
On CT, haemangiomas are normally
well-defined hypodense masses with peripheral nodular enhancement post-contrast and centripetal fill-in on delayed scans.
153
Haemangioma on MRI
The lesions are also classically high signal on T2W imaging (Fig 1), with the degree of signal increasing as you increase the time to echo (TE) parameter of the sequence.
154
the second most common benign tumour of the liver
Focal nodular hyperplasia
155
what is focal nodular hyperpalsia?
thought to be formed as a response to vascular malformation. comprises an arrangement of normal hepatocytes, Kupffer cells and bile ducts in an abnormal pattern.
156
focal nodular hyperplasia and COCP association
You should note that there is no proven association with the oral contraceptive pill, but the lesion may regress if usage of the pill is ceased.
157
focal nodular hyperplasia on CT
CT, FNH demonstrates arterial contrast enhancement except for the central scar. The lesion then becomes hypo/isoattenuating in the portal venous phase. The central scar enhances on delayed scans in up to 80% of cases or may remain hypoattenuating
158
Central scar is classic for focal nodular hyperplasia but can also be found in
central scar is classic, it is not pathognomic and can also be found in fibrolamellar HCC, adenoma, and hepatic necrosis.
159
what are the types of hepatic adenomas
Inflammatory Hepatic nuclear factor (HNF) 1 alpha-mutated Beta catenin-mutated Unclassified hepatic
160
what are the complications of hepatic adenomas?
infarction haemorrhage malignant transformation
161
What are hepatic adenomas associated to?
Adenomas are thought to be linked to glycogen storage diseases and also the oral contraceptive pill. Stopping the latter is thought to sometimes cause regression of the lesion.
162
hepatic adneomas US appearance and why?
well-defined mixed echogenicity lesions due to their varying component. Because of this, their appearances are often non-specific.
163
hepatic adenomas on MRI
high signal on T2 (Fig 1) and low signal on T1 (Fig 2).
164
Nucklear medicine and Kuppfer cells
Kuppfer cells uptake the radioisotope. So lesions with high kuppfer cells appear as bright
165
common anatomy mimics in the liver for lesions?
adjacent to falciform ligament perfusion mimics are in the congested liver, which gives a mottled, inhomogeneous appearance
166
common causes of fatty infiltration of the liver
Obesity Toxins: Alcohol, Amiodarone, Chemotherapy Steroids Malnutrition Hepatitis Chronic illness: Diabetes, Congestive heart failure, Tuberculosis Glycogen storage disorders
167
Focal fatty change normally affects which parts of the lvier
caudate lobe, right lobe, perihilar region
168
how to tell fatty focal change from a mass lesion?
look at the vessels, do they pass through it freely?
169
which MRI sequence is useful for fatty liver?
in and out phase sequence
170
focal fatty SPARING is common where?
falciform ligament and the gallbaldder fossa
171
in cirrhotic livers what are the other types of mass lesions that can be found?
regenerating nodules are found
172
Location of focal nodular hyperplasia?
subcapsular
173
FNH on non contrast T2W imaging
bright central scar
174
FNH - type of early arterial enhancement?
There is arterial enhancement though a tortuous feeding artery and a spoke-wheel pattern of internal vessels. Later, there is centrifugal filling.
175
low kpffer cell lesions?
haemangioma and adeonoma are low in Kupffer cells
176
Simple cysts are associated with what?
Tuberosclerosis
176
Simple cysts are associated with what?
Tuberosclerosis
177
Which liver lesions have a centralvscar
FNH Fibromellar HCC Adenoma Hepatic necrosis
178
two types of HCC
HCC Fibromellar HCC
179
Typical enhancement characteristics of HCCs on arterial-phase imaging
Hepatocellular carcinomas are typically hyperenhancing in the arterial phase
180
Typical enhancement characteristics of HCCs on venous-phase imaging
n the venous phase, an HCC is usually hypointense to the surrounding liver. Hepatocellular carcinomas often display an enhancing peripheral rim in the venous phase, due to a pseudocapsule.
181
The appearance of HCC on ultrasound:
Is usually cirrhotic liver Is non-specific Is a focal, solid lesion May be hyper- or hypoechoic Is that the lesion may be very small and similar to haemangiomas
182
T or F Hepatocellular carcinomas enhance with extracellular contrast similarly to the enhancement on CT
T
183
diffusion restirction is typical for which liver lesion
HCC
184
what is LI- RADS
LR 1 definitely benign LR5 definitely HCC
185
who does li rads apply to
patients with high risk of hcc
186
HCC lesion assessment features
Non-rim arterial phase enhancement Non-peripheral washout Enhancing capsule appearance Size Threshold growth: ≥50% increase in ≤6 months
187
Hoe best to differentiate HCC form benign lesions
dual contrast MRI
188
Poorly-differentiated HCC, metastases and adenomas do not enhance in the hepatocyte phase as they
do not contin hepatocytes
189
how to differentiate HCC from hypovascular metastases
hypoenhancement in the arterial phase compared to hyperenhancement in HCC).
190
Do malignant liver lesions take up SPIO
no
191
HCC on MRI
There is arterial enhancement with washout in the venous phase and there is a pseudocapsule The lesion usually does not take up SPIO The condition is associated with cirrhosis The condition often shows invasion of portal veins
192
FNH on MRI
Arterial enhancement but no washout A central scar that is usually progressively enhancing The lesions usually take up SPIO There is no cirrhosis There is no pseudocapsule
193
Adenoma on MRI
Arterial enhancement, variable washout The presence of a pseudocapsule No cirrhosis There is minimal SPIO uptake The lesion may contain haemorrhage The lesion may contain fat
194
MRI findings for dysplastic liver nodules
Cirrhosis No raised AFP Often take up of SPIO Bright enhancement Usually no pseudocapsule
195
MRI findings of haemangiomas
There is peripheral enhancement with gradual filling in on delayed imaging There is high signal on heavily T2W sequences Lesions are echogenic on ultrasound Lesions do not take up SPIO
196
Can you think of four or more differences between conventional HCC and fibrolamellar HCC?
Fibrolamellar HCC: Is not associated with elevated AFP Is not associated with cirrhosis Is often calcified Often has a central scar (note that the central scar in fibrolamellar HCC is non-enhancing, whereas in FNH, the scar does enhance - an important diagnostic feature) Has a better prognosis than conventional HCC Does not wash out as much as HCC - it is isointense in the venous phase
197
T or F Hepatocellular carcinomas are hyperenhancing in the arterial phase
T
198
Do liver cysts arterially enhance
No
199
Why is LI RADS not used in vascular disorders of the liver?
As vascular disorders can form benign nodules which can mimic HCC, LI-RADS should not be applied in:
200
What are the primary liver tumours?
Hepatoma Intra-hepatic cholangiocarcinoma Haemangioendothelioma Angiosarcoma Biliary cystadenocarcinoma Hepatic lymphoma
201
Liver mets from which cnacers?
Gastro-intestinal (GI) adenocarcinomas - stomach, pancreas, small bowel, colon Breast carcinoma Bronchogenic carcinoma mlanoma Pancreatic islet cell tumours Lymphoma (Hodgkin's and non-Hodgkin's) Gastro-intestinal stromal tumours (GISTs)
202
When is biopsy of a liver lesion conducted
If ultrasound shows widespread lesions consistent with unresectable metastases, biopsy may be performed.
203
Certain tumours have arterially enhancing metastases, with these an arterial phase scan (25-30 seconds) should be added. These tumours are
neuroendocrine, renal cell carcinomas and thyroid tumours.
204
Can you list four indications for performing a liver MRI when looking for metastases?
Inconclusive CT/ultrasound Patient has contraindications to CT contrast Rising CEA with normal CT in someone with history of colorectal cancer Patient for resection of colorectal metastases: MRI may identify further metastases
205
how does SPIO help image livers?
taken up by normal liver (which goes dark) and so will show mets easily (not taken up by mets)
206
Why is SPIO best imaged in T2*
It is best imaged on T2* sequences as this utilises susceptibility artefact to create increased signal drop out in the normal liver, so that the metastases become more conspicuous, as they do not take up SPIO.
207
how does cholangiocarcinoma invade?
along the bile ducts
208
what are the three types of cholangiocarcinoma
Mass-forming: usually large and well-defined Periductal-infiltrating: often spiculate Intraductal: often multiple
209
CT appearances of intrahepatic cholangiocrcinoma
May be calcified May have intrahepatic dilatation Peripheral enhancement on arterial phase Gradually fills in on delayed images Fibrous tissue may become hyperintense on delayed images Need delayed images or the tumour may not be adequately identified Periductal and intraductal forms may only show biliary dilatation with no mass Capsular retraction is often present
210
cholangiocrcinoma bet seen in what CT contrast phase
Late venous - 10 minutes
211
Crohns disease - behaviour types
Inflammatory (non-stricturing, non-penetrating) Stricturing Fistulating (penetrating)
212
Smoking link with UC and Crohns
increases crohns but decreases UC
213
Acute severe pancreatitis can be associated with organ failure and local complications such as
necrosis (with infection), pseudocyst or abscess.
214
What is a pancreatic Acute pseudocyst
is a collection of pancreatic juice enclosed in a wall of fibrous or granulation tissue that arises following an attack of acute pancreatitis.
215
How long to create a pseudocyst
4 weeks
216
commonest causes of pancreatitis?
gallstones and alcohol
217
What does atlanta criteria seperate?
Mild pancreatitis (85%) from Severe (organ failure and necrosis)
218
Severe pancreatitis involves necrosis - what are the two types of necrosis?
infected (50% mortality) sterile
219
time course of acute pancreatitis?
Proinflammatory - SIRS for two weeks Anti inflammatory - immunosupressed for two weeks
220
what is the amylase threshold for pancreatitis?
x4
221
What is US useful for in acute pancreatitis?
Ultrasound is valuable in the detection of free intraperitoneal fluid, gallstones and dilatation of the biliary tree. Gallstones important as early ERCP can be considered
222
pancreatitis acquisition type?
arterial and portal venous
223
which scores are used for pancreatitis on CT?
extent of necrosiss as percentage AND balthazar
224
Define a mild pancreatitis on CT
(also known as interstitial pancreatitis): a Balthazar score of B (enalrged) or C (inflammatory changes to surrounding fat) , without pancreatic or extrapancreatic necrosis
225
Define an intermediate pancreatitis?
intermediate pancreatitis (also known as exudative pancreatitis): a Balthazar score of D (fluid collection) or E (multiple collections), without pancreatic necrosis.
226
Severe pancreatitis is considered when there is what>
necrosis
227
when should patients with pancreatitis have their CT assessment?
All patients with acute pancreatitis should have a CT assessment between 3-10 days to try to predict the radiological severity of episode.
228
indication to re-scan a patient with pancreatitis?
Diagnostic uncertainty Assessment of severe cases When clinical deterioration occurs Guidance for interventional procedures For follow-up and monitoring of complications
229
Usually the whole pancreatic gland is involved in pancreatitis. How often and for what reason is it only parital??
In up to 18% of cases, however, a focal area of inflammation can develop. This is thought often to be associated with bile duct stones.
230
complications of pancreatic pseudocyst?
Compression of adjacent structures, which can cause pain and jaundice Spontaneous rupture, which can cause pancreatic ascites or even peritonitis Infection, which can lead to abscess formation
230
complications of pancreatic pseudocyst?
Compression of adjacent structures, which can cause pain and jaundice Spontaneous rupture, which can cause pancreatic ascites or even peritonitis Infection, which can lead to abscess formation
231
only reliable CT sign indicating infected necrosis of pancreatitis
small gas bubbles in the peripancreatic collection
232
differentials when considering acute pancreatitis?
Pancreatic ductal adenocarcinoma Autoimmune pancreatitis Peptic ulcer disease with posterior perforation Pancreatic lymphoma
233
intra and extra hepatic duct dilatation with swollen pancreas
can be due to the pancreaittis. not necessarily just gallstones
234
in acute pancreatitis - portal vein thrombosis can lead to
subsegmental portal hypertension, splenic enlargement and distal variceal formation.
235
typical punctate calcification across the upper abdomen on a plain film is diagnostic of
chronic pancreatitis
236
The presence of calcification is much more likely when the chronic pancreatitis is caused by
alcohol
237
US appearance of chronic pancreatitis?
Alterations of the size and echotexture of the gland Focal masses Calcification Pancreatic duct dilatation Pseudocyst formation
238
EUS findings for chronic pancreatitis
Echogenic foci within the gland Focal areas of reduced echogenicity within the gland Increased echogenicity/thickness of the main pancreatic duct wall Accentuation of the glands lobular pattern Cysts Irregular contour of the main pancreatic duct Dilatation of the main pancreatic duct Side duct dilatation
239
CT findings for chronic pancreatitis
Echogenic foci within the gland Focal areas of reduced echogenicity within the gland Increased echogenicity/thickness of the main pancreatic duct wall Accentuation of the glands lobular pattern Cysts Irregular contour of the main pancreatic duct Dilatation of the main pancreatic duct Side duct dilatation
240
What is the considered measurement for atrophic pancreas?
1cm in tail - AP 1.5cm in the head
241
How big is the duct in chronic panreatitis
Dilatation of the pancreatic duct and the secondary radicles to greater than 3 mm is a feature of chronic pancreatitis
242
What vascular complications can occur with chronic pancreatitis?
Vascular complications of chronic pancreatitis, such as occlusion of the splenic vein, with development of segmental portal hypertension or pancreatitic pseudoaneurysms are well-demonstrated
243
What would you see on MRI of chronic pancreatitis?
most common MRI finding in chronic pancreatitis is a diminished signal on T1 weighted fat suppressed imaging with a heterogeneous enhancement pattern and areas of signal void, corresponding to the areas of punctate calcification. can get side duct ectasia dilated main duct
244
What is a chronic pancreatitis pseudo cyst? How will the wall enhance with contrast?
well demarcated and unilocular collection if the wall is thick then is will enhance after contrast
245
How long does it take to develop a pseudocyst after acute pancreatitis?
6-8 weeks
246
What happpens if a pseduocyst ruptures into the peritoneum?
can develop pancreatic ascites
247
When should pseudocysts be operated on?
greater than 6cm or sometimes for pain
248
How does a pancreatic pseudoaneurysm form after acute or chronic pancreatitis? Surgical mortality?
walls of the peripancreatic vessels are exposed to pancreatic enzymes resulting from the glandular inflammation. These enzymes lead to wall degradation with the possibility of subsequent haemorrhage. The vessels most commonly involved are the: Splenic artery 30-50% Gastroduodenal artery 10-15% Superior and inferior pancreaticoduodenal arteries 10% Surgical mortality 15-40%
249
How can chronic pancreatitis mess up the portal vein?
inflammation can cause a thrombosis also can cause stenosis
250
risk factors for pancreatic adenocarcinoma
smoking
251
where is most pancreatic adeno found?
head (80%)
252
why is pain a poor prognostic indicator for pancreatic Ca?
infiltrated the retroperitoneal nerves
253
Why is pancreatic phase an early acquisition?
The pancreas will enhance early, malignant (adneo) will be delayed compared to this 40 seconds instead of 65 seconds
254
Differentials for a solid mass in the pancreas?
Chronic pancreatitis Groove pancreatitis Autoimmune pancreatitis Metastases to the pancreas Non-functioning neuroendocrine tumours Distal cholangiocarcinoma
255
Causes of SBO
adhesions (505) External or internal hernias (15%) Malignancy (15%)
256
SBO mechanical - two types
Simple - one or several points along the bowel. Closed loop - two adjacents points in close proximity
257
why differentiate between simple and closed mechanical obstrcution?
in closed the intervening mesentry (blood vessels) can also be obstructed
258
what is the definition of strangulation ?
A closed loop obstruction associated with intestinal ischaemia.
259
Small bowel wall thickness
less than 2mm normally
260
Causes of small bowel target sign on CT
Ischaemic bowel Intramural haemorrhage Inflammatory bowel disease Henoch-Schönlein purpura Infective enterocolitis Pseudomembranous enterocolitis Radiation enterocolitis Portal hypertensive enteropathy
261
CT features of uncomplicated Crohn's disease
Comb sign: dilatation of parallel mesenteric vessels perpendicularly entering an actively inflamed bowel segment (the vessels mimic the teeth of a comb) Misty mesentery (streaking of the perienteric fat indicating hyperaemia/inflammation) Stenosis Pre-stenotic dilatation/obstruction
262
MRI bowel in crohns - what to assess?
Lesion site Lesion extent (length) Number of strictures and their degree (based on pre-stenotic dilatation) Maximum bowel wall thickness Bowel wall signal intensity Signal intensity of fibrofatty proliferation on fat-suppressed images (oedema/hyperaemia) Local complications, for example local free fluid, phlegmons, abscesses, or fistulas
263
What are the differentials for crohns on CT
Acute ileitis Appendicitis Mesenteric adenitis (viral or bacterial, self-limiting) Infectious ileocaecitis, for example tuberculosis or other (Yersinia, Salmonella, Shigella, Campylobacter) Eosinophilic gastroenteritis (rare, eosinophilia, responds to steroids)
264
What portion of pancreatic Ca are pancreatic ductal adenocarcinoma
>90%
265
How to divide the other tumours of pancreas?
by tissue type
266
Pancreatic cancer tissue type
Epithelial, indeterminate, non-epithelial
267
Pancreatic epithelial origin tumours
Duct cell tumours (ductal adeno (>90%). also get benign epithelial cyst which is uncommon. Endocrine cell tumours, exocrine tumours and variant carcinoma of duct cell origin
268
What are the types of variant cacrinoma of duct cell origin ?
Cystic lesions: Mucinous cystic neoplasm and serous cystadenoma (microcystic) Pleomorphic giant cell carcinoma Adenosquamous carcinoma Intraductal papilloma Mucinous adenocarcinoma
269
Epithelial endocrine cell tumours in pancreatic cnacer
Insulinoma Gastrinoma Non-functioning islet cell tumour Glucagonoma VIPoma Somatostatinoma
270
Exocrine cell tumours as part of epithelial pancreatic cnacners
Acinar cell carcinoma Acinar cystadenocarcinoma Pancreaticoblastoma
271
Pancreatic cancer of indeterminate origin include
solid and papillary epithelial neoplasm (SPEN). Small cell carcinoma.
272
Pancreatic cancer - non epithelial origin tumours
Sarcoma Dermoid cyst Lymphangioma Leiomyosarcoma Haemangiopericytoma Malignant fibrous histiocytoma Lymphoepithelial cyst Lipoma Schwannoma/paraganglioma
273
What are most pancreatic cystic lesions
pseudocysts
274
Differential list for cystic lesions of the pancreasa?
Pseudocyst (most common) Mucinous cystic neoplasm Serous cystadenoma Cystic islet cell neoplasm Solid and papillary epithelial neoplasm Giant cell tumour Acinar cystadenocarcinoma Cystic teratoma Lymphangioma Haemangioma Paraganglioma Epithelial cyst, associated with von Hippel-Lindau (VHL) disease, cystic fibrosis and adult polycystic disease Ms Scagleph
275
Pancreatic cystic neoplasm - usually affect who?
female, 40 - 60 pancreatic tail
276
What are IPMT in pancreatic mucinous cystic neoplasm
Intraductal papillary mucinous tumours. Malignnat but low indolent course. Men over 65
277
Serous cystadenoma in pancreatic tumours is idnetified by what features?
Large, inumerable cysts, central calcification is common.
278
Give examples of variant carcinomas of duct cell origin in pancreatic cancer? What is a feature that can look like cysts?
Pleomorphic giant cell carcinoma Adenosquamous carcinoma Microadenocarcinoma Mucinous adenocarcinoma Anaplastic carcinoma The feature is necrosis.
279
Pancreatic endocrine tumours - list
Insulinoma Gastrinoma Non-functioning islet cell tumours Glucagonoma Vasoactive intestinal peptide-screening tumours (VIPomas) Somatostatinoma
280
What is whipples triad?
hypoglycaemic on fasting fasting blood sugar less than half normaly rapid relief of symptoms with glucose infusion. seen in insulinoma
281
Gastrinoma causes what?
Zollinger-Ellison syndrome
282
Solid and papillary epithelial neoplasm pancreatic Ca affects who?
young females
283
Small bowel malignancy presenting features
Abdominal pain Gastro-intestinal (GI) bleeding Nausea and/or vomiting Weight loss Diarrhoea Abdominal mass
284
Common sdmall bowel malignancies
Adenocarcinoma Carcinoid Lymphoma Gastro-intestinal stromal tumours (GIST)
285
Rare small bowel malignancies
Liposarcoma Neurosarcoma Angiosarcoma Haemangioendothelioma Fibrosarcoma
286
conditions which increase risk of small bowel cancer?
Adenomatous polyps Coeliac disease (usually duodenum or jejunum) Crohn's disease (distal ileum) Peutz-Jeghers syndrome (duodenal adenocarcinoma) Neurofibromatosis (ileum) Ileal conduit or ileocystoplasty (adjacent to anastomosis) Ileostomy after colectomy (ileocutaneous junction) Duodenal or jejunal bypass surgery Lynch syndrome II Congenital bowel duplication
287
how does jejunal and ileal adeno spread on CT?
adenocarcinomas may be heterogeneous in attenuation and show moderate IV contrast enhancement. Adenocarcinoma may extend into the mesentery and metastasise to local lymph nodes, liver, peritoneum and ovaries. Bulky lymphadenopathy is rare.
288
Where do abdominal carcinoid tumours
neuroendocrine amine precursor uptake and decarboxylation cells derived from the different embryonic divisions of the gut
289
Carcioid constitues what proportion of small bowel malignancies and where are they most commonly found?
Small bowel and appendix Quarter
290
Carcinoid in the duodenum (rare) can be associated with what conditons?
ay be associated with Zollinger-Ellison syndrome or neurofibromatosis
291
Carcinoid metastases are related to what facotr?
Size
292
Carcinoid mets where?
liver, lymph and bone
293
features of haemangioma on US
hyperechoic no hypoechoic rim no flow on dopplers
294
features of haemangioma on MRI
T2 bright shine through for all types of haemangioma
295
types of haemangioma
tpyical giant sclerosed high flow haemangiomatosis (rare)
296
Giant haemangioma whill fill in or not?
no, too large can look like a scar
297
sclerosed hamangioma - how to diagnose?
loss of cavernous hamengioma charachteristiscs as retracted in post infarction. progressive infilling
298
list of lesions with capsular retration
metasases (treated) Intrahepatic cholangiocarcinoma sclerosed haemangioma epithelioid haemangioendothelioma
299
haemangiomatosis is what
replacement of liver parenchyma by multiple haemangiomas
300
high flow haemangiomas features
fill rapidly wedge shaped THAD due to perfusion changes
301
FNH is caused by what
hyperplastic response to a vascular insult
302
FNH scar is what on MRI
high T2 signal
303
US FNH
hyper or hypo echoic spoke wheel present
304
FNH on CT and MRI
stealth - pretty isointense
305
FNH with contrast
massive arterial enhancement NO WASHOUT
306
what is whashout
liver lesion is darker than parenchyma in portal venous or delayed
307
what is fade post contrast mean?
liver lesion becomes less bright than arterial phase but is never darker than background liver
308
FNH on MRI, what happens
similar to CT arterial enhancement
309
OATP receptors exist on what?
hepatocytes
310
MOAT receptors exist on
bile canaliculus
311
Does FNh express OATP
yes
312
tpyes of FNH on HBP with HSCA
hyperintense ring pattern
313
which liver lesions can demonstrate a central "scar" ?
FNH fibromellar HCC giant haemangioma any large lesion with a central component/necrosis
314
HC adenomas grow in repsonse to
steroids (exogenous or indogenours)
315
HA vs FNH - what do you do?
need MRI as otherwise very similar
316
HA vs FNH on MRI?
HA does not have OATP and so will be dark on MRI contrast
317
subtypes of HA
HNF 1 inactivated HA inflammatory HA B catenin acitivateded HA non specific HA
318
Appearance of HNF1a HA
Fat in lesion gene for getting rid of fat has been removed
319
appearance of Inflammatory HA
T2 bright Atoll sign (Island rim sign) Can mimic FNA high bleeding risk
320
appearance of B catenin HA
High risk of HCC No specific sign may show washout
321
Liver metastases T2 -
bright
322
Liver mets - do they have OATP?
No therefore dark on contrast MRI
323
Liver arterial rim type enhancement think
liver mets
324
Hypervascular liver mets types
RCC Thyroid Neuroendocrine melanoma choriocarcinoma
325
Sequences for liver mets what do you use
DWI with primovist
326
T2 shine through on ADC can be a result of
central necrosis
327
Intra hepatic cholangiocarcinoma ICCA risk factors
Cirrhosis Hep B and C
328
ICCA appearance
rim arterial enhacnement capsule retration satelllite nodule cloud like infilling of the lesions
329
infilling of haemangioma vs ICCA
haemangioma infills from outside in ICCA is cloud like
330
hepatic AML what proportion of fat
can be fat rich or fat poor
331
Differentials for fat containing liver mass
HCC HNF 1 HA dysplastic nodule (cirrhosis) Hepatic AML
332
HCC - fibromellar affects who?
young adults
333
fibromellar HCC presents as
large well define with a scar
334
Features of Fibromellar HCC on imaging
washout heterogenous compared to FNH Central T2 dark central scar calcification low signal in HB phase
335
Epithelioid haemangioendothelioma what is it
rare low grade malignancy multiple lesions / multifocal
336
how does features of haemangioma image look like
multiple lesions geographical capsular retraction ++
337
who do we screen for HCC
High risk people cirrhotics non cirrhotic HBV HCV and fibrosis NAFLD and fibrosis
338
What is a positive Liver US HCC screen
1cm lesion in liver. (hypo or hyper) CT or MRI next if less than 1cm, do 3 monthly USS intervals
339
main thing for diagnosing HCC on imaging
Non rim Arterial phase enhancement enhancing capsule nonperipheral washout threshold growth
340
how can HCC be diagnosed (lesions structure)
due to vascular lesion angiogenesis unpaired arteries. Late arterial phase hyperenhancement
341
HCC venous changes?
hepatic vein to portal vein drainage reduced portal vein blood supply rapid drainage of contrast - washout
342
liver lesion washout seen in
HCC dysplastic nodules
343
HCC capsule - what is it
thin rim around the lesion
344
HCC threshold growth is what
50% growith in 6 months
345
Types of HCC
Early progressed nodule in nodule angioinvasive infiltrating
346
Early HCC
less than 2cm no capsule no vascular changes hard to diangose
347
progressed HCC
the typical blood supply changes capsule charachteristic
348
ancillary features of HCC
mosaic arhcitecutre corona enhancement - early contrast of surrounding liver, get satellite nodules here
349
Fat in HCC
common good indicator of Hepatocellular origin
350
DWI HCC will show what and why?
HCC are densely packed cells true restriction though if well differentiated may not show restriction
351
OATP expression on HCC
the more progressed the HCC the less OATP is expressed
352
cirrhotic nodules also called
regenerative nodules
353
macroregenerative nodules appearance
big and benign T1 bright T2 dark (iron uptake) normal vessels pass through
354
low grade dysplastic nodules are only seen in what phase
HB phase due to fat they still haev some OATP expression
355
dark HB phase lesion differential list
HCC (early and progressed) dysplastic nodules Cholangiocarcinoma
356
ICCA apperance
rim enhancement cloud like infilling washout
357
confluent hepatic fibrosis what is it
extensive fatty fibrosis with volume loss extends to the hilum normally triangular T2 bright scar tissue
358
peribiliary cysts in the cirrhotic liver develop from
peribiliary glands