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AA ST2 > Gastroenterology > Flashcards

Gastroenterology Flashcards

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
Q

1-year-survival for metastatic oesophageal cancer

A

20%

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26
Q

UPPER GI imaging is mostly for what purpose?

A

staging and response to treatment.

Endoscopy and biopsy are done for the symptoms

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27
Q

what are the oesophagus landmarks for the three parts

A

oharynx to aortic arch

aortic arch to inferior pulmonary vein

inferior pulmonary vein to GOJ

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28
Q

risk factors for oesophgeal SCC

A

smoking and alcohol
age - over 40
afrocaribbean
radiotherapy
hot drinks

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29
Q

Oesophageal SCC is associated with what other cancers?

A

Head and neck SCC - staging often includes the neck

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30
Q

Oesophageal SCC is most common in which part of the oesophagus?

A

middle - 50%

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31
Q

What is Barretts

A

rrett’s oesophagus: This is a condition where oesophageal stratified squamous cell epithelium undergoes metaplasia to columnar epithelium.

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32
Q

Patients with high grade dysplasia are given what options?

A

Surgey - oesophagectomy - are considered - 30% will develop cancer.

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33
Q

Once oesophageal tumour is confirmed, further investigations can be considered to aid staging:

A

Positron emission tomography (PET)/CT
Endoscopic ultrasound

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34
Q

Oesophageal CT tumours

A

Oesophageal tumours usually show as thickening of the oesophageal wall. The oesophagus proximal to the tumour may be dilated and contain food residue.

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35
Q

what is diagnostic for achalasia? physiology teting

A

high pressure scphincter that doesn’t relax.

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36
Q

biochemical indicators of iron deficiency anaemia

A

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)

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37
Q

The serum ferritin correlates well with iron stores, but it can also be elevated with…. ?

A

liver disease, inflammatory conditions, and malignant neoplasms.

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38
Q

Common causes of occult GI blood loss

A

Aspirin NSAID 10-15%
Colonic carcinoma 5-10%
Gastric carcinoma 5%
Benign gastric ulceration 5%
Angiodysplasia 5%

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39
Q

Risk factors of colon cancer

A

Genetic - FAP
IBD - UC and diet

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40
Q

How is colon cancer staged?

A

TNM

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41
Q

Colon cancer - 80%of all colon cancers are what stage at presentation?

A

T3 - Tumour extends beyond the muscle layer into pericolic or perirectal tissue

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42
Q

Fro colon staging scan what parameters should be used?

A

Oral contrast. IV contrast with delay of 25s thorax and 60 s for abdo pelvis

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43
Q

Colon cancer when can MRI be used?

A

distal sigmoid and upper rectum

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44
Q

Colon cancer when can PET CT be used?

A

recurrence if markers going back up. Detectin of extrahepatic disease if undergoing hepatic recetion for metastasis

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45
Q

Colorectal TNM - what is the N staging

A

N0 - none
N1 three or less
N2 - four or mroe

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46
Q

streaky change in the fat surrounding the sigmoid colon, which may be a result of ???

A

peritumoural inflammation or infiltration of tumour into the surrounding fat.

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47
Q

Colorectal cancer staging - lymph node size cut offs?

A

if >1cm likely malignanct involvement.
If under then likely inflammatory.

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48
Q

Colon cancer relationship of lung and liver mets?

A

If lung mets then normally there will be liver mets first

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49
Q

Colorectal cancerr - why do MRI?

A

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

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50
Q

Low rectal tumours an achieve wider dissemination - why?

A

bypoass the liver capillary netowrk that captures other cells

or lymphatic spread

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51
Q

Colorectal cancer - R2 meaning

A

there is macroscopic involvement of tumour resection margin.

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52
Q

Colorectal cancer - R1 meaning

A

indicates that there is microscopic involvement of the resection margin or that the tumour comes within 1 mm of the margin.

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53
Q

Colorectal cancer - R0 meaning

A

R0 indicates that there was a margin of at least 1 mm of normal tissue between the tumour and the resection margin.

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54
Q

Path report - V1

A

Vascular invasion.

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55
Q

Vascular invasion of colon cancer seen on what modality?

A

MRI - if greater than 3mm

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56
Q

Patients with lymph node involvement at surgery are usually offered are usually offered what?

A

adjuvant chemotherapy to reduce the risk of recurrent disease.

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57
Q

Colon cancer - metastatic locations

A

27% of patients develop liver metastases, approximately two thirds are identified at presentation and the other third present in next 3 years.

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58
Q

Colon liver mets appear as what on CT? and why?

A

hypovascular and so best seen as hypodense on portal venous phase study.

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59
Q

Colon liver mets appear as what on MRI? and why?

A

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

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60
Q

Do mets take up MR contrast?

A

no

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61
Q

Colon cancer - Right-sided tumours recur within …..

A

para-aortic nodes adjacent to the superior mesenteric artery (SMA),

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62
Q

Colon cnacer - left-sided tumours metastasis

A

to the para-aortic nodes adjacent to the origin of the inferior mesenteric artery (IMA).

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63
Q

why are liver and lung mets excised?

A

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.

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64
Q

How is MRI used to differnetiate recurrence at an anastomosis?

A

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

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65
Q

Hydronephrosis post colon cancer surgery?

A

Sinister sign for recurrence

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66
Q

IN colon cancer when is MR used?

A

if there is a known liver met and no extra hepatic mets then can be used to aid surgical approach

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67
Q

Chemo in the use of cancer treatment - 3 types what are they>

A

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

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67
Q

what are diverticula?

A

herniations of mucosa and submucosa through the colonic wall.

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68
Q

which points are suscepitble to divertiucla?

A

Where the vasa recta penetrate

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69
Q

two types of diverticlosis

A

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

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70
Q

Diverticulitis CT features

A

Diverticula
Fat stranding
Centipede sign (hyperaemic engorged vasa recta)
Arrow head sign
Wall thickening >4 mm

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71
Q

How to diverticula bleeds occur?

A

They occur through arterial blood supply - thinnning of the vasa recta

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72
Q

External anal sphincter is made of what muscle?

A

Striated muscle

Squeezed to withold defecation

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73
Q

internal anal sphincter is made of what@

A

smooth muscle
85% of resting anal pressure

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74
Q

What muscle lies between the EAS and IAS ?

A

interspincteric plane - longitudinal muscle

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75
Q

On US - smooth muscle is generally what kind of pattern?>

A

hyporeflective

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76
Q

what are the two causes of incontinence>

A
  1. Disruption of the sphincter muscles

childbirth but can also occur secondary to surgical procedures, trauma, etc.

  1. Atrophy of the sphincter muscles
    This may be due to ageing or the effect of pudendal nerve stretching during pregnancy and childbirth.
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77
Q

what are the two syndromes of anal spinchter atrophy?

A

IAS atrophy or ‘degeneration’ where the IAS is thinned and difficult to visualise
EAS atrophy where the EAS is thinned and replaced by fat

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78
Q

Fistula in ano is believed to arise from ??????

A

chronic infection of the anal glands.

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79
Q

‘Parks classification of sphincters is what?

A

Intersphincteric
Transsphincteric
Suprasphincteric
Extrasphincteric

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80
Q

How to treat fistulas in anus?

A

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

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81
Q

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:

A

Transsphincteric
Supralevator
Extrasphincteric

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82
Q

Supralevator sepsis in anal fistulas is important to note - why?

A

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

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83
Q

T or F

MR imaging is as accurate as clinical examination for classification of fistula in ano

A

F
MR imaging is far superior.

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84
Q

T or F
The main role of MR imaging is the pre-operative detection of areas of sepsis

A

T
It has been shown that MR imaging can detect sepsis that would otherwise be missed.

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85
Q

T or F
Sphincter division is greater for a transsphincteric fistula than intersphincteric fistula

A

T
When laying open an intersphincteric fistula the EAS is not divided.

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86
Q

T or F
The internal opening of a suprasphincteric fistula is higher than an extrasphincteric fistula

A

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.

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87
Q

T or F
It has been shown that pre-operative MR imaging can reduce subsequent fistula disease

A

T
By up to 75% in complex cases.

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88
Q

Liver is created in which mesentry?

A

ventral

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89
Q

falciform ligament become what?

A

ligamentem teres

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90
Q

Special blood supply of caudate lobe?

A

frm left and right hepatic arteries.
Venous drainage straight to IVC

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91
Q

Oesophageal staging type

A

TNM

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92
Q

Oesophagus lymph node drainage?

A

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.

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93
Q

Location of Oesophageal mets?

A

liver and lung being the most common sites. Other sites include brain, bone, and intra-abdominal organs.

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94
Q

When is PET /CT FDG used in oesophageal cancer?

A

Proximal to GOJ
if no mets found on CT then PET is done with diangostic laparoscopy and endoscopic ulrasoun

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95
Q

normal oesophageal wall thickness

A

is less than 3 mm thick

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96
Q

How to tell T staging?

A

Very difficult
if outer edge against fat is irregular assume T3.

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97
Q

Oesophageal cancer lymph node size cut off?

A

10mm
though some groups are 6mm like supraclavicular

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98
Q

Features of a benign node

A

Benign nodes tend to be oval, triangular, flat or kidney shaped

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99
Q

features of malignant node

A

fatty core replaced by malignant tissue, spherical, hypoechoic, well defined

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100
Q

Oesphageal T staging

A

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/

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101
Q

Fluorouracil (5 FU)) can produce what side effect

A

coronary spasm

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102
Q

reasons for neo adjuvant therapy

A

sterilise lymph nodes
down stage the disease
reduce chance of spread

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103
Q

post chemo CT reviews what?

A

Size of primary
size of lymphadenopathy
any mets / response

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104
Q

Gastric cancer risk factors

A

low fruit and veg
smoked food, salted foods

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105
Q

Gastric cancer signs and symptoms

A

Indigestion
nausea and vomitting
dysphagia
postprandial fullness

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106
Q

Gastric cancer late complicaitons

A

pathologic perotneal and pleural effusions
GOT obstruction
bleeding

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107
Q

Duodenal cancer - risk facotrs

A

coeliac disease
crohns
colonic polyps

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108
Q

Duodenal cancers are mostly

A

Adenocarcinomas

others are carcinoid and sarcomas

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109
Q

how does H Pylori cause gastric cancer

A

Atrophic gastritis leads to atrophy, metaplasia, dysplasia and then malignancy.

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110
Q

Pernicious anaemia gives a higher risk of what

A

gastric malignancy

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111
Q

Relationship of mgastric polyps to gastric malignancy

A

gastric polyps are less common than malignancy. x30 cancer is more common than polyps

Most polyps are inflammatory.

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112
Q

duodenum - where is most common for adneocarcinoma?

A

third part

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113
Q

mets to duodenum are from what cancers?

A

melanoma, breast and lung

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114
Q

most common benign tumour f the stomach

A

leiomyomas

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115
Q

less common benign cancers of the stomach

A

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

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116
Q

Hamartomas occur in patients with

A

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)

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117
Q

Adenomatous polyps occur in patients with:

A

Familial polyposis coli (the majority of these patients have gastric polyps)
Gardner’s syndrome (osteomas, soft tissue tumours, dental anomalies)

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118
Q

what are the three types of gastric volvulus?

A

Mesentero-axial
organo-axial
vertical

most common - organo axial. axis from cardia to pylorus

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119
Q

what are the three types of gastric volvulus?

A

Mesentero-axial
organo-axial
vertical

most common - organo axial. axis from cardia to pylorus

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120
Q

Duodenum divertiucla are assocaited with what?

A

small bowel overgrwoth and malabsorption

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121
Q

oesophagus - what level does striated uscle turn into smoth muslce?

A

around aortic arch - xzone of transition

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122
Q

Achalasia is characterised as…..

A

aperistalsis of the oesophagus with associated lower oesophageal dysfunction.

reduced ganglionic cells in myenteric plexus.

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123
Q

radiographic appearance of oesophagus onf nutcracker syndrome

A

normal

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124
Q

myenteric plexus can also become damaged simulating achalasia in

A

chronic Chagas’s disease

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125
Q

Chagas’s disease is by

A

Trypanosome cruzi and is endemic in Central and South America. Reduvid bug.

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126
Q

How does scleraderma affect the bowel?

A

Scleroderma is an autoimmune condition that leads to the atrophy and fibrosis of the smooth muscle layer of the bowel

dilates the oesohpagus

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127
Q

Technetium-99m (99mTc) as pertechnetate is cleared from the circulation into the

A

thyroid, the choroid plexus of the brain, the salivary glands and the normal gastric mucosa.

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128
Q

How is octreotide used for neuro endocrine tumours

A

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.

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129
Q

FDG is labelled with what for the Nuc med scans

A

Flu 18

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130
Q

Simple cysts and peoples age

A

become more frequent in lder age

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131
Q

Simple cysts are associated with other diseases

A

Tuberous sclerosis
Polycystic kidney disease (approximately 30% of patients also have liver cysts)
Polycystic liver disease (auto-dominant)
Von Hippel-Lindau (VHL) syndrome

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132
Q

Can you list three sonographic criteria that allow this lesion to be called a simple cyst?

A

Anechoic/water echogenicity
Posterior acoustic transmission
A well-defined or imperceptible wall

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133
Q

Simple cyst on CT - HU should be

A

10 or less

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134
Q

Simple cyst on MRI

A

low signal on T1W spin-echo (SE) images, and very high signal on T2W images, as shown in Fig 1.

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135
Q

US appearance of complex cysts

A

A thick wall
Internal septa
Haemorrhage
Debris
Calcification

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136
Q

Name the types of benign liver cystic lesions?

A

Biliary cystadenoma
Hydatid
Multiple biliary hamartomas

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137
Q

Where to biliary cystadenomas arise from?

A

Bile ducts, occur often in the right lobe

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138
Q

Symptoms of biliary cystadenomas?

A

abdominal pain

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139
Q

Characteristics of biliary cystadenomas?

A

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.

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140
Q

Risk of biliary cystadenomas?

A

can have malignant transformation

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141
Q

What is hydatid disease?

A

Hydatid disease is a multi-system condition effecting the bowel, liver, lungs, spleen, kidney, bone and central nervous system (CNS).

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142
Q

Complications of hydatid?

A

Jaundice. Other complications include rupture, infection and anaphylaxis.

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143
Q

How does hydatid appear on imaging?

A

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

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144
Q

What treatment is used ofr hydatid cysts ahead of srgery?

A

albendazole

145
Q

Multiple biliary hamartomas, also known as

A

von Meyenburg complexes,

146
Q

what are multiple biliary hamartomas

A

Lesions comprise small groups of dilated bile ducts.

147
Q

US appearances of multiple biliary hamartomas

A

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
Q

What is most common benign focal liver lesion?

A

haemangioma

149
Q

Two types of haemangioma?

A

typical and giant

150
Q

features of typical haemangiomas

A

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
Q

features of giant haemangioma

A

these are uncommon, >5 cm in size and may be symptomatic with risk of haemorrhage and thrombosis

152
Q

On CT, haemangiomas are normally

A

well-defined hypodense masses with peripheral nodular enhancement post-contrast and centripetal fill-in on delayed scans.

153
Q

Haemangioma on MRI

A

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
Q

the second most common benign tumour of the liver

A

Focal nodular hyperplasia

155
Q

what is focal nodular hyperpalsia?

A

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
Q

focal nodular hyperplasia and COCP association

A

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
Q

focal nodular hyperplasia on CT

A

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
Q

Central scar is classic for focal nodular hyperplasia but can also be found in

A

central scar is classic, it is not pathognomic and can also be found in fibrolamellar HCC, adenoma, and hepatic necrosis.

159
Q

what are the types of hepatic adenomas

A

Inflammatory
Hepatic nuclear factor (HNF) 1 alpha-mutated
Beta catenin-mutated
Unclassified hepatic

160
Q

what are the complications of hepatic adenomas?

A

infarction
haemorrhage
malignant transformation

161
Q

What are hepatic adenomas associated to?

A

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
Q

hepatic adneomas US appearance and why?

A

well-defined mixed echogenicity lesions due to their varying component. Because of this, their appearances are often non-specific.

163
Q

hepatic adenomas on MRI

A

high signal on T2 (Fig 1) and low signal on T1 (Fig 2).

164
Q

Nucklear medicine and Kuppfer cells

A

Kuppfer cells uptake the radioisotope. So lesions with high kuppfer cells appear as bright

165
Q

common anatomy mimics in the liver for lesions?

A

adjacent to falciform ligament
perfusion mimics are in the congested liver, which gives a mottled, inhomogeneous appearance

166
Q

common causes of fatty infiltration of the liver

A

Obesity
Toxins: Alcohol, Amiodarone, Chemotherapy

Steroids
Malnutrition
Hepatitis
Chronic illness: Diabetes, Congestive heart failure, Tuberculosis

Glycogen storage disorders

167
Q

Focal fatty change normally affects which parts of the lvier

A

caudate lobe, right lobe, perihilar region

168
Q

how to tell fatty focal change from a mass lesion?

A

look at the vessels, do they pass through it freely?

169
Q

which MRI sequence is useful for fatty liver?

A

in and out phase sequence

170
Q

focal fatty SPARING is common where?

A

falciform ligament and the gallbaldder fossa

171
Q

in cirrhotic livers what are the other types of mass lesions that can be found?

A

regenerating nodules are found

172
Q

Location of focal nodular hyperplasia?

A

subcapsular

173
Q

FNH on non contrast T2W imaging

A

bright central scar

174
Q

FNH - type of early arterial enhancement?

A

There is arterial enhancement though a tortuous feeding artery and a spoke-wheel pattern of internal vessels. Later, there is centrifugal filling.

175
Q

low kpffer cell lesions?

A

haemangioma and adeonoma are low in Kupffer cells

176
Q

Simple cysts are associated with what?

A

Tuberosclerosis

176
Q

Simple cysts are associated with what?

A

Tuberosclerosis

177
Q

Which liver lesions have a centralvscar

A

FNH
Fibromellar HCC
Adenoma
Hepatic necrosis

178
Q

two types of HCC

A

HCC

Fibromellar HCC

179
Q

Typical enhancement characteristics of HCCs on arterial-phase imaging

A

Hepatocellular carcinomas are typically hyperenhancing in the arterial phase

180
Q

Typical enhancement characteristics of HCCs on venous-phase imaging

A

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
Q

The appearance of HCC on ultrasound:

A

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
Q

T or F

Hepatocellular carcinomas enhance with extracellular contrast similarly to the enhancement on CT

A

T

183
Q

diffusion restirction is typical for which liver lesion

A

HCC

184
Q

what is LI- RADS

A

LR 1 definitely benign

LR5 definitely HCC

185
Q

who does li rads apply to

A

patients with high risk of hcc

186
Q

HCC lesion assessment features

A

Non-rim arterial phase enhancement
Non-peripheral washout
Enhancing capsule appearance
Size
Threshold growth: ≥50% increase in ≤6 months

187
Q

Hoe best to differentiate HCC form benign lesions

A

dual contrast MRI

188
Q

Poorly-differentiated HCC, metastases and adenomas do not enhance in the hepatocyte phase as they

A

do not contin hepatocytes

189
Q

how to differentiate HCC from hypovascular metastases

A

hypoenhancement in the arterial phase compared to hyperenhancement in HCC).

190
Q

Do malignant liver lesions take up SPIO

A

no

191
Q

HCC on MRI

A

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
Q

FNH on MRI

A

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
Q

Adenoma on MRI

A

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
Q

MRI findings for dysplastic liver nodules

A

Cirrhosis
No raised AFP
Often take up of SPIO
Bright enhancement
Usually no pseudocapsule

195
Q

MRI findings of haemangiomas

A

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
Q

Can you think of four or more differences between conventional HCC and fibrolamellar HCC?

A

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
Q

T or F

Hepatocellular carcinomas are hyperenhancing in the arterial phase
A

T

198
Q

Do liver cysts arterially enhance

A

No

199
Q

Why is LI RADS not used in vascular disorders of the liver?

A

As vascular disorders can form benign nodules which can mimic HCC, LI-RADS should not be applied in:

200
Q

What are the primary liver tumours?

A

Hepatoma

Intra-hepatic cholangiocarcinoma
Haemangioendothelioma
Angiosarcoma
Biliary cystadenocarcinoma
Hepatic lymphoma

201
Q

Liver mets from which cnacers?

A

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
Q

When is biopsy of a liver lesion conducted

A

If ultrasound shows widespread lesions consistent with unresectable metastases, biopsy may be performed.

203
Q

Certain tumours have arterially enhancing metastases, with these an arterial phase scan (25-30 seconds) should be added. These tumours are

A

neuroendocrine, renal cell carcinomas and thyroid tumours.

204
Q

Can you list four indications for performing a liver MRI when looking for metastases?

A

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
Q

how does SPIO help image livers?

A

taken up by normal liver (which goes dark) and so will show mets easily (not taken up by mets)

206
Q

Why is SPIO best imaged in T2*

A

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
Q

how does cholangiocarcinoma invade?

A

along the bile ducts

208
Q

what are the three types of cholangiocarcinoma

A

Mass-forming: usually large and well-defined
Periductal-infiltrating: often spiculate
Intraductal: often multiple

209
Q

CT appearances of intrahepatic cholangiocrcinoma

A

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
Q

cholangiocrcinoma bet seen in what CT contrast phase

A

Late venous - 10 minutes

211
Q

Crohns disease - behaviour types

A

Inflammatory (non-stricturing, non-penetrating)
Stricturing
Fistulating (penetrating)

212
Q

Smoking link with UC and Crohns

A

increases crohns but decreases UC

213
Q

Acute severe pancreatitis can be associated with organ failure and local complications such as

A

necrosis (with infection), pseudocyst or abscess.

214
Q

What is a pancreatic Acute pseudocyst

A

is a collection of pancreatic juice enclosed in a wall of fibrous or granulation tissue that arises following an attack of acute pancreatitis.

215
Q

How long to create a pseudocyst

A

4 weeks

216
Q

commonest causes of pancreatitis?

A

gallstones and alcohol

217
Q

What does atlanta criteria seperate?

A

Mild pancreatitis (85%) from Severe (organ failure and necrosis)

218
Q

Severe pancreatitis involves necrosis - what are the two types of necrosis?

A

infected (50% mortality)

sterile

219
Q

time course of acute pancreatitis?

A

Proinflammatory - SIRS for two weeks

Anti inflammatory - immunosupressed for two weeks

220
Q

what is the amylase threshold for pancreatitis?

A

x4

221
Q

What is US useful for in acute pancreatitis?

A

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
Q

pancreatitis acquisition type?

A

arterial and portal venous

223
Q

which scores are used for pancreatitis on CT?

A

extent of necrosiss as percentage

AND
balthazar

224
Q

Define a mild pancreatitis on CT

A

(also known as interstitial pancreatitis): a Balthazar score of B (enalrged) or C (inflammatory changes to surrounding fat) , without pancreatic or extrapancreatic necrosis

225
Q

Define an intermediate pancreatitis?

A

intermediate pancreatitis (also known as exudative pancreatitis): a Balthazar score of D (fluid collection) or E (multiple collections), without pancreatic necrosis.

226
Q

Severe pancreatitis is considered when there is what>

A

necrosis

227
Q

when should patients with pancreatitis have their CT assessment?

A

All patients with acute pancreatitis should have a CT assessment between 3-10 days to try to predict the radiological severity of episode.

228
Q

indication to re-scan a patient with pancreatitis?

A

Diagnostic uncertainty
Assessment of severe cases
When clinical deterioration occurs
Guidance for interventional procedures
For follow-up and monitoring of complications

229
Q

Usually the whole pancreatic gland is involved in pancreatitis.

How often and for what reason is it only parital??

A

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
Q

complications of pancreatic pseudocyst?

A

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
Q

complications of pancreatic pseudocyst?

A

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
Q

only reliable CT sign indicating infected necrosis of pancreatitis

A

small gas bubbles in the peripancreatic collection

232
Q

differentials when considering acute pancreatitis?

A

Pancreatic ductal adenocarcinoma
Autoimmune pancreatitis
Peptic ulcer disease with posterior perforation
Pancreatic lymphoma

233
Q

intra and extra hepatic duct dilatation with swollen pancreas

A

can be due to the pancreaittis. not necessarily just gallstones

234
Q

in acute pancreatitis - portal vein thrombosis can lead to

A

subsegmental portal hypertension,
splenic enlargement and
distal variceal formation.

235
Q

typical punctate calcification across the upper abdomen on a plain film is diagnostic of

A

chronic pancreatitis

236
Q

The presence of calcification is much more likely when the chronic pancreatitis is caused by

A

alcohol

237
Q

US appearance of chronic pancreatitis?

A

Alterations of the size and echotexture of the gland
Focal masses
Calcification
Pancreatic duct dilatation
Pseudocyst formation

238
Q

EUS findings for chronic pancreatitis

A

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
Q

CT findings for chronic pancreatitis

A

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
Q

What is the considered measurement for atrophic pancreas?

A

1cm in tail - AP
1.5cm in the head

241
Q

How big is the duct in chronic panreatitis

A

Dilatation of the pancreatic duct and the secondary radicles to greater than 3 mm is a feature of chronic pancreatitis

242
Q

What vascular complications can occur with chronic pancreatitis?

A

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
Q

What would you see on MRI of chronic pancreatitis?

A

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
Q

What is a chronic pancreatitis pseudo cyst?

How will the wall enhance with contrast?

A

well demarcated and unilocular collection

if the wall is thick then is will enhance after contrast

245
Q

How long does it take to develop a pseudocyst after acute pancreatitis?

A

6-8 weeks

246
Q

What happpens if a pseduocyst ruptures into the peritoneum?

A

can develop pancreatic ascites

247
Q

When should pseudocysts be operated on?

A

greater than 6cm or sometimes for pain

248
Q

How does a pancreatic pseudoaneurysm form after acute or chronic pancreatitis?

Surgical mortality?

A

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
Q

How can chronic pancreatitis mess up the portal vein?

A

inflammation can cause a thrombosis

also can cause stenosis

250
Q

risk factors for pancreatic adenocarcinoma

A

smoking

251
Q

where is most pancreatic adeno found?

A

head (80%)

252
Q

why is pain a poor prognostic indicator for pancreatic Ca?

A

infiltrated the retroperitoneal nerves

253
Q

Why is pancreatic phase an early acquisition?

A

The pancreas will enhance early, malignant (adneo) will be delayed compared to this

40 seconds instead of 65 seconds

254
Q

Differentials for a solid mass in the pancreas?

A

Chronic pancreatitis
Groove pancreatitis
Autoimmune pancreatitis
Metastases to the pancreas
Non-functioning neuroendocrine tumours
Distal cholangiocarcinoma

255
Q

Causes of SBO

A

adhesions (505)
External or internal hernias (15%)
Malignancy (15%)

256
Q

SBO mechanical - two types

A

Simple - one or several points along the bowel.

Closed loop - two adjacents points in close proximity

257
Q

why differentiate between simple and closed mechanical obstrcution?

A

in closed the intervening mesentry (blood vessels) can also be obstructed

258
Q

what is the definition of strangulation ?

A

A closed loop obstruction associated with intestinal ischaemia.

259
Q

Small bowel wall thickness

A

less than 2mm normally

260
Q

Causes of small bowel target sign on CT

A

Ischaemic bowel
Intramural haemorrhage
Inflammatory bowel disease
Henoch-Schönlein purpura
Infective enterocolitis
Pseudomembranous enterocolitis
Radiation enterocolitis
Portal hypertensive enteropathy

261
Q

CT features of uncomplicated Crohn’s disease

A

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
Q

MRI bowel in crohns - what to assess?

A

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
Q

What are the differentials for crohns on CT

A

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
Q

What portion of pancreatic Ca are pancreatic ductal adenocarcinoma

A

> 90%

265
Q

How to divide the other tumours of pancreas?

A

by tissue type

266
Q

Pancreatic cancer tissue type

A

Epithelial, indeterminate, non-epithelial

267
Q

Pancreatic epithelial origin tumours

A

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
Q

What are the types of variant cacrinoma of duct cell origin ?

A

Cystic lesions: Mucinous cystic neoplasm and serous cystadenoma (microcystic)
Pleomorphic giant cell carcinoma
Adenosquamous carcinoma
Intraductal papilloma
Mucinous adenocarcinoma

269
Q

Epithelial endocrine cell tumours in pancreatic cnacer

A

Insulinoma
Gastrinoma
Non-functioning islet cell tumour
Glucagonoma
VIPoma
Somatostatinoma

270
Q

Exocrine cell tumours as part of epithelial pancreatic cnacners

A

Acinar cell carcinoma
Acinar cystadenocarcinoma
Pancreaticoblastoma

271
Q

Pancreatic cancer of indeterminate origin include

A

solid and papillary epithelial neoplasm (SPEN). Small cell carcinoma.

272
Q

Pancreatic cancer - non epithelial origin tumours

A

Sarcoma
Dermoid cyst
Lymphangioma
Leiomyosarcoma
Haemangiopericytoma
Malignant fibrous histiocytoma
Lymphoepithelial cyst
Lipoma
Schwannoma/paraganglioma

273
Q

What are most pancreatic cystic lesions

A

pseudocysts

274
Q

Differential list for cystic lesions of the pancreasa?

A

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
Q

Pancreatic cystic neoplasm - usually affect who?

A

female, 40 - 60
pancreatic tail

276
Q

What are IPMT in pancreatic mucinous cystic neoplasm

A

Intraductal papillary mucinous tumours. Malignnat but low indolent course. Men over 65

277
Q

Serous cystadenoma in pancreatic tumours is idnetified by what features?

A

Large, inumerable cysts, central calcification is common.

278
Q

Give examples of variant carcinomas of duct cell origin in pancreatic cancer? What is a feature that can look like cysts?

A

Pleomorphic giant cell carcinoma
Adenosquamous carcinoma
Microadenocarcinoma
Mucinous adenocarcinoma
Anaplastic carcinoma

The feature is necrosis.

279
Q

Pancreatic endocrine tumours - list

A

Insulinoma
Gastrinoma
Non-functioning islet cell tumours
Glucagonoma
Vasoactive intestinal peptide-screening tumours (VIPomas)
Somatostatinoma

280
Q

What is whipples triad?

A

hypoglycaemic on fasting
fasting blood sugar less than half normaly
rapid relief of symptoms with glucose infusion.

seen in insulinoma

281
Q

Gastrinoma causes what?

A

Zollinger-Ellison syndrome

282
Q

Solid and papillary epithelial neoplasm pancreatic Ca affects who?

A

young females

283
Q

Small bowel malignancy presenting features

A

Abdominal pain
Gastro-intestinal (GI) bleeding
Nausea and/or vomiting
Weight loss
Diarrhoea
Abdominal mass

284
Q

Common sdmall bowel malignancies

A

Adenocarcinoma
Carcinoid
Lymphoma
Gastro-intestinal stromal tumours (GIST)

285
Q

Rare small bowel malignancies

A

Liposarcoma
Neurosarcoma
Angiosarcoma
Haemangioendothelioma
Fibrosarcoma

286
Q

conditions which increase risk of small bowel cancer?

A

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
Q

how does jejunal and ileal adeno spread on CT?

A

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
Q

Where do abdominal carcinoid tumours

A

neuroendocrine amine precursor uptake and decarboxylation cells derived from the different embryonic divisions of the gut

289
Q

Carcioid constitues what proportion of small bowel malignancies and where are they most commonly found?

A

Small bowel and appendix

Quarter

290
Q

Carcinoid in the duodenum (rare) can be associated with what conditons?

A

ay be associated with Zollinger-Ellison syndrome or neurofibromatosis

291
Q

Carcinoid metastases are related to what facotr?

A

Size

292
Q

Carcinoid mets where?

A

liver, lymph and bone

293
Q

features of haemangioma on US

A

hyperechoic
no hypoechoic rim

no flow on dopplers

294
Q

features of haemangioma on MRI

A

T2 bright shine through

for all types of haemangioma

295
Q

types of haemangioma

A

tpyical
giant
sclerosed
high flow
haemangiomatosis (rare)

296
Q

Giant haemangioma whill fill in or not?

A

no, too large

can look like a scar

297
Q

sclerosed hamangioma - how to diagnose?

A

loss of cavernous hamengioma charachteristiscs as retracted in post infarction.

progressive infilling

298
Q

list of lesions with capsular retration

A

metasases (treated)
Intrahepatic cholangiocarcinoma

sclerosed haemangioma

epithelioid haemangioendothelioma

299
Q

haemangiomatosis is what

A

replacement of liver parenchyma by multiple haemangiomas

300
Q

high flow haemangiomas features

A

fill rapidly
wedge shaped THAD due to perfusion changes

301
Q

FNH is caused by what

A

hyperplastic response to a vascular insult

302
Q

FNH scar is what on MRI

A

high T2 signal

303
Q

US FNH

A

hyper or hypo echoic

spoke wheel present

304
Q

FNH on CT and MRI

A

stealth - pretty isointense

305
Q

FNH with contrast

A

massive arterial enhancement

NO WASHOUT

306
Q

what is whashout

A

liver lesion is darker than parenchyma in portal venous or delayed

307
Q

what is fade post contrast mean?

A

liver lesion becomes less bright than arterial phase but is never darker than background liver

308
Q

FNH on MRI, what happens

A

similar to CT
arterial enhancement

309
Q

OATP receptors exist on what?

A

hepatocytes

310
Q

MOAT receptors exist on

A

bile canaliculus

311
Q

Does FNh express OATP

A

yes

312
Q

tpyes of FNH on HBP with HSCA

A

hyperintense
ring pattern

313
Q

which liver lesions can demonstrate a central “scar” ?

A

FNH
fibromellar HCC
giant haemangioma

any large lesion with a central component/necrosis

314
Q

HC adenomas grow in repsonse to

A

steroids (exogenous or indogenours)

315
Q

HA vs FNH - what do you do?

A

need MRI as otherwise very similar

316
Q

HA vs FNH on MRI?

A

HA does not have OATP and so will be dark on MRI contrast

317
Q

subtypes of HA

A

HNF 1 inactivated HA
inflammatory HA
B catenin acitivateded HA
non specific HA

318
Q

Appearance of HNF1a HA

A

Fat in lesion
gene for getting rid of fat has been removed

319
Q

appearance of Inflammatory HA

A

T2 bright
Atoll sign (Island rim sign)
Can mimic FNA

high bleeding risk

320
Q

appearance of B catenin HA

A

High risk of HCC

No specific sign

may show washout

321
Q

Liver metastases
T2 -

A

bright

322
Q

Liver mets
- do they have OATP?

A

No

therefore dark on contrast MRI

323
Q

Liver
arterial rim type enhancement

think

A

liver mets

324
Q

Hypervascular liver mets

types

A

RCC
Thyroid
Neuroendocrine
melanoma
choriocarcinoma

325
Q

Sequences for liver mets

what do you use

A

DWI with primovist

326
Q

T2 shine through on ADC can be a result of

A

central necrosis

327
Q

Intra hepatic cholangiocarcinoma
ICCA

risk factors

A

Cirrhosis
Hep B and C

328
Q

ICCA appearance

A

rim arterial enhacnement
capsule retration
satelllite nodule

cloud like infilling of the lesions

329
Q

infilling of haemangioma vs ICCA

A

haemangioma infills from outside in

ICCA is cloud like

330
Q

hepatic AML
what proportion of fat

A

can be fat rich or fat poor

331
Q

Differentials for fat containing liver mass

A

HCC
HNF 1 HA
dysplastic nodule (cirrhosis)
Hepatic AML

332
Q

HCC - fibromellar affects who?

A

young adults

333
Q

fibromellar HCC presents as

A

large well define with a scar

334
Q

Features of Fibromellar HCC on imaging

A

washout

heterogenous compared to FNH

Central T2 dark central scar

calcification

low signal in HB phase

335
Q

Epithelioid haemangioendothelioma

what is it

A

rare low grade malignancy

multiple lesions / multifocal

336
Q

how does features of haemangioma image look like

A

multiple lesions
geographical
capsular retraction ++

337
Q

who do we screen for HCC

A

High risk people

cirrhotics
non cirrhotic HBV
HCV and fibrosis
NAFLD and fibrosis

338
Q

What is a positive Liver US HCC screen

A

1cm lesion in liver. (hypo or hyper)
CT or MRI next

if less than 1cm, do 3 monthly USS intervals

339
Q

main thing for diagnosing HCC on imaging

A

Non rim Arterial phase enhancement

enhancing capsule
nonperipheral washout
threshold growth

340
Q

how can HCC be diagnosed

(lesions structure)

A

due to vascular lesion
angiogenesis

unpaired arteries. Late arterial phase hyperenhancement

341
Q

HCC venous changes?

A

hepatic vein to portal vein drainage

reduced portal vein blood supply

rapid drainage of contrast -
washout

342
Q

liver lesion washout seen in

A

HCC
dysplastic nodules

343
Q

HCC capsule - what is it

A

thin rim around the lesion

344
Q

HCC threshold growth is what

A

50% growith in 6 months

345
Q

Types of HCC

A

Early
progressed

nodule in nodule
angioinvasive
infiltrating

346
Q

Early HCC

A

less than 2cm
no capsule
no vascular changes

hard to diangose

347
Q

progressed HCC

A

the typical blood supply changes

capsule charachteristic

348
Q

ancillary features of HCC

A

mosaic arhcitecutre

corona enhancement
- early contrast of surrounding liver, get satellite nodules here

349
Q

Fat in HCC

A

common
good indicator of Hepatocellular origin

350
Q

DWI HCC will show what and why?

A

HCC are densely packed cells
true restriction

though if well differentiated may not show restriction

351
Q

OATP expression on HCC

A

the more progressed the HCC the less OATP is expressed

352
Q

cirrhotic nodules also called

A

regenerative nodules

353
Q

macroregenerative nodules

appearance

A

big and benign
T1 bright
T2 dark (iron uptake)
normal vessels pass through

354
Q

low grade dysplastic nodules are only seen in what phase

A

HB phase

due to fat they still haev some OATP expression

355
Q

dark HB phase lesion differential list

A

HCC (early and progressed)
dysplastic nodules
Cholangiocarcinoma

356
Q

ICCA apperance

A

rim enhancement
cloud like infilling
washout

357
Q

confluent hepatic fibrosis

what is it

A

extensive fatty fibrosis with volume loss

extends to the hilum
normally triangular

T2 bright scar tissue

358
Q

peribiliary cysts in the cirrhotic liver develop from

A

peribiliary glands

AA ST2 (14 decks)

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