Oesophagogastric Flashcards
1
Q
Describe the musculature of the oesophagus
A
In two layers as is the norm throughout the GI tract
- Outer longitudinal
- Inner circular
Upper third is striated
Lower third is smooth muscle
Middle third is mixed
- There is a gradual transition in muscle type
2
Q
Describe the mucosa of the oesophagus
A
Stratified squamous non keratinizing
Muscularis mucosae absent in uppermost part and thick in lower part
Mucous secreting glands at upper and lower parts
3
Q
Management of bleeding oesophageal varices
A
Banding
- Recommended first line therapy
Sclerotherapy
- high rebleed rates compared with banding and may increase portal pressures
Tamponade
- Not good, use only if absolutey necessary
- High risk of serious complications in inexperienced hands.
- Dual balloon system is preferable- inflate in stomach and gentle traction
- Aim transfer-
- high rebleed rates (50%)
- Aim transfer-
Terlipressin
- Vasopressin analogue
- Induces sphlancnic vasoconstriction
- 3-4% mortality reduction
- Octreotide is another (less effective) option
Antibiotics (broad spectrum)
- A significant percentage of patients will have variceal bleeding due to decompensation associated with sepsis
- Emperic braod spectrum antibiotics significantly reduce the rebleeding risk
Shunting
- TIPS
- Excellent bleeding and rebleeding control
- 50% rate of encephalopathy within the year
- Open shunting
- Selective distal splenorenal
- Less risk of late encephalopathy and shunt occlusion but high morbidity and mortality in cirrosis from surgery
Beta Blockers and ISMN
- Non selective beta blocker (nadolol)
- Decreases rebleeding risk
- Combination of ISMN and beta blockade is superior
Acid suppression
- PPI and Sucralfate
4
Q
Gastrin
A
Secreted by G cells in gastric antrum
Acts to increase
- Gastic motility
- Gastric acid production
5
Q
Management of chylothorax
A
Tube thoracostomy
Medium chain triglyceride diet or TPN
Octreotide
6
Q
What is the role for antireflux treatments in Barretts oesophagus
A
Medical therapy
- Has recently been shown to improve outcomes in Barretts
- High dose better than low dose
- Combined with aspirin (if not using an NSAID already) is superior still
Antireflux surgery
- 1 RCT of PPI vs surgery has shown reduction in the length of Barretts segment.
- No evidence of reduced malignancy risk
- Symptomatic management
7
Q
What is the role for ablation in Barretts
A
Photodynamic therapy (PDT) and RFA both have been shown to reduce the risk of adenocarcinoma by 50% in individuals with high grade dysplasia
There is also a role for ablation in LGD as it prevents progression to HGD
There is no evidence for ablation in non dysplastic Barretts
8
Q
What is Barretts Oesophagus
A
Barrett’s Oesophagus (BO) is a premalignant condition of the oesophagus defined as the presence of metaplastic columnar epithelium, which endoscopically appears as salmon pink mucosa, extending above the gastro-oesophageal junction (GOJ) and into the tubular oesophagus, thereby replacing the stratified squamous epithelium that normally lines the distal oesophagus.
9
Q
What is the histological definition of Barretts oesophagus
A
Differing definitions are given in guidelines from Europe and the USA.
It is generally agreed that Barrett’s Oesophagus is characterised by metaplastic columnar mucosa replacing normal oesophageal squamous mucosa,
- At this time clinical studies are contradictory about whether histologically-proven intestinal metaplasia (IM) with morphologically typical goblet cells should be necessary for its diagnosis
- Intestinal type metaplasia is the only subtype which is clearly shown to clearly increase the adenocarcinoma risk
- American guidelines require IM for the diagnosis
- British do not and any columnar metaplasia is adequate for the diagnosis
- Cancer council Australia gives seperate recommendations for each.
- 1-3cm, no IM then single repeat at 3-5 years and stop if still no IM
- 1-3cm, IM, repeat endoscopy every 3-5 years
- >3cm always for surveillance every 2-3 years
- Intestinal type metaplasia is the only subtype which is clearly shown to clearly increase the adenocarcinoma risk
Higher number of biopsies correlate with more accurate diagnosis of IM
10
Q
Histology from lower oesophageal biopsy of an area of salmon pink mucosal change
A
This shows columnar epithelial change with goblet cells consistent with barretts and intestinal type metaplasia
11
Q
How is the GOJ identified on endoscopy
A
Proximal extent of the gastric folds is the definition used in the prague classification
- Termination of the pallisade vessels is an acceptible secondary measure
Barretts >1cm is the generally accepted definition of actually being present
12
Q
Prague Criteria
A
13
Q
What are the recommendations for biopsy in Barretts
A
The Seattle protocol
- Careful assessment for any areas of ulceration or nodularity
- Use narrow band imaging as an adjunct
- These should undergo targeted biopsy
- Then random 4 quadrant biopsies at 2cm intervals, unless:
- known or suspected dysplasia then quadrantic biopsies every 1cm
Forceps should be placed perpendicular to the surface then endoscopic suction to collapse the lumen
Spraying dilute adrenaline may be of assistance
14
Q
Surveillance of Barretts
No dysplasia or malignancy
A
Short (<3cm)
- 3-5 years
Long
- 2-3 years
15
Q
Barretts surveillance
indefinite for dysplasia
A
BO SURVEILLANCE PROTOCOL
INDEFINITE FOR DYSPLASIA ON BIOPSY
The changes of indefinite for dysplasia on biopsy should be confirmed by a second pathologist, ideally an expert gastrointestinal pathologist. If indefinite for dysplasia is confirmed, then the following endoscopic surveillance is recommended:
Repeat endoscopy in 6 months with Seattle protocol biopsies for suspected dysplasia (biopsy of any mucosal irregularity and quadrantic biopsies every 1cm) on maximal acid suppression.
If repeat shows no dysplasia then follow as per non-dysplastic protocol.
If repeat shows low grade or high grade dysplasia or adenocarcinoma then follow as per protocols for these respective conditions.
If repeat again shows confirmed indefinite for dysplasia, then repeat endoscopy in 6 months with Seattle protocol biopsies for suspected dysplasia (biopsy of any mucosal irregularity and quadrantic biopsies every 1cm).
16
Q
Barretts oesophagus surveillance:
Low grade dysplasia
A
Should be confirmed by a second pathologist
- Ideally an expert gastrointestinal pathologist.
- If low grade dysplasia is confirmed, then:
- Repeat endoscopy every 6 months with Seattle protocol biopsies for dysplasia
- biopsy of any mucosal irregularity and quadrantic biopsies every 1cm.
- If two consecutive 6 monthly endoscopies with Seattle dysplasia biopsy protocol show no dysplasia, consider reverting to a less frequent follow up schedule.
- Repeat endoscopy every 6 months with Seattle protocol biopsies for dysplasia
17
Q
BO surveillance
high grade dysplasia
A
refer to specialist centre
consider ablation
18
Q
How is duodenal polyposis classified
A
19
Q
Histological features of dysplasia in Barretts
A
Cytometry- Nuclear shape and size
Architecture- Cellular crowding
20
Q
What is the risk of progression to adenocarcinoma in Barrett’s without dysplasia
A
0.33% per annum
21
Q
What are the rates of progression to adenocarcinoma in Barretts with dysplasia
A
Low grade dysplasia
- 1% per annum
High grade dyslasia
- 6-7% per annum
22
Q
Is surveillance in Barretts effective
A
No
but there is no better alternative yet
Most societies recommend surveillance
23
Q
How would you manage Barretts with HGD
A
Refer to a specialist centre for consideration of EMR or ablation
- EMR provides opportunity for histology
- Halo (RFA) is the most common form of ablation
Surgery also has a role
- Especially long segment
- Multifocal disease
- HH
- Patient preference
24
Q
Barretts with active oesophagitis
A
Can’t be accurately called, esp dysplasia
Treat the oesophagitis and rescope in 6 months with Seattle protocol biopsies again
25
Siewert Classification
26
What are the recommended staging and preoperative investigations in adenocarcinoma of the oesophagus
Staging
* Endoscopy and biopsy
* CT CAP
* EUS
* Consider EMR
* Consider staging laparoscopy esp in T3/4 disease
* In our intsitution we are using PET routinely in the preoperative staging
Preoperative
* Frailty assessment
* CPEX (or at least lung function studies)
* Consider echo
* Nutritional assessment
27
What did the FLOT4 study show
FLOT then surgery then FLOT is essentially equivalent to conventional CRT in oesophageal cancer
28
Oesophageal Stenting considerations in adenocarcinoma
Not before RTX
* Stent will migrate
Position of tumour
* too close to crichopharyngeus will not be tolerable
Type
* Partially covered is preferable
Use fluoroscopy in its placement
29
What is the role for surgery in oesophageal SCC
PCR rate with definitive chemorads is only ~50%
Therefore there remains a role particularly in young and fit patients
30
Gastric GIST intro statement
Gastric GISTs are the most cvommon malignancy of mesenchymal orign of he GI tract and account for ~1% of all GI malignancies.
They are submucosal lesions and arise most frequently in the stomach and small bowel but can arises in the entire GI tract, omentum, mesentery or peritoneum
Broad spectrum of disease from benign to malignant
Arise in the interstitial cells of Cajal
Most possess KIT or PDGFRA mutations
31
What is the distribution of GIST tumours by site of origin
Stomach 60%
SB 30%
Rectum 3%
Remainder from rest of GI tract, omentum, mesentery or peritoneum
32
GIST genetics
85% c-KIT or PDGFRA
12-15% Wild type
5% Congenital
* Carney complex
* NF1
33
What are the cellular markers for GIST tumours
CD117
DOG1
34
What are the recommended staging investigations in GIST tumours
CT CAP
Endoscopy and biopsy
EUS and biopsy
MRI to assess local invasion where pertinent
Genetic markers including exon site testing (Exon 11)
(there is no established role for PET currently)
35
Principles of surgery in GIST tumours
R0 resection is all that is required
Multivisceral resection is appropriate where necessary
LN resection is not needed
Aim to maintain organ function as best as possible- Wedge resection etc where possible
36
What is the recommended adjuvant therapy in GIST tumours
Which patients should recieve it
Imatinib
* Rule of 5's
* 5cm
* \>5 mitoses/50HPF
* High risk sites of disease
* Exon 11
* Exon 9 at higher dose
* The duration of therapy is debatable
* Current NZ guidelines are for lifelong therapy in high risk disease
* Trials have shown 3 things
* Improved survival at 3 years
* High rates of recurrence upon cessation within that 3 years
* beyond is not yet well studied
* Imatinib induces cellular quiescence but not death
37
GIST prognostic variables
Size
* \<2
* 2-5
* 5-10
* \>10
Site
* Stomach (best)
* Jejunum/ileum
* Duodenum
* Rectum (worst)
Mitotic rate
* 5 or less per 50 HPF
* \>5 per 50 HPF
38
Discuss the pertinent genetic factors in adjuvant therapy for GIST tumours
The adjuvant therapy of choice in GIST tumours is a TKI
* Imatinib
80% have KIT mutations
* of those with no KIT mutation some (maybe a third) have mutations in PDGFRA
* both are receptor tyrosine kinases
12% will be wild type with no KIT or PDGFRA mutation
Exon 11 (the most common site) mutations are the most responsive to imatinib
Exon 9 mutations are also responsive but at a higher dose
39
Is there a role for surveillance post GIST resection
there is no established protocol or survival benefit to post resection surveillance
40
LN stations in gastric cancer
41
What is a D1 vs D2 Lymphadenectomy in gastric cancer
Which is preferred
D1- Nodal stations 1-6 (perigastric only)
D2- Nodal stations 1-12
Sydney RPA group retrospective analysis suggests better outcomes in spleen and panc preserving D2 resection (2018 WJO)
42
What are the 2 most common causes of PUD
NSAIDS
H. Pylori
43
H pylori virulence factors
Flagellated
* burrow into mucus,
* maintian microenvironment
Chemotaxis
* Toward less acidic environment
Urease production
* Converts urea into ammonia and water
* Increases pH
Vac-A
* Not all strians
* Induces vacuolation and cell death
Cytotoxin-associated gene (cagA)
* Improves adherence
44
Helicobacter pylori
45
Complications of H. Pylori infection
Gastritis
PUD
MALT lymphoma
Gastric adenocarcinoma
As an interesting aside H.Pylori may be actually be protective against oesophageal cancer
46
What is the pathophysiology of NSAID induced PUD
NSAIDs are COX inhibitors
* Predominant effect is due to COX-1 inhibition
* Prevent prostaglandin synthesis
* Impairs the mucoprotective layer
47
What are the landmarks of the gastrinoma triangle
CHD/cystic/CBD junction
D2/D3 Junction
Junction of the body and neck of pancreas
48
Gastrin levels in Zollinger- Ellison syndrome
Diagnostic
* \>10x upper limit of normal (1000pg/ml), and;
* pH \<2
* No further testing required
Equivocal
* 1-10x upper limit of normal
* May be pathologic or related to PPI
* Confirmatory testing off PPI
* If remains equivocal- Secretin stimulation test
* Normal G cells are inhibited but gastrinoma cells are stimulated
49
What is the appropriate dosing and regimen for PPI in UGI bleeding
Omeprazole 80mg IV stat. then either
* 8mg/hour infusion or:
* 40mg IV every 12 hours
50
How is the risk of rebleeding on endoscopy best classified
The Forrest classification
51
The Chicago classification
Classification of functional oesophageal disorders based on high resolution manometry findings
IRP- Integrated relaxation pressure
DCI- Distal contractile integral
DL- Distal Latency
52
How is achalasia defined on Chicago classification findings
Achalasia is defined by aperistalsis and abnormal LES relaxation (IRP \> 15 mmHg).
Subclassified into:
* Type I:
* incomplete LES relaxation
* aperistalsis
* absence of esophageal pressurization.
* Type II:
* incomplete LES relaxation
* aperistalsis
* panesophageal pressurization in at least 20% of swallows.
* Type III:
* incomplete LES relaxation
* premature contractions (DL \< 4.5 seconds) in at least 20% of swallows.
53
Interpret these oesophageal HRM findings
54
What is the incidence of achalasia
2.5/100000
Increases with age
55
What are the treatment options for achalasia
Botox
Dilatation
POEM
Hellers myotomy
56
What impact can Scleroderma have on the oesophagus
Smooth muscle atrophy
Functional oesophageal disorder with weak peristalsis
Also prone to severe reflux which may be refractory to medical management and require partial fundoplication
57
Schatzki ring
Distal oesophageal stricture
short
B ring on barium
proximal is stratified squamous, distal side is columnar
Benign
Usually respond well to dilatation
58
Eosinophillic oesophagitis:
Epidemiology
Pathogenesis
Presentation
Investigation
Uncommon 1:1000
Pathogenesis:
* Likely allergic
* possibly food intolerance vs peptic
Presents as:
* dysphagia
* stuck food bolus
Diagnosis:
* Endoscopy
* Friable
* Ringed oesophagus
* Sometimes referred to as feline oesphagus on contrast studies but this doesn't seem to be widely used and sometimes refers to normal mucosal folds
* Histology
* \>15 eosinophils per HPF
59
Eosinophillic oesophagitis management
PPI
Dietary elimination
Steroid (topical)
Dilatation for strictures
60
Management of peptic strictures
Ensure it is not a cancer!
Acid supression and reflux management
Dilatation
* Savary-Gillard
* Sequential (3 size) dilatators over guidewire
* TTS Balloon (Through the scope)
61
Gastric gancer:
Epidemiology
Risk factors
4th most common cancer
* Most common in Japan
Risks
* Low socioeconomic status
* Smoking
* H. Pylori
* Age
* Occupatinal exposure
* Coal
* Pottery
* FHx
* especially CDH1, Hereditary diffuse gastric cancer
* Pernicious anaemia
62
What are the routine recommended staging investigations in gastric cancer
OGD and biopsy
EUS and biopsy if linitus plastica suspected
CT CAP
Staging laparoscopy and cytologic lavage (T2 and above)
MDM
No established/validated role for PET at present
63
What is the significance of the Siewert classification
Siewert grade is based on the position of the epicentre of the cancer
Siewert I
* always managed as oesophageal
Siewert II
* If tumour is below OGJ and does not extend to it:
* managed as stomach
* If extends to OGJ:
* Managed as oesophageal
Siewert III
* Always managed as gastric whether tumour extends to the OGJ or not
64
T staging of gastric cancer
T1 Tumour above muscularis propria
* T1a Tumour invades lamina propria or muscularis mucosae
* T1b Tumour invades submucosa
T2 Tumour invades muscularis propria
T3 Tumour penetrates subserosal tissue without invasion of visceral peritoneum or adjacent structures
T4 Tumour breaches serosa
* T4a Tumour penetrates serosa (visceral peritoneum) but not into adjacent structures
* T4b Tumour directly invades adjacent organs or structures
65
N staging of gastric cancer
What is considered adequate lymph node harvest in gastric cancer for staging
N1
* Metastases in 1-2 regional lymph nodes
N2
* Metastases in 3-6 regional lymph nodes
N3
* Metastases in 7+ regional lymph nodes
At least 16 nodes, 30 or more is desirable
66
Management of T1 gastric cancer
Risk of LN mets is 3% in T1a disease
* EMR and ESR are reasonable treatment options
Risk of LN mets is ~20% in T1b (submucosal invasive) disease
* Surgery
67
the MAGIC trial
NEJM 2006
* A sentinel study in the treatment of gastric, OGJ and lower oesophageal cancer
* Surgery and epirubicin, cisplatin and 5-FU- 3 cycles of both neoadjuvant and adjuvant therapy
* vs
* Surgery alone
* Significant 5 year survival benefit to perioperative therapy
* 36%
* vs
* 23%
68
FLOT4 trial
Journal of clinical oncology 2017
* 4 cycles of FLOT both pre and post surgery for gastric and GOJ adenocarcinoma is superior to MAGIC
* 50 vs 35 months median survival
* It should be noted that this survival outcome is similar to that seen in the CROSS trial with combined neoadjuvant chemoradiotherapy (48 months)
69
Surgical principles in oncologic gastic surgery
Total or subtotal are the only appropriate operations
At least 5cm margin
Left gastric pedicle should be taken with any operation
D2 lymph node resection is superior (spleen and pancreas preserving resection of nodal basins 1-12)
At least 16 lymph nodes (30 is desirable)
70
Dumping syndrome:
Early dumping
Secondary to hyperosmolar intestinal content
* Large fluid shifts
* Intravascular hypovolaemia
* Secondary sympathetic response
* Symptoms
* Abdominal pain
* Diarrhoea
* Nausea
* Tachycardia
* Management
* Behavioural modifications and education usually effective
* Avoid simple carbohydrates
* increase complex carbohydrate, protein and fibre
* Small frequent meals
* Separate food and fluids by 30 mins
71
Dumping syndrome:
Late dumping
Secondary to hypoglycaemia after ingestion ogf food
* Likely hormonally mediated
Symptoms
* Hypoglycaemic symptoms
* Decreased LOC
* Confusion
* Abdominal pain
* Diarrhoea
* Nausea
* Tachycardia
Management
* Behavioural modifications and education usually effective
* Avoid simple carbohydrates
* increase complex carbohydrate, protein and fibre
* Small frequent meals
* Separate food and fluids by 30 mins
* Unlike early dumping medications may be necessary (and may be effective)
* Nifedipine
* Acarbose
* Octreotide
72
How can oesophageal reflux be classified
73
What are " alarm symptoms" in reflux
Weight loss
Dysphagia
Anaemia
Failure of response
74
How is oesophageal reflux diagnosed and scored objectively
The DeMeester score
* a composite score of the acid exposure during 24 or 48 hour ambulatory pH monitoring that has been used since 1970s to categorize patients as GERD+ or GERD-.
* 6 parameters
* Percent total time pH \< 4
* Percent Upright time pH \< 4
* Percent Supine time pH \< 4
* Number of reflux episodes
* Number of reflux episodes ≥ 5 min
* Longest reflux episode (minutes)
* Composite score \> 14.72 indicates reflux
75
How does a fundoplication decrease reflux
Increase LOS pressure
Reconstitute the normal angle
Reduces frequency of LOS relaxations
76
Gastric volvulus:
Mesenteroaxial volvulus
77
Gastric volvulus:
Organoaxial volvulus
78
Specific risks of fundoplication
Inability to burp and vomit
Slipped wrap
* Stomach above wrap
Recurrent HH
* Stomach and wrap in chest
Dysphagia
Redo
Vagus injury
Injury to accessory left hepatic artery
79
Classes of obesity
Class I
* BMI 30-35
Class II
* BMI 35-40
Class III
* BMI 40-50
Super Obese
* BMI \>50
80
Define excess weight loss
Excess weight above a BMI of 25
81
Main medical impacts of morbid obesity
Type II diabetes
Cardiovascular risk/hypertension
Obstructive sleep apnoea
Reflux
* carcinoma of the oesophago-gastric junction and obesity
82
Psychosocial impact of obesity
* Low self-esteem
* Low self confidence
* Reduced employability
* Depression
* Decreased libido
* Social isolation
* Discrimination
83
How does obesity increase the risk of malignancy
Systemic factors
* insulin resistance
* elevated insulin, mildly elevated glucose
* GH/IGF-1 axis
* GH, IGF1
* hypertriglyceridemia
* high VLDL/LDL
* low HDL
* renin-angiotensin system
* ang II and AT1R, transactivation of receptor tyrosine kinases
Local Factors
* low grade inflammation
* TNF, IL-6, IL-1B
* endocrine function
* increased leptin, adiponectin, PEDF
* steroid hormones
* increased aromases
* increased oestrogens
* decreased testosterone
* lipid metabolism
* lncreased lipolysis, increased lipogenesis
84
Standard indications for bariatric surgery
BMI \>40
BMI \>35 with metabolic complications of obesity
85
Key aspects of history in bariatric surgery
1. Age, Weight, BMI, comorbidity
1. DIABETES – mild? Severe? Insulin dependent?
2. Reflux – mild? Severe? Controllable with PPIs?
3. Previous abdominal/gastric surgery?
4. Meds – blood thinners? NSAIDs? Steroids?
5. Alcoholism, drugs, cigs
6. Misc – cirrhosis, IBD, Barrett’s etc.
86
Preoperative studies and consults in bariatric surgery
Sleep study
Nutritional screen
* Vitamins A, D, B12
* PTH
* Fe, Zn
Dietician
Psychologist
Consider gastroscopy
H. pylori testing and eradication
87
LA grading of reflux oesophagitis
Grade A
* Mucosal break(s) ≤5 mm, without continuity across mucosal folds
Grade B
* Mucosal break(s) \>5 mm, without continuity across mucosal folds
Grade C
* Mucosal break(s) continuous between ≥2 mucosal folds, involving \<75% of the esophageal circumference
Grade D
* Mucosal break(s) involving ≥75% of the esophageal circumference
88
What is the Seattle protocol
endoscopic recommendations for biopsy in Barretts
4 quadrant every 2cm if no dysplasia
4 quadrant biopsies every 1cm if dysplasia
Labelled clearly
89
Management of low grade dysplastic Barretts
SURF trial compared surveillance vs ablation
Reduced risk of progression to HGD and invasive cancer
But no survival benefit when compared with surveillance
90
Management of T1a Oesophageal adenocarcinoma
OG surgeon
MDT
endoscopic vs surgery
* Similar outcomes in survival
* Increased risk of local recurrence with endoscopy
* Less morbidity
91
Sleeve leak dilatation
Consider (Talbot says perform) dilatation of the incisura in every patient with a sleeve leak.
92
Name an extremely rare cause of persistent hyperinsulinemic hypoglycemia in adults.
The cause of the functional dysregulation in adults is unknown but should be considered in hypoglycaemia post bariatric surgery as a differential for dumping.
Histologically almost always characterized by a proliferation of abnormal β cells throughout the entire pancreas
Nesidioblastosis
93
Nesidioblastosis
Nesidioblastosis is an extremely rare cause of persistent hyperinsulinemic hypoglycemia in adults.
The cause of the functional dysregulation in adults is unknown but should be considered in hypoglycaemia post bariatric surgery as a differential for dumping.
Histologically nesidioblastosis is almost always characterized by a proliferation of abnormal β cells throughout the entire pancreas
94
Metabolic requirements in bariatrics
95
What is the technique for laparoscopic management of internal hernia post RYGB
Ports
* Umbilical Hassan
* RUQ and LLQ
Run bowel in 3 directions
* ICV to Jejunojejunostomy
* Gastrojej to Jejunojejunostomy
* Jejunojejostomy to ligament of Treitz
96
What is the Seattle protocol
A standardised recommendation and protocol for biopsies of the distal oesophagus in Barretts oesophagus
* biopsy of any mucosal irregularity and quadrantic biopsies every 2cm unless known or suspected dysplasia then quadrantic biopsies every 1cm
97
Australian cancer council decision tree for Barrett's oesophagus
98
Endoscopic landmarks in the oesophagus and their distances
99
What is the clinical triad associated with Boerhaaves
Vomiting
Pain
Subcutaneous emphysema
In that order and actually only seen in around 20%, more often present with shock and chest pain
100
What genetic variant of H. pylori is associated most strongly with gastic cancer
CagA positive
Found with a very high prevalence in Japan
101
Who should receive neoadjuvant treatment in gastric cancer
Stage 2 with any high risk features
102
What is the definition of malnutrition
103
D levels in gastrectomy surgery
104
CROSS Trial
Neoadjuvant chemoradiotherapy and surgery vs surgery alone for oesophageal and junctional cancers
* Significant survival advantage to neoadjuvant therapy with median survival of 48 vs 24 months
105
Sleeve leak subclassification:
Type 3
Free perforation with peritonitis
106
Sleeve leak subclassification:
Type 2
107
Sleeve leak subclassification:
Type 1
phlegmon with no drainable collection
108
Sleeve leak subclassification:
Type 4
