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FRACS study > Oesophagogastric > Flashcards

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
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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

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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%)

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
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4
Q

Gastrin

A

Secreted by G cells in gastric antrum

Acts to increase

  • Gastic motility
  • Gastric acid production
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5
Q

Management of chylothorax

A

Tube thoracostomy

Medium chain triglyceride diet or TPN

Octreotide

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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
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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

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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.

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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

Higher number of biopsies correlate with more accurate diagnosis of IM

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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

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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

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12
Q

Prague Criteria

A
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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

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14
Q

Surveillance of Barretts

No dysplasia or malignancy

A

Short (<3cm)

  • 3-5 years

Long

  • 2-3 years
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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).

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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.
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17
Q

BO surveillance

high grade dysplasia

A

refer to specialist centre

consider ablation

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18
Q

How is duodenal polyposis classified

A
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19
Q

Histological features of dysplasia in Barretts

A

Cytometry- Nuclear shape and size

Architecture- Cellular crowding

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20
Q

What is the risk of progression to adenocarcinoma in Barrett’s without dysplasia

A

0.33% per annum

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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
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22
Q

Is surveillance in Barretts effective

A

No

but there is no better alternative yet

Most societies recommend surveillance

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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
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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

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25
Q

Siewert Classification

A
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26
Q

What are the recommended staging and preoperative investigations in adenocarcinoma of the oesophagus

A

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
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27
Q

What did the FLOT4 study show

A

FLOT then surgery then FLOT is essentially equivalent to conventional CRT in oesophageal cancer

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28
Q

Oesophageal Stenting considerations in adenocarcinoma

A

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

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29
Q

What is the role for surgery in oesophageal SCC

A

PCR rate with definitive chemorads is only ~50%

Therefore there remains a role particularly in young and fit patients

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30
Q

Gastric GIST intro statement

A

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

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31
Q

What is the distribution of GIST tumours by site of origin

A

Stomach 60%

SB 30%

Rectum 3%

Remainder from rest of GI tract, omentum, mesentery or peritoneum

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32
Q

GIST genetics

A

85% c-KIT or PDGFRA

12-15% Wild type

5% Congenital

  • Carney complex
  • NF1
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33
Q

What are the cellular markers for GIST tumours

A

CD117

DOG1

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34
Q

What are the recommended staging investigations in GIST tumours

A

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)

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35
Q

Principles of surgery in GIST tumours

A

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

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36
Q

What is the recommended adjuvant therapy in GIST tumours

Which patients should recieve it

A

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
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37
Q

GIST prognostic variables

A

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
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38
Q

Discuss the pertinent genetic factors in adjuvant therapy for GIST tumours

A

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

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39
Q

Is there a role for surveillance post GIST resection

A

there is no established protocol or survival benefit to post resection surveillance

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40
Q

LN stations in gastric cancer

A
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41
Q

What is a D1 vs D2 Lymphadenectomy in gastric cancer

Which is preferred

A

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)

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42
Q

What are the 2 most common causes of PUD

A

NSAIDS

H. Pylori

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43
Q

H pylori virulence factors

A

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
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44
Q
A

Helicobacter pylori

45
Q

Complications of H. Pylori infection

A

Gastritis

PUD

MALT lymphoma

Gastric adenocarcinoma

As an interesting aside H.Pylori may be actually be protective against oesophageal cancer

46
Q

What is the pathophysiology of NSAID induced PUD

A

NSAIDs are COX inhibitors

  • Predominant effect is due to COX-1 inhibition
  • Prevent prostaglandin synthesis
    • Impairs the mucoprotective layer
47
Q

What are the landmarks of the gastrinoma triangle

A

CHD/cystic/CBD junction

D2/D3 Junction

Junction of the body and neck of pancreas

48
Q

Gastrin levels in Zollinger- Ellison syndrome

A

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
Q

What is the appropriate dosing and regimen for PPI in UGI bleeding

A

Omeprazole 80mg IV stat. then either

  • 8mg/hour infusion or:
  • 40mg IV every 12 hours
50
Q

How is the risk of rebleeding on endoscopy best classified

A

The Forrest classification

51
Q

The Chicago classification

A

Classification of functional oesophageal disorders based on high resolution manometry findings

IRP- Integrated relaxation pressure

DCI- Distal contractile integral

DL- Distal Latency

52
Q

How is achalasia defined on Chicago classification findings

A

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
Q

Interpret these oesophageal HRM findings

A
54
Q

What is the incidence of achalasia

A

2.5/100000

Increases with age

55
Q

What are the treatment options for achalasia

A

Botox

Dilatation

POEM

Hellers myotomy

56
Q

What impact can Scleroderma have on the oesophagus

A

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
Q

Schatzki ring

A

Distal oesophageal stricture

short

B ring on barium

proximal is stratified squamous, distal side is columnar

Benign

Usually respond well to dilatation

58
Q

Eosinophillic oesophagitis:

Epidemiology

Pathogenesis

Presentation

Investigation

A

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
Q

Eosinophillic oesophagitis management

A

PPI

Dietary elimination

Steroid (topical)

Dilatation for strictures

60
Q

Management of peptic strictures

A

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
Q

Gastric gancer:

Epidemiology

Risk factors

A

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
Q

What are the routine recommended staging investigations in gastric cancer

A

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
Q

What is the significance of the Siewert classification

A

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
Q

T staging of gastric cancer

A

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
Q

N staging of gastric cancer

What is considered adequate lymph node harvest in gastric cancer for staging

A

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
Q

Management of T1 gastric cancer

A

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
Q

the MAGIC trial

A

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
Q

FLOT4 trial

A

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
Q

Surgical principles in oncologic gastic surgery

A

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
Q

Dumping syndrome:

Early dumping

A

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
Q

Dumping syndrome:

Late dumping

A

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
Q

How can oesophageal reflux be classified

A
73
Q

What are “ alarm symptoms” in reflux

A

Weight loss

Dysphagia

Anaemia

Failure of response

74
Q

How is oesophageal reflux diagnosed and scored objectively

A

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
Q

How does a fundoplication decrease reflux

A

Increase LOS pressure

Reconstitute the normal angle

Reduces frequency of LOS relaxations

76
Q

Gastric volvulus:

Mesenteroaxial volvulus

A
77
Q

Gastric volvulus:

Organoaxial volvulus

A
78
Q

Specific risks of fundoplication

A

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
Q

Classes of obesity

A

Class I

  • BMI 30-35

Class II

  • BMI 35-40

Class III

  • BMI 40-50

Super Obese

  • BMI >50
80
Q

Define excess weight loss

A

Excess weight above a BMI of 25

81
Q

Main medical impacts of morbid obesity

A

Type II diabetes

Cardiovascular risk/hypertension

Obstructive sleep apnoea

Reflux

  • carcinoma of the oesophago-gastric junction and obesity
82
Q

Psychosocial impact of obesity

A
  • Low self-esteem
  • Low self confidence
  • Reduced employability
  • Depression
  • Decreased libido
  • Social isolation
  • Discrimination
83
Q

How does obesity increase the risk of malignancy

A

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
Q

Standard indications for bariatric surgery

A

BMI >40

BMI >35 with metabolic complications of obesity

85
Q

Key aspects of history in bariatric surgery

A
  1. Age, Weight, BMI, comorbidity
  2. DIABETES – mild? Severe? Insulin dependent?
  3. Reflux – mild? Severe? Controllable with PPIs?
  4. Previous abdominal/gastric surgery?
  5. Meds – blood thinners? NSAIDs? Steroids?
  6. Alcoholism, drugs, cigs
  7. Misc – cirrhosis, IBD, Barrett’s etc.
86
Q

Preoperative studies and consults in bariatric surgery

A

Sleep study

Nutritional screen

  • Vitamins A, D, B12
  • PTH
  • Fe, Zn

Dietician

Psychologist

Consider gastroscopy

H. pylori testing and eradication

87
Q

LA grading of reflux oesophagitis

A

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
Q

What is the Seattle protocol

A

endoscopic recommendations for biopsy in Barretts

4 quadrant every 2cm if no dysplasia

4 quadrant biopsies every 1cm if dysplasia

Labelled clearly

89
Q

Management of low grade dysplastic Barretts

A

SURF trial compared surveillance vs ablation

Reduced risk of progression to HGD and invasive cancer

But no survival benefit when compared with surveillance

90
Q

Management of T1a Oesophageal adenocarcinoma

A

OG surgeon

MDT

endoscopic vs surgery

  • Similar outcomes in survival
  • Increased risk of local recurrence with endoscopy
  • Less morbidity
91
Q

Sleeve leak dilatation

A

Consider (Talbot says perform) dilatation of the incisura in every patient with a sleeve leak.

92
Q

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

A

Nesidioblastosis

93
Q

Nesidioblastosis

A

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
Q

Metabolic requirements in bariatrics

A
95
Q

What is the technique for laparoscopic management of internal hernia post RYGB

A

Ports

  • Umbilical Hassan
  • RUQ and LLQ

Run bowel in 3 directions

  • ICV to Jejunojejunostomy
  • Gastrojej to Jejunojejunostomy
  • Jejunojejostomy to ligament of Treitz
96
Q

What is the Seattle protocol

A

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
Q

Australian cancer council decision tree for Barrett’s oesophagus

A
98
Q

Endoscopic landmarks in the oesophagus and their distances

A
99
Q

What is the clinical triad associated with Boerhaaves

A

Vomiting

Pain

Subcutaneous emphysema

In that order and actually only seen in around 20%, more often present with shock and chest pain

100
Q

What genetic variant of H. pylori is associated most strongly with gastic cancer

A

CagA positive

Found with a very high prevalence in Japan

101
Q

Who should receive neoadjuvant treatment in gastric cancer

A

Stage 2 with any high risk features

102
Q

What is the definition of malnutrition

A
103
Q

D levels in gastrectomy surgery

A
104
Q

CROSS Trial

A

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
Q

Sleeve leak subclassification:

Type 3

A

Free perforation with peritonitis

106
Q

Sleeve leak subclassification:

Type 2

A
107
Q

Sleeve leak subclassification:

Type 1

A

phlegmon with no drainable collection

108
Q

Sleeve leak subclassification:

Type 4

A

FRACS study (13 decks)

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