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FRCS General Section 1/2 > OG > Flashcards

OG Flashcards

1
Q

Who should receive a 2 week wait OGD referral?

A

Dysphagia
Weight loss with reflux/abdo pain/dyspepsia
Upper abdominal mass

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2
Q

How many biopsies for suspicious mucosal lesions at OGD?

A

6-8

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3
Q

What is the characteristic finding in achalasia

A

Loss of ganglion cells in Auerbachs plexus

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4
Q

What is the classification of Peptic Ulcers

A

Modified Johnson
1. body of stomach (not associated with acid hyper secretion) (50%)
2. Body in combination with duodenal ulcers (acid ++) (25%)
3. Pyloric channel within 3cm of pylorus (acid ++) (20%)
4. Proximal GOJ <10%)
5. Chronic NSAID use

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5
Q

What are the characteristics of Gastric lymphoma?

A

5% of gastric malignancies - mostly B cell lymphomas
May regress with H Pylori eradication
More commonly are metastatic

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6
Q

What is Plummer Vinson syndrome?

A

Oesophageal web with Iron deficiency –> dysphagia

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7
Q

What is the most common site of benign gastric ulcer?

A

Lesser curve (50%)

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8
Q

Dilation of oesophageal cancer carries what risk of perforation?

A

4-6%

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9
Q

What are the characteristic histological findings of Schatzki rings?

A

They are typically found at the OG junction, with oesophageal mucosa above and columns epithelium below

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10
Q

What lymph nodes are removed in a D1 gastric resection?

A

Stations 1-7

Lesser/Greater curve + Left gastric

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11
Q

What lymph nodes are removed at a D2 gastric resection?

A

D1 stations (1-7) + 8-12

8 - Common hepatic
9 - Coeliac
10 - Splenic hilum
11 - Spenlic artery
12 - Hepatoduodenal ligament

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12
Q

What lymph nodes are removed at a D3 gastric resection?

A

D1 (1-7) + D2 (8-12) + 14-15

14 -root of SMA
15 - middle colic

(nb - not 13, posterior to pancreatic head)

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13
Q

What comprises a D4 gastric resection?

A

D1 (1-7) + D2 (8-12) + D3 (14-15) + 16

16- Para-aortic nodes

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14
Q

How are BMI categories altered in asian patients?

A

reduced by 2.5

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15
Q

What are the weight loss service tiers in the NHS?

A

Tier 1 - community based
Tier 2 - Advice from GP and medication (Orlistat, Mysimba [naltrexone/burprenorphine], Saxenda [liraglutide]
Tier 3 - Specialist weight management (MDT)
Tier 4 - Bariatric surgery

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16
Q

What are the NICE criteria for bariatric surgery?

A

1) BMI≥40 or 35-40 with significant disease (T2DM/HTN)
2) All appropriate measures undertaken and failed
3) Intensive Tier 3 management available (completed with weight loss ≥5%)
4) Patient generally fit for anaesthesia
5) Person commits for need to follow up

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17
Q

How wide is stomach typically left behind after a sleeve gastrectomy?

A

About 4cm

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18
Q

How long are the biliarypancreatico and ailmentary limbs typically made in a gastric bypass (for weight loss)?

A

BP 50cm
Ailmentary 100cm

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19
Q

Which bariatric surgery procedure has the greatest long term weight loss?

A

Total At 10 years:

Bypass 25%
Sleeve 17%
Band 14%

Excess body weight loss At 5 years:

Bypass 63%
Sleeve 53%
Band 48%

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20
Q

What follow up do patients undergoing bariatric surgery require?

A

For all - nutrition and CNS for 1 year
For bands - inflation increments
For sleeves and bypass - micronutrients, with regular monitoring of FBC, U&E, LFT, Folic acid, Ca, PTH, Vitamin D, Lipids, B1, B12, Vitamin A,EK

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21
Q

What advice is given re pregnancy after bariatric surgery?

A

Avoid for 12 months due to risk of foetal malnutrition

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22
Q

What late complications are typically associated with a gastric band (5)?

A

1) Port / tubing issues-Port replacement or shortening of tube
2) Oesophagitis-OGD +/-deflation or removal
3) Slippage-AXR +/-water soluble contrast- repositioning or removal
4) Gastric pouch-Water soluble contrast swallow/ OGD-Deflation +/-gradual refilling or removal
5) Erosion-Removal

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23
Q

What late complications are typically associated with a sleeve gastrectomy?

A

Reflux oesophagitis-OGD- PPI +/- convert to Roux en Y
Stricture- Endoscopic dilatation
Twist/ kink- convert to Roux en Y

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24
Q

What late complications are typically associated with a gastric bypass?

A

Marginal ulcer-Smoking cessation, avoid NSAIDS, PPI, consider anastomosis revision
Anastomotic stricture-Endoscopic dilatation
Internal hernia-Laparoscopy and reduction of hernia, closure of spaces

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25
Q

In what proportion of cases of mid 1/3 SCC will cervical lymph nodes be positive?

A

17%

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26
Q

Where are lymph node metastases most frequently seen in oesophageal adenocarcinomas?

A

Left gastric (17) - 24% and paraesophaeal stations (8M/8L) - 18%

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27
Q

What is the lymph node metastasis rate for T1a oesophageal cancer?

A

M1 - epithelial layer 0%
M2 - invasion of lamina propria 0%

M3 SCC - Invasion of muscularis mucosae 0-8%
M3 AC - Invasion of muscularis mucosae 1.8-4.5%

Overall SCC 0-3%
Overall AC 1.3-2%

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28
Q

What is the lymph node metastasis rate for T1b Oesophageal cancer?

A

Through muscularis mucosae:
SCC
SM1 (superficial 1/3) 8-33%
SM2 (middle 1/3) 17-30%
SM3 (Deep 1/3) 36-69%

Overall 26-50%

AC

SM1 (superficial 1/3) 0-22%
SM2 (middle 1/3) 0-35%
SM3 (Deep 1/3) 26-78%

Overall 22-41%

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29
Q

What is the most frequently occurring benign oesophageal tumour?

A

Leiomyoma (75%)

Others such as fibromas, neuromuscular tumour and NETS are very rare

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30
Q

How do oesophageal leiomyomas tend to present?

A

Incidental finding on OGD. Tend to have more symptoms >5cm, dysphagia and reflux

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31
Q

Where do oesophageal leiomyomas most frequently occur?

A

Distal 2/3 of oesophagus, 5% multiple

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32
Q

What is the most useful investigation for Leiomyoma of the oeosophagus?

A

EUS - typical appearance with no invasion of muscularis layer. Biopsies are often non-diagnostic and can disrupt tissue planes prior to resection

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33
Q

What is the histological findings of a leiomyoma?

A

Bundles of interlacing smooth muscle cells,

well-demarcated by adjacent tissue or by a definitive capsule

Tumour cells have blunt ended elongated nuclei with minimal atypic and few mitotic figures

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34
Q

What is the optimum treatment of oesophageal leiomyomas?

A

<5cm surveillance
>5cm or symptomatic - can be approach left or right thorax, muscle layer split and lesion enucleated

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35
Q

What is Menetriers disease?

A

Rare form of acquired gastropathy
Characteristic - foveolar hyperplasia + absent oxyntic glands
Giant rugal folds >1cm persisting after insufflation
Antral sparing
Diagnosed on deep biopsies (pit to gland ratios)
Risk of malignancy of 10% at 1 year

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36
Q

What is the most common origin cell of a gastric lymphoma?

A

Metastatic non gastric primary

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37
Q

For primary gastric lymphoma, which is the most common cell type?

A

B cell lymphomas

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38
Q

How frequent is reflux disease in Western populations?

A

20%

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39
Q

What are the characteristics of a normal lower oesophageal sphincter?

A

3-4cm with pressure of 10-25mmHg

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40
Q

What drug characteristically enhances contraction of the LOS?

A

Metoclopramide vagally mediated

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41
Q

What factors may relax the LOS

A

Alcohol, smoking and caffeine

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42
Q

In early GORD, which is the most common pathological mechanism of reflux?

A

Increased transient post prandial LOS relaxations (rather than fall in LOS pressure).

In late GORD, the LOS pressure reduces (?repeated acid exposure), exacerbated by decreased intra-abdominal sphincter length (obesity) and crural weakness and HH

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43
Q

How is a reflux episode defined during pH monitoring?

A

When pH<4

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44
Q

What factors are measured in pH monitoring (6)?

A

Number of reflux episodes (pH<4) - Normal <50
%total time<4 (<5%)
%upright time<4 (<8%)
%supine time<4 (<3%)

Number episodes >5 minutes (<3)
Longest reflux time

Demeester score >14.7 considered pathological

Most useful is total reflux time and symptom correlation

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45
Q

What types of wrap are used with a fundoplication?

A

Nissen - posterior 360
Toupet - posterior 270
Dor - anterior 180
Watson - anterior 120

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46
Q

What are the grades of varices?

A

Grade 1 - varices the collapse to air insufflation
Grade 2 - varices between 1 and 3
Grade 3 - varices large enough to occlude lumen

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47
Q

What primary prophylaxis for bleeding is required for Grade 2 varices

A

Non-selective beta blocker - e.g. Propranolol or nadolol.
Band ligation only for rebreeding. Repeat 7-14days until gone

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48
Q

What are the types of gastritis (5)?

A

Type A - autoimmune (antral sparing, parietal cell antibodies, hypochlorhydria, loss of IF and B12, elevated gastrin levels)

Type B - antral (H.pylori)

Reflux - bile reflux (chronic inflammation, foveolar hyperplasia –> Prokinetics)

Erosive - NSAIDS(/etoh, COX1)

Stress - diffuse ulceration following hypotension (most sensitive GIT)

(Menetriers disease - gross hypertrophy, premalignant)

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49
Q

In what percentage of patients with gastric ulceration is H.pylori implicated?

A

60%

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50
Q

What are the characteristics of H.pylori organism?

A

Gram negative helical rod
Microaerophillic
Produces urease enzyme (hydrolyses urea –> NH3)
NH3 affects astral G cells –> release of gastrin

Cannot colonise native duodenal mucosa, but can induce metaplasia then colonise and inflame.

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51
Q

What is the risk of peptic ulcer in patient with H.pylori?

A

10-20% (1-2% risk of gastric cancer , <1% MALT lymphoma)
Decreased risk of Oesophageal adenocarcinoma

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52
Q

What are the testing strategies for H.pylori (5)?

A

1) C13/C14 breath tests - diagnosis/confirmation of eradication (cannot be used if Abx <4 weeks)
2) Blood IgG - initial diagnosis only
3) Rapid urease testing (Clo) diagnosis and confirm eradication - 80-95% sens, 90-100% spec
4) Histology (gold standard, resource intensive)
5) Culture (gold standard, resource intensive, difficult)
6) Stool antigen test

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53
Q

What is the characteristic change seen with Barrett’s oesophagus?

A

Metaplastic change from stratified squamous to columnar gastric epithelium.

Three types - intestinal (high risk), cardiac and fundal

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54
Q

How can Barrett’s be subdivided?

A

Long >3cm and short segment <3cm

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55
Q

What is the recommended initial treatment of oeosophagitis (if severe)?

A

Full dose (e.g. 40mg oemp/esomep) for 8 weeks - if fails switch or go high dose

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56
Q

How long after PPIs will a h.pylori stool or breath test be accurate?

A

2 weeks

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57
Q

What is the upper oesophageal sphincter comprised of?

A

Cricopharyngeus and proximal oesophageal musculature

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58
Q

What are the 4 types of hiatus hernia?

A

1 sliding (95%)
2 paraoesophageal
3 mixed
4 giant

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59
Q

What is the evidence for LARS?

A

LOTUS trial 2011 JAMA - less reflux symptoms but more dysphagia, bloating flatulence
REFLUX trial 2013 BMJ - Better QoL, less anti reflux meds,

Rickenbacker Meta-analysis - less symptoms, better QoL, but significant still on antacids

Watsons group
- 20 year follow up - no benefit to short gastric division
- Nissen probably has less reflux but more side effects than anterior wraps
- No benefit to prophylactic mesh

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60
Q

What are the characteristic physiological findings of Achalasia?

A

1) Absence of swallow-induced relaxation of the LOS
2) Absence of peristalsis along oesophageal body

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61
Q

What is the investigation of choice for Achalsia?

A

High resolution manometry (>normal resolution)
Intraluminal circumferential pressures at 1cm over 26cm

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62
Q

What is the most diagnostic measurement for Achalasia?

A

HRM - Supine integrated relaxation pressure (IRP) >15mmHg

SIRP - mean of 4s of maximal relaxation at beginning of UES relaxation, referenced to gastric pressure

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63
Q

What Types of achalsia are there?

A

Chicago Classification
Type 1 - Abnormal median IRP, 100% failed peristalsis
Type 2 - Abnormal median IRP, 100% failed peristalsis, ≥20% swallows with pan oesophageal peristalsis
Type 3 - Abnormal median IRP ≥20% swallows with presmature/spastic contraction + no evidence of peristalsis

Type 1 Classic
Type 2 Achalasia with oesophageal compression
Type 3 Spastic

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64
Q

Which type of achalsia has the most favourable prognosis?

A

Type 2 >Type 1 >Type 3

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65
Q

What scoring system is used for Achalasia symptoms?

A

Eckardt score

Good outcome if ≤3, poor ≥3.
Composite of dysphagia, regurgitation, chest pain and weight loss

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66
Q

What is the 5 year success rate of Pneumatic Dilatation for achalasia?

A

90% 1 year, 86% 2 years, 82% 5 years, 50% 10 years

25-33% need repeat within 5 years

Graded PD using 30–>35–>40 balloons

Risk of perforation of about 5%

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67
Q

What evidence for POEM vs Heller vs PD

A

Ponds 2019 JAMA - 2 year treatment success 92% POEM 54% PD

Werner 2019 NEJM - 2 year treatment success equivalent POEM/Heller+Dor
Higher reflux POEM, Higher complications Heller

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68
Q

What is the treatment failure rate of LHM in different types of Achalasia?

A

Type 1 14.6%
Type 2 4.7%
Type 3 30.4%

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69
Q

What length of myotomy should be performed for a LHM

A

8cm - 6cm proximal to GOJ and 2-3cm distal

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70
Q

What is the risk of SCC in patients with Achalsia?

A

Increased 10-50 times

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71
Q

What are the differences between Idiopathic achalasia and Chagas disease?

A

In Chagas disease both excitatory and inhibitory neurones are lost (cf IA - inhibitory only) and the LES pressure is variable

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72
Q

What is the Los Angeles Classification for oesophagitis? (4)

A

A - one fold <5mm
B - one fold >5mm
C - multiple folds <75% circumference
D - multiple folds >75% circumference

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73
Q

What is the Prague Criteria for Barrett’s oesophagus?

A

C/M extent + Islands

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74
Q

What is the Paris Criteria for oesophageal lesions?

A

Descriptive of anatomical appearance I-III
I raised
2 flat
3 excavated

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75
Q

What is the increased risk of OAC in patients with Barretts?

A

OR of 11.3, 0.33% annual incidence in non-dysplastic

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76
Q

What surveillance should patients with Barrett’s oesophagus undergo?

A

BSG guidelines

Non-dysplastic
<3cm - 3-5 years
≥3cm 2-3years

Quadrantic biopsies every 2cm (Seattle protocol every 1cm is no better)

Dysplastic (2 GI Pathologists)
Indefinite - repeat 6 months with maximal acid suppression
LGD - repeat 6 months, if confirmed probably should have RFA (42% HGD at 4 years)
HGD - ESD>EMR/RFA (40% risk of adenocarcinoma)

EUS often unhelpful

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77
Q

What medical treatment should patients with Barrett’s oesophagus receive?

A

High dose PPI (80mg esomeprazole)
?Aspirin

ASPECT trial 2018 says better for high dose PPI than low dose in preventing composite of HGD, OAC and death.

?Aspirin

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78
Q

What is are the points of FB impaction in the oesophagus

A

1) Hypopharynx (cricopharynxgeus)
2) Upper thoracic oesophagus (Aortic arch, low pressure zone at transition between striated and smooth muscle fibres)
3) LOS

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79
Q

In what proportion of patients with impacted oesophageal foreign bodies it there an underlying structural abnormality?

A

25% - stricture, HH, web, Schatzki ring, eosinophilic oesophagitis, achalasia, tumours

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80
Q

What is the characteristic finding seen after ingestion of Ammonia?

A

Superficial haemorrhagic gastritis evolving over 24-48 hours

NB airway burns from vapour

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81
Q

What is the best diagnostic test for transmural necrosis after caustic ingestion?

A

Contrast CT at 3-6 hours > OGD - WSES guidelines
Looking for absence of post-contrast wall enhancement

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82
Q

What classification systems for caustic ingestion exist?

A

CT
Grade 1 - homogenous enhancement of wall without oedema/fat stranding
Grade 2a - enhancement of oesophageal mucosa with oedema and enhancement of outer wall –> target
Grade 2b - no enhancement of mucosa (necrotic)
Grade 3 - no post contrast wall enhancement

Zargar’s Endoscopic
Grade 0 - normal
Grade 1 - superficial mucosal oedema and erythema
Grade 2 - mucosal ulceration (2a superficial, 2b deep)
Grade 3 - transmural ulceration with necrosis (3a Focal, 3b Extensive)
Grade 4 - perforation

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83
Q

What is the optimum management of Caustic ingestion?

A

Type 1 -2 (CT) –> NOM
If deterioration, repeat CT
Grade 1 - discharge 24-48 hours no follow up
Grade 2a - <20% risk of strictures
Grade 2b - >80% risk of strictures

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84
Q

What is the lifetime risk of oesophageal Adenocarcinoma after caustic ingestion?

A

7%

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85
Q

What is the most common cause of oesophageal perforation?

A

Iatrogenic - diltation, VBL, sclerotherapy - mostly in hypopharynx (60%)
Boerhaave (15%) lower 1/3 usually on Left border, large defect
Rare - trauma, malignancy, FB, caustics

10-20% mortality

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86
Q

What scoring systems can be used to help predict success of NOM in oesophageal perforation

A

Altorjay criteria

Early, well, contained, no esophageal disease, close observation possible

Pittsburgh classification

Well, young patients, with contained leak, early presentation and no cancer

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87
Q

When is surgery ideally performed for oesophageal perforation (if necessary)

A

within 24 hours - mortality 10% vs 30% after

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88
Q

How is a thoracic oesophageal perforation repaired?

A

Thoracotomy
Two layer repair with suturing of mucosa and muscularis (25-50% failure rate)
Buttress if possible +/- T-tube
Need to extend muscular incision as mucosal injury will be greater

Feeding jejunostomy + gastric decompression

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89
Q

What percentage of GOJ cancer have peritoneal metastases?

A

Up to 15%

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90
Q

In what circumstances can a T1b AC of the esophagus be managed by ESD?

A

ESMO guidelines 2016
SM1 - <500um invasion, L0,V0, G1/2, <20mm diameter)

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91
Q

Which trials are investigating the treatment of presurgery complete responders to CRT in AC oesophagus?

A

ESOstrate and SANO

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92
Q

What is the Siewert staging system for GOJ tumours?

A

Siewert 1 - Tumour epicentre 1-5cm above anatomic GOJ
Siewert 2 - Tumour epicentre 1cm above to 2cm below anatomic GOJ
Siewert 3 - Tumour epicentre 2-5cm below GOJ - treat as gastric

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93
Q

What is the RCT evidence for a minimally invasive approach to oesophagectomy?

A

TIME Trial (2012 Lancet) – open vs MIO (56 vs 59) – Pulmonary infection RR 0.30

MIRO Trial (2019 NEJM) – open vs hybrid (104 vs 103) – major complications OR 0.31, pulmonary 18 vs 30%. Survival not different QOL better up to 2 years post-surgery (when most patients die)

ROMIO trial awaited

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94
Q

What is the most common type of gastric polyp?

A

Fundic gastric polyps

Usually <0.5cm, commonly associated with HP
Small malignancy risk, polypectomy if >1cm
Can be associated with polyposis syndromes if multiple

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95
Q

What is the risk of malignancy in 1 2cm gastric adenomatous polyp?

A

50%

Often associated with chronic gastric metaplasia

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96
Q

What are the BSG guidelines for gastric polyps?

A

• Sample all types
• Biopsy of intervening mucosa
• Eradicate H.Pylori
• Remove if dysplastic, adenomatous or symptomatic
• Repeat gastroscopy at 1 year if dysplastic and not removed or high risk

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97
Q

What is the probability of stricture formation when EMR >50% circumference

A

2/3

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98
Q

How frequently is Barretts seen on OGD for reflux symptoms?

A

15-20%

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99
Q

Which radioactive material is typically used for brachytherapy of the oesophagus?

A

Iridium -192

100
Q

Where are pulsion diverticulae most common in the oesophagus?

A

distal oesophagus, right posterolateral wall

101
Q

What is chronic afferent loop syndrome?

A

Abdominal pain after eating where an afferent (BP) loop is compressed for mechanical reasons and progressively enlarges causing pain.

Relieved by vomiting, which will be bile

102
Q

What interventional procedure at OGD has the highest risk of perforation?

A

Stent placement 5-25%

103
Q

What proportion of patients with systemic sclerosis have oesophageal involvement?

A

Systemic sclerosis - skin thickening, skin oedema, with 80% oesophageal involvement
Smooth muscle atrophy at LOS

104
Q

What are the manometric findings of Nutcracker Oesophagus?

A

High amplitude contractions with normal peristalsis

105
Q

What tests should be sent if a chylothorax is suspected?

A

Presence of chylomicrons
TG>110mg/dL
Cholesterol<200mg/dL

Fluid to serum cholesterol ratio <1 and TG ratio>1

106
Q

When might an endoscopic approach be appropriate for gastric cancers?

A

JGCA
- T1a non ulcerated, differentiated <2cm - EMR/ESD
- T1a with ulceration <3cm - ESD

107
Q

Where is the pH electrode placed?

A

5cm above manometrically determined upper border of LOS

108
Q

What is the most common soft tissue sarcoma?

A

A GIST

109
Q

What are the most common mutations associated with GISTs?

A

KIT or PDGFRA,

More rarely NF1 and BRAF

NB
Carney Triad syndrome (gastric GIST, paraganlgioma, pulmonary chondroma)
Carney-Stratakis syndrome
Type 1 NF
Familial GIST

110
Q

What is the standard management of GISTs <2cm

A

Serial imaging - without biopsy

For larger tumours an EUS guided biopsy for diagnosis is helpful, small risk of seeding

111
Q

What diagnostic stains are useful for GISTs?

A

only 1% are immunonegative for CD117 and DOG1

If doubt, molecular analysis for KIT1/PDGFRA

112
Q

What are proven prognostic factors for GISTs?

A

Mitotic rate
Tumour size
Tumour site (Gastric>Rectal/SB)
Presence/absence of rupture

Combined in modified NIH classification - v.low, low, intermediate, high risk

113
Q

For localised GIST, when should Imatinib be given?

A

Neoadjuvant If immediate primary resection is difficult or morbid
Adjuvant for 3 years if high risk

114
Q

What is the treatment of metastatic/recurrent GIST?

A

Imatinib –> Sunitinib –> Regorafenib

Exon 11 normal
Exon 9 - double dose imatinib
Exon 17 - regorafenib

115
Q

What is the risk of lymph node positivity according to T stage in oesophageal cancer?

A

T1a - 0-3%
T1b - 25%
T2 - 50%
T3 - 80%
T4 - 100%

116
Q

What are the Lauren types of gastric adenocarcinoma and which has the best prognosis?

A

Intestinal and Diffuse - Intestinal better prognosis (20% vs 10% at 5 years)

Intestinal has M:F of 2:1 (Diffuse equal) and higher age of detection (55 vs 45)

117
Q

In which Lauren type of Gastric Adenocarcinoma are signet cells seen?

A

Diffuse type

Due to prominent mucin production within storm and outside glands.

118
Q

In which cells are the problem in Pernicious anaemia?

A

The parietal cells failing to produce sufficient IF (gastric antrum)

119
Q

What is the lymph node metastasis rate for T1b oesophageal tumours?

A

sm1 = 6% AC 27% SCC
sm2 = 23% AC 36% SCC
sm3 = 58% AC 55% SCC

120
Q

What is the normal stomach pH?

A

About 2

121
Q

Where is gastric acid produced?

A

Oxyntic glands of Parietal cells of stomach, maintained by H/K ATPase

122
Q

In which phase is most gastric acid secreted?

A

Cephalic phase (smell/taste) –> vagal stimulation of gastrin and acid (30%)

Gastric phase (distension) –> low H+/peptides and gastrin release (60%)

Intestinal phase (food in duodenum) –> high acid/distension/hypertonic in duodenum inhibits gastric acid secretion (10%)

123
Q

What factors increase gastric acid secretion (3)?

A

Vagal nerve stimulation
Gastrin release
Histamine release from enterochromaffin like cells

124
Q

What hormones decrease gastric acid production? (3)

A

Somatostatin (via decreased histamine)
Cholecystokinin
Secretin

125
Q

Where is gastrin produced?

A

G cells in antrum of stomach

126
Q

What are the effects of gastrin release?

A

Increase HCl, pepsinogen and IF secretion
Increases gastric motility

127
Q

Where is CCK produced?

A

I cells in upper SI, released in response to partially digested proteins and TGs

128
Q

What are the effects of CCK?

A

Promotes digestion
-Pancreatic enzyme release (exocrine/endocrine)
-Contraction of GB and SOD relaxation
-DECREASED gastric emptying

129
Q

Where is secretin released?

A

S cells in SI

in response to acidic chyme and FAs

130
Q

What are the effects of secretin?

A

Counteracts acidity
-Increases exocrine pancreatic secretion
-inhibits acid/pepsinogen secretion

131
Q

What are the effects of VIP?

A

Digestion
-Stimulates secretion by pancreas/intestines
-inhibits acid/pepsinogen

132
Q

Where is Somatostatin produced?

A

D cells in pancreas and stomach

133
Q

What are the effects of somatostatin?

A

Decreases acid/pepsin/gastrin
Decreases pancreatic enzyme secretion
Decreases insulin and glucagon
Inhibits trophic effects of gastrin

STIMULATES gastric mucous production

134
Q

Where is gastric inhibitory peptide secreted?

A

K cells of duodenum an jejunum

in response to FAs and glucose

135
Q

What are the effects of GIP?

A

Mostly increased insulin release
Small decrease in gastric acid release

136
Q

What effect dose vagal stimulation have on gastric emptying?

A

Increases it (nb vagotomy –> pyloroplasty)

137
Q

Which hormones increase (1) and decrease (3) gastric emptying?

A

Increase - gastrin
Decrase - GIP, CCK, Enteroglucagon

138
Q

Which type of gastrojejunostomy empties most effectively?

A

Posterior retrocolic

139
Q

What is Hereditary Diffuse gastric cancer?

A

CDH 1 mutation
Average age diagnosis of 38
Associated with lobular Brest cancers and cleft lip
60-70% risk of cancer

140
Q

What bacteria are involved in cholecystitis?

A

Primarily chemical, but secondary infections from gut

-E.Coli, Kelbsiella and Step Faecalis (aerobic)
-Bacteroides fragilis, clostridia (anaerobic)

Often mixed

141
Q

What is the muscular composition of the oesophagus?

A

Overall - external longitudinal, inner circular

For external
Top 1/3 - voluntary striated
Middle 1/3 - striated and smooth
Bottom 1/3 - smooth muscle

142
Q

How many sequential oesophageal dilatation should be attempted in 1 sitting?

A

No more than 3

143
Q

When should fluoroscopic guidance be used for oesophageal stricture dilatation?

A

High risk
- post radiation/caustic
- impassable endoscopically
- long, angulated or multiple

144
Q

When should contrast studies be performed after oesophageal dilatation?

A

Not routinely, only if chest pain, fever, breathlessness or tachycardia

145
Q

How frequently should dilatation be performed for stricture?

A

Weekly or bi-weekly until ≥15mm dilator placed

146
Q

What size of pneumatic balloon should be used in achalasia?

A

30mm, with build up to 35 and 40mm

147
Q

What are typical indications for oesophageal dilatation?

A

Achalsia
Post-radiation
Caustic ingestion
Post-operative/post-endoscopic
Eosinophilic oesophagitis
Schatzki’s ring (if symptomatic)
Peptic strictures

148
Q

Where do Dieulafoy’s lesions most commonly occur?

A

In the stomach submucosa - large tortuous arteriole

149
Q

When should the urea 13c breath test and helicobacter stools antigen tests not be performed?

A

Within 2 weeks of PPI
Within 4 weeks of antibacterial treatment

150
Q

What is the triple therapy for H.Pylori?

A

No allergy:
1st line PPI + Amox + Clari or metronidazole (7/7)
2nd linePPI + Amox + metronidazole or Clari (other choice) (7/7)

3rd line - PPI + Bismuth subsalicylate + 2 x antibiotics or rifabutin

Pen allergy:
1st PPI + Clari + Metro (7/7)
2nd PPI + Metro + levo

151
Q

In which patients should an open approach to repair of peptic ulcer be adopted?

A

Unstable, severe CV comorbidity, especially if old

152
Q

What factors contribute to the prevention of GORD (6)?

A

1) Crura
2) Oblique Angle of GOJ
3) Apposition of mucosal folds
4) Phreno-oesophageal ligament
5) Intra-abdominal pressure compressing intra-abdominal oesophagus
6) High pressure zone of LOS

153
Q

Where is gastric cancer most common in the West?

A

Proximally (distally in East)

154
Q

Which blood group has an increased incidence of gastric cancer?

A

A

155
Q

What influence do KIT and DOG positivity have on prognosis for GIST?

A

None

156
Q

When is a PET CT not useful for OG cancers?

A

-Obvious metastatic disease
-T1a Oesophageal cancer
-Gastric cancer unless suspecting occult metastatic disease

157
Q

When should patients with a BMI of 30-35 be referred for consideration for bariatric surgery?

A

Recent diagnosis of T2DM

158
Q

What length of Roux Limbs should be used for a cancer reconstruction?

A

50cm BP
50cm Alimentary

159
Q

What conditions produce foveolar hyperplasia?

A

Reflux gastritis (resection or cholecystectomy)
NSAIDS
Alcohol

160
Q

What is Gurvits syndrome?

A

Acute oesophageal necrosis.

M:F in 6th decade, DKA

161
Q

What is the most common type of gastric polyp?

A

Fundic (75%) - may be more common in patients on acid suppression

162
Q

What are some risk factors for gastric cancer?

A

STK11 (Peutz Jaegers)
Helicobacter
EBV
Smoking
Low fibre diet
CDH-1 (1-3% of cancers, 60-70% risk)

163
Q

What is Jackhammer oesophagus?

A

A specific type of Nutcracker oesophagus (hyper contractile) - with a distal contractile interval of >8000

164
Q

What conditions are associated with eosinophilic oesophagitis?

A

Asthma, coeliac disease

Get trachealisation or concentric rings with white plaques in oesophagus

165
Q

How should post ERCP bleeding be treated?

A

Re-ERCP and treatment

166
Q

What is the most common site of a peptic ulcer?

A

Duodenum 2 -3x more than stomach

167
Q

Where is the primary site of intestinal sodium reabsorption?

A

Jejunum

168
Q

What are the regions of the mediastinum?

A

Superior
Inferior - posterior/anterior/middle

169
Q

What are the contents of the superior mediastinum?

A

Arteries (4)
-Arch of aorta
-right brachiochephalic
-left subclavian
-left common carotid arteries
Veins (3)
-SVC
-right brachiocephalic
-left braciocephalic
Organs (3)
-Oesophagus
-Trachea
-Thymus
Nerves (3)
-Left recurrent laryngeal
-Phrenic
-Vagus

Other
-Thoracic duct

170
Q

What are the contents of the anterior mediastinum?

A

Fat + LN + thymus

171
Q

What are the contents of the middle mediastinum?

A

-Pericardium
-Heart
-Aortic root
-Arch of azygos vein
-Main bronchi

172
Q

What are the contents of the posterior mediastinum

A

Oesophagus
Aorta
Azygos vein
Thoracic duct
Vagus nerve
Sympathetic nerve trunks
Splanchnic nerves

173
Q

How is the thoracic duct related to the oeosphagus?

A

Mostly posterior - passes to left at T5

174
Q

What is a specific contraindication for sleeve gastrectomy?

A

Barretts

175
Q

What vitamin deficiencies can be seen post bypass?

A

Vitamin B3/12/1
Vitamin D

176
Q

What is Wernickes triad?

A

Thiamine

Ophthalmoplegia, cerebellar dysfunction, confusion

177
Q

What is the most important vitamin deficiency post bariatric surgery?

A

Thiamine - short half life of body stores 9-18 days

178
Q

Which nerves are divided in a highly selective vagotomy?

A

Nerves of Laterjet

179
Q

How many segments does each lung contain?

A

10

180
Q

How many lobes are in each lung?

A

Right - 3 (oblique/transverse fissures)
Left - 2 (lingual)

181
Q

How should patients with small GISTS be treated?

A

If <2cm, surveillance with annual EUS (BSG 2017)

182
Q

How should patients with NSAID associated ulcers and H.pylori be treated?

A

2 months of PPI, stop NSAID, then first line eradication regime

183
Q

How long after decontamination should gastroscopes be used?

A

Within 3 hours

184
Q

What factor would suggest that GISTS are completely insensitive to TKIs?

A

c-KIT wild type

185
Q

What treatment is given for KIT exon 17 GISTS?

A

Regorafenib

186
Q

What treatment is given for KIT exon 9 GISTS?

A

Imatinib - may benefit given dose escalation as well

187
Q

What is the minimum examination time for Barretts screening?

A

7 minutes

188
Q

How long should patients be observed post dilatation?

A

2 hours

189
Q

What medication can reduce the risk of stricturing after large EMRs?

A

Oral prednisone

190
Q

What is the incidence of H.Pylori in perforated duodenal ulcer?

A

90-95% so treat empirically

191
Q

What histo stain would be more consistent with carcinoma than lymphoma?

A

Pancytokeratin

192
Q

from where does the right gastric artery arise?

A

Proper hepatic (53%)
Common hepatic (20%)

193
Q

What is the size of the gastric pouch in bariatric procedures?

A

Band/Bypass - 20ml
Sleeve 150-200ml

194
Q

What are the diagnostic criteria for chylothorax?

A

Triglyceride >110mg/dl
Cholesterol <200mg/dL
Presence of chylomicrons

Use medium chain fatty acids

195
Q

Why should surgery be offered for the treatment of morbid obesity?

A
  • Global epidemic with cost to NHS of >£5billion/year
  • Reduced life expectancy of patients due to CVD, DM, NASH, Malignancy and others
  • Bariatric surgery has been shown to be the only effective treatment for weight loss/maintenance
  • Also has profound metabolic effects including reversal of T2DM - Stampede trial
196
Q

What is the rate of progression of non-dysplastic Barrett’s to cancer?

A

0.22-0.38% per year

197
Q

Who should patients with Barrett’s with gastric metaplasia be managed?

A

Repeat biopsies, if short segment and confirmed Gastric –> discharge

198
Q

How should patients with Barretts with LGD be managed?

A

Repeat OGD in 6 months, if confirmed –> Ablation
If absent, repeat at further 6 month interval

199
Q

What is the anatomy of the thoracic duct?

A
  • Drains lymph from the lower half of the body and abdomen at the cisterna-chyli (L1/L2)
  • Runs superiorly along the right side of the vertebral column
  • Runs in posterior mediastinum and crosses to left at about T4/T5
  • Behind the left brachiocephalic vein and drains into the left subclavian

Transports about 2-4L of Chyle per day
Cons mx of chyle leak unlikely to be successful if >1L/day
Diet of Medium chain triglycerides (absorbed directly into portal venous system)

200
Q

How does H.Pylori damage the stomach?

A

-Production of urease, ammonia, acetaldehyde and mucolytics
-Attract inflammatory cells and produce free radicals
-Cause acute and chronic gastritis
-Chronic superficial gastritis progresses to atrophic gastritis, intestinal metaplasia, dysplasia and cancer

201
Q

What are the common complications of gastrectomy?

A

Immediate - Leak, duodenal stump blow out, haemorrhage
Late - dumping syndrome (early/late), vitamin deficiencies esp Vit B12 and Fe

Early dumping - fluid shifts from glucose in intestines
Late dumping - rebound hypoglycaemia

202
Q

How should acid suppression be managed prior to pH monitoring?

A

Stop-
PPI 7 days
H2 3 days
antacids 1 day

203
Q

How is a POEM performed?

A

GA
2cm longitudinal mucosal incision
Submucosal tunnel created similar to an ESD passing over OGJ to 3cm of stomach
Myotomy of circular layer of muscle performed keeping longitudinal layer intact

204
Q

What is the normal Phi Angle?

A

4-58 degrees

205
Q

Where might Internal Herniae occur after bypass surgery?

A

1) Peterson’s space - between transverse colon mesentery and gastrojejunostomy
2) Small bowel mesenteric defect at JJ
3) If retrocolic –> through mesocolic defect

206
Q

What follow up should patients endoscopically treated for HGD receive?

A

3 monthly for 1 year and yearly thereafter

207
Q

How is EMR performed?

A

Sedation/GA
Excision margins marked with APC
Injected with mixture of adrenaline/gelofusine - if lifts, amenable to EMR
Mucosectomy device applies a rubber band to create a pseudo polyp and then excised

208
Q

How would you perform a subtotal gastrectomy?

A
  • Laparoscopic approach with 4 ports and liver retractor
  • Dissection of greater omentum from transverse colon running from 1st short gastric to right gastroepiploic pedicle which is ligated with clips
  • Division of posterior gastric adhesions including splenic artery nodes (11p)
  • Division of gastrohepatic ligament and isolation/ligation of right gastric artery
  • Mobilisation of 1st part of duodenum and division with a linear stapler
  • Dissection of lymphatic tissue from CHA, coeliac axis and hepatoduodenal ligament (8/9/12)
  • Left gastric artery then ligated at its origin (7)
  • Dissection along lesser curve including pericardiac nodes
  • Division of specimen 5cm proximal to tumour
  • Reconstruction with roux-en-y technique
    —- Division of jejunum at 50cm (BP Limb)
    —-50cm further jejunum taken and anastomosis of BP limb to jejunum at this level with linear stapler and closure of enteroenterostomy
    —-Antecolic, ante gastric Gastrojejunostomy created with linear stapler and closure of gastroenterostomy
    —-Closure of mesenteric defects with permanent suture
    —-Drain to duodenal stump
209
Q

What is a MALT lymphoma?

A

Low grade lymphoma from gastric mucosa-associated lymphoid tissue
Form of B cell non-Hodgkin’s lymphoma

210
Q

From which cell type do GISTS arise?

A

Interstitial cells of Cajal

211
Q

How should patients with an excised GIST be followed up?

A

High risk - 3 monthly for 2 years then 6 monthly for 2 years then annually
Intermediate risk - 3months post op, then 6 monthly for 2 years then annually
Low risk - 3 months post op then clinical

212
Q

What is impedance monitoring?

A

Change of resistance to electric current when a bolus passes between two sensors
Liquids - high conductance (ions)
Gas - low conductance

213
Q

How is the oesophagus approached in the neck?

A
  • Left side of neck with head extends and turned to right
  • Incision on anterior border lower 1/2 of SCM
  • SCM dissected free from sternohyoid to identify internal jugular vein
  • Anterior Omohyoid belly identified and divided
  • Middle thyroid vein ligated and deep cervical fascia opened
  • Carotid sheath retracted laterally
  • Blunt dissection onto oesophagus via NGT.
214
Q

What size circular stapler is used for Oesophageal anastomosis?

A

25mm (strictures if less than this)

215
Q

What is Ghrelin?

A

Orexigenic hormone produced by fungus
Reduced by sleeve –> reduced hunger

216
Q

How would you perform an Ivor-Lewis Oesophagectomy?

A

Minimally invasive approach
—- Abdominal phase - 4 ports, liver retractor
- Mobilisation of greater omentum with careful preservation of gastroepiploic arcade and division of short gastrics above this to hiatus
- Partial Kocherisation of duodenum to mobilise pylorus to hiatus
- Dissection of lymphatic tissue and ligation of LGA at origin
- Mobilisation of lesser curve of stomach including lymph nodes and wide dissection hiatus
- Sling oesophagus with Jaques catheter and dissect up into mediastinum as far as possible including pleural strip
- Divide stomach 5cm distal to tumour creating tubularised conduit
- Suture divided specimen to conduit
- Feeding jejunostomy and close
—-Thoracic phase - 4 ports, single-lung ventilation, semi-prone right chest
- Continue pleural strip superiorly to azygos vein and divide between hemoloks
- Dissection of oesophagus including paraoesophagheal and carinal lymph nodes until free
- Ligate thoracic duct if identified
- Divide oesophagus proximally with linear stapler
- Open chest, extract specimen, prepare conduit
- Circular stapled anastomosis using Orville 25mm
- Passage of NGT past anastomosis and fixation at nose
- Gastrostomy excised with linear stapler and removed
- 2 x chest drain close

217
Q

How is anaemia defined and initially investigated

A

Hb <12 Female, <13 Male
Microcytic, normocytic, macrocytic
OGD + Colonoscopy + D2 biopsies x 4 for coeliac + Urinalysis/micro

218
Q

If initial investigations for IDA are negative how should you proceed?

A

BSG guidelines 2021 - trial of iron therapy
If recurrent or refractory –> Capsule endoscopy
Consider dummy capsule to exclude strictures (dissolvable material) with RFID

219
Q

In patients undergoing investigation for IDA, when can a colonoscopy be safely omitted?

A

OG cancer diagnosed at OGD

220
Q

What are the expected outcomes after LARS?

A

REFLUX 30% taking PPIs at 5 years
LOTUS 5 year symptom remission of 90%
Watson 20 year follow up - 90% satisfaction, 10% revision
-Satisfaction 90%
-Revision 10%

221
Q

How is high resolution manometry conducted?

A
  • Dedicated physiologist
  • 32 sensor catheter
  • Positioned at LES for 5 minutes
  • 10 wet swallows of 10ml water
  • Chicago V4 - 10 solid bolus swallows
  • Measurement of oesophageal peristalsis and LES function
222
Q

What is measured at high resolution manometry?

A

Identify basal LES pressure and PIP/Hiatus hernia
Measure IRP >15 abnormal
Assess peristaltic waves and short/long peristaltic defects
Contractile deceleration point (point when speed of waveform decreases)

Important measurements
IRP <15
DCI 450-5000
CVF <9cm/s

223
Q

How are SEMS inserted?

A
  • Either in CEPOD or IR with fluoroscopy available, usually under GA
  • Visualisation of lesion
  • Passage of guidewire beyond lesions and confirmation of position with fluoroscopy. May need to balloon up if not big enough
  • Target landing zone identified on fluoroscopy and marked on surface
  • Scope withdrawn and stent inserted
  • Position confirmed and guidewire removed
  • Stent deployed and visualised endoscopically

Cook stents
- Length of 8-14cm and diameter of 20mm
- Colon up to 35mm diameter

224
Q

How should perforated oesophageal cancer be managed?

A

If not resectable –> SEMS
If resectable best served by resection
Could exclude and bypass

Outcomes poor

225
Q

How should perforated gastric cancer be managed?

A

With an R0 resection
If R0 not achievable then median survival a few months

226
Q

What is the COMMANDO operation?

A

Combined mandibulectomy and neck dissection operation
(Tongue malignancy)

Glossessctomy, hemimandibulectomy, block dissection of cervical nodes

227
Q

How should patients with symptoms after LARS be managed?

A

–Distinguish between Failure (never worked), dysfunction (better then worse) or complication (new symptoms)

Technical causes
– intrathoracic migration - OGD/Barium – revision
– torsion – Barium – revision
– Crural stenosis - OGD/Barium – revision
– oesophageal pathology (eosinophilic oesophagitis/motor disorders)
– HH recurrence/failed wrap

Horgan classification for failed Fundoplication
Type 1 - GEJ herniated through hiatus +/- fundoplication
Type 2 - Paraoesophageal hernia component from redundant fundoplication
Type 3 - malformation of fundoplication

Treatment
Ix – OGD + biopsies, Barium, Manometry/pH
If failed or new symptoms, consider re-do surgery
If dysphagia and no anatomical abnormalities consider prokinetics or dilatation

228
Q

What are the risks of complications after oesophagectomy?

A

ESOdata 3000 patients
30d mortality - 2.5%
Any comp - 60%
Major comp(3b-5) 16.8%

Anastomotic Leak 11%
Chyle leak 5%
RLN injury 4.2%
Respiratory 27.8%
Cardiac 16.8%

229
Q

What are the risks of complications after gastrectomy?

A

DUCA 2019 1600

30d mortality 4.4%
Any complication 43%
Major complication 20%

Anastomotic Leak 9%
Respiratory 17%
Cardiac 5%
Chyle leak 2%

230
Q

What are the risk of RLN after oesophagectomy?

A

McKeown (14%) or Transhiatal (2%)
Thermal injury, stretching, compression
Significant increase in risk of pulmonary complications, tracheostomy
>50% present after aspiration
may require medialisation

231
Q

What is sucralfate?

A

Aluminium salt
Binds to positively charged proteins in exudates locally forming a thick viscus coating for ulcers, also reduces pepsin and increases bicarb
FDA approved for DU healing
Can be used for dyspepsia, radiation proctitis, diversion colitis, stress ulcer prophylaxis
Negligible side effects - constipation (avoid in ESRF)

232
Q

What is the course of the vagus nerve?

A

Exits cranium via jugular foramen (with IX and XI), passing in carotid sheath.
R+L deviate at base of neck

–Right passes anterior to SCA and posterior to SCJ entering the thorax. RRLN hooks underneath RSCA
—Posterior vagal trunk in chest
–Left passes inferiorly between L CCA/SCA into thorax. LRLN hooks underneath arch of aorta
—Anterior vagal trunk in chest (branches from both form oesophageal plexus)

233
Q

How should a perforation at LARS be managed?

A

If intra-operative - primary repair and drain and confirm healing with WSCS
If post-op - oesophagus –> drain +/- primary repair +/- T-Tube +/- SEMS
stomach –> primary repair or resection

234
Q

What is the cause of diarrhoea post LARS?

A

Vagotomy
Small bowel bacterial overgrowth
Bile salt malabsorption

235
Q

What is the differential diagnosis of dysphagia?

A

Intrinsic
- Stricture (benign peptic, malignant, leiomyoma)
- Eosinophilic oesophageal ring or Plummer Vinson syndrome
Food bolus
- Zenkers diverticulum

Neurological/motility
- Stroke, dementia, MS
- Achalasia, DES, Scleroderma

Extrinsic
- Mediastinal mass
- LAH
- Dysphagia lusoria

236
Q

What is the arterial and venous supply of the stomach?

A

Venous
– LGE and Short gastrics –> Splenic vein (nb is joined by IMV)
– RGE –> SMV
– LG and RG –> Portal vein

237
Q

After dCRT, where is a salvage Esophagectomy useful?

A

dCRT uses 50Gy (vs 30-41.4 NA)
Failure rate of 38% local, 13% regional and 16% distal

NACRT vs dCRT two trials in 2005/2007 - improved local control but no difference in overall survival (but very high operative mortality of 9-10%)

If loco regional recurrence then may be useful

Avoid anastomosis in irradiated fields, consider 3 phase.
Risk of airway injury/anastomotic break down. May need to consider a colonic interposition.

NEEDS trial recruiting CRT + Surgery vs CRT + salvage if needed

238
Q

What is Tylosis?

A

Palmoplantar keratosis associated with leukoplakia and Oesophageal SCC
AD inheritance, Howel-Evans Syndrome
RHBDF2 gene –> EGFR

239
Q

What is Bloom syndrome?

A

Abnormality of BLM gene, DNA repair
Leukaemia, Lymphoma, Oesophageal SCC
Short, T2DM

240
Q

What is Fanconi Anaemia?

A

AR inheritance, more common in Ashkenazi Jews
AML, physical abnormalities
mucosal SCCs including Oesophageal not cured by BMT

241
Q

What is hereditary diffuse gastric cancer?

A

CDH 1 gene, AD inheritance
Diffuse Gastric cancer + Lobular breast cancer

242
Q

What is the pathophysiology seen in dumping syndrome?

A

Early - hyperosmolar nutrients in small bowel –> fluid shifts
–> reduction in plasma volume, tachycardia, syncope, along with distension of bowel, pain, diarrhoea

Late - Rapid glucose absorption –> Exaggerated GLP1 and insulin –> autonomic and neurogylcopenic symptoms

243
Q

What is the Mandard tumour regression grade?

A

1 - fibrosis only
2- isolated tumour cells
3 - fibrosis outgrowing tumour
4 - tumour outgrowing fibrosis
5 - no regression

244
Q

What is the key molecular marker seen in SCC oesophagus?

A

p53 mutation 80%
over expression cyclin D1 20-40%

245
Q

What are the different zones of the oesophagus?

A

Cervical - lower border of cricoid to thoracic inlet (to 18cm)
Upper 1/3 - 18-24cm
Middle 1/3 - 24-32cm
Lower 1/3 - 32-40cm

FRCS General Section 1/2 (13 decks)

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