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CHAPTER 3 | STOMACH AND DUODENAL DISORDERS
17. A 34- year- old woman presented with nausea, intermittent vomiting,
bloating, and 5kg weight loss over three months. She had gastrooesophageal reux disease, for which she took omeprazole, but no
other past medical history. Examination revealed epigastric distension
and a succussion splash.
Investigations:
Haemoglobin 130 g/ L
Creatinine 67 µmol/ L
Thyroid stimulating hormone 1.16 munit/ L
Fasting glucose 4.5mmol/ L
Gastroscopy Normal
MR enterography Normal
What is the most appropriate investigation to make a diagnosis?
A. 3C breath testing
B. Barium follow through
C. Scintigraphic gastric emptying at two hours
D. Scintigraphic gastric emptying at four hours
E. Wireless capsule motility testing
18. A 68- year- old man with Parkinson’s disease on levodopa was admitted
with vomiting and abdominal pain.
Which of the following anti- emetics is the rst- line treatment for nausea
and vomiting in patients with Parkinson’s disease?
A. Domperidone
B. Haloperidol
C. Metoclopromide
D. Ondansetron
E. Prochlorperazine
19. A 45- year- old woman attended her general practitioner with recurrent
nausea and vomiting associated with travel. She had tried cyclizine to no
eect.
What is the next choice of medication for her motion sickness?
A. Betahistine
B. Hyoscine
C. Metoclopromide
D. Ondansetron
E. Prochlorperazine
CHAPTER 3 | QUESTIONS
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20. A 56- year- old man was referred for a gastroscopy with symptoms
of dyspepsia and upper abdominal pain. His history included coeliac
disease (CD) for which he maintained a gluten- free diet.
Investigations:
Gastroscopy Fig. 3.6
Urease breath test Negative
49
Fig.3.6 Endoscopic image of stomach. See also Plate 8
Image courtesy of Dr Tim Ambrose, Oxford University Hospitals NHS Foundation Trust
What is the most likely diagnosis?
A. Granulomatous gastritis
B. Haemorrhagic gastritis
C. H.pylori- associated gastritis
D. Lymphocytic gastritis
E. Upper GI Crohn’s disease
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CHAPTER 3 | STOMACH AND DUODENAL DISORDERS
21. A 56- year- old man was referred to the gastroenterology clinic with
epigastric pain, anorexia, and weight loss. Abdominal examination was
unremarkable. He had peripheral oedema to the mid shins.
Investigations:
Haemoglobin 130 g/ L
White cell count 9.0 × 109/ L
Platelet count 387 × 109/ L
Albumin 28 g/ L
C- reactive protein 9 mg/ L
Gastroscopy Markedly thickened gastric folds primarily of the
body and fundus. Gastric biopsies taken.
Histology Foveolar hyperplasia
What is the most likely diagnosis?
A. Chronic gastritis
B. Gastric adenocarcinoma
C. Lymphoma
D. Ménétrier’s disease
E. Zollinger– Ellison syndrome
22. A patient had undergone a gastroscopy to investigate iron- deciency
anaemia. Their GP had received the duodenal histology result showing
‘intraepithelial lymphocytosis and normal villous architecture’, and
asked whether this meant that the patient had coeliac disease.
In which other condition can duodenal intraepithelial lymphocytosis be
present?
A. All the listed options
B. Crohn’s disease
C. Giardiasis
D. NSAID enteropathy
E. Small intestinal bacterial overgrowth
CHAPTER 3 | QUESTIONS
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23. A 69- year- old man was referred for a gastroscopy and colonoscopy
to investigate iron deciency anaemia. He denied any symptoms. His
background included ischaemic heart disease and hypertension.
Investigations:
Gastroscopy A mass was seen in the second part of the
duodenum (Fig. 3.7)
Histology (duodenal mass) Small tubular glands lined by eosinophilic
absorptive epithelium with pseudostratied
hyperchromatic nuclei; no evidence of
dysplasia.
CD10 and CDX positive
Colonoscopy Sigmoid diverticulae only
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Fig.3.7 Endoscopic image of second part of duodenum. See also Plate 9
Image courtesy of Dr Tim Ambrose, Oxford University Hospitals NHS Foundation Trust
What is the most likely diagnosis?
A. Coeliac disease
B. Crohn’s disease
C. Duodenal adenocarcinoma
D. Duodenal adenoma
E. Duodenal lymphoma
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CHAPTER 3 | STOMACH AND DUODENAL DISORDERS
24. At the latest endoscopy user group meeting, the key performance
measures for upper GI endoscopy are published for each endoscopist.
Which of the following is a key performance measure for gastroscopy?
A. Accurate documentation of indications after therapeutic upper gastrointestinal (UGI)
endoscopy
B. Accurate photo documentation of anatomical landmarks and abnormal ndings
C. Documentation of distance from incisors to gastro oesophageal junction (GOJ), in
centimetres
D. Documentation of patient comfort score
E. Minimum seven- minute procedure time for index gastroscopy
25. A 57- year- old taxi driver with pancreatic cancer attended the
emergency department with profuse vomiting and metabolic alkalosis.
Asuccussion splash was elicited on examination.
Investigations:
CT abdomen and pelvis Distended stomach with evidence of gastric outlet
obstruction secondary to duodenal obstruction
What is the most appropriate immediate next step?
A. Decompression with large- bore nasogastric tube
B. Gastrojejunostomy
C. Gastroscopy and duodenal stent insertion
D. Gastroscopy and nasojejunal tube insertion
E. Parenteral nutrition
from locally advanced pancreatic cancer
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chapter
STOMACH AND DUODENAL
DISORDERS
3
ANSWERS
1. E. Urea breath test
• NSAIDs and H.pylori are independent risk factors for PUD
• Routine testing and treating of H.pylori prior to starting NSAIDs is indicated in those with a
history of PUD
NSAIDs and H.pylori are independent risk factors for PUD. However, both can have additive
eects on the risk of peptic ulcer bleeding. Studies have shown that H.pylori eradication is
associated with a reduced incidence of peptic ulcer in new NSAID users but not in chronic users.
Atest and treat strategy is not recommended in all patients prior to starting NSAIDs. However, it is
justiable in those with a history of PUD.
Full- dose PPIs in high- risk patients (age >60, past history of PUD, concomitant oral steroids or
oral anticoagulants, comorbidity, and requirement for prolonged use of NSAIDs) is recommended.
COX– 2 inhibitors, such as celecoxib, have fewer GI side eects. However, their use has to be
balanced against the recognized risk of cardiovascular events.
Malfertheiner P, Megraud F, O’Morain CA etal. (on behalf of the European Helicobacter and
Microbiota Study Group and Consensus panel). Management of Helicobacter pylori infection— the
Maastricht V/ Florence Consensus Report. Gut. 207 Jan;66():6– 30. Doi:0.36/ gutjnl- 206- 32288.
2. B. H.pylori infection
• Rapid urease testing may give false negative results in patients on PPI therapy
• PPI therapy is associated with an elevated serum gastrin
Rapid urease testing (e.g. a CLO test) sensitivity is well recognized as being compromised by acidsuppressing therapy, and patients should ideally withhold these medications for two weeks prior
to testing. If patients are still taking their medication at the time of endoscopy, there is a risk of
obtaining false negative results. PPI treatment is also associated with an elevated serum gastrin due
to the interruption of the normal negative feedback loop.
The most likely diagnosis is of a false negative rapid urease test in a patient with H.pylori infection,
and this patient should be oered non- invasive H.pylori testing o PPI treatment.
ZES is a cause of peptic ulceration in 0.%– % of cases. Features suggestive of ZES include:
• severe or resistant ulceration in the absence of NSAIDs or H.pylori infection
• unusual sites of ulceration (e.g. D2 or more distally)
• diarrhoea
Best of Five MCQs for the European Specialty Examination in Gastroenterology and Hepatology. Thomas Marjot, Colleen G C McGregor,
Tim Ambrose, Aminda N De Silva, Jeremy Cobbold, and Simon Travis, Oxford University Press (2021). © Oxford University Press.
DOI: 10.1093/oso/9780198834373.003.0003
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CHAPTER 3 | STOMACH AND DUODENAL DISORDERS
• large gastric folds
• fasting serum gastrin levels >,000 pg/ ml (o PPI treatment)
Fasting serum gastrin levels can be intermediate in ZES so, if there is strong suspicion clinically,
the next step would be a secretin provocation test. Other causes of intermediate elevated fasting
serum gastrin levels include atrophic gastritis, pernicious anaemia, gastric outlet obstruction (GOO),
renal failure, and small bowel resection.
HIV infection predisposes to cytomegalovirus (CMV) and herpes simplex virus, which can cause
ulcers resistant to standard treatment. Crohn’s disease is characterized by transmural ulceration,
although this is uncommon in the upper GI tract. Tuberculosis is a rare cause of ulceration. The
normal blood tests make these diagnoses less likely.
Malfertheiner P, Megraud F, O’Morain CA etal. (on behalf of the European Helicobacter and
Microbiota Study Group and Consensus panel). Management of Helicobacter pylori infection—
the Maastricht V/ Florence Consensus Report. Gut. 207 Jan;66():6– 30. Doi:0.36/
gutjnl- 206- 32288.
3. C. Low body mass index
• Failure of rst- line H.pylori eradication regimens occurs in at least 20% of patients
• Insucient gastric acid suppression contributes signicantly to treatment failure
• Raised BMI and active smoking confer lower eradication rates due to reduced drug
bioavailability
Failure of rst- line treatment regimens occurs in more than 20% of patients. Contributory
factors are multifactorial:host genetic factors, H.pylori virulence factors, antimicrobial resistance,
compliance with therapy, and duration of therapy.
Factors associated with treatment failure are discussed below:
• Primary antimicrobial resistance is increasing worldwide. Resistance patterns vary between
regions because of diering antibiotic usage, treatment regimens, and disease prevalence.
Amoxicillin rates are low in Europe, the US, Japan, and China in contrast to signicantly higher
rates in South Korea and Iran. Clinicians must bear in mind the primary antimicrobial resistance
patterns for their local population before deciding on empirical treatment.
• Acid suppression studies show that higher- dose twice- daily PPI regimens are associated with a
higher eradication rate when compared with standard regimens. Intra- gastric acid suppression
enables H.pylori to enter its growth phase, thereby increasing its vulnerability to antibiotics
targeting its replicative cycle.
• Virulence factors of H.pylori:certain H.pylori strains produce highly immunogenic CagA protein
and VacA toxin, both of which result in more severe gastric inammation. Studies signicantly
correlate severe gastric inammation with treatment success. It is postulated that severe
inammation increases drug bioavailability through increased mucosal perfusion.
• Host IL- β polymorphism:eradication rates are signicantly better in patients with the IL- β- 5
T/ T genotype compared with the C/ C and C/ T genotypes.
• BMI and smoking:an elevated BMI (>25kg/ m2) and smoking are associated with lower
eradication rates, thought to be due to lower drug bioavailability.
• Treatment duration:a longer treatment duration (0– 4days) is more ecacious than a seven-
day regimen, with eradication rates increased by 4%– 6%.
Song M, Ang T.Second and third line treatment options for Helicobacter pylori eradication. World J
Gastroenterol. 204 Feb 4; 20(6):57– 528. Doi:0.3748/ wjg.v20.i6.57.
CHAPTER 3 | ANSWERS
Billroth I gastrectomy for gastric ulcer
not stomach
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4. E. Resection of the gastric antrum, formation of a gastrojejunostomy, and closure
of the rst part of the duodenum and gastric outow
A. Is as described
B. Is a vagotomy and pyloroplasty
C. Is a Roux- en- Y gastric bypass
D. Is a pyloromyotomy.
Fig. 3.8 shows both the Billroth Iand Billroth II gastrectomy.
1/3
2/3
Gastric ulcer
Billroth II gastrectomy for duodenal ulcer
Duodenum
1/3
Stoma
2/3
Duodenal ulcer
Rest of cut end of
stomach closed to
produce ‘valved’
Duodenal ulcer left in situ
anastomosis which
narrows stoma and
perhaps directs
Duodenal stump oversewn
pancreatico-biliary
secretions to jejunum,
Fig.3.8 Billroth I and Billroth II gastrectomy
Reproduced from Essential Surgery Problems, Diagnosis and Management, 3rd edition, Burkitt HG and Quick CGR, Figure4.,
p.223. Copyright Elsevier 200
Burkitt HG, Quick CGR, Essential Surgery Problems, Diagnosis and Management, 3rd edition, 200, Elsevier.
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CHAPTER 3 | STOMACH AND DUODENAL DISORDERS
5. C.Iron
• Anaemia post gastrectomy may be multifactorial– iron, B2, or folate deciency
• Hypochlorhydria post gastrectomy results in reduced iron absorption
• Folate deciency is exacerbated by B2 deciency
Iron deciency is the most common vitamin deciency post gastrectomy, and occurs approximately
0years before the onset of vitamin B2 deciency (because the body has substantial reserves of
B2). Gastric acid is required for the solubilization of ferric iron to form ferrous iron. Therefore,
hypochlorhydria post gastrectomy results in reduced iron absorption. Vitamin B2 deciency
occurs because of the reduction in intrinsic factor, which is secreted by the parietal cells of the
stomach. Folate deciency has also been documented, and may be exacerbated by vitamin B2
deciency because the latter is required to convert inactive methyltetrahydrofolic acid to the active
tetrahydrofolic acid. Vitamin D deciency with subsequent osteoporosis has also been implicated.
Following partial gastrectomy, 30%– 40% of patients experience long- term side eects. The risk of
malignant change in the gastric remnant is 3% over 5years. Dumping syndrome tends to present
within three months of surgery, but can resolve within one year post- operatively. It occurs in 25%–
50% of patients, but causes signicant symptoms in 5%– 0%.
A Billroth II gastrectomy is the surgical procedure of choice for a duodenal ulcer, whereas the
Billroth Iis used for a gastric ulcer.
Rogers C.Postgastrectomy nutrition. Nutr Clin Pract. 20;26:26– 36.
Doi: 0.77/08845336400070.
6. C. Three years
• Extensive atrophic gastritis and intestinal metaplasia (IM) are precancerous conditions because
they constitute the background in which dysplasia and intestinal- type gastric adenocarcinoma
develop
• For adequate staging and grading, at least four non- targeted biopsies of two topographic sites
should be taken; additional targeted biopsies of lesions should also be taken
• Helicobacter pylori eradication is important to slow progression to cancer
The histopathological slide (Fig. 3.9) demonstrates gastric body mucosa with an almost complete
absence of specialized gastritis glands, extensive intestinal metaplasia, and focal pyloric metaplasia.
No H.pylori organisms are seen.
High- risk features predisposing to GC include the following:
• Membership of a high- risk ethnic population (e.g. East Asian ethnicity)
• Residence in, or migration from, a high- risk geographic location
• Family history of GC
• Dysplasia on biopsy
• Extensive IM on biopsies; the extent of IM is probably more important than the metaplastic
subtype
• Operative Link on Gastritis Assessment (OLGA) or Operative Link on Gastric Intestinal
Metaplasia (OLGIM) Stage III or IV
Pyloric
inammatory inltrate
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metaplasia
Extensive intestinal
metaplasia
CHAPTER 3 | ANSWERS
Plasma cell rich
57
Fig.3.9 Histology specimen from stomach body
Image courtesy of Dr Eve Fryer, Consultant Histopathologist, Oxford University Hospitals NHS Foundation Trust
The European Society of Gastrointestinal Endoscopy (ESGE) recommends that patients with
extensive atrophy and/ or intestinal metaplasia should receive follow- up oesophago- gastroduodenoscopy assessment every three years after diagnosis. There is no specic treatment for
atrophic gastritis or IM. However, H.pylori eradication may lead to partial regression of atrophic
gastritis. Although it does not reverse intestinal metaplasia, it may slow progression to neoplasia.
Dinis- Ribeiro M etal. Management of precancerous conditions and lesions in the stomach (MAPS).
Endoscopy. 202;44:74– 94. Doi:0.055/ s- 003- 2949.
7. C. Repeat the gastroscopy with excision of polyps >1cm
• Fundic gland polyps are the most prevalent type of gastric epithelial polyp
• The number, location and size of the largest polyp should be clearly documented
• Adenomatous polyps should be resected, when appropriate, because of the signicant
malignant potential
Gastric epithelial polyps can be classied as three types:fundic gland polyps (FGPs), hyperplastic
polyps, and adenomatous polyps. FGPs are the most prevalent type of epithelial polyp. They are
typically small (<cm), multiple, and located in the fundus and body. Their colour is usually the
same as the surrounding mucosa. They are not usually associated with an increased risk of cancer
unless in the context of familial adenomatous polyposis (FAP). However, larger polyps (>cm)
have been shown to be dysplastic in approximately 2% of patients. Routine tissue sampling of FGPs
(<cm) is not required. Unlike hyperplastic and adenomatous polyps, there is no association with
H.pylori infection. FGPs are associated with long- term PPI use, however, and regress once PPI
treatment is stopped. One should question the diagnosis of FGPs if they appear ulcerated, >cm,
or are in an antral location. Such atypical features warrant excision.
Hyperplastic polyps are typically small, single, or few in number. They are red, domeshaped, and smooth. Associated with H.pylori infection, gastric atrophy and gastric intestinal
metaplasia, these polyps regress on eradication of H.pylori. Hyperplastic polyps are potentially
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