Unit 556

December 2018

Digestive

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Digestive
Unit 556 December 2018

About this activity 2

Case 1 Linda has lower abdominal pain 4

Case 2 Karen has chronic gastrointestinal symptoms 8

Case 3 Russell has heartburn 15

Case 4 Ethel decides to take aspirin 19

Case 5 Omar and Felicity have abdominal pain 23

Multiple choice questions 28

The five domains of general practice

Communication skills and the patient–doctor relationship

Applied professional knowledge and skills
Population health and the context of general practice
Professional and ethical role
Organisational and legal dimensions
About this activity check Digestive
About this activity
The Gut Foundation estimates that half
of the Australian population experiences
some type of digestive issue in any
12-month period.1 In 2013–14,
gastrointestinal disorders in Australia
amounted to approximately $3.5 million
in admitted patient care.2
Irritable bowel syndrome affects
approximately 10% of the Australian
population at any point in time, and
40% of people at some stage in
their lives.3
Diverticular disease affects
approximately 65% of people aged
>70 years.4 Five per cent of patients
who are affected by diverticular disease
develop diverticulitis, and careful
management is required to prevent
reoccurrence.4
Gallstones, which are present in
25–30% of the Australian population
aged >50 years,5 are asymptomatic in
up to 80% of affected patients;6
however, some cases progress to
complications such as cholecystitis,
which may require cholecystectomy.7
It is estimated that gastro-oesophageal
reflux disease affects 7.5% of the
population;8 although rarely a life-
threatening disease, patients
experience a significant decrease in
quality of life.9
Although the incidence of peptic ulcer
disease is falling as a result of the
success in eradicating Helicobacter
pylori, the use of low-dose aspirin,
which has recently become
recommended for the prevention of
cardiovascular disease,10 increases the
risk of stomach ulcers and bleeding.11
This edition of check considers the
management of various digestive issues
in general practice.
References
1. The Gut Foundation. Sydney: The Gut
Foundation, 2018. Available at www.
gutfoundation.com.au [Accessed
21 November 2018].
2. Australian Institute of Health and
Welfare. Australian health expenditure—
Demographics and diseases: Hospital
admitted patient expenditure 2004–05
to 2012–13. Cat. no. HWE 69. Canberra:
AIHW, 2017.
2
3. Linedale EC, Andrews JM. Diagnosis and
management of irritable bowel
syndrome: A guide for the generalist.
Med J Aust 2017;207(7):309–15.
doi: 10.5694/mja17.00457.
4. McSweeney W, Srinath H. Diverticular
disease practice points. Aust Fam
Physician 2017;46(11):829–32.
5. Gastroenterological Society of Australia.
Melbourne, GESA, 2018. Available at
www.gesa.org.au/resources/patients/
gallstones [Accessed 21 November 2018].
6. Stinton LM, Shaffer EA. Epidemiology of
gallbladder disease: Cholelithiasis and
cancer. Gut Liver 2012;6(2):172–87.
7. Gurusamy K, Samraj K, Gluud C,
Wilson E, Davidson BR. Meta-analysis of
randomized controlled trials on the
safety and effectiveness of early versus
delayed laparoscopic cholecystectomy
for acute cholecystitis. Br J Surg
2010;97:141–50.
8. Harrison C, Britt H, Miller G,
Henderson J. Prevalence of chronic
conditions in Australia. PLoS One
2013;8(7):e67494. doi: 10.1371/journal.
pone.0067494.
9. Tack J, Becher A, Mulligan C,
Johnson DA. Systematic review: The
burden of disruptive gastro-oesophageal
reflux disease on health-related quality of
life. Aliment Pharmacol Ther
2012;35(11):1257–66.
doi: 10.1111/j.1365-2036.2012.05086.x.
10. Bibbins-Domingo K, US Preventive
Services Task Force. Aspirin use for the
primary prevention of cardiovascular
disease and colorectal cancer: US
Preventive Services Task Force
Recommendation Statement. Ann
Intern Med 2016;164(12):836–45. doi:
10.7326/M16-0577.
11. Sostres C, Lanas A. Low dose aspirin,
H.  Pylori infection, and the risk of upper
gastrointestinal bleeding. Med J Aust
2018;209(7):297–98. doi: 10.5694/
mja18.00742.
Learning outcomes
At the end of this activity, participants
will be able to:
• identify the signs and symptoms of
diverticulitis
• discuss the process of diagnosing
irritable bowel syndrome
• outline the risk factors for the
development of peptic ulcers
• summarise the management of
gastric reflux
• describe a possible treatment plan
for cholecystitis.
Authors
Michael Crawford (Case 5) MBBS,
FRACS, MMed (Clin Epi) is a specialist
laparoscopic and hepatobiliary and
transplant surgeon at Royal Prince
Alfred, Lifehouse and the Mater
Hospitals in Sydney. He has a particular
interest in advanced laparoscopic
surgery and liver transplant. He is
currently the Head of Liver Transplant
Surgery at Royal Prince Alfred Hospital.
Hooi Ee (Case 3) MBBS, PhD, FRACP
is a gastroenterologist at Sir Charles
Gairdner Hospital, Western Australia,
with a clinical interest in complex
general luminal gastroenterology and
hereditary gastrointestinal cancer
syndromes. He is also a co-author of
national colorectal cancer guidelines on
population screening, genetic risks and
polyp surveillance.
Ruelan Furtado (Case 5) MBBS(Hons),
FRACS, MPhil is a Senior
Hepatopancreaticobiliary (HPB) Fellow
at Royal Prince Alfred Hospital. He has
trained as a Fellow at Fiona Stanley
Hospital and Nepean Hospital. He has
an interest in laparoscopic hepato-
pancreatic surgery and endoscopic
retrograde cholangiopancreatography.
Gerald Holtmann (Case 2) MD, PhD,
MBA, FRACP, FRCP is the Director of
Gastroenterology and Hepatology at
the Princess Alexandra Hospital in
Brisbane. He trained clinically at the
University Hospital Essen, Germany
and the Mayo Clinic, Rochester,
Minnesota. He is a Fellow of the Royal
College of Physicians (London), the
Royal Australasian College of
Physicians (Sydney) and the Australian
Academic of Health and Medical
Sciences. He has a research focus in
the field of neurogastroenterology and
has led pathophysiology research in the
field of gastrointestinal disorders for
nearly two decades. He is the author of
>250 peer-reviewed original papers,
and his work has been cited more than
20,000 times. Besides his medical
qualification, he has obtained a MBA
and serves on the boards of various
healthcare organisations.
Kevin Ooi (Case 1) MBBS(Hons),
FRACS is a consultant colorectal
 Digestive check About this activity

surgeon at Strathfield Private, BMI body mass index

Bankstown-Lidcombe and Fairfield CRP C-reactive protein
District hospitals in Sydney. He has an CT computed tomography
interest in both benign and malignant IBD inflammatory bowel disease
colorectal conditions. He is also a IBS irritable bowel syndrome
conjoint lecturer with the University of ERCP endoscopic retrograde
NSW. cholangiopancreatography
FBC full blood count
Ayesha Shah (Case 2) MBBS, FRACP
FGIDs function gastrointestinal
is a junior academic gastroenterologist.
disorders
After completing her MBBS at Mumbai
FODMAPs fermentable
University, she completed basic
oligosaccharides,
physician training and advanced
disaccharides, and
training in Gastroenterology and
monosaccharides and polyols
Hepatology in Brisbane, Queensland.
GORD gastro-oesophageal reflux
She also completed a two-year
disease
Fellowship in Motility/Inflammatory
H2RA H2-receptor antagonist
Bowel Disorders and is now a consultant
LFT liver function test
at the Department of Gastroenterology
NSAID nonsteroidal anti-
at the Princess Alexandra Hospital. Her
inflammatory drug
research interests are focused on the
OTC over-the-counter
interrelationship between
PPI proton pump inhibitor
gastrointestinal function and gut
PMS premenstrual syndrome
microbiome. In parallel to her clinical
SIBO small intestinal bacterial
responsibilities, she is a PhD candidate
overgrowth
at the University of Queensland. She
STI sexually transmissable
also serves on Metro South Human
infection
Research Ethics Board.
UTI urinary tract infection
Neville Yeomans (Case 4) BA(Hons),
MBBS, MD, DSc (hc), FRACP, AGAF is
Emeritus Professor at Western Sydney
University and the University of
Melbourne. He was Director of
Gastroenterology and Professor of
Medicine at Melbourne’s Western
Hospital for almost 20 years and has
had a long-standing interest in peptic
ulcer and its causes. He has served on
an advisory panel for Pfizer, which
provided the funding for the FDA-
mandated trial mentioned near the end
of Case 4.

Peer reviewers
Ashwin C Garg BSc(Med), MBBS,
GradDipBiomedEng (UNSW), FRACGP,
DipChildHealth is a general practitioner
at North Strathfield Medical Practice
and a RACGP OSCE examiner.

Ronald McCoy MBBS(Hons) is

Education Strategy Senior Advisor at
the RACGP.

Abbreviations
APREE ASPirin in Reducing Events
in the Elderly

3
Case 1 check Digestive

CASE You request blood tests, which show a white cell count of

1
14.8 x 109/L and a C-reactive protein (CRP) level of 80 mg/L.
Her electrolytes and liver function tests (LFTs) are normal. You
Linda has lower abdominal pain refer Linda for an abdominal and pelvic computed
tomography (CT) scan with contrast (Figure 1).
Linda, 50 years of age, presents to your practice for the
first time with left-sided lower abdominal pain. The pain
started three days ago and she has not opened her
bowels since; however, she is passing flatus. She
normally opens her bowels every two days. She has not
had any rectal bleeding, diarrhoea, weight loss or urinary
symptoms. Linda has mild hypertension, is obese, and
smokes 15 cigarettes a day. She has had no prior surgery
or endoscopy. When asked about her family history, she
tells you that her mother had breast and colon cancers.

Question 1
What information would you focus on in your physical
examination?

Figure 1. Linda’s abdominal and pelvic computed tomography scan

with contrast

Question 3
What does the abdominal CT scan show? How would you
manage Linda?

Question 2
What are your differential diagnoses? How would you proceed
to investigate Linda’s symptoms?

Question 4
Linda asks if there is anything she can do to prevent this from
happening again. What would you advise her?

Further information

Clinically, Linda does not look unwell. Her temperature is

37.6°C, blood pressure is 160/81 mmHg and her heart rate is
96 beats per minute. Linda’s height is 162 cm and weight is
92 kg (body mass index [BMI]: 35.1 kg/m2). Her abdomen is
soft but tender in the left lower abdominal quadrant. There is
no peritonism or flank tenderness. A urine dipstick analysis
shows no trace of nitrates or blood.

4

Question 5
Linda asks whether she needs to have a colonoscopy, as she
previously accompanied her mother for her endoscopies and
cancer treatment. How would you respond to her query?
Further information
Linda took your medical advice and completed her course of oral
antibiotics. You reviewed her two weeks after the initial attack
and she was feeling much better. Linda has also made an
appointment to see a specialist for colonoscopy as per your
referral. However, she presents back to your clinic eight weeks
later with worsening lower abdominal pain and a fever of 38.4˚C.
She is very tender over her left lower abdomen. Her repeat blood
tests show a white cell count of 17.8 x 109/L and a CRP level
of 183 mg/L. A repeat abdominal CT scan (Figure 2) shows a
recurrent sigmoid diverticulitis with an associated pelvic abscess.
Figure 2. Linda’s repeat abdominal computed tomography scan
with associated pelvic abscess (arrow)
Question 6
How would you manage Linda’s case now?
Digestive check Case 1
CASE 1 Answers
Answer 1
A full physical examination is required: take note of
whether the patient looks well or unwell during the
consultation and obtain her vital signs, temperature and
weight. Note any peripheral signs of cachexia, jaundice or
anaemia. During your abdominal examination, confirm
the area of tenderness and check for peritonism or any
palpable mass. Remember to also palpate for flank
tenderness (pyelonephritis) and complete the assessment
with a digital rectal examination. Rectal tumours can
sometimes be large enough to cause large bowel
obstruction. You may also ask the patient about the
consistency of the stool and presence of any rectal
bleeding. Check for any offensive vaginal discharge to
exclude sexually transmissible infections (STIs), and
obtain a urine sample to check for urinary tract infection
(UTI) or faecal particulate.
Answer 2
Differential diagnoses could include the following:
• acute sigmoid diverticulitis
• UTI, pyelonephritis
• gynaecological cause (eg pelvic inflammatory disease,
acute salpingitis, cystic ovarian lesions)
• acute colitis (usually pain with rectal bleeding and
diarrhoea – infective, ischaemic, inflammatory bowel)
• irritable bowel syndrome
• malignancy causing bowel obstruction (rare).
Investigations should include:
• urinalysis, urine cultures
• vaginal swabs if relevant
• blood tests (ie full blood count [FBC], electrolytes,
LFTs, CRP, and iron studies as a marker of occult
faecal blood loss)
• abdominal and pelvic CT scan with contrast.
Answer 3
Figure 1 shows an axial CT image with a thickening of the
sigmoid colon, with associated mesenteric stranding that
is indicative of acute inflammation. There is diverticulosis
affecting this segment of the colon, most likely consistent
with acute uncomplicated sigmoid diverticulitis. There is
no associated collection or free fluid. There is oral
contrast in the small intestines, and the intestinal calibre
is normal. In complicated sigmoid diverticulitis, there
could be CT features of large bowel obstruction from a
stricture or phlegmon, perforation (localised or free),
abscess formation or fistulating disease involving a
neighbouring organ.
5
Case 1 check Digestive
Linda’s condition can be safely managed initially in an
outpatient setting with simple analgesia, oral antibiotics
and plenty of fluids with electrolyte replacement. She can
have a light diet if she can tolerate it or when her
symptoms begin to improve. There is an increasing trend
to manage uncomplicated acute diverticulitis in an
outpatient setting with little supportive therapy.1 There is
recent evidence to suggest antibiotics may not be
necessary in mild-to-moderate uncomplicated
diverticulitis; the American Gastroenterology Association
(AGA) guidelines now recommend selective antibiotic use
on the basis of patient circumstances.1 Australia’s
Therapeutic Guidelines recommend oral amoxycillin +
clavulanate (875/125 mg) twice daily for five days for
patients with systemic features (eg fever, elevated white
cell count) or failing conservative medical measures.2 Linda
may not require oral antibiotics as her diverticulitis is
uncomplicated and she does not have other at-risk medical
conditions such as diabetes, organ impairment or
immunosuppression. However, it is still common to see
antibiotics prescribed in clinical practice in Australia.
Answer 4
Recurrent attacks can occur in 20–25% of patients despite
complete remission after an acute attack of diverticulitis.3 You
will need to assess and address Linda’s risk factors, and
recommend the necessary changes. The risk factors for
symptomatic diverticular disease include lifestyle, dietary and
anthropometric factors.
A high-fibre diet is still recommended in many guidelines for
the prevention and treatment of diverticular diseases, despite
the lack of high-quality evidence. However, improving dietary
fibre intake has been associated with decreased risk of
developing symptomatic diverticular disease in cohort
studies.4,5 Consumption of a vegetarian diet was associated
with a 31% lower risk of admission to hospital or death from
diverticular disease, when compared with a diet that included
meat.6 Nuts, seeds or popcorn are safe to be consumed, as no
relationship has been found between their consumption and
the development of diverticulitis or diverticular bleeding.7
Smoking is associated with a moderate increase in the risk of
developing symptomatic diverticular disease, when compared
with people who do not smoke.8 Two large cohort studies
have shown that increased physical activity is associated with
reduced risk of acute diverticulitis.9,10 Women who are obese
are at increased risk of attacks and complication of the
disease, compared with individuals who are not obese.9,10
Another recent systematic review failed to find any benefit
from probiotics and 5-aminosalicylic acid in preventing
recurrent diverticulitis.11
Answer 5
A colonoscopy is not recommended in the acute setting
because of concerns about perforation during the carbon
dioxide insufflation required for the procedure. However, a
colonoscopy can be performed at approximately six to eight
weeks following resolution of a patient’s acute attack. A
number of guidelines recommend routine colonoscopies after
6
an episode of acute diverticulitis to confirm the diagnosis and
exclude malignancy,12,13 which is a common practice in
Australia as well.
The recommendation to conduct routine colonoscopies after
acute diverticulitis is currently being challenged, as routine
colonoscopies place a huge resource burden on our current
healthcare system. A recent systematic review and meta-
analysis has found that the pooled proportional estimate of
malignancy detected was 1.6%; in those with uncomplicated
diverticulitis, the risk estimate drops to 0.7%.14 This study
suggested that routine colonoscopy may not be necessary,
particularly if the patient has had a normal colonoscopy
within the past three years. In this case, Linda’s personal and
family history of bowel cancer will be important to determine
her risk and need for a colonoscopy. As this was her first
attack, and she is 50 years of age and has a family history of
cancer, Linda should be referred to a specialist for a
subsequent colonoscopy.
Answer 6
In cases of systemic unwellness or complicated diverticular
disease evident on CT scan, patients should be hospitalised for
intravenous antibiotics, bowel rest and surgical consultation.
The initial management of diverticulitis complicated with
abscess formation has gradually moved away from emergency
surgery (with or without stoma formation) to a more
conservative approach involving antibiotics and CT-guided
percutaneous drainage. Localised abscess formation (>3 cm)
associated with diverticulitis can be successfully drained by
radiology in approximately 50% of cases.15 Although the
evidence from literature is weak, there is a slight trend for this
group to go on to develop chronic or recurrent diverticular
symptoms. Ultimately, the decision for elective colonic resection
can be made after joint consultation with a colorectal surgeon.
Conclusion
Linda had a successful percutaneous drainage and treatment
in hospital and was discharged home a week later after her
pelvic CT scan showed resolution of the abscess. She now
awaits her colonoscopy.
References
1. Strate LL, Peery AF, Neumann I. American Gastroenterological
Association Institute technical review on the management of acute
diverticulitis. Gastroenterology 2015;149(7):1950–76.e12.
doi: 10.1053/j.gastro.2015.10.001.
2. Expert Group for Gastrointestinal: Diverticular disease. In: eTG
complete [Internet]. Melbourne: Therapeutic Guidelines
Limited, 2018.
3. Hupfield L, Burcharth J, Pommergaard HC, Rosenberg J. Risk
factors for recurrence after acute colonic diverticulitis:
A systematic review. Int J Colorectal Dis 2017;32(5):611–22.
doi: 10.1007/s00384-017-2766-z.
4. Crowe FL, Balkwill A, Cairns BJ, et al. Source of dietary fibre and
diverticular disease incidence: A prospective study of UK women.
Gut 2014;63(9):1450–56. doi: 10.1136/gutjnl-2013-304644.
5. Aldoori WH, Giovannucci EL, Rimm EB, et al. Prospective study of
physical activity and the risk of symptomatic diverticular disease in
men. Gut 1995;36(2):276–82.
 Digestive check Case 1

6. Crowe FL, Appleby PN, Allen NE, Key TJ. Diet and risk of
diverticular disease in the Oxford cohort of European Prospective
Investigation into Cancer and Nutrition: Prospective study of
British vegetarians and non-vegetarians. BMJ 2011;343:d4131.
doi: 10.1136/bmj.d4131.
7. Strate LL, Liu YL, Syngal S, Aldoori WH, Giovannucci EL. Nuts,
corn and popcorn consumption and the incidence of diverticular
disease. JAMA 2008;300(8):907–14. doi: 10.1001/jama.300.8.907.
8. Hjern F, Wolk A, Hakansson N. Smoking and the risk of
diverticular disease in women. Br J Surg 2011;98(7):997–1002.
doi: 10.1002/bjs.7477.
9. Hjern F, Wolk A. Hakansson N. Obesity, physical inactivity and
colonic diverticular disease requiring hospitalization in women:
A prospective cohort study. Am J Gastroenterol 2012;107(2):296–
302. doi: 10.1038/ajg.2011.352.
10. Strate LL, Liu YL, Aldoori WH, Giovannucci EL. Physical activity
decreases diverticular complications. Am J Gastroenterol
2009;104(5):1221–30. doi: 10.1038/ajg.2009.121.
11. Unlu C, Daniels L, Vrouenraets B, Boermeester MA. Systematic
review of medical therapy to prevent recurrent diverticulitis. Int J
Colorectal Dis 2012;27(9):1131–36. doi: 10.1007/s00384-012-1486-7.
12. Rafferty J, Shellito P, Hyman NH, Buie WD, Standards Committee
of American Society of Colon and Rectal Surgeons. Practice
parameters for sigmoid diverticulitis. Dis Colon Rectum
2006;49(7):939–44.
13. Anderson JC, Bundgaard L, Elbrond H, et al. Danish national
guidelines for treatment of diverticular disease. Dan Med J
2012;59(5):C4453.
14. Sharma P, Eglinton T, Hilder P, Frizelle F. Systematic review and
meta-analysis of the role of routine colonic evaluation after
radiologically confirmed acute diverticulitis. Annals of Surgery
2014;259(2):263–72.
15. Lamb M, Kaiser A. Elective resection versus observation after non-
operative management of complicated diverticulitis with abscess:
A systematic review and meta-analysis. Dis Colon Rectum
2014;57(12):1430–40. doi: 10.1097/DCR.0000000000000230.

7
Case 2 check Digestive

CASE Further information

2
The results of Karen’s previous investigations were as follows.
Karen has chronic
2017: Normal gastroscopy with normal gastric and small
gastrointestinal symptoms
bowel biopsy, and a normal colonoscopy with normal colonic
Karen, 56 years of age, presents with a 10-year history of biopsies. There was no evidence of lactose intolerance.
chronic gastrointestinal symptoms, mainly altered bowel
2016: Normal cross-sectional imaging, including computed
habits – predominantly constipation with intermittent
tomography (CT) of abdomen and pelvis, and magnetic
loose stools. She has difficulties evacuating her bowel,
resonance enterography.
which is associated with lower abdominal discomfort.
Karen also complains of severe bloating and meal- Karen’s recent stool analyses and blood tests (coeliac and
related abdominal discomfort. Her symptoms worsened Helicobacter pylori serology, inflammatory markers, thyroid
18 months ago, with no identifiable aggravating cause function test, electrolytes, full blood count, liver function tests,
such as infectious gastroenteritis, overseas travel or iron stores, B12 and folate) were all unremarkable.
intake of medication (eg nonsteroidal anti-inflammatory
drugs [NSAIDs]) except for increased personal stress.

Karen also tells you that she has had multiple Question 3
investigations in the past; however, these tests did not
How can you confidently diagnose IBS in general practice?
reveal a structural or organic cause for her symptoms,
Are the previously outlined tests necessary for the diagnosis
and she was diagnosed with irritable bowel syndrome
of IBS?
(IBS). She does not have any other medical
comorbidities, has not had any abdominal surgery, and is
not on any regular medication except some aperients as
required. She does, however, have generalised anxiety
disorder and has been reviewed by a psychologist in the
past. Karen does not have a family history of
gastrointestinal malignancy, inflammatory bowel disease
(IBD) or coeliac disease. Her body mass index (BMI) is
26 kg/m2 and physical examination is unremarkable.

Question 1
What are your differential diagnoses? On the basis of the
information provided, can you confirm the diagnosis of IBS?

Further information

Karen also complains of extra-intestinal symptoms such as

insomnia, back pain, fatigue, headaches, and symptoms
worsened by anxiety and stress.

Question 4
Is there any association between functional gastrointestinal
disorders (FGIDs) and psychiatric comorbidities?
Question 2
What are the next steps in your approach? What are some of
the alarm gastrointestinal symptoms to consider?

8
 Digestive check Case 2

Question 5 Further information

Are there any possible overlaps between the different FGID types? Karen underwent a glucose breath test and the results are
shown in Figure 1.

100

90

80

Hydrogen/methane level (ppm)

70

60
Methane (CH4)
50

40
Question 6
How would you treat and manage Karen’s IBS? What would 30
Cut off H2
you tell her?
20

10 Hydrogen (H2)

0
0 20 40 60 80 100 120
Time (mins)

Figure 1. Karen’s glucose breath test results

The results of the glucose breath test were positive for

small intestinal bacterial overgrowth (SIBO), as the rise over
base for breath methane is >10 ppm. Karen has a positive
Further information diagnosis for methane-positive SIBO.

Karen attends your practice three months later and tells you
that she had some improvements with the outlined treatment Question 8
plan, which included 30 minutes of moderate intensity exercise,
What is SIBO? Does SIBO play a part in the pathophysiology
a trial of avoiding food containing high levels of fermentable
of IBS?
oligosaccharides, disaccharides, and monosaccharides and
polyols (FODMAPs) and an increased intake of soluble fibre.
However, she still has significant bloating and constipation.
Karen has also taken your advice and has been regularly
visiting her psychologist, where she has noticed significant
improvements in her mood and anxiety.

Question 7
Are there any other tests that would be helpful in guiding
Karen’s treatment? Question 9
What is the treatment for SIBO?

9
Case 2 check Digestive
CASE 2 Answers
Answer 1
On the basis of Karen’s history, the common differential
diagnoses would include:
• colorectal cancer (unlikely in this age group)
• overlap of IBS and functional dyspepsia
• SIBO
• microscopic colitis
• coeliac disease
• somatisation disorder
• pelvic floor dyssynergia
• new-onset inflammatory bowel disease (though very unlikely).
Based on information provided, the diagnosis of IBS can
be confirmed.
Answer 2
Although Karen has had chronic gastrointestinal symptoms
and was previously diagnosed with IBS, her symptoms have
worsened over the past 18 months. Thus, the next step
would be to look out for any alarm gastrointestinal
symptoms on history.
A list of alarm gastrointestinal systems that require urgent
referral to a gastroenterologist for further evaluation is
Box 1. Alarm gastrointestinal symptoms that require urgent
referral to a gastroenterologist for further evaluation1
• Symptom onset after 50 years of age
• Severe or progressively worsening symptoms
• Unexplained weight loss
• Nocturnal diarrhoea
• Family history of organic gastrointestinal disease
• Rectal bleeding or melaena
• Unexplained iron deficiency anaemia
• Positive faecal occult blood test
• Palpable abdominal mass or lymphadenopathy
Box 2. Rome IV criteria for diagnosing irritable bowel
syndrome1
• Symptoms have no biochemical or structural cause
• Recurrent abdominal pain for ≥1 day per week in the past three
months associated with two or more of the following:
–– Related to defecation
–– Onset associated with a change in stool frequency
–– Onset associated with change in stool form
10
available in Box 1. In patients aged >50 years, it would be
necessary to rule out malignancy and other relevant organic
diseases (ie microscopic colitis, IBD, celiac disease) with new-
onset (worsening) bowel symptoms.
While Karen has severe or very severe symptoms, she has
had comprehensive diagnostic work-up. In addition, the
symptoms have persisted or relapsed over an extended
period of time. It is therefore extremely unlikely that a
malignancy is the cause of her symptoms. However, further
specialised management might be required since treatment
in the primary care setting has failed.
Answer 3
You can confidently establish that Karen has an FGID, most
likely IBS, based on the use of the Rome IV criteria. FGIDs
are disorders of the function of the gastrointestinal tract and
can affect any part of the tract. The Rome IV criteria,1 which
are derived from a consensus process by a multinational
group of experts in functional gastrointestinal disorders, are
used for diagnosing IBS in general practice. However, while
the Rome III and Rome IV criteria are still considered the
gold standard for the conduct of clinical trials, they are not
widely used in the clinical setting and their value has
recently been challenged.2 In addition, in the clinical setting,
many patients present with an overlap of diseases
(eg functional dyspepsia and IBS). Thus, while the Rome
criteria initially have been developed to categorise FGID
with the intention to guide therapy, there is now evidence
that overlapping symptom clusters are a feature of patients
with severe symptom manifestations.3
For patients who have symptoms meeting the Rome IV
criteria and no alarm features as noted in Box 1, the clinician
should make a positive diagnosis of IBS without resorting to
a battery of tests. In the majority of patients without alarm
symptoms, an IBS diagnosis can be made without invasive
tests like endoscopy. Some targeted tests should be ordered
to exclude IBD (normal stool calprotectin) and coeliac
disease (serology) in patients presenting with chronic
unexplained gastrointestinal symptoms.
On the basis of the Rome IV criteria,1 IBS is classified into
four subtypes (Figure 2) according to the predominant
disorder in the bowel habits:
• IBS with diarrhoea (IBS-D)
• IBS with constipation (IBS-C)
• IBS with mixed symptoms of constipation and
diarrhoea (IBS-M)
• unsubtyped IBS (IBS-U).
According to Figure 2, given Karen predominantly has
constipation with intermittent loose stools, she is likely to
have IBS-C.
Answer 4
A wide range of extra-intestinal symptoms such as
psychiatric and psychological conditions (eg anxiety,
 Digestive check Case 2

depression) are highly prevalent in patients with FGIDs Answer 5

(Figure 3).4 Therefore, FGIDs have been conceptualised as
While the Rome criteria have been developed to categorise
disturbances of the brain–gut axis in the absence of
patients with otherwise unexplained (functional)
organic pathology.5 Psychological trauma including
gastrointestinal disorders, it has emerged that patients –
childhood abuse is frequently observed in female patients
particularly those with severe disease manifestations –
with IBS-C and should be carefully explored.6 If a patient
frequently report an overlap between the various distinct
has FGIDs associated with evidence of comorbid
FGID types (ie functional constipation, functional
psychiatric conditions that interfere with activities of daily
dyspepsia, functional diarrhoea, functional heartburn, IBS).
living, specialised psychiatric or psychological counselling
Therefore, patients with severe symptoms may report IBS-
should be facilitated.
type symptoms plus functional dyspepsia.3,4

Functional dyspepsia (ie upper gut FGIDs) and IBS (ie lower
gut FGIDs) can often co-exist in the same patient and be
unrecognised and under-reported. This can have significant
treatment implications; therefore, it is vital to take a
comprehensive medical history from the patient. It is
important to ask open-ended questions relating to the upper
and lower gut, especially as patients often only report certain
symptoms that are most troublesome or have the biggest
impact on their quality of life. For example, the presenting
complaint may be constipation; however, this may be
associated with upper gastrointestinal symptoms like
postprandial pain and fullness, which could indicate an
overlap with functional dyspepsia.

It seems unlikely that Karen has overlap with the other FGIDs,
because as she has lower gut symptoms that are consistent
Figure 2. Irritable bowel syndrome subtypes according to stool form1
with a diagnosis of IBS, and she does not have symptoms
BM, bowel movement
meeting diagnosis criteria of disorders such as functional
dyspepsia or gastro-esophageal reflux disease, which would
indicate an overlap.

Answer 6
Establishing an empathic, therapeutic doctor–patient
pelvic pain Chron
ronic ic p
relationship is the most important step in the management
Ch ros
nce tat
ra a u sea H e iti of FGIDs. Any FGID treatment begins by explaining the
ole N artb s
t urn
condition/diagnosis to the patient and confirming the
in

a
si
ve
od

An
ra

absence of any sinister pathology responsible for the

on

Fo

ep

cti

x ie
sp
si

ve
ers

longstanding gastrointestinal symptoms.

res

dy

iar

ty

IBS-U
blad
sord

al

rho
Desp

io n

ea

der

You should encourage Karen to increase her intake of

Eating di

Funct

soluble fibre (psyllium husk), which can improve her

dysfunc n
trio

IBS-C IBS-M IBS-D constipation and bloating.7 She should also be reviewed
Fibromy

and receive education about FODMAPs, which are present

GO R
Inco

in stone fruits, legumes, lactose-containing foods and

ntin
algi

ual

artificial sweeteners. Avoiding high FODMAPs-containing

sex
en
as

ce
ynd

or

food has a minor beneficial effect, particularly with

io

ti p
at

tile
ro

Pe ns
m

Co
ec

Ch lvic
abdominal discomfort and bloating.7
e

Er

ro floo S
nic r dy
ssynergia
fat PM
igu mes Karen could also be referred for psychological and behavioural
e sy o
mdrome Pain syndr
treatment. Effective psychological and behavioural treatment
Somatisation interventions may include cognitive behavioural therapy,
hypnosis, psychotherapy and stress management, and should
Psychiatric disorders
be considered in patients with moderate-to-severe symptoms
Functional non-gastrointestinal disorders
who fail to respond to medical treatment or those in whom
Functional gastrointestinal disorders
stress, or psychological comorbidity, may be affecting their
Irritable bowel syndrome (IBS)
gastrointestinal symptoms.8 It is important to enable the
Figure 3. Functional gastrointestinal disorders and overlap syndromes4 patient to cope with the symptoms. Low-dose tricyclic
GORD, gastro-oesophageal reflux disease; PMS, premenstrual syndrome antidepressants are often effective in patients who have failed
to respond to other measures.8

11
Case 2 check Digestive
It is important to note, however, that the placebo response
rate across randomised controlled trials of pharmacological
therapies in IBS treatment is 30–40%.3 This may reflect
spontaneous fluctuations of symptoms.
Answer 7
You could refer Karen to undergo a glucose breath test,
which is covered by the Medicare Benefit Schedule and
could be used indirectly to diagnose SIBO. GPs can
refer any patient presenting with unexplained
gastrointestinal symptoms that suggest SIBO for this
non-invasive test.
The glucose breath test is based on the principle that
human cells are not capable of producing hydrogen (H2)
or methane (CH4) gas. The presence of these gases in
the human breath indicates the metabolism of (non-
digested) carbohydrates by gut bacteria.4 After oral
ingestion of various carbohydrate substrates (most
commonly glucose or lactulose), hydrogen and methane
can be measured in exhaled breath using gas
chromatography or other techniques, and are reported
in ppm.9 The glucose breath test, which is used
commonly in clinical practice for diagnosing SIBO, has
a sensitivity of 62.5% and a specificity of 81.7%.10
A positive result for SIBO on glucose breath test is
defined as a rise of ≥20 ppm of breath hydrogen and
≥10 ppm of breath methane over the baseline level for
each individual patient.11
Central processing of information,
personality traits, anxiety, depression
Acute or chronic stressor
Life experiences
Antibiotics
Control of gut function and nutrient intake
Environment
Gastrointestinal infections
Diet
Methanogenic flora affecting transit, bile acid metabolisms
Figure 4. Proposed pathophysiology of irritable bowel syndrome18
12
Answer 8
There is growing evidence that dysbiosis (alteration in the
composition, density and the function of the intestinal
microbes) of the gut microbiota is associated with the
pathogenesis of intestinal and extra-intestinal disorders.7
The most recognised small intestinal dysbiosis is SIBO, which
has been identified as a condition that is defined by an
excessive and/or abnormal type of bacteria in the small
bowel.12,13 SIBO is frequently associated with gastrointestinal
symptoms such as bloating, distension, flatulence, abdominal
discomfort, diarrhoea and weight loss.14 SIBO overlaps with
other gastrointestinal disorders and symptoms, often making
it unclear if it is the cause, consequence or an epiphenomenon
in relation to the other disorder.15
For decades, researchers have believed the underlying disease
mechanisms of IBS to be centered on alterations of
gastrointestinal motility16 and visceral sensory function.17
However, in recent years, the focus has shifted to several
other mechanisms that could potentially explain the
pathophysiology of IBS (Figure 4).5,18 More recently, through
the use of real-time polymerase chain reaction and 16S sRNA
gene sequencing, studies have shown a role for dysbiosis of
the duodenal microbiota in IBS.19,20 A systematic review and
meta-analysis of nine studies showed methane on breath
testing is more common in patients with functional
constipation or C-IBS, compared with non-constipated
controls.21 Furthermore, there is experimental and clinical
evidence that methane appears to inhibit gastrointestinal
motility and gastrointestinal transit.22
Regulation of gut function (motility, sensory secretion)
Genes
Visceral afferent function
Gastrointestinal immune system
Gastrointestinal microbiome

Answer 9
As a proof of concept, several investigators have treated SIBO
in patients with IBS with antibiotics and probiotics. The
majority of these studies have shown symptomatic
improvement in a significant proportion of patients with IBS
and SIBO. This was thought to be due to the impact of the
antimicrobial therapy on SIBO.23 A systematic review and
meta-analysis of 10 studies found that antibiotic treatment
resulted in breath test normalisation in patients with
symptoms attributable to SIBO, and breath test normalisation
correlated with clinical response.24
While antibiotic therapy (eg a 14-day course of
amoxycillin 875 mg and clavulanic acid 125 mg) could be
considered and would likely result in a temporary (global)
symptom improvement and normalisation of the
methane-positive glucose breath test, it is debatable
whether this will result in a ‘cure’ of the symptoms. In the
future, non-absorbable antibiotics (ie rifaximin, which is
currently not approved in Australia for this indication)
might be used for treatment of SIBO.
Conclusion
FGIDs are defined as disturbances of the brain–gut axis in
the absence of organic pathology. In the clinical setting, IBS
can be confidently diagnosed without the need for extensive
investigations, particularly in younger patients with long-
lasting symptoms without alarm symptoms.
The pathophysiology of FGIDs is complex, multifactorial and
thus far incompletely understood. There has been a
paradigm shift in recent years, and specific abnormalities,
including alterations of gastrointestinal sensory function and
brain–gut interactions or changes of the gastrointestinal
microbiome, have been identified.
While there is currently no cure for IBS, establishing a
therapeutic doctor–patient relationship remains the
cornerstone in the management of FGIDs. Complementary
and alternative medicines are popular in many countries for
treatment of FGIDs. However, unless efficacy and safety
have been proven in appropriate clinical trials (complying
with standards for ‘normal’ medications), their benefit can be
questioned. In Australia, peppermint oil and the herbal
preparation STW5 are available as evidence-based
treatments for FGID. Since herbal extracts contain many
different active ingredients, it has been suggested that they
can offer a theoretical advantage over medications that
target a single mechanism.25 Targeted interventions with
spasmolytics, probiotics, central-acting drugs (ie tricyclic
antidepressants) or evidence-based herbal medications can
provide relief for most patients; however, the patients’ ability
to cope with the symptoms and to overcome the fear that a
life-threatening disease is the cause for the chronic
symptoms is critical. Besides pharmacologic and lifestyle
interventions, there is substantial evidence that
psychological interventions (eg cognitive behavioural
therapy) are effective to relieve the symptom burden.
Digestive check Case 2
Resources for patients
• Low FODMAP Diet – Gastroenterological Society of
Australia, www.gesa.org.au/resources/patients/low-
fodmap-diet
• Irritable Bowel Syndrome – Gastroenterological Society of
Australia, www.gesa.org.au/resources/patients/irritable-
bowel-syndrome
Resources for doctors
• Management of IBS:
–– Ford AC, Lacy BE, Talley NJ. Irritable Bowel Syndrome.
N Engl J Med 2017;376(26):2566–78. doi: 10.1056/
NEJMra1607547.
• Therapeutic Guidelines, https://tgldcdp.tg.org.au/
etgcomplete
• Structured Assessment of Gastrointestinal Symptoms
Scale (SAGIS):
–– SAGIS is a questionnaire that assesses 22
gastrointestinal symptoms and five extra-intestinal
symptoms. Response items are on a five-point Likert
scale from no problem to very severe problem.
• Koloski NA, Jones M, Hammer J, et al. The Validity of a
New Structured Assessment of Gastrointestinal
Symptoms Scale (SAGIS) for evaluating symptoms in the
clinical setting. Dig Dis Sci. 2017 Aug;62(8):1913–22.
doi: 10.1007/s10620-017-4599-6. Epub 2017 May 27.
References
1. Lacy BE, Mearin F, Chang L, et al. Bowel disorders.
Gastroenterology 2016; pii: S0016-5085(16)00222-5.
doi: 10.1053/j.gastro.2016.02.031.
2. Holtmann GJ, Talley NJ. Inconsistent symptom clusters for
functional gastrointestinal disorders in Asia: Is Rome burning?
Gut 2018;67:1911–15. doi: 10.1136/gutjnl-2017-314775.
3. von Wulffen M, Talley NJ, Hammer J, et al. Overlap of irritable
bowel syndrome and functional dyspepsia in the clinical setting:
Prevalence and risk factors. Dig Dis Sci 2018. doi: 10.1007/
s10620-018-5343-6.
4. Enck P, Aziz Q, Barbara G, et al. Irritable bowel syndrome. Nat
Rev Dis Primers 2016;2:16014. doi: 10.1038/nrdp.2016.14.
5. Holtmann G, Shah A, Morrison M. Pathophysiology of functional
gastrointestinal disorders: A holistic overview. Digestive
Diseases 2017;35(suppl 1):5–13. doi: 10.1159/000485409.
6. White DL, Savas LS, Daci K, et al. Trauma history and risk of the
irritable bowel syndrome in women veterans. Aliment Pharmacol
Ther 2010;32(4):551–61. doi: 10.1111/j.1365-2036.2010.04387.x.
7. Rao SS, Yu S, Fedewa A. Systematic review: Dietary fibre and
FODMAP-restricted diet in the management of constipation and
irritable bowel syndrome. Aliment Pharmacol Ther 2015
Jun;41(12):1256–70. doi: 10.1111/apt.13167.
8. Ford AC, Quigley EM, Lacy BE, et al. Effect of antidepressants
and psychological therapies, including hypnotherapy, in irritable
bowel syndrome: Systematic review and meta-analysis. Am J
Gastroenterol 2014;109:1350–65. doi: 10.1038/ajg.2014.148.
9. Christman NT, Hamilton LH. A new chromatographic instrument
for measuring trace concentrations of breath-hydrogen.
J Chromatogr 1982;229:259–65.
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Case 2 check Digestive

10. Gasbarrini A, Corazza GR, Gasbarrini G, et al. Methodology and

indications of H2-breath testing in gastrointestinal diseases: The
Rome Consensus Conference. Aliment Pharmacol Ther 2009;29
Suppl 1:1–49. doi: 10.1111/j.1365-2036.2009.03951.x.
11. Rezaie A, Buresi M, Lembo A, et al. Hydrogen and nethane-
based breath testing in gastrointestinal disorders: The North
American Consensus. Am J Gastroenterol 2017;112:775–84.
doi: 10.1038/ajg.2017.46.
12. Corazza GR, Menozzi MG, Strocchi A, et al. The diagnosis of
small bowel bacterial overgrowth. Reliability of jejunal culture
and inadequacy of breath hydrogen testing. Gastroenterology
1990;98:302–9.
13. Bouhnik Y, Alain S, Attar A, et al. Bacterial populations
contaminating the upper gut in patients with small intestinal
bacterial overgrowth syndrome. Am J Gastroenterol
1999;94:1327–31.
14. Grace E, Shaw C, Whelan K, et al. Review article: Small
intestinal bacterial overgrowth – Prevalence, clinical features,
current and developing diagnostic tests, and treatment. Aliment
Pharmacol Ther 2013;38:674–88. doi: 10.1111/apt.12456.
15. Quigley EM, Abu-Shanab A. Small intestinal bacterial
overgrowth. Infect Dis Clin North Am 2010;24:943–59, viii–ix.
doi: 10.1016/j.idc.2010.07.007.
16. Sullivan MA, Cohen S, Snape WJ, Jr. Colonic myoelectrical
activity in irritable-bowel syndrome. Effect of eating and
anticholinergics. N Engl J Med 1978;298:878–83.
17. Ritchie J. Pain from distension of the pelvic colon by inflating a
balloon in the irritable colon syndrome. Gut 1973;14:125–32.
18. Holtmann GJ, Ford AC, Talley NJ. Pathophysiology of irritable
bowel syndrome. Lancet Gastroenterol Hepatol 2016;1(2):133–46.
doi: 10.1016/S2468-1253(16)30023-1.
19. Kerckhoffs AP, Samsom M, van der Rest ME, et al. Lower
bifidobacteria counts in both duodenal mucosa-associated and
fecal microbiota in irritable bowel syndrome patients. World J
Gastroenterol 2009;15:2887–92.
20. Kerckhoffs AP, Ben-Amor K, Samsom M, et al. Molecular
analysis of faecal and duodenal samples reveals significantly
higher prevalence and numbers of Pseudomonas aeruginosa in
irritable bowel syndrome. J Med Microbiol 2011;60(2):236–45.
doi: 10.1099/jmm.0.022848-0.
21. Kunkel D, Basseri RJ, Makhani MD, et al. Methane on breath
testing is associated with constipation: A systematic review and
meta-analysis. Dig Dis Sci 2011;56(6):1612–18. doi: 10.1007/
s10620-011-1590-5.
22. Attaluri A, Jackson M, Valestin J, et al. Methanogenic flora is
associated with altered colonic transit but not stool
characteristics in constipation without IBS. Am J Gastroenterol
2010;105:1407–11. doi: 10.1038/ajg.2009.655.
23. Simren M, Barbara G, Flint HJ, et al. Intestinal microbiota in
functional bowel disorders: A Rome foundation report. Gut
2013;62(1):159–76. doi: 10.1136/gutjnl-2012-302167.
24. Shah SC, Day LW, Somsouk M, et al. Meta-analysis: Antibiotic
therapy for small intestinal bacterial overgrowth. Aliment
Pharmacol Ther 2013;38:925–34. doi: 10.1111/apt.12479.
25. Madisch A, Holtmann G, Plein K, et al. Treatment of irritable bowel
syndrome with herbal preparations: Results of a double-blind,
randomized, placebo-controlled, multi-centre trial. Aliment
Pharmacol Ther 2004;19(3):271–79.

14
 Digestive check Case 3

CASE Question 3

3
What are the indicators for referral for further investigations
Russell has heartburn (eg endoscopy)?

Russell, an IT consultant of Anglo-Celtic ethnicity aged

46 years, presents to your practice with a two-year
history of increasing heartburn and acid regurgitation at
the back of his throat. The discomfort sometimes
spreads throughout his chest and occasionally can be
felt in his back. His symptoms initially occurred
monthly, but in the last year have occurred daily, usually
after meals and soon after going to bed. The symptoms
worsen with rich spicy meals like beef curry or large
meat servings at barbecues, which Russell enjoys. He
always consumes beer and/or wine with his dinner.

Russell self-diagnosed his condition to be reflux and

for the last year has been using over-the-counter
(OTC) antacids with good relief. However, he is
concerned about needing daily doses, sometimes two
to three times per day.
On further questioning, he admits to occasionally feeling
a delay in food passing through the low sternal level, but
without actual sticking or needing to wash it through
with fluid. There is no anorexia or haematemesis. Russell
tells you that he gained 20 kg of weight in the past 10
years, and his weight is currently 110 kg. His height is
180 cm, and his body mass index (BMI) is 34 kg/m2.
Question 1
What are the likely and important diagnoses to consider?
Further information
After eight weeks of proton pump inhibitor (PPI) treatment,
Russell felt that the degree of burning had improved by 50%,
but there was little change to the frequency of events. The
improvements were felt in the first four weeks but had now
reached a plateau. He still needs antacids three to four days
per week for breakthrough symptoms. Russell’s dysphagia
has improved, occurring half as often, but has not
disappeared completely.
Russell has tended to avoid hot curries and large meat-rich
meals, with benefits noted at the time. He has also tried to
reduce his alcohol intake, being able to have two alcohol-free
nights per week; however, he still has six to eight standard
drinks per night on Fridays and Saturdays. He understands
that losing weight is an important goal.

Question 4
Given Russell’s current state of health, would you consider
referring him for an endoscopy? Would you consider
additional pharmacotherapy (eg increasing PPI dose or adding
H2-receptor antagonists [H2RAs] or prokinetic agents)?

Question 2
What would be the appropriate initial approach to
managing Russell?

Further information

Russell underwent upper gastrointestinal endoscopy while

still on his standard PPI treatment and was found to have
multiple short linear-distal oesophageal reflux erosions
without confluence. He was also found to have a 2 cm

15
Case 3 check Digestive
segment of Barrett oesophagus and a short (3 cm) sliding
hiatus hernia. There was no stricture and no evidence of
eosinophilic oesophagitis. The gastric and duodenal mucosa
were normal. Russell’s gastric tissue urease test was negative
for Helicobacter pylori, but the biopsies of the Barrett segment
confirmed intestinal metaplasia without dysplasia.
Question 5
How should Russell now be managed in terms of his
symptoms and Barrett oesophagus?
Further information
After four weeks of twice-daily PPI, Russell feels that his
symptoms are much better controlled. His dysphagia has also
resolved, and he no longer needs antacid supplementation.
His weight remains unchanged, but he continues to be wary
of dietary indiscretions. He is able to maintain two alcohol-
free nights per week but still consumes excessive quantities
on other nights. His sleep has improved, and he has fewer
nocturnal and supine reflux episodes.
Russell found a lot of online information about his diagnosis
and is happy to undergo surveillance for Barrett oesophagus.
However, he has some concerns about the long-term use of
PPIs and also wants to discuss surgery.
Question 6
What will you tell Russell about long-term PPI use? Is he a
candidate for anti-reflux surgery?
16
CASE 3 Answers
Answer 1
Russell appears to be correct in his self-diagnosis of gastro-
oesophageal reflux disease (GORD). The most common
presenting symptoms of GORD are heartburn (a burning
sensation); retrosternal, rising discomfort; and regurgitation
(the occurrence of sour-tasting, acidic gastric contents in the
back of the throat or mouth without a vomiting action).1–3 The
refluxate is described as tasting like vomitus.
His symptom of minor dysphagia is very common with GORD
but can also occur with complications of GORD (eg peptic
stricturing from scarring).2 The intermittent, non-progressive
nature of his dysphagia without anorexia and weight loss
makes a malignancy unlikely, and it is not a sufficient trigger
for endoscopy. However, this presentation requires careful
prospective observation. Other alarm symptoms include
recurrent vomiting, anaemia, haematemesis or melaena.1
A differential diagnosis to GORD is eosinophilic oesophagitis,
an allergic condition with wide-ranging symptoms, although
dysphagia is the most predominant symptom. There is often a
history of atopy (eg eczema, allergic rhinitis, asthma) and a
history of intermittent food bolus obstruction. Although more
frequent in males, it remains much less common than
GORD.2,3
A careful assessment for exertional exacerbation of chest pain
is important to exclude angina, and appropriate assessment is
recommended if there is any concern.2,3
Answer 2
As GORD is the likely diagnosis, a trial of acid suppression
such as PPIs and H2RAs is warranted, because the antacids
are not providing adequate relief, their effects are not
sustained, they do not effect healing or prevent complications
and patients often do not want to keep taking medication
many times throughout the day. H2RAs produce less acid
suppression than PPIs and are clinically less effective. As
Russell’s symptoms suggest some severity, and treatment
should aim to effect rapid improvement, partly to provide
confirmation of the diagnosis, a PPI at standard dose should
be used. A four-week initial course is reasonable until the
patient experiences significant symptom improvement, but
may be extended to eight weeks if improvements are slower.
Once symptoms are tolerable, therapy can be reduced in
dosage or used on an ‘as needed’ basis. Dosing should be
made half to one hour before a meal for maximal
effectiveness. Adverse events like headache and diarrhoea are
uncommon (2%).1,3–5
As Russell’s dysphagia is minor, without progression or other
alarm features, it is reasonable to assess response to therapy
prior to investigation.
Russell can also consider non-pharmacological treatments to
improve his reflux symptoms. He has many opportunities to
address lifestyle factors, especially weight reduction.1,3–5

Elevating the head of his bed is also recommended, but is
usually instituted later because of the inconvenience. General
advice, although unproven in efficacy, includes:1
• reducing consumption of fat, protein, coffee, alcohol,
chocolate, and acidic and spicy food
• reducing meal sizes
• avoiding food and drinks within 2–3 hours of lying down,
exercise or bedtime
• drinking fluids between meals
• stopping smoking
• limiting provoking foods and drinks.
Answer 3
Endoscopy is unnecessary and not recommended as a routine
diagnostic test for GORD, although it is frequently requested.
In patients with uncomplicated cases of GORD, clinical
diagnosis and institution of therapy are appropriate initial
steps.1,3,5
Endoscopy is only recommended if the patient exhibits
indications of alarm features, including significant dysphagia,
odynophagia, haematemesis, melaena, iron deficiency
anaemia, weight loss or persistent vomiting.1 Endoscopy is
also recommended if there is an inadequate response to
standard PPI doses after four to eight weeks.
Testing for H. pylori is recommended if reflux symptoms
overlap with dyspepsia, epigastric discomfort, pain and
bloating. If detected, eradication therapy is recommended.
Endoscopy is not recommended for patients who test positive
for H. pylori unless alarm symptoms are present, if there is a
first-degree relative with gastric cancer or the patient was
born in a region with high gastric cancer prevalence.6
Additionally, endoscopy is indicated if diagnostic clarification
is required – for example, when reflux is thought to be
responsible for dental erosions, globus sensation, sore throat,
vocal hoarseness, laryngitis, cough and wheeze. These latter
symptoms are frequently attributed to GORD even though
there is an overdiagnosis of GORD as the major contributing
factor for these symptoms.7
Answer 4
If Russell’s PPI response had been satisfactory, endoscopy
would be unnecessary. However, his response to PPI therapy
is inadequate and he has ongoing minor dysphagia, albeit still
at low likelihood of being due to malignancy. Therefore,
elective endoscopy is indicated to determine if PPI dose
escalation is warranted. Russell’s age, BMI and ethnicity also
increase his risk of Barrett oesophagus, which adds further
impetus for endoscopy.1
While the addition of H2RAs and/or prokinetic agents
(eg metoclopramide, domperidone) are commonly practised
for refractory reflux symptoms, the benefits are transient
because of tachyphylaxis (H2RAs) or minimal and associated
with increased adverse events (prokinetics).4,8
Digestive check Case 3
Answer 5
The endoscopic findings confirm ongoing acid ulceration on a
standard PPI dose. The most effective next step is to use a
twice-daily PPI and ensure Russell takes the medication
30–60 minutes before meals. H2RAs can further maintain a
raised gastric pH; a nocturnal dose may help, but loses
effectiveness after one to two weeks. A start–stop approach
may overcome the H2RA-induced tachyphylaxis – for
instance, alternating one week on and one week off therapy.4,8
Barrett oesophagus is characterised by the replacement of the
distal squamous oesophageal mucosa with columnar mucosa
containing histological intestinal metaplasia. While
considered pre-malignant, the risk of progression to high-
grade dysplasia or cancer is very low (0.2% per annum). The
diagnosis of Barrett oesophagus likely causes
disproportionate anxiety and excessive surveillance. Current
Australian guidelines recommend:9
• treatment with PPIs to control reflux symptoms
• surveillance endoscopy every three to five years for short-
segment disease (<3 cm)
• surveillance endoscopy at two-yearly to three-yearly
intervals for long-segment involvement, which has greater
risk of progression to cancer.
More intensive surveillance and a consideration of ablative
therapy are indicated if dysplasia is found on histology.
However, Barrett surveillance has not been shown to reduce
mortality, and the cost effectiveness is inconsistent.9
Answer 6
Russell will likely be required to continue on long-term
treatment with PPIs for his condition. Attempts should be
made to reduce his dosing, but it is common for the
symptoms to quickly deteriorate with lower doses, and
frequent re-escalation will be needed. Weight reduction
should be strongly encouraged, and appropriate weight-loss
strategies effected.
Although there have been growing concerns about the risk of
long-term PPI use, including kidney disease, dementia,
osteoporosis, pneumonia and Clostridium difficile infections,
the quality of these studies is low.10 Thus, long-term PPI use
for reflux control remains recommended, along with titrating
dose to symptoms. This is especially important in Russell’s
case, as he has a good correlation between endoscopic
findings and symptoms, and also has Barrett oesophagus.
Nonetheless, the lowest possible dose should be used.
Anti-reflux surgery is rarely performed, largely due to the
effectiveness of PPI therapy in reducing the symptoms.
The least invasive surgical option is laparoscopic
fundoplication, and it is most successful at a high-volume
operative centre. Laparoscopic fundoplication is usually
indicated for patients refractory to, or intolerant of, medical
therapy.4,11 It is also useful for correcting a significant
anatomical defect such as a large hiatus hernia with
associated volume reflux effects. However, laparoscopic
17
Case 3 check Digestive

fundoplication has not been shown to reduce Barrett
oesophagus or prevent consequent adenocarcinoma.9,11
Patient selection is critical, and the procedure is most
effective for patients with classical reflux symptoms that
correlate with objective reflux events (by pH monitoring) who
have a good response to PPI therapy. However, dysphagia can
be a problem in >10% of cases after the surgical procedure.
Failure to respond to PPI therapy is not an automatic
indication for surgery, as these patients need careful
evaluation to ascertain if symptoms are actually due to reflux
events. Oesophageal hypersensitivity and functional heartburn
are functional disorders resembling reflux that do not respond
to further acid suppression. Various motility disorders can
also present with reflux-like symptoms. Identification of these
conditions (eg with oesophageal manometry) indicates a likely
poor response to surgery. Thus, a specialist assessment is
recommended prior to referral for anti-reflux surgery.
7. Madanick RD. Extraesophageal presentations of GERD: Where is
the science? Gastroenterol Clin North Am 2014;43(1):105–20.
doi: 10.1016/j.gtc.2013.11.007.
8. Fass R. Approach to refractory gastroesophageal disease in adults.
In: Post TW, editor. Waltham, MA: UpToDate, 2018.
9. Whiteman DC, Appleyard M, Bahin FF, et al. Australian clinical
practice guidelines for the diagnosis and management of Barrett’s
esophagus and early esophageal adenocarcinoma. J Gastroenterol
Hepatol 2015;30(5):804–20. doi: 10.1111/jgh.12913.
10. Freedberg DE, Kim LS, Yang YX. The risks and benefits of long-
term use of proton pump inhibitors: Expert Review and Best
Practice Advice From the American Gastroenterological
Association. Gastroenterology 2017;152(4):706–15. doi: 10.1053/j.
gastro.2017.01.031.
11. Schwaitzberg SD. Surgical management of gastroesophageal reflux
in adults. In: Post TW, editor. Waltham, MA: UpToDate, 2018.

Given Russell’s good response to medical therapy as well as

his presenting mild dysphagia, which is likely to be due to a
non-specific acid-induced dysmotility, he should not be
recommended for surgical management. Russell should be
strongly encouraged to address lifestyle factors, especially
weight reduction.

Conclusion

GORD is common, and management should begin with a trial

of acid suppression and attempts to address exacerbating
factors. Endoscopy should be reserved for patients with alarm
symptoms or those who are refractory to PPI therapy. Patients
should be reassured that PPI use is very safe and the evidence
for uncommon significant long-term complications is weak.
Nonetheless, the lowest effective doses are recommended,
including intermittent dosing.

Patients who remain refractory to high-dose PPIs should be

referred for specialist review where further assessments to
correlate symptoms to reflux events (eg pH monitoring) or
motility abnormalities (manometry) can be undertaken. If
necessary, surgical management may be considered, but
patient selection is critical.

References
1. Expert Group for Gastrointestinal. Gastrointestinal: Gastro-
oesophageal reflux. In: eTG complete [Internet]. Melbourne:
Therapeutic Guidelines Limited, 2018.
2. Kahrilas PJ. Clinical manifestations and diagnosis of
gastroesophageal reflux in adults. In: Post TW, editor. Waltham,
MA: UpToDate, 2018.
3. Keung C, Hebbard G. The management of gastro-oesophageal
reflux disease. Aust Prescr 2016;39(1):6–10.
4. Gyawali CP, Fass R. Management of gastroesophageal reflux
disease. Gastroenterology 2018;154(2):302–18. doi: 10.1053/j.
gastro.2017.07.049.
5. Kahrilas PJ. Medical management of gastroesophageal reflux
disease in adults. In: Post TW, editor. Waltham, MA:
UpToDate, 2018.
6. Expert Group for Gastrointestinal. Gastrointestinal: Helicobacter
pylori infection. In: eTG complete [Internet]. Melbourne:
Therapeutic Guidelines Limited, 2018.

18
 Digestive check Case 4

CASE Question 3

4 Ethel decides to take aspirin

What advice would you give Ethel about continuing the use of
low-dose aspirin?

Ethel, aged 66 years, decided to put herself on

prophylactic aspirin (half a 300 mg tablet daily) after
her father died recently from a myocardial infarction
at the age of 89 years. She had read on an online blog
that the use of aspirin can stop her from developing
cardiovascular disease. Ethel suffers from some pain
in her right knee, particularly when going down stairs,
for which she takes paracetamol intermittently. You
recently completed a comprehensive health check on
her, and at that stage you did not believe she had
cardiac risk factors. She is normotensive, non-diabetic
and a non-smoker, with a normal lipid profile and no
cardiac symptoms. Ethel made this appointment to
ask your opinion about her taking aspirin. She has
heard it can cause stomach ulcers but is not sure how Further information
often this side effect occurs.
Despite your advice that aspirin might do more harm than
good, Ethel decides she wants to continue taking it. She
has also heard that it might reduce the risk of some
Question 1 cancers and, since she needs to help care for her grandson
who has a disability, wants to try to maximise her chances
Has Ethel’s father’s cardiac death significantly increased her
of staying healthy.
cardiac risk status?

Question 4
Accepting that continuing to take aspirin is Ethel’s choice,
could you give her any advice that would reduce her risk of
developing an ulcer?

Question 2
What advice would you give Ethel about the chances of her
getting a peptic ulcer if she continues long-term use of low-
dose aspirin?

Further information

Ethel follows your advice and is now taking the 100 mg

aspirin tablet you prescribed, but she decides against adding
a proton pump inhibitor (PPI). Her son conducted a Google
search about peptic ulcers and told her that two Australian
researchers won the Nobel Prize in Physiology or Medicine for
discovering that many stomach ulcers are caused by a
bacterium called Helicobacter pylori. Ethel is a little nervous
about the possibility that she might develop an ulcer, and she
wonders whether she should be tested for H. pylori. She has
not been diagnosed with a peptic ulcer in the past.

19
Case 4 check Digestive
Question 5
What advice would you give her?
Further information
A little over a year later, you receive a telephone call at the
practice from Ethel’s husband. He informs you that Ethel has
just had two large, loose, very black and smelly bowel actions,
and she is feeling faint. He asks if you can make a house call.
Question 6
What would you do in this situation?
Further information
When Ethel reaches hospital, she is mildly shocked (blood
pressure 100/60 mmHg, with a postural drop of 20 mmHg,
and a pulse of 105 beats per minute). She is transfused and
has an early endoscopy. An actively bleeding ulcer is seen in
the gastric antrum during endoscopy. The endoscopist
manages to obtain haemostasis by injecting adrenaline into
the ulcer base then applying endoscopic clips. The rapid
urease test on a biopsy elsewhere in the antrum is negative
for H. pylori. The aspirin is stopped and Ethel is started on an
eight-week course of a PPI to heal the ulcer. There is no
further bleeding and she is discharged home three days later.
Three months later, she visits you to ask whether she should
start aspirin again.
20
Question 7
What advice would you give her about starting on aspirin again?
Further information
A year goes by and Ethel consults you for worsening pain in her
right knee. On examination, there is discomfort and crepitus on
movement. She has similar but less marked features in the
other knee. You undertake appropriate diagnostic
investigations and confidently diagnose osteoarthritis. Her daily
walks with the dog are becoming more difficult, although some
weeks are not too bad.
Paracetamol is no longer giving her any effective relief, and she
asks if you can prescribe something stronger. Ethel mentions
that her son (who conducted another Google search) told her
some arthritis drugs can cause heart attacks or stomach ulcers.
Ethel wonders whether some drugs might be safer than others.
Question 8
What advice would you give her?
CASE 4 Answers
Answer 1
If Ethel’s father died from a myocardial infarction in the
absence of obvious cardiac disease earlier in his life, it does
not significantly increase his daughter’s current cardiac risk.
The British Heart Foundation and The Royal Australian
College of General Practitioners (RACGP) advise that her

father would need to have been diagnosed with cardiovascular
disease before the age of 55 years (and 65 years of age for
women) for her to be labelled as having a family history of
cardiovascular disease.1,2 In addition, the information you
already have about Ethel, when entered into the Australian
absolute cardiovascular disease risk calculator, indicates she
has only about a 1% chance of developing cardiovascular
disease in the next five years.3
Answer 2
Peptic ulcers, more often gastric than duodenal, occur very
frequently in people taking low-dose aspirin. One study found
a point prevalence of 7% in volunteers who agreed to an
endoscopy, most of whom were asymptomatic. Over the
course of a whole year, the incidence of these ‘endoscopic
ulcers’ is probably nearer to about 20–30%.4
It is now clear that asymptomatic nonsteroidal anti-
inflammatory drug (NSAID) and aspirin ulcers, which are
often quite small, come and go. The problem arises if one
happens to erode a submucosal artery; the annual incidence
of this occuring is somewhere between 0.2% and 1%.5
Answer 3
The recent large ASPirin in Reducing Events in the Elderly
(ASPREE) trial, carried out mainly in Australia and the US,
found that low-dose aspirin was of doubtful benefit for
primary prophylaxis – that is, for individuals without evidence
of overt cardiovascular disease. The trial was conducted in
individuals aged ≥70 years with no evidence of cardiovascular
disease. Almost 20,000 participants were randomised to
receive either 100 mg aspirin daily or a placebo for almost five
years. The rate of cardiovascular events in those receiving
aspirin was almost identical to those given placebo. However,
the aspirin group had approximately a 40% higher rate of
major haemorrhage.6 Thus it is appropriate to advise Ethel
that she should seriously consider discontinuing the aspirin.
Answer 4
The risk of developing ulcers with long-term aspirin use is
dose-related. The optimal dose for vascular prevention is
nearer to 100 mg daily, so you could prescribe Ethel with one
of the Australian formulations with a 100 mg dose. While
some patients prefer an enteric-coated formulation, there is
little evidence this is less ulcerogenic than uncoated aspirin.
It would also be worth discussing the use of a PPI as
co-therapy, although the main disadvantage would be the
additional cost. PPIs are generally very well tolerated, with the
only well-proven side effect being an increase in risk of enteric
infections such as travellers’ diarrhoea.7 Other possible long-
term risks such as increased fracture incidence and renal
insufficiency have been raised by some case-control studies,
but these studies have been unable to rule out confounders.8
In the absence of data from randomised controlled trials,
these possible risks should be seen as speculative. If Ethel
happened to have gastro-esophageal reflux disease (GORD)
as well, the addition of a PPI would be an added benefit to her.
Studies using 20 mg/day and 40 mg/day of esomeprazole
Digestive check Case 4
found a 70–90% reduction in endoscopic ulcers during six
months’ follow-up. Epidemiologic studies have also found a
reduction in ulcer haemorrhage of the same order with a
variety of PPIs.9–11
Answer 5
A recent meta-analysis found that patients who are infected
with H. pylori were about 2.5 times more likely to develop a
gastroduodenal ulcer bleed while taking low-dose aspirin than
uninfected patients.12 However, the number-needed-to-treat
to prevent one bleed per year is high – somewhere between
100 and 1000.
Since Ethel has no particular risk factors for peptic ulcers,
other than her age and the low-dose aspirin, it may not be
cost-effective to test her for the bacterium. If you did decide to
proceed with conducting a test, a breath test (13C or 14C-urea)
is more specific and sensitive than serology, but the latter is
probably more convenient for you to order and simpler for her
to do.
Answer 6
Based on the described presentation, this is almost certainly
a case of melaena, and very likely caused by a bleeding ulcer.
Your first advice would be to recommend Ethel’s husband
call an ambulance to take her to a hospital with a 24-hour
gastroenterology service. If time permits you to make the
house call while the ambulance is on its way, you would be
giving pastoral care to a patient you know well. Of course, if
there was a risk of delay in the ambulance arriving, the better
advice might be for the husband to drive Ethel to hospital if
he has a car.
Answer 7
Since there was no good indication to take aspirin in the first
place, the recent bleed is a strong reason to recommend that
Ethel does not take aspirin (assuming she has not developed
cardiovascular disease in the meantime).
Patients who developed a bleeding ulcer while taking
NSAIDs or low-dose aspirin are at least 10 times more likely
to have a subsequent ulcer bleed if they recommence
NSAIDs or aspirin.13
Answer 8
It is probably a little early to consider referring Ethel for a
possible knee replacement. However, it would be useful to go
through a shared decision-making process using a decision
support tool for knee osteoarthritis (eg www.safetyandquality.
gov.au/wp-content/uploads/2018/05/Designed-draft-DST-
for-OAK-for-consultation-April-2018.pdf). If she decides on
medical management, you would advise weight loss if she is
overweight. You would be likely to try a NSAID to manage the
pain, as well as recommend gentle regular walking within the
limits of her pain. Other advice – for example, cycling and
hydrotherapy as per the RACGP’s Guideline for the
management of knee and hip osteoarthritis – would also be
worthwhile.14 Since she already had an ulcer bleed while
21
Case 4 check Digestive
taking another NSAID (aspirin), and her risks of further ulcer
bleeds have significantly increased, there is a definite
advantage in using co-treatment with a PPI, and probably
choosing a COX-2 selective NSAID (coxib) to further reduce
the ulcer risk.
A recent very large Prospective Randomized Evaluation of
Celecoxib Integrated Safety versus Ibuprofen or Naproxen
(PRECISION) trial randomised patients with an established or
increased risk of cardiac disease plus osteoarthritis to receive
celecoxib (100 mg twice daily), ibuprofen (600–800 mg three
times daily) or naproxen (375–500 mg twice daily). It found no
increase in cardiovascular events in patients taking the coxib,
but these patients had substantially fewer clinically significant
gastrointestinal events than those on the nonselective
NSAIDs. It is important to note that all patients also received
a PPI (esomeprazole 20 mg or 40 mg daily).15,16
In conclusion, current international guidelines recommend
that someone needing an NSAID who is at high
gastrointestinal risk (such as Ethel, who has proven she is in
that category due to her bleed) should either receive a coxib or
a conventional NSAID plus a PPI. The recent CONCERN trial
suggests that the safer option is to use both a coxib and a
PPI.17 Celecoxib is the only coxib licensed in Australia, and
100 mg twice daily was the dose used in CONCERN. The
likelihood of her having another bleed in the future is low. But
if it did occur, knee replacement may become an attractive
option instead of NSAIDs, if deteriorating arthritis had not led
to it already.
Resources for doctors
• Therapeutic Guidelines Gastrointestinal, ‘Preventing
NSAID-induced ulcers’: These guidelines are still useful, but
they and other international guidelines now need revision as
a result of the FDA-mandated PRECISION study. In
particular, the UK National Institute for Health and Care
Excellence (NICE) guidelines (last updated February 2018)
no longer reflect best evidence.
Resources for patients
• Helicobacter pylori (H. pylori) – Gastroenterological Society
of Australia’s ‘Health information fact sheets’, www.gesa.
org.au/resources/patients/health-information-fact-sheets
References
1. British Heart Foundation. Family history. London: British Heart
Foundation [date unknown]. Available at www.bhf.org.uk/
informationsupport/risk-factors/family-history [Accessed
12 November 2018].
2. The Royal Australian College of General Practitioners. Guidelines
for preventive activities in general practice. 9th edition. East
Melbourne, Vic: 2018.
3. The Heart Foundation. Absolute risk. Melbourne: National Heart
Foundation of Australia [date unknown]. Available at www.
heartfoundation.org.au/for-professionals/clinical-information/
absolute-risk [Accessed 12 November 2018].
4. Yeomans ND, Lanas AI, Talley NJ, et al. Prevalence and incidence
of gastroduodenal ulcers and erosions during treatment with
vascular protective doses of aspirin. Aliment Pharmacol Ther
2005;22:795–801.
22
5. Serrano P, Lanas A, Arroyo MT, et al. Risk of upper gastrointestinal
bleeding in patients taking low-dose aspirin for the prevention of
cardiovascular diseases. Aliment Pharmacol Ther
2002;16(11):1945–53.
6. McNeil JJ, Wolfe R, Woods RL. Effect of aspirin on cardiovascular
events and bleeding in the health elderly. N Engl J Med
2018;379:1509–18.
7. Bavishi C, Dupont HL. Systematic review: The use of proton pump
inhibitors and increased susceptibility to enteric infection. Aliment
Pharmacol Ther 2011;34(11–12):1269–81.
doi: 10.1111/j.1365-2036.2011.04874.x.
8. Kinoshita Y, Ishimura N, Ishihara S. Advantages and
Disadvantages of Long-term Proton Pump Inhibitor Use.
J Neurogastroenterol Motil. 2018;24(2):182–196. doi: 10.5056/
jnm18001.
9. Yeomans ND, Lanas A, Labenz J, et al. Efficacy of esomeprazole
(20 mg once daily) for reducing the risk of gastroduodenal ulcers
associated with continuous use of low-dose aspirin. Am J
Gastroenterol 2008;103:2465–73.
10. Scheiman JM, Devereaux PJ, Herlitz J, et al. Prevention of peptic
ulcers with esomeprazole in patients at risk of ulcer development
treated with low-dose acetylsalicylic acid: A randomised,
controlled trial (OBERON). Heart 2011;97:797–802.
11. Lanas A, Garcia-Rodriguez LA, Arroyo MT, et al. Effect of
antisecretory drugs and nitrates on the risk of ulcer bleeding
associated with nonsteroidal anti-inflammatory drugs, antiplatelet
agents and anticoagulants. Am J Gastroenterol 2007;102:507–15.
12. Ng J, Yeomans ND. Helicobacter pylori infection increases the risk
of upper gastrointestinal bleeding with low-dose aspirin: A meta-
analysis. Med J Aust 2018;209:306–11.
13. Lai KC, Lam SK, Chu KM, et al. Lansoprazole for the prevention of
recurrences of ulcer complications from long-term low-dose
aspirin use. N Engl J Med 2002;346:2033–38.
14. The Royal Australian College of General Practitioners. Guideline
for the management of knee and hip osteoarthritis. 2nd edition.
East Melbourne, Vic: 2018.
15. Nissen, SE, Yeomans ND, Solomon DH, et al. Cardiovascular
safety of non-steroidal anti-inflammatory drugs in patients with
chronic arthritis. N Engl J Med 2016;375: 2519–29.
16. Yeomans ND, Graham DY, Husni ME, et al. Randomised clinical
trial: Gastrointestinal events in arthritis patients treated with
celecoxib, ibuprofen or naproxen in the PRECISION trial. Aliment
Pharmacol Ther 2018;47:1453–63.
17. Chan FKL, Ching JYL, Tse YK, et al. Gastrointestinal safety of
celecoxib versus naproxen in patients with cardiothrombotic
diseases and arthritis after upper gastrointestinal bleeding
(CONCERN): An industry-independent, double-blind, double-
dummy, randomised trial. Lancet 2017;389(10087):2375–82.
doi: 10.1016/S0140-6736(17)30981-9.
 Digestive check Case 5

CASE Question 3

5
How would your management and treatment plan be affected
Omar and Felicity have if Omar’s clinical picture was more of biliary colic (chronic
abdominal pain cholecystitis and waxing and waning pain in the right upper
quadrant brought on by eating fatty food) and the ultrasound
Omar, 65 years of age, presents with a three-day
report showed gall bladder polyps without stones?
history of right upper quadrant pain of his abdomen.
He notes that he has lost his appetite and feels ‘off’,
and has felt nauseated and been vomiting. Omar’s
clinical notes show he had a coronary bypass graft
four years ago, and he has a history of high
cholesterol, diabetes and prostatism.

On examination, Omar looks unwell. He struggles to

get on the examination table and winces on
palpation of the right upper quadrant of the
abdomen. He is unable to take a full breath while you
press on the right upper quadrant. His mucous
membranes are dry, his heart rate is 95 beats per
minute, and he has a temperature of 37.8˚C. Further information

You send Omar for some blood tests, and the blood tests
return with a white cell count of 18,000 x 109/L, C-reactive
protein (CRP) of 86 mg/L and bilirubin of 50 μmol/L. The
Question 1 ultrasound shows gallstones, a thickened gall bladder with a
bile duct diameter of 12 mm and dilated intrahepatic ducts.
What is your clinical suspicion? What diagnostic work-up
would you perform on Omar?

Question 4
Given Omar’s blood test and ultrasound report, what does the
clinical picture suggest? How should he be managed?

Question 2
Question 5
Would a computed tomography (CT) scan be useful for Omar?
Would your management and treatment plan be different if
the obstruction were above the common bile duct but below
the intrahepatic ducts?

23
Case 5 check Digestive

Further information Further information

Omar’s colleague, Felicity, is female, aged 38 years and comes Felicity presents to you prior to surgery with a positive
to see you today. She has no significant past medical history, pregnancy test. Based on her menstrual history, she is in the
and she presents with a two-day history of intermittent first trimester.
epigastric and right upper quadrant pain. Felicity noticed that
initially she had attacks only after consuming fatty foods, but
now almost any food seems to bring on an attack. The pain Question 8
radiates to her back, and dissipates after an hour when
How does pregnancy affect the timing of surgery?
treated with simple analgesia. Physical examination reveals a
soft abdomen, and you refer Felicity for basic investigations
(ie blood tests including liver function tests, full blood count
and electrolytes and an upper abdominal ultrasonography).

You follow up with Felicity after two days. She tells you that
during this time, her pain has had the same pattern and she is
having daily attacks. Ultrasonography shows gallstones, but
there is no sign of acute cholecystitis. The ultrasound shows
that there is a stone impacted in Hartman’s pouch, the
junction between the gall bladder and the cystic duct.

Question 6 Further information

What would be your diagnosis of Felicity? It was decided, in conjunction with the specialist and Felicity,
that she would undergo laparoscopic cholecystectomy.
Felicity has an uncomplicated laparoscopic cholecystectomy
with an overnight stay.

Question 9
What advice would you give Felicity?

Further information

Felicity is concerned that she may have to wait three months

for surgery after being placed on a waiting list, as she does
not have any private health insurance.

Question 7
What would you advise Felicity? What would her CASE 5 Answers
management plan include?

Answer 1
Patients who present with right upper quadrant pain,
nausea, vomiting, a high temperature and Murphy’s sign (ie
inhibition of inspiration by pain on palpitation) should be
highly suspected of having acute cholecystitis. Acute
cholecystitis is an inflammation of the gall bladder, and is
most often caused by gallstones, although this is not
always necessary.

Tests can be performed to 1) exclude common differential

diagnoses such as cardiac ischaemia, pneumonia, a

24

perforated ulcer and urinary tract infection, and 2) support
the diagnosis of cholecystitis. Typical tests investigating
other potential causes would include electrocardiography,
chest X-ray, urinalysis and blood tests, including those
listed below.
The diagnosis of acute cholecystitis should be made on the
basis of clinical features, which is supported by the results of
ultrasonography.
Given that Omar is showing signs of dehydration and is
clearly unwell, it would be prudent to send Omar to a hospital,
where the work-up could be done, and management initiated.
The following lab tests should be performed:
• Inflammatory markers – raised white cell count, CRP and
erythrocyte sedimentation rate could confirm an infection.
• Liver function tests (LFTs) – important as these may
indicate signs of biliary obstruction, which can occur in
cholangitis or when an impacted gallstone obstructs the
common hepatic duct (Mirizzi syndrome).1
• Electrolytes and sugars – checked and managed,
particularly as Omar has a history of diabetes, and when
there are early signs of dehydration.
• A troponin level – helpful to rule out myocardial infarction.
Imaging is essential to confirm the diagnosis of acute
cholecystitis. Most patients with a convincing history and
examination, as seen with Omar, and particularly with the
positive Murphy’s sign, are best served with ultrasonography
as this has high sensitivity and specificity for gallstones and
cholecystitis.2 The ultrasound can also show features of
unexpected liver disease (ie cirrhosis or an abscess).
Furthermore, the ultrasound will image the bile duct; while
there is a low chance (around 30%) of actually seeing a bile
duct stone when present due to overlying gas, it can give a
clue to the presence of bile duct stones by detecting a
dilation of the bile ducts.3
Answer 2
A CT scan is not recommended as a first-line investigation for
a patient such as Omar and is unnecessary for therapeutic
decisions if the ultrasound has already shown the suspected
pathology. A CT scan would be useful if another pathology
was suspected, the ultrasound was not convincing or when
ultrasonography is unavailable. While abdominal CT is an
informative radiographic imaging tool for many conditions, the
assessment of the gall bladder is poor, and sensitivity is low
for gallstones.
The role of a CT scan (with intravenous and oral contrast) is
two-fold. First, it can help to identify or rule out other
pathology such as appendicitis, perforated ulcer,
pyelonephritis or pneumonia if the ultrasound is unclear or
unavailable. Second, it can show complications of
cholecystitis such as an abscess, perforation or phlegmon, as
well as biliary obstruction. Its sensitivity for acute cholecystitis
is less than with ultrasonography. Thus, only a small
proportion of patients are served best by both tests.2
Digestive check Case 5
Answer 3
Biliary colic and a gall bladder polyp are common and reflect
the reality of polyp diagnosis. A gall bladder polyp is diagnosed
sonographically as a nodule that produces no shadow and does
not move once the patient is rolled. Conversely, a gallstone
classically casts an acoustic shadow and moves.
The vast majority of gall bladder ‘polyps’ suggested by
ultrasound are in fact inflammatory pseudopolyps caused
by tiny cholesterol stones.4 These are managed by the same
rules as biliary colic with gallstones, and an elective
cholecystectomy can be advised. It is rare for these to grow
beyond around 8 mm, and the pathologist usually will not
report a polyp, because it is rubbed away in the retrieval
and preparation.
Adenomatous polyps are rare, but can be pre-malignant. The
risk for malignancy is strongly associated with size, and
appears to be measurable after a polyp is >20 mm measured
on ultrasound.5 Given non-adenomatous polyps rarely reach
10 mm, this is used as a cut-off to recommend
cholecystectomy in patients with asymptomatic polyps. The
caveat is that patients with inflammatory bowel disease or
primary sclerosing cholangitis should have their gall bladder
removed (even for small polyps) because of their increased
risk of biliary cancer. A useful flowchart-like algorithm is
presented in the European guidelines.5
If there were gall bladder polyps found on the ultrasound, it
would be recommended that Omar have ultrasonography
performed every six months for two years to ensure that there
is no growth beyond 10 mm.5 Stones sometimes become
apparent during this period of observation. If there is no
growth at two years, then we can be confident that these are
pseudopolyps and can be left alone unless symptoms occur.
Answer 4
Omar’s blood tests show signs of systemic inflammation, and
the ultrasound shows gall bladder thickening, both of which
are indicative of cholecystitis in this setting.
An important finding on ultrasonography is that there are
signs of biliary obstruction, which is highlighted by the dilated
bile duct (normally <6 mm)6 and raised bilirubin. Omar’s
management and potential complications are therefore
substantially more complicated than ‘simple’ cholecystitis. He
is likely to have cholangitis from stones in the common bile
duct. Given Omar’s age and comorbidities, these results
suggest he should be managed in hospital, even if he did not
appear unwell. His initial management should be
resuscitative, and intravenous fluids and antibiotics should be
initiated while specialist opinion is sought.
While a cholecystectomy will be important for Omar in the
future, the most pressing and immediate problem is his
cholangitis. The management of cholangitis is antibiotics
combined with biliary decompression.7 Biliary decompression
is most commonly performed by endoscopic retrograde
cholangiopancreatography (ERCP), with sphincterotomy and
removal of the offending stone.
25
Case 5 check Digestive
However, in patients with ischaemic heart disease and those
who are on antiplatelet or anticoagulants, urgent biliary
drainage has risks of bleeding or cardiac events.8 These risks
can be reversed to some degree with vitamin K or blood
products; however, this cannot always be done, as some
agents have no effective reversal, and in some cases, reversing
anticoagulation presents too high a risk.
ERCP is still performed in patients with ischaemic heart
disease and those who are on antiplatelet or anticoagulants,
although sphincterotomy and stone extraction is sometimes
omitted. Instead, the pus is allowed to drain alongside a
plastic stent. The plastic stents should be removed before two
months have elapsed, otherwise they too can get blocked and
lead to another episode of cholangitis. Sphincterotomy and
stone extraction are often performed at a second, elective
ERCP, when antiplatelets can be omitted.
Answer 5
If the obstruction is above the common bile duct but below the
intrahepatic ducts, the most likely cause is Mirizzi syndrome.
This occurs when a large gallstone becomes impacted at the
cystic/bile duct junction and occludes the common hepatic
duct, leading to biliary obstruction. The differential diagnosis is
a malignancy of the gall bladder or bile ducts. Cross-sectional
imaging with a CT scan or magnetic resonance imaging is
useful to exclude features of malignancy.
Management of Mirizzi syndrome is usually complex. A
cholecystectomy can sometimes be performed to resolve the
situation. However, there is often severe inflammation of the
bile duct, or even fistula between the common bile duct and
gall bladder. Other management approaches, including a
partial or subtotal cholecystectomy with or without biliary
procedures, are commonly undertaken. Decompression of the
infected biliary tree is mandatory, and this is usually achieved
through biliary stenting. In rare cases, bile duct reconstruction
using biliary-enteric anastomosis is required.
Answer 6
On the basis of her presentation and investigation results,
Felicity is likely to have refractory biliary colic. This often
occurs when a stone is impacted in the neck of the gall
bladder, causing pain and intolerance to meals. Some
patients in this scenario do not develop classical features of
cholecystitis on imaging.
Answer 7
Patients with this slightly unusual presentation of gallstones,
where the pain pattern is frequent and brought on by even
seemingly non-fatty foods, should be managed with expedited
cholecystectomy, and referral for semi-urgent
cholecystectomy is appropriate. Patients should be advised to
present to the emergency department if the pain increases,
fails to settle or if a fever develops. This type of presentation
can be a harbinger of acute cholecystitis.
In the meantime, management comprises analgesia and
avoidance of fatty foods. It is worth reminding patients that
26
fatty foods include ‘healthy’ fats such as avocado, nuts and
olive oil. Analgesia for biliary colic includes paracetamol,
nonsteroidal anti-inflammatory drugs and, in some cases,
opiates if other choices have not proven effective. Some
patients report symptomatic relief with antispasmodics.9
Answer 8
Biliary colic during pregnancy is quite common. Historical
data suggest that open cholecystectomy during the first
trimester is associated with high rates of spontaneous
abortion or complications for the fetus or mother, and those
in the third trimester are technically difficult and associated
with early labour.10 This has led many to consider
cholecystectomy during pregnancy for only the most
serious cases, and to confine it to the second trimester
wherever possible.
Reviews have found reasonable evidence that laparoscopic
procedures (as opposed to the historical open surgery) are
safe in any stage of pregnancy.10 Although there is uncertainty
of the potential long-term effects on the unborn child, there is
no evidence that laparoscopic surgery causes problems. In
fact, it may be safer for the unborn child than untreated
cholecystitis or complications of gallstones.
The Society of American Gastrointestinal and Endoscopic
Surgeons guidelines suggest pregnancy in any term is not an
absolute contraindication for cholecystectomy.11 There
should be a conversation with the managing obstetric team
and the surgical team about the patient, and risks and
benefits need to be weighed. For instance, a mild, single
attack of biliary colic might be managed conservatively until
after birth, whereas acute cholecystitis or choledocholithiasis
might be managed with surgery.
The use of intra-operative radiation should be minimised; if it
is required, there should be shielding of the fetus in place.
This sometimes means that an intraoperative
choledochoscopy will be used in preference to ERCP to clear
common bile duct stones if present.
Answer 9
It would be important to give Felicity information on:
• time off work
• wound management
• driving
• diet
• pain control.
Time off work
Time off work after cholecystectomy would depend on the
patient and work factors. In an uncomplicated operation,
most healthy patients will return to reasonable levels of
physical activity within two to three days. A week off
sedentary work is typically recommended, and most patients
will feel a little more fatigued than usual for one to two
weeks. Patients should not engage in lifting items >10 kg for

six weeks after surgery to allow for strengthening of the scar
tissue to prevent hernia formation.
Wound management
Dressings can be removed approximately seven days after the
surgery. Showering is safe with most waterproof hospital and
over-the-counter dressings. After the dressings come off,
there is usually a scab on the wounds, and patients can
shower but are not encouraged to use soaps directly onto the
wounds for a few more days. They can swim once the scab is
replaced by a dry scar (around two to three weeks).
Driving
Patients should not drive while under the influence of
medications such as strong analgesia that could affect their
ability, or while physically unable to safely control a vehicle.
While laparoscopic surgery leads to a more rapid recovery
than open surgery, there is still some pain, and most patients
will not drive for a few days after surgery.
Diet
Following cholecystectomy, there is no need for a diet change
in the vast majority of patients. Some patients will notice that
they have slightly more frequent bowel motions, but
troublesome diarrhoea is rare.
Pain management
Regular paracetamol and a short course of NSAIDs are the
key to pain control post-cholecystectomy for up to a week or
so. A short course of opiate analgesia is necessary in a
minority of patients who find that non-opiate pain relief is not
strong enough. However, persistent or worsening pain is
unusual and should be investigated.
If pain persists, possible differential diagnoses include bile
leak (although this is usually evident within days of the
surgery), retained bile duct stone, spasm of the sphincter of
Oddi, wound pain and causes unrelated to the biliary system
or surgery. In up to 5–10% of patients, the gall bladder was not
the cause of the pre-operative pain; therefore, the pain can
persist after cholecystectomy. Pain at this stage is often
termed post-cholecystectomy syndrome.
Blood tests, including inflammatory markers and LFTs,
should be performed to look for signs of infection or
obstruction of the biliary tree. Imaging with ultrasonography
or CT scan can determine the presence of collections or
dilated bile ducts.
It would be worthwhile to contact Felicity’s surgeon at this
stage, as they could give advice about what to do next.
Typically, a referral to a gastroenterologist is required, who
will work through a differential that will include peptic ulcer
disease, gastritis and gastro-oesophageal reflux. Rarer
functional causes exist, such as irritable bowel syndrome or
sphincter of Oddi dysfunction; however, these can be a
challenge to diagnose and treat.
Digestive check Case 5
Resources for patients
• ECI patient factsheet – Gallstones, www.aci.health.nsw.gov.
au/__data/assets/pdf_file/0009/273744/gallstones-ed-
patient-factsheet-2015.pdf
• Better health channel: Gallbladder – gallstones and surgery,
www.betterhealth.vic.gov.au/health/
conditionsandtreatments/gallbladder-gallstones-and-surgery
• Baiu I, Hawn MT. Gallstones and biliary colic. JAMA
2018;320(15):1612, https://jamanetwork.com/journals/
jama/fullarticle/2707462
References
1. Chen H, Siwo EA, Khu M, Tian Y. Current trends in the
management of Mirizzi Syndrome: A review of the literature.
Medicine (Baltimore) 2018;97(4):e9691.
2. Pinto A, Reginelli A, Cagini L, Coppolino F, Ianora A, Bracale R,
Giganti M, Romano L. Accuracy of ultrasonography in the
diagnosis of acute calculous cholecystitis: Review of the literature.
Crit Ultrasound J 2013;5(Suppl 1):S11.
3. Stott MA1, Farrands PA, Guyer PB, Dewbury KC, Browning JJ,
Sutton R. Ultrasound of the common bile duct in patients
undergoing cholecystectomy. J Clin Ultrasound 1991;19(2):73–76.
4. Vivian SJ, Furtado R, Falk G. Ultrasound ‘gallbladder polyps’: A
midleading description best rephrased. Sonography
2015;2(3):57–60.
5. Wiles R, Thoeni R, Barbu S, et al. Management and follow-up of
gallbladder polyps: Joint guidelines between the European
Society of Gastrointestinal and Abdominal Radiology (ESGAR),
European Association for Endoscopic Surgery and other
Interventional Techniques (EAES), International Society of
Digestive Surgery - European Fedoration (EFISDS) and European
Society of Gastrointestinal Endoscopy (ESGE). Eur Radiol
2017;27(9):3856–66.
6. Bruneton J, Roux P, Fenart D, Carmella E, Occelli J. Ultrasound
evaluation of common bile duct size in normal adult patients and
following cholecystectomy. A report of 750 cases. Eur J Radiol
1981;1(2)171–72.
7. ASGE Standards of Practice Committee, Maple J. Ikenberry S,
Anderson M, et al. The role of endoscopy in the management of
choledocholithiasis. Gastrointest endosc 2011;74(4):731–41.
8. Oh H, ElHajj I, Easler J, et al. Post-ERCP bleeding in the era of
multiple antiplatelet agents. Gut Liver 2018;12(2):214–18.
9. Johnston M, Fitzgerald J, Bhangu A, Greaves N. Prew C, Fraser I.
Outpatient management of biliary colic: A Prospective
observational study of prescribing habits and analgesia
effectiveness. Int J Surg 2014;12(2):169–76.
10. Sedaghat N, Cao A, Eslick G, Cox M. Laparoscopic versus open
cholecystectomy in pregnancy: a systematic review and meta-
analysis. Surg endosc 2017;31(2):673–79.
11. Pearl J, Price R, Tonkin A, Richardson W, Stefanidis, D. SAGES
guidelines for the use of laparoscopy in pregnancy. Surg Endosc
2017;31(10)3767–82. doi: 10.1007/s00464-017-5637-3.
27
Multiple choice questions check Digestive

A. Consume a high-fibre diet

ACTIVITY ID 148174
B. Avoid nuts and seeds
Digestive C. Take an omega-3 fatty acid supplement

This unit of check is approved for six Category 2
points in the RACGP QI&CPD program. The
expected time to complete this activity is three
hours and consists of:
• reading and completing the questions for each
case study
–– you can do this on hard copy or by logging on
to the gplearning website, http://gplearning.
racgp.org.au
D. There is no evidence that diet has any impact
Case 2 – Li Hui
Li Hui, 32 years of age, suffers from two years of alternating
diarrhoea and constipation, and intense bouts of abdominal pain.
Question 3
Which of the following symptoms requires urgent referral to a
gastroenterologist?

• answering the following multiple choice questions A. Symptom onset <50 years of age
(MCQs) by logging on to the gplearning website, B. Family history of inflammatory bowel disease
http://gplearning.racgp.org.au
C. Unexplained weight gain
–– you must score ≥80% before you can mark the
D. New onset haemorrhoids
activity as ‘Complete’

• completing the online evaluation form.

Further information
You can only qualify for QI&CPD points by
Following further investigations, referrals and management,
completing the MCQs online; we cannot process
Li Hui is diagnosed with irritable bowel syndrome (IBS).
hard copy answers.

If you have any technical issues accessing this Question 4

activity online, please contact the gplearning
helpdesk on 1800 284 789.
If you are not an RACGP member and would like to
access the check program, please contact the
gplearning helpdesk on 1800 284 789 to purchase
access to the program.
Case 1 – Dimitrious
Which of the following is a recommended component
of IBS management?
A. Increased intake of insoluble fibre
B. Elimination of gluten-containing foods
C. Increased intake of foods containing high levels of
fermentable oligosaccharides, disaccharides, and
monosaccharides and polyols (FODMAPs)
D. Trial of psychological interventions

Dimitrious, 60 years of age with a history of recurrent sigmoid

diverticulitis, presents with five days of left-sided abdominal Case 3 – Dylan
pain. His son’s wedding is in three days and he reports feeling
Dylan, 19 years of age, presents with retrosternal discomfort
stressed. On examination, his body temperature is 37˚C, blood
after meals despite two months of 20 mg pantoprazole twice
pressure is 140/80 mmHg and heart rate is 85 beats per
daily prescribed by another general practitioner. He runs a
minute. The abdomen is soft and he is tender in the left iliac
scuba-diving business in Phuket and Boracay. Doug prefers a
fossa. The full ward test is negative.
non-alcoholic, vegan diet.

Question 1
Question 5
What is the most appropriate management step?
Which of the following would be the most appropriate next
A. Oral fluids while awaiting computed tomography scan results management step?

B. Intravenous amoxicillin 1 g twice daily in hospital
C. Oral amoxicillin + clavulanic acid 875/125 mg twice daily
D. Intravenous fluids and light diet
Question 2
Dimitrious asks you whether there are any dietary changes he
should implement. What is the most appropriate dietary
advice for diverticular disease?
A. Increase proton pump inhibitor (PPI) dosage
B. Test for Helicobacter pylori
C. Consider reflux surgery
D. Adjust dietary intake with dietician supervision
Further information
Dylan tests negative for H. pylori on urea breath testing. He
returns with persistent symptoms and requests an endoscopy.

28
 Digestive check Multiple choice questions

Question 6 Further information

Which of the following is not an indication for endoscopy? You recommend Brenda undergo several investigations, which
she declines. The following year, Brenda and her family move
A. Iron deficiency anaemia
to Germany. On a trip back to Australia, she reports she has
B. Family history of gastric cancer been diagnosed with ‘a non-symptomatic gall bladder growth’
while overseas and is worried about cancer. You review her
C. Significant weight gain
results, which suggest a 5 mm polyp on ultrasound. You
D. Recurrent vomiting discuss this finding with her.

Case 4 – Eden Question 10

Eden, a final-year medical student, is attending your clinic as Which of the following is the most appropriate management
her general practice placement. She asks your opinion on the for an asymptomatic 5 mm gall bladder polyp?
use of low-dose aspirin as primary prophylaxis.
A. Biopsy to rule out malignancy

Question 7 B. Emergency cholecystectomy

Based on the findings of the Aspirin in Reducing Events in the C. Ultrasonography every six months
Elderly (ASPREE) trial, which of the following is true of low-
D. Investigation for Crohn’s disease
dose aspirin?

A. Reduces the rate of cardiovascular events

B. Increases the rate of bowel cancer

C. Increases the rate of major haemorrhage

D. Reduces the rate of deep vein thrombosis

Question 8
Which of the following will reduce the risk of developing gastric
ulcers and bleeding in patients taking aspirin as prophylaxis?

A. Enteric-coated aspirin formulation

B. Dose adjustment to 75 mg aspirin twice daily

C. Empiric treatment for H. pylori

D. Co-therapy with a PPI

Case 5 – Brenda
Brenda, 36 years of age, presents with a history of three bouts
of abdominal pain over the last year. She reports each episode
as starting around 9 pm, with intense epigastric pain
accompanied by sweating and nausea. All episodes resolved
spontaneously. The first bout occurred after her birthday
dinner. She attended an emergency department following the
most recent episode but left without being seen. Examination
is unremarkable, except for a body mass index of 26 kg/m3.
Brenda’s father underwent coronary artery bypass grafting
earlier this year.

Question 9
What is the most likely diagnosis of Brenda’s symptoms?

A. Biliary colic

B. Acute myocardial infarction

C. Pancreatitis

D. Cholangitis

E. Gastroenteritis

29
Independent learning program for GPs

Independent learning program for GPs