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CHAPTER 5 | PANCREATICDISORDERS
15. A 45- year- old male publican presented to the emergency department
with one month of worsening episodic, sudden onset, severe upper
abdominal pain, post- prandial vomiting, and weight loss.
Investigations:
Haemoglobin 13 g/ L
White cell count 15.1 × 10⁹/ L
Serum C- reactive protein (CRP) 120 mg/ L
Serum bilirubin 25 µmol/ L
Serum alanine transferase (ALT) 50 U/ L
Serum alkaline phosphatase (ALP) 120 U/ L
Serum amylase 180 U/ L
CT abdomen with contrast Focal thickening and abnormal enhancement of
the second portion of the duodenum with an
enlarged pancreatic head
Gastroscopy Duodenal wall oedema and stenosis from D1 to
D2.
Duodenal histology Brunner’s gland hyperplasia with multiple spindle
Which of the following statements regarding this condition is correct?
A. Endoscopic stenting of the minor papilla is the mainstay of treatment
B. High- dose prednisolone is the optimal rst- line therapy
C. Pancreatoduodenectomy is often required
D. Serum levels of CA 9- 9 are often elevated
E. Serum levels of IgG4 are often elevated
cells
CHAPTER 5 | QUESTIONS
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16. A 70- year- old man presented with abdominal pain and weight loss.
On clinical examination, he was jaundiced. Observations including
temperature, heart rate, and blood pressure were all unremarkable. He
had no comorbidities and his performance status was 0.
Investigations:
CT triple phase pancreas 3cm solid mass in the head of the pancreas,
highly suspicious for pancreatic carcinoma. No
locoregional lymph nodes or metastatic disease.
Mild common bile duct dilatation (8mm) but no
intrahepatic biliary dilatation.
CT chest Normal
Haemoglobin 120 g/ L
White cell count 4 × 109/ L
Platelet count 252 × 109/ L
International normalized ratio (INR) 1.0
Serum bilirubin 75 µmol/ L
Serum alanine transferase (ALT) 35 U/ L
Serum alkaline phosphatase (ALP) 150 U/ L
Serum C- reactive protein (CRP) 3 mg/ L
What is the next best intervention for this patient?
A. EUS
B. ERCP
C. Percutaneous biopsy of pancreatic mass
D. Staging laparoscopy
E. Whipple procedure
17. Which of the following statements about CA 19- 9 is correct?
A. Alevel ≥500 U/ ml is diagnostic of pancreatic adenocarcinoma
B. Is unable to be produced by % of the population
C. Level is elevated in 50% of patients with advanced pancreatic adenocarcinoma
D. Level is not elevated in hepatocellular carcinoma
E. Level positively correlates with serum bilirubin
18. Which syndrome is most associated with the development of pancreatic
neuroendocrine tumours (p- NETs)?
A. Familial adenomatous polyposis
B. Lynch syndrome
C. Multiple endocrine neoplasia type
D. Multiple endocrine neoplasia type 2A
E. Multiple endocrine neoplasia type 2B
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CHAPTER 5 | PANCREATICDISORDERS
19. Which of the following pancreatic cystic neoplasms has the lowest
malignant potential?
A. Branch duct intraductal papillary neoplasm
B. Cystic pancreatic endocrine neoplasm
C. Main duct intraductal papillary neoplasm
D. Mucinous cystic neoplasms
E. Serous cystadenoma
20. A 50- year- old man was incidentally noted to have a pancreatic cystic
lesion on a CT abdomen performed to investigate diverticulitis.
Asubsequent MRCP was performed.
Investigations:
MRCP 20mm cystic lesion in the head of the pancreas with connection to the
pancreatic duct consistent with branch duct intraductal papillary mucinous
What is the next best management strategy?
A. Discharge with no follow- up required
B. Surgical resection
C. Surveillance at six months, one year, and then annually with magnetic resonance
imaging (MRI)
D. Surveillance with MRI after one year
E. Symptom- based follow- up
neoplasm (IPMN). The main pancreatic duct is dilated to 11mm
chapter
5
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PANCREATICDISORDERS
5
ANSWERS
1. C. Gallstone related
• Gallstones are responsible for 40% of acute pancreatitis
• A>3- fold elevation of ALT in the presence of acute pancreatitis has a positive predictive value
of 95% in diagnosing acute gallstone pancreatitis
• Hypertriglyceridemia is not thought to be a risk for acute pancreatitis at levels below
mmol/ L
Although alcohol is thought to account for >30% of cases of acute pancreatitis, there is nothing in
the question stem to suggest a history of excessive alcohol consumption. There is also no history of
recent new medication that makes drug- related pancreatitis unlikely. Although an ampullary tumour
is possible, the young age of the patient and no family history of pancreatic malignancy make this a
less likely diagnosis. The patient has hypertriglyceridemia. However, the serum triglyceride level is
insuciently elevated to cause acute pancreatitis. Even in the context of a normal calibre common
bile duct, the presence of gallstones within the gallbladder of a patient with acute pancreatitis and
no other more likely aetiology should prompt further investigation of gallstone- related disease.
Furthermore, an elevated ALT ≥3- fold— the upper limit of normal in the presence of acute
pancreatitis— has a positive predictive value of 95% in diagnosing acute gallstone pancreatitis.
Sleisenger and Fordtran’s Gastrointestinal and Liver Disease. 0th ed. 2 vols, 206. Chapter58:Acute
Pancreatitis.
2. B. It is a dose- independent complication
• Two to three per cent of patients with inammatory bowel disease (IBD) treated with
azathioprine will develop azathioprine- induced pancreatitis
• It usually manifests as mild disease within one month of treatment initiation and rapidly
improves on treatment withdrawal
Azathioprine- induced pancreatitis is an idiosyncratic, dose- independent drug reaction aecting
2%– 7% of treated patients with IBD. Risk factors associated with its onset include female gender,
cigarette smoking, glucocorticoid exposure, and certain human leukocyte antigen polymorphisms.
There is no association with polymorphisms in the thiopurine methyltransferase enzyme. The
temporal relationship between initiation of azathioprine and symptom onset usually helps clarify
the diagnosis, with most cases occurring within one month of commencing treatment. Other
potential causes of acute pancreatitis in IBD must also be considered, however, including drugrelated pancreatitis (e.g. 5- aminosalicylates, metronidazole), choledocholithiasis (with increased
prevalence of gallstones in Crohn’s disease), and from related autoimmune conditions (primary
sclerosing cholangitis and autoimmune pancreatitis). In most cases, the pancreatitis is mild and
Best of Five MCQs for the European Specialty Examination in Gastroenterology and Hepatology. Thomas Marjot, Colleen G C McGregor,
Tim Ambrose, Aminda N De Silva, Jeremy Cobbold, and Simon Travis, Oxford University Press (2021). © Oxford University Press.
DOI: 10.1093/oso/9780198834373.003.0005
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rapidly responds to azathioprine withdrawal. There is a high rate of recurrence with azathioprine
re- introduction.
Ledder O, Lemberg DA, Day AS. Thiopurine- induced pancreatitis in inammatory bowel diseases.
Expert Rev Gastroenterol Hepatol. 205 Apr;9(4):399– 403. Doi:0.586/ 747424.205.992879.
3. B. Diclofenac
• The risk of PEP is 3.5% in unselected cases
• The European Society of Gastrointestinal Endoscopy (ESGE) recommends 00 mg rectal
diclofenac or indomethacin for all patients undergoing ERCP unless contraindicated
PEP is the most common complication of ERCP occurring in 3.5% of patients. Most cases are mild–
moderate but death occurs in 3%. Patient risk factors for PEP include functional biliary sphincter
disorder (formerly Sphincter of Oddi dysfunction, female gender, and previous pancreatitis.
Procedural risk factors include prolonged cannulation attempts, pancreatic guidewire passage, and
pancreatic injection. ESGE 204 guidelines recommend the routine administration of diclofenac or
indomethacin either pre- or post- procedure. The estimated number needed to treat to prevent
one episode of pancreatitis is 5. Both glyceryl trinitrate and somatostatin have conicting evidence
to support their use with heterogeneity of dosages or routes of administration used in dierent
trials. The other medications listed are ineective in reducing PEP.
Dumonceau JM, Andriulli A, Elmunzer BJ etal. Prophylaxis of post- ERCP pancreatitis:European
Society of Gastrointestinal Endoscopy Guideline. Endoscopy. 204 Sep;46(9):799– 85. Doi:0.055/
s- 0034- 377875.
4. A. Abdominal ultrasound
• All patients with acute pancreatitis should have an abdominal ultrasound at presentation to
look for gallstones as the underlying aetiology
• Early CT imaging does not help prognosticate or improve outcomes but can be useful after 72
hours in deteriorating patients to exclude pancreatic necrosis and/ or collections
International Association of Pancreatology (IAP)/ American Pancreatic Association (APA) guidelines
recommend the use of ultrasound abdomen for all patients presenting with acute pancreatitis to
establish the possibility of a gallstone aetiology, although an ALT level >50 U/ L within 48 hours
after symptoms onset discriminates biliary pancreatitis with a positive predictive value of >95%.
Contrast CT in acute pancreatitis is indicated in cases of diagnostic uncertainty to help conrm
disease severity based on clinical predictors, and in the setting of clinical deterioration where
pancreatic necrosis and peripancreatic uid collections amenable to surgical/ radiological
intervention may be identied. These complications take several days to manifest and therefore
optimal timing for initial CT assessment is at least 72– 96 hours after onset of symptoms. Early CT
does not add to prognostic scoring systems or improve clinical outcome.
IAP/ APA Evidence- based guidelines for the management of acute pancreatitis. Pancreatology. 203 Jul–
Aug;3(4 Suppl 2):e– 5. Doi:0.06/ j.pan.203.07.063.
5. C. 750 ml Ringer’s lactate over one hour
• In acute pancreatitis, Ringer’s lactate decreases the incidence of systemic inammatory
response syndrome (SIRS) compared with resuscitation with normal saline
CHAPTER 5 | ANSWERS
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• Meta- analysis has demonstrated no evidence to support the routine use of antibiotic
prophylaxis in patients with severe acute pancreatitis
There have been few head- to- head trials on the eects of dierent uid regimes on outcomes in
acute pancreatitis. However, there is randomized control data suggesting that resuscitation with
Ringer’s lactate decreases the incidence of SIRS compared with resuscitation with normal saline.
The use of HES is discouraged because it has been found to increase the rates of renal failure and
mortality, as compared with Ringer’s lactate in patients with severe sepsis. Note that Ringer’s lactate
is very similar but not identical to Hartmann’s solution. Although uid resuscitation is important,
particularly in severe acute pancreatitis, there is randomized control evidence that overly aggressive
resuscitation can increase morbidity and mortality. Patients resuscitated with uid infusion rate of
5– 0 ml/ kg/ h experienced less need for mechanic ventilation, abdominal compartment syndrome,
sepsis, and mortality as compared with patients assigned to receive infusion rates of 0– 5 ml/ kg/h.
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IAP/ APA Evidence- based guidelines for the management of acute pancreatitis. Pancreatology. 203 Jul–
Aug;3(4 Suppl 2):e– 5. Doi:0.06/ j.pan.203.07.063.
patients with severe acute pancreatitis.
6. B. Enteral feeding via nasogastric tube
• The presence of SIRS at baseline and 48 hours helps grade severity of pancreatitis, predict
outcome, and guide approach to nutritional management
• In severe pancreatitis, dened by the presence of SIRS, enteral feeding reduces systemic
infections, multi- organ failure, and mortality
Determining the optimal nutritional strategy in acute pancreatitis requires an assessment of
severity. Despite a range of validated predictive scoring systems, the joint international guidelines
recommend using the presence of SIRS to dene severe pancreatitis because of its widespread
familiarity and simplicity. SIRS is dened by the presence of two or more of the following
criteria:() temperature <36oC or >38oC (2)heart rate >90/ min, (3)respiratory rate >20/ min,
and (4)white blood cells >2 or >0% bands. Persistent SIRS (>48 hours) carries a 25% mortality
compared with 8% mortality for transient SIRS.
In mild– moderate pancreatitis, oral feeding with a full solid diet can start as soon as clinically
tolerated. In those intolerant to oral feeding, enteral tube feeding (using standard polymeric
formulae) should be commenced within 24– 48 hours of admission. In severe pancreatitis, dened
by the presence of SIRS, enteral tube feeding (via either a nasojejunal or nasogastric tube) is the
preferred route and has been proven to reduce systemic infections, multi- organ failure, need
for surgical intervention, and mortality. While placement of a nasogastric feeding tube is more
straightforward, a number of patients will not tolerate nasogastric feeding because of delayed
gastric emptying and may require nasojejunal tube placement. Parenteral nutrition is reserved for
patients who do not meet nutritional requirements via the oral or enteral route. Where parenteral
is indicated, parenteral L- glutamine should also be supplemented because it may reduce infection
rates and mortality.
Arvanitakis M, Ockenga J, Bezmarevic M etal. ESPEN guideline on clinical nutrition in acute
and chronic pancreatitis. Clin Nutr. 2020 Jan 22. pii:S026- 564(20)30009- . Doi:0.06/
j.clnu.2020.0.004.
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7. C. Within 24 hours
• In patients with gallstone pancreatitis and coexisting cholangitis, an ERCP should be performed
urgently (<24 hours)
• In patients with gallstone pancreatitis without cholangitis, the need and timing of ERCP remain
unclear
The role and timing of ERCP in acute gallstone pancreatitis is controversial and was subject to
Cochrane systematic review and meta- analysis in 202. This demonstrated that routine ERCP
(<72 hours) did not signicantly aect mortality or local/ systemic complications, regardless of
pancreatitis severity compared with conservative treatment alone. Furthermore, no statistically
signicant eect of the timing of ERCP (<24 hours vs <72 hours) on mortality was demonstrated.
Therefore, in uncomplicated gallstone pancreatitis, it is reasonable to treat conservatively for at
least the rst 48 hours.
However, meta- analysis did clearly demonstrate that early ERCP (<24 hours) improved mortality
and local and systemic complications in patients with acute gallstone pancreatitis and co- existing
cholangitis, which is evident in this case (jaundice, fever, choledocholithiasis, and common bile duct
dilatation).
IAP/ APA Evidence- based guidelines for the management of acute pancreatitis. Pancreatology. 203 Jul–
Aug;3(4 Suppl 2):e– 5. Doi:0.06/ j.pan.203.07.063.
8. C. EUS- guided transmural drainage
• Most pancreatic pseudocysts can be managed conservatively with drainage only required for
cases with symptoms, obstructive complications, or pseudocyst infection
• EUS- guided transmural stenting represents the best and safest method of achieving pseudocyst
drainage
The MRCP image shows a large pancreatic pseudocyst (Fig. 5.3; arrow). Pancreatic pseudocysts
complicate 0%– 20% and 20%– 40% of cases of acute and chronic pancreatitis respectively. In
CP, the risk of pseudocysts is particularly high with underlying alcohol aetiology. Up to 70% of
pseudocysts will resolve spontaneously, particularly following an episode of acute pancreatitis, and,
even without resolution, most pseudocysts rarely lead to signicant symptoms or complications.
Most pseudocysts can therefore be managed conservatively with intervention reserved for patients
with symptoms (usually abdominal pain) or complications including biliary and/ or gastric outlet
obstruction, pseudocyst bleeding, or infection. In these problematic cases, a range of treatment
modalities are available. Traditionally, a surgical cystogastrostomy was performed, which involved an
open or laparoscopic procedure to create an anastomosis between the lumen of the cyst cavity and
the stomach. However, endoscopic approaches are now preferred, yielding similar technical success
rates with lower rates of complications. Conventional endoscopic drainage involves visualizing
the pseudocyst bulge in the gastric wall, advancing a guidewire into the pseudocyst cavity, and
deploying one or more plastic stents. While this can safely be used for visibly bulging pseudocysts,
most pseudocysts are now drained under EUS guidance to allow safer access and a decrease in
complications. Trials comparing percutaneous versus endoscopic drainage have demonstrated
equivalent technical success rates but a decreased re- intervention rate and shorter hospital stays
among patients drained endoscopically.
Tyberg A, Karia K, Gabr M etal. Management of pancreatic uid collections:a comprehensive review
of the literature. World J Gastroenterol. 206 Feb 2;22(7):2256– 2270. Doi:0.3748/ wjg.v22.i7.2256.
Fig.5.3 MRCP image showing pancreatic pseudocyst (arrow)
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CHAPTER 5 | ANSWERS
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9. D. Pancreas divisum
• Pancreas divisum results from failure of ventral and dorsal pancreatic ducts to fuse, and occurs
in 4%– 4% of the population
• Poor pancreatic drainage through the minor papilla can result in recurrent pancreatitis
• Annular pancreas is characterized by pancreatic tissue wrapping around the descending
duodenum, and can rarely cause duodenal obstruction and ulceration
Pancreas divisum is the most common congenital pancreatic ductal abnormality occurring in 4%–
4% of the population. It is characterized by a failure of the dorsal and ventral pancreatic anlage to
fuse during gestation resulting in two separate duct systems:the dorsal pancreatic duct (Santorini
duct) directly entering the minor papilla, and the ventral duct (Wirsung) entering the major papilla.
In most cases, there is no communication between the two ducts with most of the pancreas
drained via the dorsal duct and minor papilla (Fig. 5.2). Most patients are asymptomatic. However,
it can be associated with recurrent pancreatitis due to inadequate pancreatic drainage. Up to 26%
of patients with idiopathic recurrent pancreatitis have pancreas divisum. Annular pancreas is a much
rarer anomaly (/ 20,000 people) in which a band of pancreatic tissue surrounds the descending
duodenum, either completely or incompletely, and is in continuity with the head of the pancreas.
The anomaly is often discovered incidentally in asymptomatic patients although it can be associated
with duodenal stenosis and ulceration, acute pancreatitis, and biliary obstruction.
Yu J, Turner MA, Fulcher AS etal. Congenital anomalies and normal variants of the pancreaticobiliary
tract and the pancreas in adults:Part2, Pancreatic duct and pancreas. AJR Am J Roentgenol. 2006
Dec;87(6):544- 553.
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Fig.5.4 MRCP image showing pancreas divisum
10. E. S- cells in the duodenum
• Secretin and Cholecystokinin (CCK), produced by duodenal S- cells and enteroendocrine cells
respectively, promote secretion of bicarbonate- rich uid and digestive enzymes from the
pancreas
• Secretin- stimulated MRCP improves pancreatic duct distension and signaling, and can be used
to help characterize anatomical abnormalities
The acinar cells of the exocrine pancreas are radially orientated around a central lumen into which
>2L of bicarbonate- rich uid containing digestive enzymes and proenzymes are secreted each day.
This secretion is upregulated both by neural stimulation from the vagus nerve and from humoral
factors, principally secretin and CCK. Secretin is produced by duodenal S- cells in response to low
luminal pH derived from the transit of acidic gastric secretions. Secretin stimulates the pancreatic
acinar cells and duodenal Brunner’s glands to secrete neutralizing water and bicarbonate, as well
as to directly downregulate acid production by gastric parietal cells. The exogenous administration
of intravenous secretin during MRCP image acquisition can improve pancreatic duct visualization
by increasing duct calibre and signal intensity. Secretin- stimulated MRCP therefore has a role in the
detection and characterization of pancreatic duct abnormalities, communications with stulae or
pseudocysts, and in Sphincter of Oddi dysfunction.
CCK is produced by duodenal enteroendocrine cells in response to a meal, and promotes the
production and secretion of digestive enzymes from the exocrine pancreas. CCK also increases
hepatic bile production, stimulates the contraction of the gallbladder, and induces Sphincter of Oddi
relaxation. CCK- stimulated cholescintigraphy, which involves assessment of gallbladder contractility
and emptying after injection of CCK, and a radiolabelled tracer can be used in carefully selected
cases to investigate functional gallbladder disorders.
The endocrine pancreas is comprised of alpha, beta, delta, and epsilon cells that produce glucagon,
insulin, somatostatin, and ghrelin respectively.
Kumar V, Abbas A, Aster J.Robbins & Cotran Pathologic Basis of Disease. 0th ed. June 2020.
CHAPTER 5 | ANSWERS
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11. E. Progression to CP after a single attack of acute pancreatitis occurs in 10% of
patients.
• Alcohol consumption is the most common cause of CP
• Pancreatic insuciency is best managed with pancreatic enzyme replacement with dose
uptitrated to control maldigestion- related symptoms (e.g. steatorrhoea, weight loss)
• All patients with CP should be screened for osteoporosis at baseline with dual- energy X- ray
absorptiometry (DEXA)
CP is accompanied by the progressive destruction of both islet cells and acinar tissue.
Malabsorption only becomes evident once >90% of pancreatic acinar tissue has been destroyed.
Progression to CP following a single attack of acute pancreatitis occurs in 0%. The most common
aetiology for CP is alcohol excess with smoking and genetic mutations also signicant risk factors.
Hereditary pancreatitis should be considered in young patients with otherwise unexplained CP and
carries a signicantly elevated risk of secondary pancreatic cancer. Pancreatic calcication occur in
>90% of patients with CP and are pathognomonic in the appropriate clinical context. Contrastenhanced CT is reported to have moderate sensitivity and very high specicity (close to 00%).
Malabsorption (exocrine insuciency), including of fat- soluble vitamins (A, D, E, and K), should be
managed with adequate pancreatic enzyme replacement therapy starting at a minimum lipase dose
of 40,000– 50,000 PhU with main meals and half that dose with snacks. This should be uptitrated as
necessary, aiming for the relief of maldigestion- related symptoms (e.g. steatorrhoea, weight loss,
atulence) and normalization of nutritional status. Monitoring for osteoporosis should be done by
DEXA scan at baseline and repeated every two years in those with osteopenia.
Löhr JM, Dominguez- Munoz E, Rosendahl J etal. United European gastroenterology evidencebased guidelines for the diagnosis and therapy of chronic pancreatitis (HaPanEU). United European
Gastroenterol J. 207 Mar;5(2):53– 99. Doi:0.77/ 205064066684695.
12. E. Vitamin deciencies can occur in the absence of steatorrhoea
• Vitamin deciencies can occur with mild– moderate pancreatic endocrine insuciency well
before the onset of steatorrhoea
• FE is not capable of excluding mild– moderate PEI
• Direct tests involving the collection of duodenal juice in response to a hormonal stimulus are
the accepted reference standard for PEI
Mild– moderate exocrine insuciency can be compensated and asymptomatic, with severe disease
(manifesting as steatorrhoea) only developing once pancreatic lipase falls <0% of normal. Patients
with ‘compensated’ PEI do, however, have an increased risk of nutritional deciencies, particularly
of fat- soluble vitamins (A, D, E, K). The most common causes of PEI include CP and cystic brosis.
Additional causes include pancreatic neoplasms, post- pancreatic resection and acute necrotizing
pancreatitis. Coeliac disease can also lead to PEI, secondary to villous atrophy and impaired CCK
production. Severe PEI and steatorrhea tend to manifest over a decade from initial diagnosis of
CP. FE is a simple test for the indirect and non- invasive evaluation of pancreatic secretion. It is not
capable of excluding mild– moderate PEI and there is no consensus regarding the threshold levels
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