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CHAPTER 3 | STOMACH AND DUODENAL DISORDERS

• Foveolar hyperplasia with corkscrew morphology and preserved linear architecture are classical histopathological ndings of MD

All the listed options are causes of thickened gastric folds. However, the combination of markedly thickened gastric folds and hypoalbuminaemia makes a diagnosis of MD the most likely. Correlation with histopathological ndings and clinical features is important to establish the correct diagnosis.

MD is a rare, acquired, hypertrophic gastropathy. Hypertrophic gastropathies refer to conditions conned to the rugae of the body and fundus, which are associated with an excessive number of mucosal epithelial cells. MD is characterized by giant gastric folds of the body and fundus, with antral sparing endoscopically, increased gastric mucus production, decreased gastric acid secretion, malnutrition, and hypoalbuminaemia secondary to protein loss in the gastric mucosa. Men are more commonly aected and typical age of onset is between 30 and 60years old. Importantly, MD may have an increased risk of GC.

Clinical presentation includes nausea, vomiting, abdominal pain, diarrhoea, weight loss, and peripheral oedema. The cause of MD is not fully elucidated. However, cases of MD have been reported in association with CMV, H.pylori infection, inammatory bowel disease, and ankylosing spondylitis, suggesting an underlying immunopathogenesis (TGF- β mediated).

Full thickness biopsy is required. Microscopic features include massive foveolar hyperplasia, which may result in mucosal thickness of ≥cm and copious thick mucus production. Foveolar epithelium has a corkscrew morphology and cystically dilated deep glands. The overall linear architecture is maintained. Oxyntic glands atrophy with reduced or absent parietal cells, resulting in an increased gastric pH. The lamina propria has a predominantly chronic inammatory cell inltrate with scattered eosinophils.

Remission may occur spontaneously in CMV- associated MD and after H.pylori eradication. There is no denitive medical treatment for MD. However, trials with anti- EGFR (cetuximab) have shown some benet. Octreotide can be used for protein loss. Total gastrectomy is reserved for patients with debilitating disease and high risk for GC.

Huh W, Coey R etal. Ménétrier’s disease:its mimickers and pathogenesis. J Pathol Transl Med. 206;50:0– 6. Doi:0.432/ jptm.205.09.5

22. A. All the listed options

• Intraepithelial lymphocytosis is dened as IELs >20 per 00 epithelial cells

• There are multiple mimickers of coeliac disease (CD)

• CD is characterized by a predominantly neutrophilic inltrate with few crypt abscesses

IELs are no more than 5– 0 per 00 epithelial cells in healthy individuals. Intraepithelial lymphocytosis is dened as IELs >20 per 00 epithelial cells. In healthy individuals, IELs localize at the base of the surface epithelium. In the presence of intraepithelial lymphocytosis, IELs are throughout the full thickness of the epithelium.

Intraepithelial lymphocytosis in the context of preserved villous architecture can present a diagnostic challenge. Histopathological ndings of CD include villous atrophy, intraepithelial lymphocytosis, increased inammatory inltrate in the lamina propria, and crypt hyperplasia. However, multiple dierentials exist for duodenal intraepithelial lymphocytosis and villous atrophy (Table 3.2). CD is characterized by a predominantly neutrophilic inltration. Neutrophilic crypt abscesses are less of a feature in CD. However, they are commonly seen in CD mimickers such as infection, peptic duodenitis, or autoimmune enteritis.

CHAPTER 3 | ANSWERS

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Table3.2 Dierentials ofduodenal intraepithelial lymphocytosis and villous atrophy

Gluten- mediated Infection Immune- mediated Drugs Other

Coeliac disease Gluten sensitivity Seronegative coeliac disease Wheat allergy

Virus (rotavirus, enterovirus, adenovirus, coronavirus, cytomegalovirus) Parasites (Giardia, cryptosporidum) Bacteria (Salmonella,

Shigella, Yersinia, Tropheryma whipplei—

Whipple’s disease) Small intestinal bacterial overgrowth

Helicobacter pylori

Immunoglobulin deciencies Food allergy Autoimmune enteritis Vasculitides Systemic autoimmune disorders (e.g. Graves’ disease, rheumatoid arthritis, psoriasis, systemiclupus erythematosus) Inammatory bowel disease

Olmesartan Non- steroidal antiinammatory drugs Proton pump inhibitors Mycophenolate mofetil Ipilimumab

Irritable bowel syndrome Peptic duodenitis Post- transplant lymphoproliferative disorders Lymphomas

Microscopic enteritis Graft vs host disease

Data from Sergi C, Shen F, Bouma G.Intraepithelial lymphocytes, scores, mimickers and challenges in diagnosing gluten- sensitive enteropathy (celiac disease). World J Gastroenterol. 207 Jan 28; 23(4):573– 589. Doi:0.3748/ wjg.v23.i4.573

Histopathological ndings of intraepithelial lymphocytosis must be interpreted with clinical history, examination, and laboratory results in mind.

Sergi C, Shen F, Bouma G.Intraepithelial lymphocytes, scores, mimickers and challenges in diagnosing gluten- sensitive enteropathy (celiac disease). World J Gastroenterol. 207 Jan 28;23(4):573– 589. Doi:0.3748/ wjg.v23.i4.573.

23. D. Duodenal adenoma

• Forty per cent of duodenal adenomas (Fig. 3.4 black asterisk) are sporadic

• Between 30% and 85% of duodenal adenomas undergo malignant transformation

• ESD has a superior complete resection and recurrence rate when compared with EMR

Fig.3.14 Endoscopic image showing duodenal adenoma

Image courtesy of Dr Tim Ambrose, Oxford University Hospitals NHS Foundation Trust

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CHAPTER 3 | STOMACH AND DUODENAL DISORDERS

Sporadic duodenal polyps are uncommon, and can be classied according to their location and histopathological subtype. Non- ampullary duodenal adenomas are common ndings in patients with FAP. Sporadic duodenal adenomas (SDA) are rare, however. Sixty per cent of duodenal adenomas are present in patients with FAP; the remaining 40% are sporadic.

Duodenal adenomas are typically multiple, sessile, and predominantly located in the distal duodenum. Between 30% and 85% of duodenal adenomas undergo malignant transformation and therefore excision, be it endoscopic or surgical, is mandatory. High- grade dysplastic lesions and large non- ampullary SDAs (≥20mm in diameter) confer an increased risk of progression to adenocarcinoma. In patients with FAP, duodenal cancer develops from pre- existing adenomas with a cumulative risk of almost 00%.

Ampullary lesions may present clinically with obstructive jaundice or pancreatitis. Non- ampullary lesions, however, are often an incidental nding at endoscopy. Endoscopic options include snare polypectomy, EMR, ESD and argon plasma coagulation (APC). Snare polypectomy is eective with an 85% eradication rate. It may be used in combination with APC. ESD has a superior complete resection rate with no recurrence when compared with EMR. However, ESD carries higher rates of perforation (6%– 50%) and bleeding when compared with EMR.

Large and/ or villous adenomas are associated with a higher rate of recurrence. Post successful resection of non- ampullary SDA, initial follow- up endoscopy is recommended at three to six months to site check for recurrence. Dedicated guidance exists for upper GI endoscopic surveillance in patients with FAP.

Surgical excision is indicated in large SDAs, with severe dysplasia, suspicious for local inltration or recurrence after complete endoscopic resection. Options include laparoscopic- assisted endoluminal surgery, laparoscopic polyp excision, duodenectomy, or pancreaticoduodenectomy. Pancreaticoduodenectomy may also be indicated in patients with FAP and severe duodenal adenomatosis.

Lim C, Cho Y.Nonampullary duodenal adenoma:current understanding of its diagnosis, pathogenesis, and clinical management. World J Gastroenterol. 206;22(2):853– 86. Doi:0.3748/ wjg.v22.i2.853.

24. B. Accurate photo documentation of anatomical landmarks and abnormal ndings

The European Society of Gastrointestinal Endoscopy (ESGE) have identied quality in upper GI endoscopy as a key priority. As such, key performance measures were dened in 206 (Table 3.3).

Bisschops R etal. Performance measures for UGI endoscopy:a European Society of Gastrointestinal Endoscopy (ESGE) Quality Improvement Initiative. Endoscopy. 206;48:843- 864. Doi:0.055/ s- 0042- 328.

CHAPTER 3 | ANSWERS

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Table3.3 Key performance measures forupper gastrointestinal endoscopy

Key performance measures Minor performance measures

• Fasting instructions prior to UGI endoscopy

• Documentation of procedure duration

• Accurate photo documentation of anatomical landmarks and abnormal ndings

• Accurate application of standardized disease- related terminology

• Application of Seattle protocol in Barrett’s surveillance

• Accurate registration of complications after therapeutic UGI endoscopy

UGI, upper gastrointestinal; ENT, ear, nose, and throat; MAPS, management of patients with precancerous conditions and lesions of the stomach.

Reproduced with permission from Bisschops R etal., Performance measures for upper gastrointestinal endoscopy:a European Society of Gastrointestinal Endoscopy (ESGE) Quality Improvement Initiative, Endoscopy, 206;48(9):843- 864. © Georg Thieme Verlag KG.

• Minimum 7- minute procedure time for rst diagnostic UGI endoscopy and follow- up of gastric intestinal metaplasia

• Minimum - minute inspection time per cm circumferential Barrett’s epithelium

• Use of Lugol chromoendoscopy in patients with a curatively treated ENT or lung cancer to exclude a second primary esophageal cancer

• Application of validated biopsy protocol to detect gastric intestinal metaplasia (MAPS guidelines)

• Prospective registration of Barrett’s patients

25. A. Decompression with large- bore nasogastric tube

• Twenty per cent of patients with pancreatic cancer develop a degree of GOO

• Stent placement or surgical bypass are treatment options in GOO

• Palliative management is the mainstay in malignant GOO

This patient has malignant GOO from pancreatic cancer. All the options are viable options. However, the appropriate immediate next step is to provide symptomatic relief with large- bore nasogastric (Ryles) tube decompression.

GOO typically develops due to progression of the pancreatic tumour resulting in extrinsic compression of the duodenum. Approximately 20% of patients with pancreatic cancer develop a degree of GOO. GOO may present with nausea, vomiting, early satiety, anorexia, or an epigastric fullness. Cross- sectional imaging conrms the diagnosis. Endoscopic assessment is key to dene the degree of obstruction and a distended, uid- lled stomach may be seen at gastroscopy. Patients often require a prolonged fast or nasogastric drainage ahead of gastroscopy. If the obstruction is incomplete, a nasojejunal feeding tube may be placed while a denitive management plan is decided.

Malignant GOO usually represents a poor prognosis. Palliative, expectant management is therefore the mainstay of treatment. Initial management includes optimal analgesia, decompression with a nasogastric tube and a plan for adequate nutrition. Endoscopic or uoroscopic stent placement across the stricture is a readily accessible option. Stents may migrate, or become blocked or compressed, however. Surgical options include bypassing the stricture with a gastrojejunostomy. It is important, though, to determine whether surgical intervention is appropriate given the burden of disease, oncological treatment, and prognosis. In selected cases, there may be a role for short- term palliative parenteral nutrition. Such management decisions necessitate a multidisciplinary approach with input from gastroenterologists, surgeons, interventional radiologists, oncologists, and palliative care sta with the patient’s wishes in mind.

McGrath C, Tsang Aetal. Malignant gastric outlet obstruction from pancreatic cancer. Case Rep Gastroenterol. 207;:5– 55. Doi.org/ 0.59/ 000480070.

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chapter

BILIARYDISORDERS

1. A 42- year- old woman presented to clinic with an incidental nding of

QUESTIONS

gallstones on ultrasound performed for another indication. She had no fever, rigors, or pain. She had a moderate alcohol intake but denied any other medical problems.

Investigations:

Serum albumin 39 g/ L Serum bilirubin 17 µmol/ L Serum alanine transferase (ALT) 42 U/ L Serum alkaline phosphatase (ALP) 104 U/ L Serum C- reactive protein (CRP) 6 mg/ L Abdominal ultrasound Three small gallstones in thin walled gallbladder

Which of the following most accurately reects the patient’s prognosis

with normal intra- and extrahepatic bile ducts.

over the next 10years?

A. Cholecystectomy is indicated to prevent symptomatic gallstones from developing

B. Fifty per cent chance of developing Mirizzi syndrome

C. Less than % chance of developing pancreatitis, cholecystitis, or biliary obstruction

D. More than 90% chance of remaining asymptomatic

E. Twenty per cent chance of developing biliary colic

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/9780198834373.003.0004

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CHAPTER 4 | BILIARYDISORDERS

2. A 64- year- old man underwent a cholecystectomy for right upper- quadrant pain.

Investigations:

Cholecystectomy specimen

The muscle wall is thickened with multiple prolapsed glands in the subserosal tissue (Rokitansky– Asho sinuses). The glands are variably dilated.

What is the most likely diagnosis?

A. Acute cholecystitis

B. Adenomyomatosis (ADM)

C. Gallbladder adenocarcinoma

D. Gallbladder empyema

E. Porcelain gallbladder

3. A 55- year- old woman was found incidentally to have gallbladder calcication on a computed tomography pulmonary angiogram (CTPA) performed to investigate a shortness of breath on the acute medical take. She did not have a pulmonary embolism and was discharged with an outpatient computed tomography (CT) abdomen. She was asymptomatic with no other comorbidities.

Investigations:

Serum bilirubin Serum alkaline phosphatase (ALP) 120 U/ L Serum alanine transferase (ALT) 18 U/ L Serum albumin 35 g/ L CT abdomen Gallbladder contains several calculi with

What is the most appropriate next step for this patient?

A. Cholecystectomy

B. Endoscopic retrograde cholangiopancreatography (ERCP)

C. Endoscopic ultrasound (EUS)

D. Magnetic resonance cholangiopancreatography (MRCP)

E. Observation

12 µmol/ L

intramural spotty calcication of the gallbladder wall.

CHAPTER 4 | QUESTIONS

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4. A 39- year- old man had a laparoscopic cholecystectomy for acute cholecystitis. Twelve hours after the operation, he developed abdominal pain although it was not peritonitic. Bile was also found in the surgical drain. CT abdomen showed no collections and ERCP demonstrated a low- grade bile leak from the duct of Luschka with no lling defects in the biliary tree.

What would be the next best management approach?

A. Conservative management with prophylactic antibiotics

B. ERCP and plastic biliary stent insertion

C. ERCP and sphincterotomy

D. Nasobiliary drainage

E. Repeat laparoscopy and surgical repair

5. A 75- year- old man presented with right upper- quadrant pain, jaundice, and fever. He had a myocardial infarction six months ago and received a drug- eluting coronary artery stent. He takes daily aspirin 75 mg, clopidogrel 75 mg, bisoprolol 5 mg and atorvastatin 80 mg. He still drives and enjoys playing golf. He remains septic despite 48 hours of intravenous co- amoxiclav and gentamicin.

Investigations:

Serum bilirubin Serum alkaline phosphatase (ALP) 317 U/ L Serum alanine transferase (ALT) 43 U/ L Serum albumin 35 g/ L International normalized ratio (INR) 1.4 Haemoglobin 120 g/ L White cell count 12 × 109/ L Platelet count 150 × 109/ L Serum C- reactive protein (CRP) 70 mg/ L Blood cultures Escherichia coli Ultrasound abdomen Common bile duct (CBD) dilatation with

MRCP (Fig. 4.1)

71 µmol/ L

probable calculi. Sludge and gallstones in non- inamed gallbladder.

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CHAPTER 4 | BILIARYDISORDERS

Fig.4.1 MRCP

What is the best treatment option for sepsis source control?

A. Broaden antimicrobial cover

B. ERCP with sphincterotomy and stone extraction

C. ERCP and plastic stent

D. Extracorporeal shock wave lithotripsy

E. Percutaneous transhepatic cholangiogram and internal– external biliary drain

CHAPTER 4 | QUESTIONS

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6. A 30- year- old woman who was 34 weeks’ pregnant presented with right upper- quadrant pain. She had a temperature of 38.2°C, heart rate 128 beats per minute and blood pressure 85/ 60mmHg.

Investigations:

Abdominal ultrasound Dilated CBD (15mm) with no obvious lling

defect and dilated intrahepatic ducts. Multiple

small stones within a thin walled gallbladder. Haemoglobin 110 g/ L White cell count 18.3 × 109/ L Platelet count 162 × 109/ L Prothrombin time 12.5 seconds Serum bilirubin 73 µmol/ L Serum alkaline phosphatase (ALP) 556 U/ L Serum alanine transferase (ALT) 67 U/ L Serum C- reactive protein (CRP) 187 mg/ L

What is the most appropriate next step in the management of this patient?

A. CT abdomen

B. ERCP

C. Expectant management

D. Induce delivery

E. MRCP

7. A 40- year- old woman presented with recurrent episodes of nocturnal right upper- quadrant pain radiating to the back, and vomiting over the past one month.

Investigations:

Serum bilirubin Serum alkaline phosphatase (ALP) 258 U/ L Serum alanine transferase (ALT) 65 U/ L Serum amylase 39 U/ L Abdominal ultrasound Several gallbladder calculi. Normal bile duct

MRCP (Fig. 4.2) EUS (Fig. 4.3)

45 µmol/ L

calibre.

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