Peptic Ulcer Disease

Question 1

What is a peptic ulcer?

Answer 1

A peptic ulcer is a break in the lining of the gastrointestinal tract, extending through to the muscular layer (muscularis mucosae) of the bowel wall.

Question 2

Where in the GI tract are gastric ulcers most common?

Answer 2

Whilst they may technically appear anywhere in the gastrointestinal tract, they are most often located on the lesser curvature of the proximal stomach or the first part of the duodenum.

Question 3

Briefly describe the pathophysiology of peptic ulcer disease

Answer 3

The normal gastrointestinal mucosa is protected by numerous defensive mechanisms, such as surface mucous secretion and HCO^3- ion release.

Peptic ulcer disease occurs when there is an imbalance between factors that protect the mucosa of the stomach and duodenum, and factors that cause damage to it.

Most commonly, this is through the presence of Helicobacter pylori (H. pylori) or Non-Steroidal Anti-Inflammatory Drug (NSAID) use.

Question 4

Why do NSAIDs lead to peptic ulcer disease?

Answer 4

NSAIDs can cause peptic ulcer formation by their action in inhibiting prostaglandin synthesis, resulting in a reduced secretion of glycoprotein, mucous and phospholipids by the gastric epithelial cells, which would otherwise normally protect the gastric mucosa.

Question 5

Briefly describe the gram stain of H. pylori

Answer 5

Gram negative spiral-shaped bacillus.

Question 6

How common is H. pylori infection in duodenal and gastric ulcers?

Answer 6

Duodenal ulcers (90%) or gastric ulcers (70%).

Question 7

How does H.pylori damage the stomach?

Answer 7

It survives in the stomach by producing an alkaline micro-environment and induces an inflammatory response in the mucosa, leading to eventual ulceration, by:

• Invoking an cytokine and interleukin-driven inflammatory response
• Increasing gastric acid secretion in both the acute and chronic phases of infection, by inducing the release of histamine which acts on parietal cells
• Damaging host mucous secretion by degrading surface glycoproteins and down-regulating bicarbonate production

Question 8

What are the risk factors for peptic ulcer disease?

Answer 8

The two main risk factors for peptic ulcers are H. pylori infection and prolonged NSAID use.

Other risk factors include corticosteroid use (when used with NSAIDs), previous gastric bypass surgery, physiological stress (such as severe burns (Curling’s ulcer) or head trauma (Cushing’s ulcer)) or Zollinger-Ellison syndrome (rare).

Question 9

What are the clinical features of peptic ulcer disease?

Answer 9

Up to 70% of peptic ulcers can be asymptomatic. For symptomatic patients, peptic ulcers can present with epigastric or retrosternal pain, nausea, bloating, post-prandial discomfort or early satiety.

Less commonly, patients may present with complications of their peptic ulcer disease, such as bleeding, perforation or gastric outlet obstruction.

Question 10

Briefly describe the NICE guidelines for referrel for urgent upper Oesophago-Gastro-Duodenoscopy (OGD)

Answer 10

NICE guidelines suggest that a referral for urgent upper Oesophago-Gastro-Duodenoscopy (OGD) should be done for patients presenting with either:

• New-onset dysphagia
• Aged >55 years with weight loss and either upper abdominal pain, reflux, or dyspepsia
• New onset dyspepsia not responding to PPI treatment

Question 11

How can the clinical features of gastric or duodenal ulcer differ?

Answer 11

Classically, any pain from a gastric ulcer is exacerbated by eating, whilst duodenal ulcers are worse 2-4 hours after eating or even alleviated by eating.

Question 12

What investigations should be ordered for peptic ulcer disease?

Answer 12

A FBC may be warranted however to assess for any potential anaemia.

Most patients, especially younger patients, should undergo non-invasive H. pylori testing, which will be either as:

• Carbon-13 urea breath test
• Serum antibodies to H. pylori
• Stool antigen test

In older patients, those with red flag symptoms, or those with ongoing symptoms despite empirical treatment, an OGD is required.

At endoscopy, any peptic ulceration seen can be biopsied, which will be sent for histology (if looks suspicious for malignancy) and for rapid urease test (the CLO test, giving an rapid result for determining presence of H. pylori).

Question 13

Briefly describe the NICE guidance on biopsies of peptic ulcer disease

Answer 13

NICE guidance recommends that all identified gastric ulcers are biopsied, due to malignant potential, and that a repeat endoscopy is performed towards the end of PPI therapy to check for resolution.

Question 14

What are the non-invasive H. pylori testing methods?

Answer 14

Non-invasive H. pylori testing, which will be either as:

• Carbon-13 urea breath test
• Serum antibodies to H. pylori
• Stool antigen test

Question 15

Why do patients need to stop medication 2 weeks before a H. pylori test?

Answer 15

Prior to any H. pylori test, patients should stop any current medical therapy for 2 weeks prior to investigation to reduce the risk of false negatives; once H. pylori is identified, no further investigations are warranted prior to starting eradication therapy.

Question 16

What is shown in image A?

Answer 16

Features of peptic ulcers on OGD: (A) peptic ulcer located in the gastric antrum

Question 17

What is shown in image B?

Answer 17

Features of peptic ulcers on OGD: (B) haemorrhaging gastric ulcer

Question 18

Briefly describe the conservative management of peptic ulcer disease

Answer 18

Any patient with suspected or confirmed peptic ulcer disease should be given lifestyle advice to reduce symptoms, such as smoking cessation, weight loss and reduction in alcohol consumption. There should also be an avoidance/ cessation of NSAIDs where possible.

Patients with suspected or confirmed ulcers can be started on a Proton Pump Inhibitor for 4-8 weeks to reduce acid production. They should be reassessed after this period for resolution of symptoms (“Test and Treat”). Those patients with a positive H. pylori test should be started on triple therapy.

Persistence of symptoms post-PPI +/- eradication therapy warrants further work-up, with first line being an urgent OGD to exclude any malignancy. Following this, other causes of treatment failure can be considered, such as failure of H. pylori eradication or Zollinger-Ellison Syndrome.

Question 19

What is the next step following persistence of symptoms post-PPI +/- eradication therapy?

Answer 19

Persistence of symptoms post-PPI +/- eradication therapy warrants further work-up, with first line being an urgent OGD to exclude any malignancy.

Following this, other causes of treatment failure can be considered, such as failure of H. pylori eradication or Zollinger-Ellison Syndrome.

Question 20

What is tiple therapy?

Answer 20

Any patient with positive H. pylori testing requires eradication therapy (also termed triple therapy), which commonly consists of a PPI with oral amoxicllin and clarithromycin or metronidazole for 7 days.

Question 21

Briefly describe the surgical management of peptic ulcer disease

Answer 21

Surgery for peptic ulcer disease is rare, except in emergencies (such as perforation) or in the management of Zollinger-Ellison Syndrome.

However, in severe or relapsing disease, either partial gastrectomy or selective vagotomy may be considered.

Question 22

What are the complications of peptic ulcer disease?

Answer 22

The main complications of peptic ulcer disease are perforation, haemorrhage, and pyloric stenosis (rare).

Question 23

What differentials should be considered for peptic ulcer disease?

Answer 23

Any condition that causes dyspepsia, chest pain, or epigastric pain can be considered a differential for peptic ulcer disease.

Important differentials to consider include acute coronary syndrome, gastro-oesphageal reflux, gallstone disease, gastric malignancy and pancreatitis,

Question 24

What is Zollinger-Ellison Syndrome?

Answer 24

Zollinger-Ellison Syndrome refers to a triad of:

1. Severe peptic ulcer disease
2. Gastric acid hypersecretion
3. Gastrinoma.

The characteristic finding is a fasting gastrin level of >1000 pg/ml.

A third of these cases are discovered as part of Multiple Endocrine Neoplasia Type 1 syndrome (Pancreas / Pituitary / Parathyroid tumours), so further investigations for MEN syndrome are often warranted.