Gastritis, Peptic ulcer disease and Dyspepsia

Question 1

What condition is known as inflammation of the gastric mucosa?

Answer 1

Gastritis

Question 2

What symptoms would you expect a patient with gastritis to present with?

Answer 2

80% are asymptomatic, leaving acid production unchanged
Those that present with symptoms include dyspeptic like symptoms such as nausea and vomiting, abdominal pain etc

Question 3

What is a complication of gastritis?

Answer 3

The inflammation of the gastric mucosa can lead to chronic gastritis, ulcer formation and then gastric cancer.
Patients with gastritis are 40 times more likely to have peptic ulcer disease which then makes them 6 times more likely to develop gastric cancer.

Question 4

What are the majority of gastritis cases due to?

Answer 4

H pylori infection (80% of cases)

Question 5

How does H pylori survive in acidic environments?

Answer 5

The bacterium hydrolyses urea to produce ammonia which is secreted around themselves, which essentially provides a buffer to the H+ ions within the stomach environment.

Question 6

How does an individual’s acid secretory status influence inflammation?

Answer 6

H pylori will burrow, using their flagella, into the gastric mucosal in areas of moderate acidity. Therefore an individual’s gastric acid secreting status which determine the area of the stomach that the H pylori bacterium migrates to by chemotaxis and causes inflammation. Two individuals with a H pylori infection you would expect to have different patterns of inflammation within the stomach.

Question 7

Describe the development of gastric and duodenal ulcers as a result of H pylori infection.

Answer 7

Initially in both types of ulcer development, H pylori begins by invading and colonising into the antrum (lower part of the stomach adjacent to the duodenum) causing chronic inflammation. This results in a decrease in somatostatin production resulting in homeostatic mechanisms being activated leading to the increase in gastrin secretion and hence gastric acid production. If there is already inflammation in the duodenum as a result of an increase in acidic production this can lead to the development of a duodenal ulcer. If not, H pylori remains within the stomach causing widespread inflammation of the GI mucosa (widespread gastritis) causing damage to cells ultimately leading to the reduction in acid production but also mucus leading to a gastric ulcer and potentially gastric cancer.

Question 8

Briefly explain the causes behind a duodenal ulcer.

Answer 8

A duodenal ulcer is caused by acid hypersecretion, often linked to genetic predisposition and an increased number of parietal cells. Inflammation due to increased acidic production in addition to H pylori infection can lead to a duodenal ulcer development.

Question 9

Briefly explain the causes behind a gastric ulcer.

Answer 9

A gastric ulcer is caused by acid hyposecretion by prolonged exposure to H pylori infection which causes widespread inflammation throughout the stomach, damaging parietal cells and reducing acid secretions.
NSAIDs reduce the protective prostaglandin production which causes a reduction of the mucus and bicarbonate protective barrier against acid injury, increasing risk of ulcer development.

Question 10

When is a patient more likely to develop a duodenal ulcer?

Answer 10

When patients have an over-production of acid within the duodenum by an increased number of parietal cells compared to average. This increased acid production within the duodenum leads to migration of H pylori bacterium there due to the chronic inflammation already present in the mucosal layer of the duodenum allowing the easier penetration into the epithelium, further initiating immune response and due to the reduced gastric protection there this can lead to the development of a duodenal ulcer.

Question 11

What is the incidence of H pylori?

Answer 11

Roughly 50% of the over 60s are infected
Almost all over 80s are

Question 12

How is H pylori spread?

Answer 12

Directed contact of an infected person’s saliva (oral-oral) , vomit (gastro-oral) or stool (faecal-oral)

Question 13

How is H pylori diagnosed?

Answer 13

Urea breath test
Stools tests

Question 14

Explain the purpose of the urea breath test.

Answer 14

Use of the urea breath test which involves the administration of radiolabelled urea to a patient and is based on the ability of H pylori’s ability to convert urea to ammonium and carbon dioxide. Therefore if H pylori is present within a patient, the carbon dioxide that is exhaled will also be radiolabelled.

Question 15

How must stools be stored prior to testing?

Answer 15

Must be stored -20 degrees before testing

Question 16

What percentage of duodenal and gastric ulcers are attributed to H pylori infections?

Answer 16

Duodenal - 90%
Gastric - 70-80%

Question 17

Which medications should be avoided prior to the testing for H pylori?

Answer 17

Lansoprazole and Omeprazole
Cimetidine and Ranitidine
Antibiotics (false negative)

Testing should not be repeated in less than 4 weeks to prior test

Question 18

What is the management strategy for H pylori?

Answer 18

Eradication of H pylori, leading to the resolution of ulcers which involves:
2 antibiotics and a PPI for 7 days

Antibiotics of choice are usually Amoxicillin plus Metronidazole or Clarithromycin (taking into account patient’s history with Metronidazole and Clarithromycin due to increased resistance and local resistance patterns)

Question 19

What percentage of the population suffers with Peptic ulcer disease?

Answer 19

10-15%

Question 20

Which ages are more commonly associated with PUD?

Answer 20

Gastric ulcers are rare under 40 whereas
Duodenal ulcers are more common between 20-50 years

Question 21

What are the underlying factors that contribute to gastric and duodenal ulcers?

Answer 21

Duodenal ulcers- genetic predisposition of increased number of parietal cells and hence acid hypersecretion

Gastric ulcers- more commonly associated with environmental factors such as smoking which leads to reduced mucosal resistance

Question 22

What is the prognosis statistics for patients with peptic ulcer disease?

Answer 22

Bleeding occurs in 10-15% of all patients with PUD

5-10% of patients with duodenal ulcer will perforate
1 in 7 of these will die

5-10% of gastric ulcers eventually found to be malignant

Question 23

What is the relapse rate in patients with gastric and duodenal ulcers?

Answer 23

60% with duodenal ulcers relapse after a year

50% with gastric ulcers relapse after 2 years

Question 24

What are some of the risk factors for peptic ulcer disease?

Answer 24

H pylori
NSAIDs
Smoking
Salt
Family history (genetics)

Question 25

What is the effect of smoking on peptic ulcer disease?

Answer 25

The increase in prevalence of peptic ulcer disease is linked to the number of cigarettes smoked.
Smoking reduces the healing rate of peptic ulcers and increases the risk of relapse

Question 26

If a parent has peptic ulcer disease, what is the increase in likelihood that their children would develop it?

Answer 26

3x more likely

Question 27

How can diet influence the development of peptic ulcer disease?

Answer 27

Salt is believed to cause parietal cell suppression leading to gastric atrophy. On the other hand antioxidants vitamins present in fresh fruits protect the specialised gastric cells from reactive oxygen species released by inflammatory cells.

Question 28

In which demographics is NSAID induced dyspepsia higher in?

Answer 28

Elderly
Smokers
Patients with a previous history of PUD

Question 29

Aside from NSAIDs which other medications can cause drug induced dyspepsia?

Answer 29

Aspirin
Corticosteroids
Bisphosphonates
SSRIs
Antibiotics
Sulfasalazine
Iron preparations
Potassium

Question 30

Which drugs are believed to lower the lower oesophageal sphincter pressure?

Answer 30

Theophylline
Calcium antagonists
Nitrates

And therefore at a predisposition to GORD

Question 31

Briefly explain how NSAIDs can cause peptic ulcer disease.

Answer 31

NSAIDs inhibit cyclo-oxygenase (COX) 1 and 2 enzymes which is responsible for the conversion of arachidonic acid into prostaglandin G2. Whilst COX-1 is the constitutive, COX-2 is only activated under inflammatory conditions and therefore responsible for production of inflammatory prostaglandins. COX-1 causes production of protective prostaglandins including those in the GI tract are responsible for gastric mucosal protection through vasodilation, stimulation, and secretion of gastroduodenal mucus and bicarbonate, and forming a protective barrier to acid injury. Where NSAIDs inhibit this enzyme, these protective prostaglandins and their protective effects are reduced against acid injury (decrease in gastroduodenal mucus and bicarbonate), increasing potential for gastritis and ulcer formation.

Question 32

Which NSAIDs have the highest risk of GI toxicity?

Answer 32

Highest risk - Piroxicam, Ketoprofen and Ketorolac

Intermediate - Indometacin, Diclofenac, Naproxen

Lower - Ibuprofen (up to 1.2g daily)

Lowest - COXIBS

Question 33

What are some of the specific symptoms of gastric ulcers?

Answer 33

Pain on eating
Epigastric pain

Question 34

What are some of the specific symptoms of duodenal ulcers?

Answer 34

Localised, dull pain in between meals and at night (able to point to it at night)
Relieved upon eating (fatty foods can aggravate it)

Question 35

What are some of the other symptoms for both gastric and duodenal ulcers?

Answer 35

Bloatedness
Nausea
Anorexia
Belching

If blood is present:
Haematemesis (blood in vomit)
Melaena (black tarry stools)