Gastritis, GORD and PUD Flashcards
1
Q
What is the pathophysiology of Barrett’s oesophagus?
A
- Premalignant condition
- Metaplastic response to mucosal injury
- Squamous becomes columnar
- Usuall intestinal with goblet cells
- Associated with benign structures but also with adenocarcinomas (3-5% lifetime risk)
- Dysplasia to carcinoma over years
- Monitored by regular endoscopy
- Ablation treatment has a role in preventing progression to cancer
2
Q
What are the features of gastric cancer?
A
- Usually more distal than proximal
- Associated with chronic gastritis
- Background atrophic mucosa, chronic inflammation, intestinal metaplasia, dysplasia
- Intestinal vs diffuse (Lauren classification)
3
Q
What are the features of diffuse gastric cancer?
A
- Individual malignant cells with mucin vacuoles (signet ring cells)
- Metastasis to ovaries (Krukenberg tumour)
- Supraclavicular lymph node (Wirchow’s node)
- Sister Joseph’s nodule (umbilical metastasis)
4
Q
What are the features of familial gastric cancer?
A
- CDH1 (E-cadherin) mutation
- Small intramucsal foci of diffuse gastric cancer may be numerous
5
Q
What are the features of autoimmune atrophic gastritis and pernicious anaemia?
A
- Malabsorption of vitamin B12
- B12 bound to salivary Haptocorrin is protected from gastric acid
- Haptocorrin is digested in duodenum
- B12 binds to intrinsic factor secreted by gastric parietal cells
- Absorbed in terminal ileum via specialised receptor
- Autoimmune destruction of parietal cells
- Anti-parietal cell antibodies in blood
- Eventual complete loss of parietal cells with pyloric and intestinal metaplasia
- Achlorhydria -> bacterial overgrowth
- Hypergastrinaemia -> endocrine cell hyperplasia/carcinoids
- Persistent inflammation -> epithelial dysplasia and may lead to cancer
6
Q
What are the features of Zollinger-Ellison Syndrome?
A
- Hypersecretion of gastrin by an endocrine tumour (gastrinoma) in pancreas or duodenum -> increased gastric acid output and severe peptic ulceration
7
Q
Helicobacter pylori
A
- Gram negative aerobic bacteria
- Produces ammonia to neutralise stomach acid - ammonia directly damages epithelial cells
- H. pylori colonises gastric mucosa -> active chronic inflammation; IL-8 from epithelial cells attracts neutrophils
- Antral-predominant gastritis -> hypergastrinaemia and duodenal ulceration
- Pangastritis -> hypochlorhydria, multifocal atrophic gastritis, IM, cancer (intestinal type)
- Tested for using:
- Urea breath test using radiolabelled carbon 13
- Stool antigen test
- Rapid urease test during endoscopy
- Eradication therapy:
- PPI
- 2 antibiotics (i.e. amoxicillin and clarithromycin) for 7 days
- Swap amoxicillin for metronidazole in penicillin allergy
8
Q
What are the features of chemical gastritis?
A
- Few inflammatory cells
- Surface congestion oedema, elongation of gastric pits, tortuosity, reactive hyperplasia/atypia and ulceration
- Antrum more than corpus
- Causes include reflux, NSAIDs, ethanol and oral iron
9
Q
Presentation of GORD
A
- Acid from the stomach refluxes through the lower oesophageal sphincter and irritates the lining of the oesophagus
- Oesophagus has a squamous epithelial lining making it more sensitive to the effects of stomach acid whilst the stomach has a columnar epithelial lining that is more protected against stomach acid
- Presentation:
- Heartburn
- Acid regurgitation
- Retrosternal or epigastric pain
- Nocturnal cough
- Hoarse voice
10
Q
Management of GORD
A
- Referral for endoscopy to assess for peptic ulcers, oesophageal or gastric malignancy
- Management:
- Lifestyle advice
- Reduce tea, coffee and alcohol
- Weight loss
- Avoid smoking
- Smaller, lighter meals
- Stay upright after meals rather than lying flat
- Acid neutralising medication when required:
- Gaviscon
- Rennie
- Proton pump inhibitors (reduce acid secretion in the stomach)
- Omeprazole
- Lansoprazole
- Ranitidine
- This is an alternative to PPIs
- H2 receptor antagonist (antihistamine)
- Reduces stomach acid
- Surgery for reflux is called laparoscopic fundoplication. This involves tying the fundus of the stomach around the lower oesophagus to narrow the lower oesophageal sphincter.
- Lifestyle advice
11
Q
Pathophysiology of peptic ulcer disease
A
- Caused by breakdown of the protective layer of the stomach and duodenum along with increase in stomach acid
- Protective layer is comprised of mucus and bicarbonate secreted by the stomach mucosa - broken down by medications (i.e. NSAIDs, steroids) and H. pylori.
- Increased acid can be a result of:
- Stress
- Alcohol
- Caffiene
- Smoking
- Spicy food
12
Q
Presentation of peptic ulcer disease
A
- Epigastric discomfort or pain
- Nausea and vomiting
- Dyspepsia
- Bleeding causing haematemesis, coffee ground vomiting and malaena
- IDA
NB - Eating typically worsens the pain of gastric ulcers and improves the pain of duodenal ulcers.
13
Q
Management of peptic ulcer disease
A
- Diagnosed by endoscopy during which a rapid urease test can be performed to check for H. pylori
- Biopsy to check for malignancy can also be undertaken
- Medical treatment is the same as GORD
14
Q
Complications of peptic ulcer disease
A
- Bleeding
- Perforation resulting in an acute abdomen and peritonitis
- Scarring and strictures of the muscle and mucosa leading to pyloric stenosis
15
Q
Presentation of oesophageal cancer
A
- Squamous cell carcinoma (more common in the developing world) typically occurring in the middle and upper thirds of the oesophagus. Associated with smoking and excessive alcohol consumption, as well as chronic achalasia.
- Adenocarcinoma (more common in the developed world) typically occurring in the lower third of the oesophagus. Arises as a consequence of metaplastic epithelium (termed Barrett’s oesophagus) which progresses to dysplasia, to eventually become malignant. Risk factors for this subtype are long-standing GORD, obesity, and high dietary fat intake.
- Patients typically present with dysphagia and weight loss.
