GORD Flashcards
What is GORD?
Gastro-oesophageal reflux disease (GORD) is where acid from the stomach refluxes through the lower oesophageal sphincter and irritates the lining of the oesophagus.
The oesophagus has a squamous epithelial lining making it more sensitive to the effects of stomach acid. The stomach has a columnar epithelial lining that is more protected against stomach acid.
Presentation?
Dyspepsia is a non-specific term used to describe indigestion. It covers the symptoms of GORD:
Heartburn
Acid regurgitation
Retrosternal or epigastric pain
Bloating
Nocturnal cough
Hoarse voice
Referral for Endoscopy?
Endoscopy can be used to assess for peptic ulcers, oesophageal or gastric malignancy if there are concerning features.
Patients with evidence of a GI bleed (i.e. meleana or coffee ground vomiting) need admission and urgent endoscopy.
Patients with symptoms suspcious of cancer should have a two-week-wait referral so that endoscopy is performed within 2 weeks. The NICE guidelines have various criteria for when to refer urgently and when to refer routinely. They key red flag features indicating referral are:
Dysphagia (difficulty swallowing) at any age gets a two week wait referral
Aged over 55 (this is generally the cut off for urgent versus routine referrals)
Weight loss
Upper abdominal pain / reflux
Treatment resistant dyspepsia
Nausea and vomiting
Low haemoglobin
Raised platelet count
Management?
Lifestyle advice
Reduce tea, coffee and alcohol
Weight loss
Avoid smoking
Smaller, lighter meals
Avoid heavy meals before bed time
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.
Test for H.pylori?
H. pylori is a gram negative aerobic bacteria. It lives in the stomach. It causes damage the epithelial lining of the stomach resulting in gastritis, ulcers and increasing the risk of stomach cancer. It avoids the acidic environment by forcing its way into the gastric mucosa. The breaks it creates in the mucosa exposes the epithelial cells underneath to acid.
It also produces ammonia to neutralise the stomach acid. The ammonia directly damages the epithelial cells. Other chemicals produced by the bacteria also damage the epithelial lining.
We offer a test for H. pylori to anyone with dyspepsia. They need 2 weeks without using a PPI before testing for H. pylori for an accurate result.
Tests
Urea breath test using radiolabelled carbon 13
Stool antigen test
Rapid urease test can be performed during endoscopy.
A rapid urease test is also known as a CLO test (Campylobacter-like organism test). It is performed during endoscopy and involves taking a small biopsy of the stomach mucosa. Urea is added to this sample. If H. pylori are present, they produce urease enzymes that converts the urea to ammonia. The ammonia makes the solution more alkali giving a positive result on when the pH is tested.
Eradication
The eradication regime involves triple therapy with a proton pump inhibitor (e.g. omeprazole) plus 2 antibiotics (e.g. amoxicillin and clarithromycin) for 7 days.
The urea breath test can be used as a test of eradication after treatment. This is not routinely necessary.
Barretts Oesophagus?
Constant reflux of acid results in the lower oesophageal epithelium changing in a process known as metaplasia from a squamous to a columnar epithelium. This change to columnar epithelium is called Barretts oesophagus. When this change happens patients typically get an improvement in reflux symptoms.
Barretts oesophagus is considered a “premalignant” condition and is a risk factor for the development of adenocarcinoma of the oesophagus (3-5% lifetime risk with Barretts). Patients identified as having Barretts oesophagus are monitored for adenocarcinoma by regular endoscopy. In some patients there is a progression from Barretts oesophagus (columnar epithelium) with no dysplasia to low grade dysplasia to high grade dysplasia and then to adenocarcinoma.
Treatment of Barretts oesophagus is with proton pump inhibitors (e.g. omeprazole). There is new evidence that treatment with regular aspirin can reduce the rate of adenocarcinoma developing however the is not yet in guidelines.
Ablation treatment during endoscopy using photodynamic therapy, laser therapy or cryotherapy is used to destroy the epithelium so that it is replaced with normal cells. This is not recommended in patients with no dysplasia but has a role in low and high grade dysplasia in preventing progression to cancer.
