Gastric Ulcers Flashcards
GERD/GORD
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.)
GORD clinical features
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
GORD referral for endoscopy
referral if concern of malignancy / concerning features
evidence of GI bleed- melena, coffe ground vomiting need admission and urgent endoscopy
suspicious of cancer urgent 2ww.
red flags: 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
GORD 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.
what is H Pylori?
gram -ve aerobic bacteria
lives int he stomach
damages the epithelial lining of the stomach - gastritis, ulcers, increases the risk of stomach cancer.
H pylori avoids the acidic environment by forcing its way into the gastric mucosa. The breaks it causes in the mucosa exposes the endothelial cells underneath to the acid
h pylori produces ammonia to neutralises stomach acid which directly damages epithelial ells.
test for H Pylori
test= need 2 weeks without using PPI to get an accurate result
urea breath test (radiolabelled carbon 13)
stool antigen test
rapid urease test (endoscopy)
CLO test (campylobacter like organism test) during endoscopy *small biopsy of stomach mucosa. add urea to sample. if hpylori is present it will produce a urease enzyme that converts urea to ammonia = alkali = positive result when test pH
erradication of H pylori
tripple therapy
PPI - omeprazole
2 abx- amoxicillin, clairthromycin for 7 days
urea breath test to test eradication after treatment
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.
