PUD & GORD
Nik Sanyal
Overview
How common is it + what are the risk
factors?
What are the symptoms and signs?
Investigations
Management
Possible exam questions
Cases
Epidemiology

Dyspepsia occurs in 40% of the population annually
and leads to a primary care consultation in 5% and
endoscopy in 1%.
Of those who undergo endoscopy:
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About 40% have functional or non-ulcer dyspepsia.
40% have gastro-oesophageal reflux
disease (GORD).
13% have ulcer disease.
2% have gastric cancer.
1% have oesophageal cancer
Aetiology
 H.
pylori.
 NSAIDs.
 Smoking.
 Alcohol.
 Steroids.
 Stress
Symptoms and Signs
 Nonspecific
and diagnosis is unreliable on
history alone
 Epigastric pain, usually postprandial - it
may sometimes be relieved by food.
 Nausea.
 Burping , bloating, distension and
intolerance of fatty food - the last is also
associated with gallstones.
Symptoms & Signs
 Heartburn
sometimes (more typically
associated with GORD).
 May cause pain radiating to the back.
 Signs may include tenderness or
succussion splash (I wouldn’t mention it
cos I wouldn’t confidently if it splashed in
my face, but you might)
 Perforation = sudden onset pain +
peritonitis, absent bowel sounds, shock
Symptoms of GORD
 Retrosternal
discomfort, acid brash regurgitation of acid or bile.
 Water brash - this is excessive salivation.
 Odynophagia (pain on swallowing) may
be due to severe oesophagitis or stricture.
 chronic cough, and asthmatic symptoms
like wheezing and shortness of breath.
 Graded A-D based on degree of mucosal
breaks
Barrett’s Oesophagus
 This
is premalignant ectopic gastric
mucosa with a change (metaplasia) from
squamous to glandular.
 Patients with chronic GORD are at
increased risk of developing the changes
of Barrett's oesophagus.
 The risk increases with longer duration and
increased frequency of gastrooesophageal symptoms.
Worrying signs
 Age
>55 + new onset dyspepsia
 Chronic GI bleed
 Dysphagia
 Weight loss
 Persistent vomiting
 Epigastric mass
 Iron deficiency anaemia
Differentials
 Gallstones
 Chronic
pancreatitis
 Cardiac e.g. MI, angina, pericarditis
 IBS
 Hepatitis
 Malignancy
 AAA
Gastric vs Duodenal Ulcer
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DU>GU
80% DU = h.pylori, 70% of GU
Duodenal ulcer — "Classic" symptoms of a
duodenal ulcer include burning, gnawing,
aching, or hunger-like pain. Eating improves
sx but then they return 2-3hrs after.
Gastric ulcer — Symptoms of a gastric ulcer
typically include pain on eating. Symptoms
are sometimes not relieved by eating or
taking antacids.
DU more likely to perforate
Investigations
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Bedside: ECG to rule out MI
Bloods: FBC to check for anaemia, raised
WCC, amylase for pancreatitis, LFTs for
gallstones
Imaging: erect CXR – free air, AXR –
constipation, cancer
Special tests:
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stool test for H.pylori (stop PPIs 1 wk before
Urea breath test – radiolabel urea + look for C13
on exhaled CO2 as H.pylori have urease.
IgG can confirm h.pylori but stays +ve for weeks
Management
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Conservative: weight loss, drink less coffee,
don’t eat just before bed, reduce alcohol,
stop smoking
Medical: If NSAID related then >90% heal with
8 wks of H2R antagonists e.g ranitidine 150mg
BD
Eradication therapy: omeprazole 20mg (BD),
amoxicillin 1g + clarithromycin 500mg BD or
metronidazole 400mg + clarithromycin 250mg
BD – antibx for 7d, PPI for 3-4 wks
Surgical: Omental patches for perforation
Complications
 Perforation
can cause acute abdomen
 Haematemesis and malaena
 Duodenal scarring leading to pyloric
stenosis
Prognosis
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Prognosis is excellent if the underlying cause
such as H. pylori infection or drugs can be
addressed.
Eradication of H. pylori decreases the ulcer
recurrence rate from 60-90% to 10-20%. This is
still higher than previously reported and this is
thought to be due to an increase in NSAIDrelated ulcers.
Those with successful eradication of GU ulcer
should be scoped for GI cancer.
Exam questions
 How
does H. pylori cause ulcers?
 How does smoking cause ulcers?
 Why do NSAIDs cause ulcers?
 If ulcers/symptoms persist despite h.pylori
eradication therapy what condition might
you consider?
 Explain to the patient an OGD

Consent for one
H
pylori causes depletion of somatostatin
from the D cells. Somatostatin normally is
released when pH is low to prevent acid
release by reducing histamine + gastrin.
 This is because the ammonia the h.pylori
releases makes the D cells think the pH is
higher than it is.
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Smoking delays healing as well as opposing
prostaglandin synthesis
NSAIDs block prostaglandin production which
are protective
May consider zollinger-ellison: excessive
production of gastrin by a tumour, stimulating
hyperplasia of the gastric acid-secreting cells
and producing a continual high acid output,
even between meals and overnight
Risks – bleeding, infection, perforation, sore
throat, complications of sedation.
THANKS
 Good
luck 