Peptic Ulcer Disease (PUD)
Epidemiology
Incidence 10%; <25% with dyspepsia have PUD; 20-60% presenting with PUD have no symptoms prior to
event; GORD more common than PUD; 30% duodenal (H pylori), 15% gastric (NSAID’s)
H pylori: spiral, G negative, urease-producing, flagellated bacterium; 10-20% infected patients develop
PUD; Present in 20-50% dyspeptic symptoms, in 90-95% duodenal ulcer, in 70% gastric ulcer; Most
common cause of PUD
NSAIDs: gastric > duodenal; 2nd most common cause of PUD; 50% patient taking NSAIDs have endoscopic
evidence of erythema, erosions, ulcers; 10% have pre-pyloric and antral ulceration; symptoms occur in
20%; 20% symptomatic patients will have normal endoscopy; especially if combined with steroids,
anticoagulants, elderly, 1st 3/12 of use, high dose, PMH PUD, co-morbidities ; COX inhibitors inhibit
healing of ulcers; pain often masked
Risk Factors
For PUD: H pylori (most common cause), NSAIDs (2nd most common cause), steroids, smoking, ETOH,
family history, stress, ZES
For malignancy: associated with chronic gastritis / gastric ulcer than duodenal; H pylori infection
For GORD: overweight, female, genetic, high fatty food intake, caffeine, nicotine, gastric outlet
obstruction
Pathophysiology
Gastropathy: epithelial cell damage and regeneration without inflammation
Gastritis: inflammation associated with mucosal injury
Ulcer: defect in mucosa extending to muscularis mucosa; stress ulcer usually on body and fundus of
stomach; gastirc ulcers  pain after eating; most ulcers on lesser curve or D1
Complications
Investigation
Penetration: in 20%; only few become clinically evident  constant pain; usually posterior duodenal
ulcers; may cause pancreatitis
Haemorrhage: in 10-20% (most common complication); usually posterior ulcer
Perforation: in 5%; associated with NSAIDs in 30-50%; 60% duodenal, 20% antral, 20% gastric; especially
common in young Asian men; sudden onset epigastric pain radiating to RIF  peritonitic
Gastric outlet obstruction: in 2%
CXR: for perforation: erect 70-80% sensitivity, lateral 85% sensitivity, decubitus 95% sensitivity; although
MCQ said 40% patients will not have free air visible on 1st XR
Endoscopy: >95% sensitivity and spec for ulcer
Do endoscopy if: >55yrs, unexplained weight loss, early satiety, V, dysphagia, anaemia, GI bleeding,
abdominal mass, anorexia, jaundice, genetic predispostion to cancer, non-responsive to acid
suppression treatment 1/52
H pylori testing: do if:  age, susceptible ethnic background, PMH/FH PUD, on NSAIDs
If negative and not on NSAIDs, then PUD unlikely
Serology: ELISA for IgG has 85% sensitivity, 80% specificity; low PPV if low prevalence; will remain +ive
for 2 year post-eradication so limited usefulness
Urease test: breath/blood tests identify patients with active disease; sensitivity and specificity 90-95%;
false negatives if antibiotics, bismuth compounds, PPI; contra-indicated in children and fertile women;
can do rapid urease tests on endoscopic samples (>90% sensitivity, >95% specificity)
Faecal Ag test: sensitivity and specificity >90%; do >1/12 after treatment to test for cure
Biopsy: done at endoscopy
Refer to gastroenterology as outpatient if: >40yrs, concerning features (anorexia, weight loss,
haematemesis, melaena, palpable abdominal mass), persistent symptoms despite treatment
Perforation: immediate OT with oversewing (maybe conservative if not gastric / colonic perforation, no
extravasation of gastrograffin, no upper GI haemorrhage); IV ampicillin + gentamicin + metronidazole;
NGT
Treat for H pylori: treatment success rate 85%; confirm cure 1/12 after treatment
1) 5/7 course:
pantoprazole 40mg BD + amoxicillin 1g BD
2) Then 5/7 course: pantoprazole 40mg BD + clarithromycin 500mg BD (resistance becoming more
common)
+ tinidazole 500mg BD (or amox / metronidazole)
H2 antagonists: OD nocte dosing regime recommended; not helpful in acute bleed; significantly better at
reducing symptoms in NON-ULCER DYSPEPSIA than omeprazole
Cimetidine: side effects = gynaecomastia, impotence, hyperprolactinaemia, CNS dysfunction; inhibits
CP450   levels of warfarin, propanolol, theophylline, diazepam, phenobarbitone, carbamazepine,
phenytoin
Ranitidine: less side effects, less drug interaction
Omeprazole: binds H/K ATPase  inhibits parietal cell proton pump Inhibits acid secretion for 24-72
hours after single dose
Side effects: ? gastrin levels   gastric cancer; dry mouth, dizziness, headache, inhibits CP450
Management
Misoprostol: PGE1 analogue; inhibits gastric acid secretion, blocks prostaglandin receptors on parietal cell,
cytoprotective for gastric mucosa; Indicated in NSAID-related disease
Sucralfate: changes to negatively charged compound when in contact with gastric acid  binds to base of
ulcer  viscous protective substance;  mucosal prostaglandin levels; adsorbs pepsin and bile acids;
QID dosing
Side effects: constipation, dry mouth,  phenytoin bioavailability
Bismuth compounds: chelates protein in ulcer slough; QID dosing; suppresses H pylori
Side effects: ammonia taste, black stool, dark tongue, chronic renal failure
Comparison of drugs:
H2 antagonists: heals 80-90% duodenal ulcers in 4-8/52
70%
gastric ulcers in 8/52 (take longer to heal)
80% relapse at 1yr if no maintenance treatment (20% with maintenance)
“antacids are as effective as H2 antagonists at healing ulcers”
Omeprazole: better early healing rates and pain relief after 2-4/52 compared with H2 antagonist (no
difference at 8/52); 80% response rate in 1/52 for gastritis
Misoprostol: similar efficacy to H2 antagonists
Sucralfate: compared to H2 antagonists: Ulcer healing rate similar, better pain relief, works better in
smokers,  relapse rate short term (no difference at 1 year)
Bismuth compounds: same efficacy as H2 antagonists; eradicates H pylori in 45% at 4/52; 95% healing
rates with metronidazole; relapse in 13% at 1 year
Prognosis
Worse outcome if H pylori negative; 5% mortality from perforation