Case History:

A 30 year old lady comes to your clinic with complaints of pain in upper abdomen on and off for past 2 months. She tells you that there is some relief of pain after eating. She also tells you that immediately after taking meal she has the feeling of fullnes of abdomen and also that she doesn’t eat as much as she used to before. On examination, there are no abnormalities except for mild epigastric tenderness. How will you manage the case?

Peptic Ulcer Disease (PUD)
  • Definition 
  • Epidemiology 
  • Etiology 
  • Clinical Manisfestations
  • Diagnosis 
  • Treatment

  • The term 'peptic ulcer' refers to an ulcer in the lower oesophagus, stomach or duodenum, in the jejunum after surgical anastomosis to the stomach or, rarely, in the ileum adjacent to a Meckel's diverticulum.
  • Acute or chronic and penetrating muscularis mucosae


The prevalence of peptic ulcer is decreasing in many Western communities as a result of widespread use of H. pylori eradication therapy but it remains high in developing countries. 
The male to female ratio for duodenal ulcer varies from 5:1 to 2:1, whilst that for gastric ulcer is 2:1 or less.

  • H. pylori
  • NSAIDs
  • Infection Cytomegalovirus ,Herpes simplex virus, Helicobacter heilmanni
  • Drug/Toxin Bisphosphonates, Chemotherapy, Clopidogrel, Crack cocaine, Glucocorticoids (when combined with NSAIDs) ,Mycophenolate mofetil, Potassium chloride
  • Miscellaneous Duodenal obstruction (e.g., annular pancreas), Infiltrating disease, Ischemia, Radiation therapy, Sarcoidosis, Crohn's disease, Idiopathic hypersecretory state

Helicobacter pylori 

The vast majority of colonised people remain healthy and asymptomatic and only a minority develop clinical disease.
Around 90% of duodenal ulcer patients and 70% of gastric ulcer patients are infected with H. pylori; the remaining 30% of gastric ulcers are due to NSAIDs.

Pathogenesis and pathophysiology of infection
The bacteria spread by person-to-person contact via gastric refluxate or vomit.
exclusively colonises gastric-type epithelium and is only found in the duodenum in association with patches of gastric metaplasia.

  • The bacterium stimulates chronic gastritis by provoking a local inflammatory response in the underlying epithelium
  • Host genetic polymorphisms :
  • expression of the proinflammatory cytokine interleukin-1β (IL-1β)
  • host inflammatory response to infection (e.g. IL-10 and TNF-α)
  • approximately 1% of infected people, H. pylori causes a pangastritis leading to gastric atrophy and hypochlorhydria. May predispose to gastric cancer
Dx of H. pylori

Non-invasive tests
  • Urea breath testing: very sensitive and widely performed
  • serology
  • Stool antigen assay
Invasive tests i.e. with endoscopic procedures
  • Biopsy urease testing
  • Brush cytology 
  • Bacterial culture and sensitivity testing

  1. Peptic ulcer 
  2. MALToma 
  3. H. pylori-positive dyspepsia 

  • 'First-line therapy is a proton pump inhibitor (12-hourly), clarithromycin 500 mg 12-hourly, and amoxicillin 1 g 12-hourly or metronidazole 400 mg 12-hourly, for 7 days. 
  • Second-line therapy is a proton pump inhibitor (12-hourly), bismuth 120 mg 6-hourly, metronidazole 400 mg 12-hourly, and tetracycline 500 mg 6-hourly, for 7 days.'

Clinical Manisfestations of PUD 
  • Postprandial fullness
  • Early satiety
  • Epigastric pain
  • Aggravated by food in gastric ulcer
  • Relieved by food in duodenal ulcer
  • Complication may be the first presentation
  • Bleeding
  • Perforation
  • Gastric  outlet obstruction


Barium meal- gastric ulcer

Gastrodudenoendoscopy – duodenal ulcer


General measures
  • Cigarette smoking, aspirin and NSAIDs should be avoided
  • Alcohol in moderation is not harmful 

Short-term management 

  • Various drugs are available
  • Antacids and alginates
  • Aluminium hydroxide, magnesium trisilicate

  • Ranitidine, cimetidine, famotidine, nizatidine

Proton pump inhibitors (PPIs
  • Omeprazole, esomeprazole, lansoprazole, pantoprazole, rabeprazole

Complex salts

  • Sucralfate

Prostaglandin analogues

  • H. pylori eradication
  • Maintenance treatment 

Usually not necessary after H. pylori eradication
A minority of pts. with relapsing disease may need it and the lowest effective dose of PPI or H2 blocker should be used


  • A rare event now because of cure of most peptic ulcers by H. pylori eradication therapy and the availability of safe and potent acid-suppressing drugs
  • Highly selective vagotomy
  • Selective vagotomy
  • Bilroth I and Bilroth II

Indications for surgery in peptic ulcer disease

  • Emergency 
  • Perforation 
  • Haemorrhage 
  • Elective
  • Complications, e.g. gastric outflow obstruction 
  • Recurrent ulcer following gastric surgery 
  • Management of complications


Gastroduodenal ulcers: have a greater incidence, admission rate and mortality.
Causes: high prevalence of H. pylori and NSAID use, and impaired defence mechanisms.
Atypical presentations: pain and dyspepsia are frequently absent or atypical so older people develop complications such as bleeding or perforation more frequently.
Bleeding: older patients require more intensive management than younger patients because they tolerate hypovolaemic shock poorly.