Peptic ulcer disease & GORD

1. Peptic ulcer disease & GORD Students4Students Hugh Tulloch ht3g10@soton.ac.uk

2. Peptic ulcer disease (PUD) • Definition: • Peptic = Peptic is an adjective that refers to any part of the body that normally has an acidic lumen • Ulcer = An ulcer is a discontinuity or break in a bodily membrane that impedes the organ of which that membrane is a part from continuing its normal functions. • Peptic ulcer is a breach in the mucosal lining of the stomach (Gastric ulcer) or duodenum (Duodenal ulcer).

3. Epidemiology Whats more common, DU or GU?? • 10-15% of adult population • DU > GU (2-3 times) • Much more common in socio-economic deprivation (increase prevalence of h. pylori) • Faecal oral transmission? uncertain

4. Aetiology What causes ulcers? • Helicobacter pylori • NSAIDs • Smoking? • Alchol?

5. Pathophysiology What is an ulcer? • Break in superficial epithelial cells penetrating down to the muscularis mucosa. Fibrous base with inflammatory cells • GU is mostly found on lesser curve near the incisura • DUs are usually found in the duodenal cap • PUD can be found in patients without H. pylori eg. If on NSAIDs or in Zollinger-Ellison syndrome

6. Pathophysiology: H. pylori What colour will H. pylori stain under gram staining? • H. pylori is a slow growing gram –ve flagellate urease-producing bacterium • The discovery of the role it plays in PUD earned a Nobel prize • Many thought that bacteria could not survive the acidic environment on the stomach

7. H. Pylori uncertainties • Although 95% of patients with duodenal ulcers have H. pylori infection and cure of infection heals the ulcer and stops ulcer recurrence… • 50% of world population is infected. Only 15% of those infected develop ulcers. • So other factors may be involved. (smoking, host factors, H. pylori genetics-Cag A/Vac A) • Ie. The reasons why a person infected with H.pyloridoes not get PUD

8. Pathology: NSAIDs Why do NSAIDs cause ulceration?? • COX-1 inhibition • COX-1 makes prostaglandins which protect the gastric mucosa • 50% of patients of regular NSAIDs will develop mucosal damage • 30% will develop ulcers • 5% will develop symptoms

9. Pathology: Zollinger–Ellison Syndrome • Zollinger–Ellison Syndrome (ZES) is caused by a non–beta islet cell, gastrin-secreting tumour of the pancreas that stimulates the acid-secreting cells of the stomach to maximal activity, with consequent gastrointestinal mucosal ulceration.

10. Signs/ symptoms • Burning epigastic pain • DU pain classically at night, worse when patient is hungry (pyloric sphincter open) • GU pain may be relieved by food (buffering of acid) • Nausea • Red flags: back pain – penetrating posterior ulcer

11. Investigationsdiagnosis of H. pylori • Non-invasive: • Serological tests. Look for IgG antibodies. Cannot be used as test of cure • 13C-Urea breath test. Ingestion of 13C Urea, followed by detection of 13CO2 • Stool antigen test. Specific immunoassay using monoclonal antibodies. • Invasive: • Biopsy urease test. Gastric biopsy is tested for urease • Culture • histology

12. investigations • If patient is young (<55) and h. pylori is detected eradication therapy can be started • If older or there are alarm symptoms (dysphagia, weight loss etc) then exclusion of cancer is required • With endoscopy

13. Complications • Haemorrhage • Perforation • DU > GU • Can be into peritoneal cavity or lesser sac • Surgery required to close perforation and drain abdomen • Gastric outlet obstruction • Projectile vomiting following meal • Oedema due to active ulcer • Scarring due to healed ulcer

14. Management • Stop smoking • Eradication therapy • 90% success • Reinfection is uncommon (1%) • 1 PPI and 2 Abx • Eg. Omeprazole + clarithromycin and amozicillin • H2 – receptor antagonists (ranitidine) can be used instead of a PPI • Bismuth is not usully given in initial regimens • Surgery – vagotomy (not used anymore)

15. Prognosis • Eradication is very effective • Test of cure (TOC) should be performed @ 6weeks

16. Gastro-oesophageal reflux disease (GORD) • chronic symptom of mucosal damage caused by stomach acid coming up from the stomach into the oesophagus •  In the Western world between 10 and 20% of the population is affected.

18. Hiatus hernias • Part of the stomach herniates into the thorax. Two different types:

19. Hiatus hernias

20. Clinical features • Heartburn – related to posture • Regurgitation • Pain with swallowing/sore throat (odynophagia) • Increased salivation (also known as water brash) • Nausea • Chest pain • Coughing

21. Differential diagnosis What is GORD commonly confused with? • Angina • 20% of cases admitted to a coronary care unit have GORD

22. Complications • Peptic stricture • Dysphagia for solid goods • Severe cases require endoscopic dilatations and long term PPI • Battett’s oesophagus • Metaplasia • Normal oesophageal squamous epithelium is replaced by metaplastic columnar mucosa.

24. Investigation • If <45 can be treated without investigation • Endoscopy to assess hiatal hernia and oesophagitis • Intraluminal pH monitoring. Excessive reflux is defined as pH < 4 for more than 4% of the time

25. Management • Conservative: • Antacids, weight loss, raise head of bed, reduce alcohol, stop smoking • Medical: • Dopamine antagonist prokinetic agents (metoclopramide/domperidone) • H2 – receptor antagonists (ranitidine) • PPI (omeprazole) • Surgical: • Laparoscopic Nissen fundoplication

26. Questions? • How do you perform a 13C-Urea breath test • What percentage of patients on NSAIDs develop GI side effects • Name two types of hiatus hernia • What can GORD be mistaken for?