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 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 Whats more common, DU or GU??

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

5. Pathophysiology 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 What is an ulcer?

6. Pathophysiology: H. pylori 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 What colour will H. pylori stain under gram staining?

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.pylori does not get PUD

8. Pathology: NSAIDs 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 Why do NSAIDs cause ulceration??

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. Investigations diagnosis of H. pylori Non-invasive: Serological tests. Look for IgG antibodies. Cannot be used as test of cure 13 C-Urea breath test. Ingestion of 13 C Urea, followed by detection of 13 CO 2 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 H 2 – 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.

17. Increased Abdominal Pressure Obesity / Pregnancy Dysfunctional LOS Failure to contract normally Hiatus Hernia Food/Drink Large meals, lots of liquid particularly alcohol or caffeine Smokers are at greater risk Dysfunctional Stomach Delayed gastric emptying

18. Hiatus hernias Part of the stomach herniates into the thorax. Two different types: Sliding Hiatus Hernia The gastroesophageal junction slides past the diaphragmatic hiatus. This is common 30% of people over 50! Only symptomatic through GORD. Rolling Hiatus Hernia A portion of the fundus herniates. The LOS remains competent below the diaphragm. Rarely gastric volvulus may result from strangulation.

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 Angina 20% of cases admitted to a coronary care unit have GORD What is GORD commonly confused with?

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) H 2 – receptor antagonists (ranitidine) PPI (omeprazole) Surgical: Laparoscopic Nissen fundoplication

26. Questions? How do you perform a 13 C-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?