1. PUD & GORD Nik Sanyal

2. Overview How common is it + what are the risk factors? What are the symptoms and signs? Investigations Management Possible exam questions Cases

3. Epidemiology  Dyspepsia occurs in 40% of the population annually and leads to a primary care consultation in 5% and endoscopy in 1%. Dyspepsia Of those who undergo endoscopy:  About 40% have functional or non-ulcer dyspepsia.non-ulcer dyspepsia  40% have gastro-oesophageal reflux disease (GORD).gastro-oesophageal reflux disease  13% have ulcer disease.  2% have gastric cancer.gastric cancer  1% have oesophageal canceroesophageal cancer

4. Aetiology  H. pylori.  NSAIDs.  Smoking.  Alcohol.  Steroids.  Stress

5. Symptoms and Signs  Nonspecific and diagnosis is unreliable on history alone  Epigastric pain, usually postprandial - it may sometimes be relieved by food. Epigastric pain  Nausea.  Burping, bloating, distension and intolerance of fatty food - the last is also associated with gallstones.

6. 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

7. 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

8. 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 gastro- oesophageal symptoms.

9. Worrying signs  Age >55 + new onset dyspepsia  Chronic GI bleed  Dysphagia  Weight loss  Persistent vomiting  Epigastric mass  Iron deficiency anaemia

10. Differentials  Gallstones  Chronic pancreatitis  Cardiac e.g. MI, angina, pericarditis  IBS  Hepatitis  Malignancy  AAA

11. Gastric vs Duodenal Ulcer  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

12. Investigations  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 :  stool test for H.pylori (stop PPIs 1 wk before  Urea breath test – radiolabel urea + look for C13 on exhaled CO 2 as H.pylori have urease.  IgG can confirm h.pylori but stays +ve for weeks

13. Management  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 H 2 R 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

14. Complications  Perforation can cause acute abdomen  Haematemesis and malaena  Duodenal scarring leading to pyloric stenosis

15. Prognosis  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 NSAID- related ulcers.  Those with successful eradication of GU ulcer should be scoped for GI cancer.

16. 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

17.  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.

18.  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.

19. THANKS  Good luck