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PUD & GORD

PUD & GORD. Nik Sanyal. Overview. How common is it + what are the risk factors? What are the symptoms and signs? Investigations Management Possible exam questions Cases. Epidemiology.

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PUD & GORD

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  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%. Of those who undergo endoscopy: • About 40% have functional or non-ulcer dyspepsia. • 40% have gastro-oesophageal reflux disease (GORD). • 13% have ulcer disease. • 2% have gastric cancer. • 1% have oesophageal 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. • 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 CO2 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 H2R antagonistse.granitidine 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 

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