Peptic Ulcer Desease (PUD), Sores in the gastrium

PUD

1. . Peptic ulcer disease (PUD) Peptic ulcer disease 08-Sep-24 PRESENTED BY MUTEGEKI ADOLF

2. Content Introduction Pathophysiology Etiology/ Risk factors Types of PUD Clinical Presentation Investigation/ Diagnostic test Complications of PUD Management Summary References.

3. INTRODUCTION Peptic ulcer disease (PUD) refers to open sores that develop on the inner lining of the stomach ( gastric ulcers ) or the upper part of the small intestine ( duodenal ulcers). These ulcers occur when the protective lining of the digestive tract is eroded, leading to exposure to stomach acid and digestive enzymes.

4. Lesion may subsequently occur into the lamina propria and submucosa to cause bleeding. – Most of peptic ulcer occur either in the duodenum, or in the stomach – Ulcer may also occur in the lower esophagus due to reflexing of gastric content – Rarely in certain areas of the small intestine

5. AETIOLOGY The primary causes of peptic ulcer disease include: Helicobacter pylori Infection: A bacterium that weakens the protective mucous coating of the stomach and duodenum, allowing acid to irritate the lining. Non-Steroidal Anti-Inflammatory Drugs (NSAIDs): Medications like aspirin, ibuprofen, and naproxen reduce the production of protective mucus, leading to increased gastric acid damage. Excessive Acid Production: Conditions like Zollinger -Ellison syndrome, where increased acid secretion causes ulcers. Other Risk Factors: Smoking, excessive alcohol consumption, stress, and genetic predisposition.

6. ETIOLOGY/ RISK FACTORS Lifestyle Smoking Acidic drinks Medications H. Pylori infection 90% have this bacterium Passed from person to person (fecal-oral route or oral-oral route) Age Duodenal 30-40 Gastric over 50 Gender Duodenal: are increasing in older women Genetic factors More likely if family member has Hx Other factors: stress can worsen but not the cause

7. Gastric ulcer Duodenal Ulcer middle age 50-60 Any age specially 30-40 Age More in female More in male Sex Same Stress job eg . Manager Occupation Epi. Can radiate to back Epigastric , discomfort Pain Immediately after eating 2-3 hours after eating & midnight Onset Eating Hunger Agg.by

8. Gastric ulcer Duodenal Ulcer Lying down or vomiting Eating Relived by Few weeks 1-2 months Duration Common(to relieve the pain) Uncommon Vomiting Pt. afraid to eat Good Appetite Avoid fried food Good , eat to relieve the pain Diet wt. Loss No wt. loss Weight 60% 40% Hematemesis 40% 60% Melena

9. PATHOPHYSIOLOGY Under normal conditions, a physiologic balance exists between gastric acid secretion and gastroduodenal mucosal defense. Mucosal injury and, thus, peptic ulcer occur when the balance between the aggressive factors and the defensive mechanisms is disrupted. Aggressive factors, such as NSAIDs,  H pylori  infection, alcohol, bile salts, acid, and pepsin, can alter the mucosal defense by allowing back diffusion of hydrogen ions and subsequent epithelial cell injury

10. Mucosal Damage: The normal gastrointestinal mucosa is protected by a layer of mucus and bicarbonate. When this protective barrier is disrupted by H. pylori, NSAIDs, or other factors, the mucosa becomes susceptible to damage from gastric acid and pepsin. Inflammation and Ulceration: Continuous exposure to acid and digestive enzymes results in inflammation and erosion, leading to ulcer formation. H. pylori also produces urease, which increases local ammonia levels, further damaging the mucosa. Impaired Healing: Persistent inflammation and damage impair the healing process of the mucosa, perpetuating ulceration.

11. PATHOPHYSIOLOGY

12. CLINICAL PRESENTATIONS Common symptoms of peptic ulcer disease include: Epigastric Pain: Burning or gnawing pain in the upper abdomen, often relieved by eating (duodenal ulcer) or worsened by eating (gastric ulcer). Nausea and Vomiting: May occur, sometimes with blood if there is ulcer bleeding. Bloating and Belching: Due to increased gas and irritation. Weight Loss: Due to avoidance of food because of pain. Complications: Such as hematemesis (vomiting blood), melena (black tarry stools), perforation, and gastric outlet obstruction

13. TYPES GASTRIC PEPTIC ULCER And DUODENAL PEPTIC ULCER

14. INVESTIGATIONS Upper Gastrointestinal Endoscopy: The gold standard for diagnosis, allowing direct visualization of the ulcer and biopsy for H. pylori detection or malignancy exclusion. H. pylori Testing: Urea Breath Test: Non-invasive test for detecting active infection. Stool Antigen Test: Detects H. pylori antigens in stool. Serology: Less accurate for current infection. Barium Meal X-Ray: May show ulcers, but less sensitive than endoscopy. Blood Tests: Including complete blood count (CBC) for anemia and liver function tests. Fasting Gastrin Levels: To rule out Zollinger -Ellison syndrome in refractory cases.

15. Stool examination for fecal occult blood. In all patients with “ Alarming symptoms ” endoscopy is required. Dysphagia. Weight loss. Vomiting. Anorexia. Hematemesis or Melena

16. COMPLICATIONS OF PEPTIC ULCERS Hemorrhage Blood vessels damaged as ulcer erodes into the muscles of stomach or duodenal wall Coffee ground vomitus or occult blood in tarry stools Perforation An ulcer can erode through the entire wall Bacteria and partially digested food spill into peritoneum=peritonitis Narrowing and obstruction (pyloric) Swelling and scarring can cause obstruction of food leaving stomach=repeated vomiting

17. MANAGEMENT LIFE STYLE MODIFICATION HYPOSECRETORY DRUG THERAPY H. pylori ERADICATION THERAPY SURGERY

18. Life style modification

19. Hyposecretory Drugs Proton Pump Inhibitors Suppress acid production Prilosec, Prevacid H2-Receptor Antagonists Block histamine-stimulated gastric secretions Zantac, Pepcid, Axid Antacids Neutralizes acid and prevents formation of pepsin (Maalox, Mylanta) Give 2 hours after meals and at bedtime Prostaglandin Analogs Reduce gastric acid and enhances mucosal resistance to injury Cytotec Mucosal barrier fortifiers Forms a protective coat Carafate/ Sucralfate cytoprotective

20. H. pylori Eradication Therapy: Triple therapy: Proton pump inhibitor . 2 Antibiotics: Metronidazole + Clarithromycin. Clarithromycin + Amoxicillin.

21. Give an antacid eg Magnesium trisilicate compound 2 tablets every 8 hours as required. Treatment for eradication of H. pylori ( Triple therapy ) Combination 1 (First line) Amoxycillin 1 g every 12 hours PLUS metronidazole 400 mg every 12 hours PLUS omeprazole 20 mg every 12 hours for two weeks Check eradication with a stool antigen test after 4 weeks

22. For bleeding and perforated ulcer Refer patient to hospital immediately for - IV fluids and blood if necessary - IV ranitidine 50 mg in 20 ml slowly every 8 hours Note: Tinidazole 500 mg every 12 hours can be used instead of metronidazole Confirm eradication with stool antigen test a month after completion of treatment; test should be negative

23. Indications: Failure of medical treatment. Development of complications High level of gastric secretion and combined duodenal and gastric ulcer. surgical Treatment Principle: Reduce acid and pepsin secretion .

24. Types of Surgical Procedures GASTROENTEROSTOMY Creates a passage between the body of stomach to small intestines. Allows regurgitation of alkaline duodenal contents into the stomach. Keeps acid away from ulcerated area

25. Types of Surgical Procedures VAGOTOMY Cuts vagus nerve Eliminates acid-secretion stimulus

26. Types of Surgical Procedures PYLOROPLASTY Widens the pylorus to guarantee stomach emptying even without vagus nerve stimulation

27. Types of Surgical Procedures ANTRECTOMY/ SUBTOTAL GASTRECTOMY Lower half of stomach ( antrum ) makes most of the acid Removing this portion ( antrectomy ) decreases acid production SUBTOTAL GASTRECTOMY Removes ½ to 2/3 of stomach Remainder must be reattached to the rest of the bowel Billroth I Billroth II

28. Billroth I Distal portion of the stomach is removed The remainder is anastomosed to the duodenum

29. Billroth II The lower portion of the stomach is removed and the remainder is anastomosed to the jejunum

30. Postoperative Care NG tube – care and management Monitor for post-operative complications

31. Post-op Complications Bleeding Occurs at the anastomosed site First 24 hours and post-op days 4-7 Duodenal stump leak Billroth II Severe abdominal pain Bile stained drainage on dressing Gastric retention WILL NEED TO PUT NG TUBE BACK IN Dumping Syndrome . Prevalent with sub total gastrostomies Early-30 minutes after meals Vertigo, tachycardia, syncope, sweating, pallor, palpitations Late – 90 min-3 hours after meals Rx: Decrease CHO intake, Eat slowly, Avoid fluids during meals, Increase fat, Eat small, frequent meals Anemia Rapid gastric empyting decreases absorption of iron Malabsorption of fat Decreased acid secretions, decreased pancreatic secretions, increased upper GI mobility

32. SUMMARY H. pylori is the most common cause of PUD and is a risk factor for gastric cancer H Pylori eradication reduces risk of disease recurrence Test-and-Treat strategy is recommended for patients with undifferentiated dyspepsia Intial evaluation with endoscopy is recommended for those with alarm symptoms or those failing treatment Optimum treatment regimens are 14d multidrug with antibiotics and acid suppressants(Triple therapy)

33. PREVENTION Avoid NSAIDs: Use alternative pain relief methods when possible or use with a PPI or misoprostol for protection. Treat H. pylori Infection: Prompt diagnosis and treatment of H. pylori can prevent recurrence. Healthy Lifestyle: Avoid smoking, excessive alcohol consumption, and maintain a balanced diet. Regular Monitoring: For patients with recurrent symptoms or high-risk factors, routine monitoring and follow-up endoscopy may be recommended. Stress Management: Although not a direct cause, managing stress can help reduce exacerbation of symptoms.