Peptic ulcer diseases-2.pptx444444444444

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1. Peptic Ulcer Disease PRESENTATION: INTERNAL MEDICINE: GROUP 3 LECTURERS:DR. SHERIFF AND DR.MARTIN

2. Mohamed lahai marrah (Leader)…..22065 Mohamed Adams jalloh ……………..22027 Bandatin wilem conteh ………………22014 Marian muyo kanu ……………………22051 Kelfala hassan dawoh ………………..22019 Foray kondeh ………………………….22056 Mohamed Alieu jalloh ………………..22026 GROUP MEMBERS

3. Definition of peptic ulcer. Location and symptoms. Types. Etiology. Pathophysiology and pathogenesis Signs & symptoms Complications ,diagnostic studies and treatment. Precautions. Aims:

4. Peptic ulcer disease (PUD) refers to ulceration of the mucosa anywhere in the GI tract exposed to acid and pepsin. Ulcers  : breaks in the mucosal surface >5 mm, with depth to the sub-mucosa . They can range in size from a few millimeters to a few centimeters The 2 most common forms/locations of PUD are Duodenal ulcer Gastric ulcer Site Lower esophagus Stomach Duodenum Introduction

5. 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.

6. Defensive Bicarbonate Mucus layer Prostaglandins Mucosal blood flow Epithelial renewal Aggressive Helicobacter pylori NSAIDs Pepsins Bile acids Smoking and alcohol PATHOPHYSIOLOGY

7. Location of peptic ulcer: Ulcer may be found : In oesophagus , stomach, duedonum jejunum at multiple levels ( Zollinger Ellison syndrome).

8. Acute Superficial erosion Minimal erosion Chronic Muscular wall erosion with formation of fibrous tissue Present continuously for many months or intermittently Types

9. Common causes of PUD Helicobacter pylori ( H.pylori ) infection Nonsteroidal Anti-inflammatory Drugs (NSAIDs) Critical illness (stress-related mucosal damage ) Uncommon causes of PUD Idiopathic (non- H.pylori , non- NSAID) Hypersecretion of gastric acid (e.g. Zollinger Ellison syndrome) Viral infections Radiation therapy Chemotherapy Etiology

10. Helicobacter pylori (HP) is a spiral shaped, gram negative, flagellated bacteria first associated with PUD in the early 1980’s Found in most people with duodenal and gastric ulcers About 95% of those with duodenal ulcers About 80% of those with gastric ulcers HP is primarily spread through the fecal to oral route Oral – oral routes Through contaminated food and water People are most often infected during childhood Helicobacter pylori

11. Mechanisms by which HP causes mucosal injury are not entirely clear but occurs through a combination of the following mechanisms: HP catalyzes urea  ammonia is produced  ammonia erodes the mucous barrier and causes epithelial damage HP produces cytotoxins HP produces mucolytic enzymes PATHOGENESIS

12. In long-term NSAID users, there is a 10% - 20% prevalence of gastric ulcers and a 2% - 5% prevalence of duodenal ulcers Mechanisms for NSAID-induced ulceration NSAIDs are weak acids and are non-ionized at gastric pH Diffuse freely across the mucous barrier into gastric epithelial cells  H + ions are liberated and cause cellular damage Aspirin is the most ulcerno-genic of all NSAIDs. Even with low dose aspirin (81-162mg/day), ulcers occur in 0.6% - 1.2% of patients per year NSAIDs

13. NSAIDs inhibit cyclooxygenase activity and therefore decrease prostaglandin production which results in a: Reduction in gastric and mucosal blood flow Decrease in mucous and bicarbonate secretion Decrease in cellular repair and replication

14. ZES is characterized by gastric acid hypersecretion and recurrent peptic ulcers that result from a gastrin -producing tumor More than 50% of gastrinomas are malignant ZES is suspected for patients with multiple ulcers and recurrent or refractory PUD often accompanied by esophagitis or ulcer complications Only accounts for 0.1% to 1% of those with duodenal ulcer Zollinger Ellison Syndrome

15. Cigarette smoking Impairs ulcer healing and increases the risk of recurrence Psychological stress Stress may induce behavioral risks such as smoking and the use of NSAIDs or may alter the inflammatory response or resistance to HP infection Dietary factors Certain foods (e.g. coffee, tea, carbonated beverages, beer, milk, spices) may cause dyspepsia but do not increase the risk of developing PUD Other factors

16. Signs &Symptoms Abdominal discomfort usually occurs in epigastric area (upper middle part of the abdomen) radiating to the back described as: dull gnawing ache comes and goes for several days pain may increase when the stomach is empty at night or half to three hours after meal. Pain is relieved by eating & antacid medication. Weight change Fatigue Bloating Chest pain Burping Nausea and Anorexia (common with gastric ulcer ) Vomiting (relieves episodes of severe pain due to evacuation of gastric acid content). Heart burn

17. Emergency symptoms: If you have any of these symptoms call your doctor right away: Sharp sudden persistent abdominal pain. Bloody or black stools. Bloody vomit or vomit that looks like coffee grounds . Dysphagia They could be signs of a serious problem such as: Perforation when the ulcer burrows through the stomach or duodenal wall.

18. Less common than duodenal ulcers Especially in chronic NSAID use Most commonly located in the lesser curvature of the antrum of the stomach More common in people greater than 60 years old Characterized by A normal to low secretion of gastric acid Back diffusion of acid is greater (chronic ) Critical pathologic process is amount of acid able to penetrate mucosal barrier H pylori is present in 50% to 70% Drugs --- Aspirin, corticosteroids, N SAIDs, reserpine , Chronic alcohol abuse, chronic gastritis Gastric Ulcers

19. Most common form of PUD It is 3 times more common than gastric ulcers Usually located in the duodenal bulb of the small intestine Most commonly occurs in people between the ages of 30 and 50 Associated with ↑ HCl acid secretion H.pylori associated in 9 0- 9 5 % of cases Diseases with ↑risk of duodenal ulcers COPD, cirrhosis of liver, chronic pancreatitis, hyperparathyroidism, chronic renal failure Duodenal Ulcers

20. 3 major complications Hemorrhage - 15% of patients with active PUD Perforation - 7% of patients with active PUD Gastric outlet obstruction Initially treated conservatively May require surgery at any time during course of therapy Complications

21. The second most common ulcer – related complications is perforation( occur in 6-7% of PUD patients) Dus tend to penetrate posteriorly in to the pancrease , leading to pancreatitis, whereas Gus tend to penetrate in to the left hepatic lobe. perforation

22. Gastric outlet obstruction is the least common ulcer-related complications,occuring in 1-2% of patients Gastric outlet obstruction

23. Endoscopy procedure Determines degree of ulcer healing after treatment Tissue specimens can be obtained to identify H. pylori and to rule out gastric cancer Tests for H.pylori Noninvasive tests Serum or whole blood antibody tests Immunoglobin G (I g G) Urea breath test C 14 breath test Fecal antigen test Invasive tests Biopsy of stomach Rapid urease test Diagnostic Studies

24. The urea breath and fecal antigen tests may be falsely negative in patients who have recently taken Antibiotics (up to 4 weeks) Bismuth compounds (up to 4 weeks) Antisecretory agents (up to 2 weeks)

25. Barium contrast studies Widely used X- ray studies Ineffective in differentiating a peptic ulcer from a malignant tumor

26. Medical regimen consists of Adequate rest Dietary modification Drug therapy Elimination of risk factors Long-term follow-up care Treatment

27. Antacids H 2 receptor blockers PPIs Antibiotics Anticholinergics Cytoprotective therapy Drug Therapy

28. Histamine receptor blocks (H 2 R blockers)- famotidine,cimetidine Used to manage peptic ulcer disease Block action of histamine on H 2 receptors ↓ HCl acid secretion ↓ conversion of pepsinogen to pepsin ↑ ulcer healing Proton pump inhibitors – pantoprazole , rabeprazole Block ATPase enzyme that is important for secretion of HCl acid Antibiotic therapy Eradicate H. pylori infection No single agents have been effective in eliminating H. pylori

29. Antacids – calcium carbonate, MgOH Used as adjunct therapy for peptic ulcer disease ↑ gastric pH by neutralizing acid Anticholinergic drugs- Dicyclomine Occasionally ordered for treatment ↓ cholinergic stimulation of HCl acid Bismuth preparations Agents Bismuth subsalicylate Bismuth exhibits antimicrobial activity against bacterial and viral gastrointestinal pathogens

30. Standard triple therapy regimen contains Amoxicillin 1000mg twice day + Clarithromycin 500mg twice a day + a PPI dosed once to twice a day Given for 10 to 14 days 14 day regimens are generally preferred as 14 day regimens significantly increases the eradication rate Bismuth-based quadruple-therapy contains Tetracycline 500mg 4 times day +Metronidazole 250-500mg 2/3 times a day + Bismuth subsalicylate 525mg 4 times a day + a PPI once or twice a day OR H 2 -receptor antagonist twice a day

31. When symptoms, ulcers, or both persist beyond 8 to 12 weeks despite conventional treatment as previously described or when several courses of H. pylori eradication therapy fail Patient should undergo an upper endoscopy to assess the situation Treatment depends on cause and may include additional H. pylori eradication attempts, higher PPI dosages, or surgery Refractory Ulcers

32. Dietary modifications may be necessary so that foods and beverages irritating to patient can be avoided or eliminated Protein considered best neutralizing food Stimulates gastric secretions Carbohydrates and fats are least stimulating to HCl acid secretion Do not neutralize well Nutritional therapy

33. < 20% of patients with ulcers need surgical intervention Indications for surgical interventions Intractability History of hemorrhage, ↑ risk of bleeding Prepyloric or pyloric ulcers Multiple ulcer sites Drug-induced ulcers Possible existence of a malignant ulcer Obstruction Surgical Treatment

34. Surgical procedures Gastroduodenostomy Gastrojejunostomy Vagotomy Pyloroplasty

35. A. Billroth I Procedure B. Billroth II Procedure

36. Thank you all