1. PEPTIC ULCER DISEASE Dr RAMBABU POPURI MD MD Asst. Professor Dept of General medicine Dept of General medicine

2. Definition A circumscribed ulceration of the gastrointestinal mucosa occurring in areas exposed to acid and pepsin and most often caused by Helicobacter pylori infection. A circumscribed ulceration of the gastrointestinal mucosa occurring in areas exposed to acid and pepsin and most often caused by Helicobacter pylori infection. More than 5mm in size More than 5mm in size Depth to the sub mucosa. Depth to the sub mucosa.

3. Peptic Ulcers: Gastric & Dudodenal

4. Comparing Duodenal and Gastric Ulcers

5. Pathogenesis of Ulcers Aggressive Factors H. pylori H. pylori Drugs (NSAIDs) Drugs (NSAIDs) acid, pepsin acid, pepsin Bile salts Bile salts Defensive Factors Mucus, bicarbonate layer Mucus, bicarbonate layer Blood flow, cell renewal Blood flow, cell renewal Prostaglandins Prostaglandins Phospholipid Phospholipid Therapy is directed at enhancing host defense or eliminating aggressive factors; i.e., H. pylori.

6. Risk factors for PUD High dose of NSAIDs High dose of NSAIDs Multiple NSAIDs Multiple NSAIDs Concomitant use of glucocorticoids &anticoagulants Concomitant use of glucocorticoids &anticoagulants Cigarette smoking Cigarette smoking Alcohol consumption Alcohol consumption

7. Genetic predisposition Blood group O –for DU Blood group O –for DU Blood group A –for GU Blood group A –for GU Psychological stress contribute to PUD Psychological stress contribute to PUD

8. Chronic disorders asso with PUD Systemic mastocytosis Systemic mastocytosis Chronic pulmonary disease Chronic pulmonary disease Chronic renal disease Chronic renal disease Cirrhosis Cirrhosis Nephrolithiasis Nephrolithiasis Hyperparathyroidism Hyperparathyroidism CAD CAD Polycythemia vera Polycythemia vera Chronic pancreatitis Chronic pancreatitis

9. Helicobacter pylori and peptic ulcer disease.

10. It has been more than 20 years since H Pylori first isolated from human stomach. More than the half of worlds population are infected (60% - 70%). Only 15% of H Pylori infected patients will develop symptomatic PUD.

11. Helicobacter pylori and peptic ulcer disease. H Pylori is now recognized as a major etiological factor of PUD: 90% of duodenal ulcers (DU) and 70% of gastric ulcers (GU) are associated with H Pylori. NSAIDs/ aspirin remain the second etiology of PUD.

12. Helicobacter pylori and peptic ulcer disease. The description of H.pylori was a major breakthrough in Gastroenterology. The recognition of H.pylori as a major pathogen changed the common beliefs about peptic ulcer disease Schwarz’s dictum: NO ACID NO ULCER has become: NO H.pylori NO ULCER.

13. Helicobacter pylori and peptic ulcer disease. H.pylori induced effects are related to distribution of gastritis H.pylori induced effects are related to distribution of gastritis H.pylori associated antral gastritis induces increased acid secretion. H.pylori associated antral gastritis induces increased acid secretion. H.pylori associated corpus gastritis induces reduced or even absent acid secretion. H.pylori associated corpus gastritis induces reduced or even absent acid secretion. Pangastritis induces no overall change in acid production. Pangastritis induces no overall change in acid production.

14. Helicobacter pylori and peptic ulcer disease. Diagnosis: Invasive methods (require endoscopy): HE stain, modified Giemsa stain, rapid urease test Non-invasive methods: serology (ELISA), 13 C or 14 C urea breath test, stool antigen test.

15. Helicobacter pylori and peptic ulcer disease.

16. H.pylori exerts several effects on gastric acid production H.pylori exerts several effects on gastric acid production Increase in basal gastrin levels. Increase in basal gastrin levels. Increase in basal acid output. Increase in basal acid output. Increase in peak acid output. Increase in peak acid output. All effects are reversed after successful eradication of H.pylori. All effects are reversed after successful eradication of H.pylori.

17. Treatment Plan: H. Pylori Medications: Triple therapy for 14 days is considered the treatment of choice. Medications: Triple therapy for 14 days is considered the treatment of choice. Proton Pump Inhibitor + clarithromycin and amoxicillin Proton Pump Inhibitor + clarithromycin and amoxicillin Can substitute Flagyl 500 mg PO bid for 14 d if allergic to PCN Goal: complete elimination of H. Pylori. Once achieved reinfection rates are low. Compliance ! Goal: complete elimination of H. Pylori. Once achieved reinfection rates are low. Compliance !

18. Signs and Symptoms of PUD Can be symptomatic Can be symptomatic anorexia, nausea, vomiting, belching, bloating, heartburn, epigastric pain (pain in the upper abdomen) anorexia, nausea, vomiting, belching, bloating, heartburn, epigastric pain (pain in the upper abdomen) awakened at night (usu. around 3am) awakened at night (usu. around 3am) duodenal ulcers duodenal ulcers epigastric pain, tenderness, burning, gnawing, aching between xiphoid process and belly button epigastric pain, tenderness, burning, gnawing, aching between xiphoid process and belly button relieved with food intake or antacids relieved with food intake or antacids gastric ulcer gastric ulcer diffuse pain over midepigastrium (midstomach) diffuse pain over midepigastrium (midstomach) worsened by food worsened by food

19. Signs and Symptoms, cont. Can also be asymptomatic Can also be asymptomatic “silent ulcer” “silent ulcer” associated with chronic NSAID use associated with chronic NSAID use

20. Complications of PUD Bleeding-15% Bleeding-15% vomited blood or black material that looks like coffee grounds vomited blood or black material that looks like coffee grounds red blood in stool usu. indicates hemorrhoids red blood in stool usu. indicates hemorrhoids if stool black or tarry, foul smelling, usu. doesn’t involve the rectum area  PUD if stool black or tarry, foul smelling, usu. doesn’t involve the rectum area  PUD the elderly can bleed w/o any prior symptoms the elderly can bleed w/o any prior symptoms Perforation, penetration -6to7% Perforation, penetration -6to7% gastric outlet obstruction-2% gastric outlet obstruction-2%

21. Physical examination Epigastric tenderness Epigastric tenderness Tachycardia & orthostatic hypotention Tachycardia & orthostatic hypotention Severly tender & board like abdomen Severly tender & board like abdomen Succusion splash- GOO-2% Succusion splash- GOO-2%

22. Diagnosis Barium meal study Barium meal study Endoscopy –most sensitive & specific Endoscopy –most sensitive & specific DD: DD: NUD NUD Proximal GI tumors Proximal GI tumors GERD GERD Biliary colic Biliary colic Chronic pancreatitis Chronic pancreatitis

23. Treatment of PUD ACID NEUTRALISING AGENTS ACID NEUTRALISING AGENTS Mg(OH)2,Al(OH)3,CaCO3,NaHCO3 Mg(OH)2,Al(OH)3,CaCO3,NaHCO3 ACID SUPPRESSING DRUGS ACID SUPPRESSING DRUGS H2 Blokers H2 Blokers PPI PPI CYTOPROTECTIVE AGENTS CYTOPROTECTIVE AGENTS Sucralfate Sucralfate Colloid bismuth subcitrate Colloid bismuth subcitrate PGE1 analogue- misoprostole 200mcg qid PGE1 analogue- misoprostole 200mcg qid

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