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PEPTIC ULCER DISEASE

PUD: definition. BREAK IN THE GASTROINTESTINAL MUCOSA EXPOSED TO GASTRIC ACID and PEPSIN MORE THAN 5 mm in diameter.MAY BE ACUTE OR CHRONIC.. EROSION . A BREAK IN THE GI MUCOSA LESS THAN 5 mm IN DIAMETER - NOT PENETRATING MUSCULARIS MUCOSA MAY OCCUR IN ACID SECRETING AND NON- ACID SECRETI

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PEPTIC ULCER DISEASE

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    1. PEPTIC ULCER DISEASE Dr Niazy Abu Farsakh

    2. PUD: definition BREAK IN THE GASTROINTESTINAL MUCOSA EXPOSED TO GASTRIC ACID and PEPSIN MORE THAN 5 mm in diameter. MAY BE ACUTE OR CHRONIC.

    3. EROSION A BREAK IN THE GI MUCOSA LESS THAN 5 mm IN DIAMETER - NOT PENETRATING MUSCULARIS MUCOSA MAY OCCUR IN ACID SECRETING AND NON- ACID SECRETING MUCOSA PERISTALSIS NOT AFFECTED HEALS RAPIDLY.

    4. Sites of PUD PUD may occur in any area where acid and pepsin are present Commonest sites: Duodenum especially first part “duodenal bulb” Stomach especially over lesser curve Other sites: Lower end of esophagus site of gastro -jejunal anastomosis Opposite to Meckel’s diverticulm

    5. AETIOLOGY OF PUD HELICOBACTER PYLORI- ASSOCIATED ULCERS NSAID-RELATED ULCERS. HYPERSECRETORY STATES: Z-E SYNDROME, IDIOPATHIC.

    6. Pathogenesis of PUD IMBALANCE BETWEEN AGGRESIVE AND DEFENSIVE FACTORS

    7. AGGRESSIVE FACTORS ACID AND PEPSIN

    8. MECHANISMS OF ACID SECRETION NERVOUS ENDOCRINOLOGICAL Gastrin PARACRINOLOGICAL GRP: increase secretion of acid Somatostatin: decreases secretion of acid Histamine : stimulates secretion of acid

    9. Role of Acid in PUD NEVER found when maximum acid output "MAO" is less than 10 mmol/hour RARE when MAO below 20 mmol/h COMMON with higher MAO rates NOT seen when fasting gastric pH is above 2.5

    10. DEFENSIVE FACTORS PROSTAGLANDINS MUCOSAL BLOOD FLOW MUCUS GEL LAYER HCO3 EPITHELIAL JUNCTIONS REGENERATION OF THE EPITHELIAL LAYER GROWTH FACTORS: EGF

    11. Epidemiology of PUD Prevalence about 5-10% Varies in different communities Higher prevalence in low socioeconomic classes and with certain diseases DU more in males: M/F: 3:1 GU equal in both sexes but increases with age FAMILY HISTORY: 3-4 increased risk . CIGARETTE SMOKING: ulceration increased EMOTIONAL DISTURBANCES and STRESS: increase gastric acid secretion

    12. CLINICAL PICTURE OF PUD Symptoms of PUD: Epigastric pain dyspepsia may be asymptomatic symptoms related to complications Signs: epigastric tenderness signs related to complications

    13. Diagnosis of PUD Clinical picture is suggestive but not diagnostic Diagnosis best by endoscopy Barium meal less helpful no role for serum gastrin or gastric acid studies in usual ulcers, indicated if ZE is suspected Evaluation for H pylori infection Gastric ulcer should be biopsied to exclude malignancy

    14. Radiology in PUD

    15. Endoscopy in PUD: GU

    16. Ulcer

    17. Gastric erosions

    18. Gastric erosions

    19. Erosive duodenitis

    20. Erosion

    21. Duodenal ulcer

    22. Duodenal ulcer

    23. Duodenal ulcer

    24. Helicobacter pylori

    25. Role of H.pylori in GI diseases Healthy subjects 20-50% Chronic active gastritis 100% Duodenal ulcer >90% Gastric ulcer 50 - 80% Gastric adenocarcinoma 90% Gastric lymphoma 85%

    26. Diagnosis of Helicobacter pylori infection Invasive( through endoscopy) Gastric biopsy and staining culture of Bx specimen Tests using urease enzyme in Bx specimens Non-invasive: Urea breath test H.pylori antibodies Stool antigen Salivary antigen

    27. Complications of PUD Hemorrhage Perforation Gastric outlet obstruction penetration in posterior ulcers

    28. GI Bleeding

    29. GI Bleeding

    30. Ulcer with recent bleed

    32. Gastric outlet obstruction

    33. Natural history of PUD PUD is a chronic episodic disease with relapses and remissions. If left untreated, 30-40 % of ulcers heal within 8 weeks. Recurrence rate without treatment is 70% during first year and 90% within 2 years. Complications develop in 20% of PUD

    34. TREATMENT OF PEPTIC ULCER DISEASE AIM OF TREATMENT: RELIEVE SYMPTOMS HEAL THE ULCER PREVENT COMPLICATIONS PREVENT RECURRENCES

    35. Life-style modification in PUD Doubtful efficacy REST RELAXATION GOOD SLEEP DIET: bland diet freuent small meals caffeine-containing beverages role of milk fat diet spices alcohol fiber vitamin E and dietary fatty acids

    36. HISTAMINE- RECEPTOR ANTAGONISTS (H2-Blockers ) CIMETIDINE 400mg b.d or 800mg at bed time RANITIDINE 150mg b.d. or 300mg at bed time FAMOTIDINE 20mg b.d. or 40mg at bed time NIZATIDINE 150mg b.d. or 300mg at bed time

    37. HISTAMINE- RECEPTOR ANTAGONISTS (H2-Blockers ) Act through blocking H2 receptors in the parietal cells Suppress nocturnal acid secretion by more than 90% Suppress 24 hour acid secretion by 50-70% Side effects : CNS effects: headache, mental confusion Reversible gynecomastia and impotence. Interaction with drugs metabolized through hepatic cytochrome P-450 microsomal enzymes

    38. ANTACIDS Rapid symptomatic relief Cheap Large amounts are required to heal ulcers leading to undesirable side effects. If taken on empty stomach; they are effective only for 10-20 minutes If taken one hour after meals they are effective for 2-3 hours. Tablet preparations are less effective than suspensions

    39. Side effects of antacids Sod bicarbonates: increases sodium load milk- alkali syndrome Aluminum compounds: constipation binds phosphates binds drugs.

    40. Side effects of antacids Magnesium compounds: diarrhea accumulation in renal failure Calcium compounds: constipation rebound hyperacidity

    41. PROTON PUMP INHIBITORS(PPIs) Suppress acid secretion by non-cometitively and irreversibly inhibiting the H+ , K+- ATPase of the gastric parietal cells Inhibit over 90%of 24-hour acid secretion Increase secretion of gastrin usually 2-3 times the baseline with proliferation and growth of ECL cells No carcinoid tumours reported to occur in man due to PPIs Heal 50% of DUs by 2 weeks, 90% in 4 weeks and almost all by 6-8 weeks.

    42. PROTON PUMP INHIBITORS(PPIs) Omeprazole: 10, 20 mg lansoprazole: 15, 30 mg pantoprazole: 20, 40 mg rabeprazole: 10, 20 mg esomeprazole:20, 40 mg Tenatoprazole: 40 mg: longer duration of action

    43. New Therapies Potasium competetive acid blockers: P-CAB: Block secretion of acid by blocking exchange of K+ by H+: still investigational AZD0865

    44. Eradication therapy for H.Pylori In vitro HP highly suggestive to many antibiotics In vivo, sensitive to the following agents: amoxycillin tetracyclin clarithromycin Metronidazole, tinidazole bismuth PPIs Second line drugs: Levofloxacin, gatifloxacin, rifabutin

    45. Eradication therapy for H.Pylori Use triple or quadruple regimen for 7-14 days. Efficacy of the regimen depends upon drugs used, compliance of patient, resistance pattern of HP in the area Relapse rate drops to less than 10% per year after successful eradication

    46. SUCRALFATE 1gm 4 times daily on empty stomach Healing rate: 70-80% within 8 weeks binds with the proteinaceous base of the ulcer increasing local mucosal production of PGs Side effects: constipation nausea reduces the absorption of some drugs binds phosphate in the gut

    47. PROSTAGLANDINS Inhibit gastric acid secretion and has cytoprotective effects They are less effective than H2- blockers side effects: abdominal cramps diarrhea not cost-effective Indicated for prophylactic use rather than for treatment

    48. Surgery for PUD Rare after introduction of effective therapeutic agents except for complications

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