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Peptic Ulcer
This document summarizes a seminar on peptic ulcer disease. It defines peptic ulcers, classifies them as acute or chronic, and discusses their etiology, including H. pylori infection and stress factors. It covers the pathogenesis of ulcers, clinical features, diagnosis including tests for H. pylori, and treatment using proton pump inhibitors, H2 receptor antagonists, and antibiotics. It also discusses complications, factors affecting treatment success, adverse drug reactions, drug interactions, and patient counseling.
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Seminar introduction on Peptic Ulcer Disease led by Walid S Momin from Pharmacy Practice.
Peptic ulcers are mucosal degeneration areas in the gastrointestinal tract exposed to acid.
Peptic ulcers classified into acute (multiple small erosions) and chronic (gastric or duodenal).
Peptic ulcer etiology includes stress, H-Pylori infection, medications, and various irritants.
H-Pylori infection can lead to gastritis and ultimately peptic ulcers.
Details on acid secretion mechanisms and factors in the pathogenesis of peptic ulcers.
Pain occurring 1-3 hours after meals, anorexia, nocturnal pain, and potential nausea.
Diagnosis of H-Pylori through non-invasive tests, invasive techniques, and biopsy methods.
Techniques for visualizing erosions and bleeding sites, including barium contrast studies.
Non-pharmacological approaches and pharmacological therapy classification for ulcers.Risks of bleeding ulcers and late complications requiring treatments like somatostatin.
Guidelines for monitoring H-Pylori treatment, patient education, and prevention strategies.
Factors contributing to unsuccessful eradication include patient compliance and antibiotic resistance.
Side effects of various treatments including PPIs, H2 antagonists, and their clinical implications.
Key references for further reading on pharmacotherapy and clinical management of ulcers.
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Peptic Ulcer
- 1. SEMINAR ON PEPTICULCER DISEASE PRESENTED BY : WALID S MOMIN 1ST YEAR M.PHARM DEPARTMENT OF PHARMACY PRACTICE
- 2. Definition : Pepticulcers are the areas of degeneration and Necrosis of gastrointestinal mucosa exposed to acid-peptic secretions. The term peptic ulcer describes a condition in which there is a discontinuity in the entire thickness of the gastric or duodenal mucosa that persists in the gastric juice. Peptic ulcer is usually represented as
- 3. CLASSIFICATION OF PEPTIC ULCERS Acute or stress ulcers : Multiple, Small mucosal erosions. Chronic ulcers: Gastric or Duodenal ulcers.
- 4. ETIOLOGY Occurs dueto imbalance between the aggressive and defensive factors. Etiological factors of Acute ulcers : A. Psychological stress B. Physiological stress Shock Severe trauma Drugs and Local irritants Cushing’s syndrome
- 5. Chronic ulcerdisease : Multifactoral, the main contributing factor is the H-Pylori infection. Acid-pepsin secretions Mucus secretion Gastritis Local Irritants Dietary factors Psychological factors Genetic factors Hormonal factors Miscellaneous factors
- 6. Viral Infections(cytomegalovirus) Radiation Chemotherapy ( e.g. hepatic artery infusions) Idioathic Vascular insufficiency Cigarette smoking
- 7. Infection •H-Pylori Infection Few months •Chronicsuperficial gastritis Years •Hyperacidity Mucosal layer erosion •Peptic ulcer
- 8. MECHANISM OF PEPTICACID SECRETION
- 9.
- 12. H-Pylori containsenzymes like urease, protease, catalase, phospholipase which damage the mucosal barrier. Basal and Maximal acid output due to various stimuli. Vagal stimulation Gastric Ulcer : Impaired gastric mucosal defenses against acid-pepsin secretions. Pathogenesis : serum gastrin levels due to ingested food leading to hyperacidity.
- 13. OTHER SUGGESTED PATHOGENESIS Acidsecretion because of parietal cell mass. Inhibition of gastric acid secretion. Hco3 - secretion in the duodenum due to H-Pylori infection causing local release of cytokins and further damage.
- 14. NSAIDS inducedpeptic ulcer : NSAIDS COX inhibition Adherence of leucocytes to mucosal endothelial cells Decreased prostagland in synthesis Superficial erosions Peptic ulcer
- 15. A numberof other factors may contribute to the development of NSAID induced mucosal injury, neurtophils adherence may damage vascular endothelium and cause reduced mucosal blood flow or may release oxygen derived free radicals and proteases. Leukotriens have stimulatory effect on neutrophils adherence. Topical irritant properties associated with the acidic properties of NSAID’s e.g. aspirin and their ability to decrease hydrophobicity of mucosal gel layer
- 16. CLINICAL FEATURES Epigastricpain Upper abdominal pain occurring 1-3 Hrs after meals and relieved by food or antacids is a classical symptom of peptic ulcer disease. Anorexia, weight loss. A typical nocturnal pain that awakens the patient from sleep. Heart burn due to acid regurgitation. Nausea may accompany the pain.
- 17. DIAGNOSIS Diagnosis ofH-Pylori infection . Non-Invasive techniques: A. Urea breath test B. Serological tests C. Stool test • Invasive techniques A. Rapid urease test B. Culture C. Histology
- 18. 13C Ureabreath test : used to demonstrate eradication of organism following treatment.
- 19. Serological test: used to detect antibodies Used in diagnosis and epidemiological studies. Stool test : Immunoassay using monoclonal antibodies for qualitative detection of H-Pylori that leads to colour change that can be detected visually or by spectrophotometer. Used in the diagnosis and monitoring efficacy of eradication therapy. Culture : Biopsies cultured on a special medium Enables sensitivity testing to determine optimum treatment or antibiotic resistance. Histology : Gastric mucosal staining, helps in the
- 20. Biopsies aredone to exclude malignancy and uncommon lesions such as crohn’s disease. Wireless capsule endoscopy : determines NSAIDS induced ulceration of small intestine. Use of gastrograffin meal: Gastrografin (Diatrizoate Meglumine and Diatrizoate Sodium Solution) is a iodinated radiopaque contrast medium for oral or rectal administration only.
- 21. Rapid ureasetest : Gastric biopsies with urea solution containing phenol Urea ammonia P H Rapid colour change
- 22. OTHER DIAGNOSTIC TESTS Esophagogastroduodenoscpy : permits direct visualization of superficial erosions and sites of active bleeding. Routine single barium contrast techniques : Fasting serum concentration studies :
- 24. TREATMENT AND MANAGEMENT Nonpharmacological therapy : I. Reduce psychological stress II. Reduce physical stress III. Cessation of cigarette smoking IV. Stop use of NSAIDS V. Avoid spicy foods, caffeine, alcohol VI. Drink plenty of water VII. Avoid fasting and maintain optimum gap between meals
- 25. Pharmacological Therapy Classificationof Drugs: 1. Proton Pump Inhibitors : e.g. omeprazole, pantaprazole,Lansoprazole. 2. H2receptor antagonists : e.g. Ranitidine, Famotidine, cimetidine 3. Sucralfate 4. Bismuth compounds 5. Antacids : systemic e.g. Sodium bicarbonate, Non Systemic e.g. Magnesium Trisilicate. 6. Prostaglandin Analogs : e.g. misoprostol, Enprostil. Anti H-Pylori drugs (Antibiotics) e.g. Amoxicillin, clarythromycin, tetracyclines.
- 26. Proton Pump Inhibitors Carried in bloodstream to the parietal cells Activation Cytosol ESCInhibition of H+ K+ ATPase Inhibit acid secretion
- 27. PPI’s differin their in their potencies. Plasma concentration is reached after 2-3 hrs. T1/2 48 Hrs. To be taken 30 minutes prior to food. 2. H2receptor antagonists : Structural analogs of histamine. pepsinogen pepsin Used in symptomatic treatment. Plasma concentration is reached within 1-3Hrs after administration. Recommended in patients with nocturnal gastric acid secretion and management of dyspepsia symptoms. ( )
- 28. Sucralfate :Basic aluminium salt of sulfated sucrose Polymerizes at pH < 4.0 by cross linking of molecules Gel Adheres to the ulcer base Precipitates surface proteins and acts as a physical barrier Antacids are contraindicated when sulfates are taken
- 29. Prostaglandin Analogs:cytoprotective properties 1. Increase mucus and bicarbonate production. 2. Increase mucosal blood flow 3. Inhibit gastrin production Antacids : ANC--- No of Meq of 1N Hcl that are brought to pH 3.5 in 15 minutes by unit dose of antacid preparation. Mgsio3 Cl- salt Cl- + HCo3 - No acid-base disturbance
- 30. COMPLICATIONS OF PEPTICULCER DISEASE BLEEDING PEPTIC ULCER : Patients with high risk of bleeding are given high dose of infusion of omeprazole ( 80 mg bolus followed by 8mg/Hr) for 72 Hrs to reduce rebleeding. LATE COMPLICATIONS OF PEPTIC ULCER: Reactive hypoglycaemia, diarrhoea, weight loss, anaemia, flushing, plapitation, sweating tachycardia, postural hypotension.
- 31. Treatment : Somatostatin analogs for reactive hypoglycaemia. Antibiotics metachlopramide Zollinger-ellison syndrome: use of octreotide, surgical.
- 32. Recommendations for Treatingand Monitoring Patients with Helicobacter pylori (HP)-Associated and Nonsteroidal Anti-inflammatory Drug (NSAID)-Induced Ulcers Assess patient allergies Assess patient use of alcohol or alcohol-containing products with metronidazole and oral birth control medications with antibiotics and counsel appropriately. Inform the patient of change in stool color when bismuth salicylate is included in an HP eradication regimen. Assess and monitor patients for potential adverse effects. Assess and monitor patients for potential drug interactions. Monitor patients for salicylate toxicity.
- 33. o Provide educationto patients who are receiving HP eradication therapy, including why antibiotic and antiulcer combinations are used, when and how to take medications, adverse effects, alarm symptoms, when to contact their health care provider, and the importance of compliance to drug treatment. NSAID-induced ulcer Recommend drug treatment Assess risk factors for NSAID-induced ulcers and ulcer-related complications, and when indicated recommend appropriate strategies for reducing ulcer risk. Assess and monitor patients for potential drug interactions and adverse effects (especially misoprostol).
- 35. FACTORS THAT CONTRIBUTETO UNSUCCESSFUL ERADICATION Poor Patient compliance Resistant organisms Increased bacterial load Missed dose in a 7 day regimen may also contribute towards failure of eradication. Tolerability Preexisting antimicrobial resistance.
- 36. ADVERSE DRUG REACTIONS Proton pump inhibitors : 1. Diarrhea 2. Headache 3. Abdominal pain 4. Nausea and vomiting 5. Microscopic colitis H2receptor antagonists : 1. Anti-androgeniceffects gynaecomastia. 2. Impotence
- 37. Bismuth chelate: 1.Neurotoxicity Sucralfate : 1. Constipation 2. Hypophosphataemia Prostaglandin analogs : 1. Diarrhea 2. Abdominal cramps 3. Uterine bleeding 4. Abortion Antacids : alkalosis, increase sodium load.
- 38. DRUG INTERACTIONS PPI’sare metabolised by cytochrome p450 isoenzymes,the affinity of individual proton pump inhibitors for these enzymes influence the incidence of clinically relevant drug interactions. E.g. omeprazole+warfarin warfarin levels. benzodiazepines + omeprazole benzodiazepines levels. PPI’s also alter the absorption of other drugs du to altered pH E.g. decreased absorption of Ketoconazole increased absorption of Digoxin Cimetidine interacts with Thiophylline, Diazepam, Flurazepam, Triazolam. All acid suppressing drugs decrease absorption of pH dependent control release tablets. Antacids interact with tetracyclines, ciprofloxacin forming insoluble complexes or chelates.
- 39. PATIENT COUNSELING Weightloss Avoid spicy foods Avoid hot beverages Maintain optimum time interval between meals Reduce psychological stress Reduce physical stress Cut off irregular eating habits Educate the patient about the current principles of therapeutic management Patient should be warned about the specific side effects to be expected from the regimen and what to do if they experience any of these side effects. Avoid drugs e.g. TCA’s, CCB’s, Anticholinergics, NSAIDS.
- 40. References Pharmacotherapy byDipiro Clinical Pharmacy and Therapeutics by Roger Walker Pharmacology by K.D Tripati Clinical Medicine by Kumar and Clark Handbook of Pathology By Harsh Mohan