GI Pharmacology. Dr. Alia Shatanawi 5/4/2018
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1 GI Pharmacology Dr. Alia Shatanawi 5/4/2018
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3 Z Gastroenterol Mar;21 Suppl: [Effect of antacids on intestinal motility]. [Article in German] Wienbeck M, Erckenbrecht J, Strohmeyer G. Abstract Disturbances of gut motility occur frequently under a highdose antacid regimen. Typical sy
4 Three pathways control parietal cell acid secretion 1. Neural stimulation via vagus nerve 2. Endocrine stimulation via secreted gastrin 3. Paracrine stimulation via released histamine H+,K+ ATPase (proton pump) Parietal cell
5 Specificity of PPI Drug absorbed in small intestine and delivered to parietal cell through the blood. Drug is protonated and trapped in acidic canaliculi. Trapping of protonated drug within the acidic canaliculi next to target enzyme. Irreversible inhibition. Full inhibition with 2:1 ratio of drug: enzyme.
6 Specificity of PPI Drug is stable at neutral ph, destroyed at low ph. Intestine absorbs drug (past the stomach) as microencapsulation dissolves. If microencapsulation disrupted before swallowing, then drug will be destroyed in stomach. When stop drug treatment, requires 4-5 days for enzyme to return to full function.
7 Proton Pump Inhibitors, PPI(1990s) Very efficacious and safe drugs. Have a major role in PUD. Omeprazole (oral). Rabeprazole (oral). Lanzoprazole (oral and IV). Pantoprazole (oral and IV). Esmoprazole (oral and IV). Formulated as prodrugs which are released in the intestine. Immediate Release Suspension results in rapid response.
8 PPI Pharmacokinetics: They are lipophilic weak bases (pka 4-5). After intestinal absorption, they diffuse across lipid membranes into acidified compartments such as the parietal cell canaliculus. The prodrug becomes protonated and concentrated more than 1000-fold within the parietal cells. There, it undergoes a molecular conversion to the active form which covalently binds the H+/K+ ATPase enzyme and inactivates it.
9 PPI Pharmacokinetics: Rabeprazole and immediate release omeprazole have faster onsets of action. Should be given one hour before meal. Have short half lives but effect lasts for 24 hours due to irreversible inhibition.
10 PPI Pharmacodynamics: Inhibit both fasting and meal-stimulated secretion because they block the final common pathway of acid secretion (90-98% of 24-hour secretion).
11 Clinical Uses: PPI Gastroesophageal Reflux (GERD): They are the most effective agents in all forms of GERD and complications. Nonulcer Dyspepsia: Modest activity % more beneficial than a placebo.
12 PPI Stress- Related Gastritis: Oral immediate- release omeprazole administered by nasogastric tube. For patients without a nasoenteric tube, IV H 2 - antagonists are preferred because of their proven efficacy. Gastrinoma and other Hypersecretory Conditions: Usually high doses of omeprazole are used.
13 PPI Peptic Ulcer Disease: They heal more than 90% of cases within 4-6 weeks. H.pylori- associated ulcers: PPI eradicate H.pylori by direct antimicrobial activity and by lowering MIC of the antibiotics. Triple Therapy: PPI twice daily. Clarithromycin 500mg twice daily. Amoxicillin 1gm twice daily,or, Metronidazole 500mg twice daily.
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15 PPI Peptic Ulcer Disease: NSAID-associated ulcers: PPIs promote ulcer healing despite continued NSAID use. Also used to prevent ulcer complications of NSAIDs. Rebleeding peptic ulcer: Oral or IV. High ph may enhance coagulation and platelet aggregation.
16 Adverse Effects: PPI General: Diarrhea, headache, abdominal pain, not teratogenic in animals, but not used in pregnancy. Reduction of cyanocobalamine absorption. Increased risk of GI and pulmonary infection.
17 PPI Adverse Effects: Increased serum gastrin levels: Hyperplasia of ECL cells. Carcinoid tumors in rats. Increase proliferative rate of colonic mucosa, but no cancer developed. Chronic inflammation in gastric body. Atrophic gastritis and intestinal metaplasia.
18 Drug Interactions: PPI May affect absorption of drugs due to decreased gastric acidity like digoxin and ketoconazole. Omeprazole can inhibit metabolism of coumadine, diazepam and phenytoin. Rabeprazole and pantoprazole have no significant interaction.
19 PPI Side Effects Generally well tolerated, and the incidence of short-term adverse effects is relatively uncommon. Headache Diarrhea abdominal pain, nausea Dizziness.. although in clinical trials the incidence of these effects with omeprazole was mostly comparable to that found with placebo. Long term the risk of a fracture increased with the length of time taking PPIs. Possibly due to reduced amount of Ca 2+ dissolved in the stomach or interference with the breakdown and rebuilding of bone by interfering with the acid production of osteoclasts.
20 Mucosal Protective Agents GI mucosal defense mechanisms: Mucus secretion. Cell-cell tight junctions; Restrict back diffusion of acid and pepsin. Epithelial bicarbonate secretion. Restitution: Cellular migration from gland neck cells seals small erosions to reestablish intact epithelium. Mucosal prostaglandins: Stimulate mucus and bicarbonate secretion.
21 Enhance mucosal protection 1. Bismuth compounds 2. Sucralfate 3. Prostaglandin analogs (misoprostol, cytotec)
22 Mucosal Protective Agents Sucralfate: Is a salt of sucrose complexed to sulfated aluminum hydroxide. In the stomach, it forms a viscous, tenacious paste that binds selectively to ulcers or erosions for up to 6 hours. The negatively charged sucrose sulfate binds to positively charged proteins in the base of ulcer or erosions, forming a physical barrier that restricts further caustic damage and stimulates prostaglandin and bicarbonate secretion.
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24 Sucralfate Clinical Use: 1 gm four times daily on an empty stomach. Reduces the incidence of GI bleeding in critically ill patients. Acid inhibitory therapies may increase the risk of nosocomial pneumonia.
25 Sucralfate Adverse Effects: It is not absorbed, so devoid of toxicity. Constipation in 2% of patients. Caution in renal insufficiency. Drug Interactions: May bind to other medications, thus impairing their absorption.
26 Mucosal Protective Agents Misoprostol: Prostaglandin Analog, a methyl analog of PGE 1. Half life 30 minutes. Given 3-4 times daily. Stimulates mucus and bicarbonate secretion and enhances mucosal blood flow. Binds to PG receptor on the parietal cells, reducing the histamine- stimulated camp production and causing modest acid inhibition. Also, stimulates electrolyte and fluid secretion, motility and uterine contractions.
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28 Mucosal Protective Agents Misoprostol: Reduces NSAIDs-induced peptic ulcers in high-risk patients. Not widely used for this purpose because of: a- side effects. b. need for multiple daily dosing. c. PPI may be as effective and better tolerated. d. Cyclooxygenase2-selective NSAIDs are an option for such patients.
29 Mucosal Protective Agents Misoprostol: Can cause diarrhea and abdominal cramping in 10-20% of patients. Should not be used in pregnancy.
30 Mucosal Protective Agents Colloidal Bismuth Compounds: Bismuth subsalicylate. Bismuth subcitrate. Bismuth dinitrate. Bismuth is minimally absorbed from GIT.
31 Mucosal Protective Agents Colloidal Bismuth Compounds: Coat ulcers and erosions, creating a protective layer against acid and pepsin. May stimulate PG, mucus and bicarbonate secretion. Bi subsalicylate inhibits intestinal PG and chloride secretion, so useful in infectious diarrhea leading to reduced liquidity and frequency of diarrhea. Have direct antimicrobial effects and binds enterotoxins, so useful in Travellers diarrhea. Have direct activity against H.pylori.
32 Mucosal Protective Agents Colloidal Bismuth Compounds: Adverse effects: Black stools and tongue. Encephalopathy: headaches, ataxia, confusion and seizures.
33 Treatment of peptic ulcers 1. Reduce gastric acid secretion from parietal cells 2. Neutralize acid in the lumen 3. Protect the mucosa from acid destruction 4. Antibiotics to eradicate Helicobacter pylori
34 Helicobacter pylori and ulcer 1. Barry J. Marshall and J. Robin Warren won Nobel Prize in Physiology or Medicine in 2005 for their discovery of the bacterium Helicobacter pylori and its role in gastritis and peptic ulcer disease. 2. a helix-shaped Gram-negative bacterium. 3. Produces large amounts of the enzyme urease molecules of which are localized inside and outside of the bacterium. Urease breaks down urea (which is normally secreted into the stomach) to carbon dioxide and ammonia which is toxic to the mucosal epithelial cells. 4. Other enzymes including protease, vacuolating cytotoxin A (VacA), and certain phospholipases damage the mucosal epithelial cells. 5. Colonization of the stomach by H. pylori results in chronic gastritis, an inflammation of the stomach lining. The inflammatory response to the bacteria induces G cells in the antrum to secrete the hormone gastrin, which travels through the bloodstream to the fundus of stomach.
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36 Antibiotics to eradicate Helicobacter pylori Clarithromycin Amoxicillin Metronidazole Tetracycline
37 Treatment of ulcers American College of Gastroenterology US Recommended Primary Therapy Eradication rates of 70-85% Clarithromycin-based triple therapy: PPI+ clarithromycin + amoxicillin or metronidazole for 14 days. Bismuth quadruple therapy: consider for penicillin allergic patients PPI or H 2 Receptor antagonist + bismuth + metronidazole + tetracycline for days.
38 Muscarinic antagonists Atropine Pirenzepine Side effcets: urinary retention xerostomia blurred vision
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40 GastroEsophageal Reflux Disease
41 GastroEsophageal Reflux Disease Heartburn; Dysphagia; chronic symptoms or mucosal damage produced by abnormal reflux of gastric contents into the esophagus. Therapy based on decreasing acidity, increasing lower esophageal sphincter tone; enhanced clearance of refluxed material.
42 GastroEsophageal Reflux Disease Treatment: 1. PPIs. 2. Coating agents Sulcralfate (Carafate) coats mucous membranes and sores to provide an additional protective barrier against stomach acid. 3. Promotility/prokinetic agents: help tighten the lower esophageal sphincter and promote faster emptying of the stomach. Metoclopramide Bethanechol. Health care providers often are reluctant to prescribe promotility agents because they have fairly significant side effects. Promotility agents also do not work as well as PPIs for most people.
43 Prokinetic agents enhancing motility of the upper GI tract useful in the treatment of GERD, especially when gastric stasis or hypomotility is involved Metoclopramide (Reglan) increases lower esophageal sphincter (LES) tone accelerates gastric emptying by enhancing motility of the upper GI tract dopamine antagonist Side effects: similar to other dopamine antagonists; hyperprolactemia; extrapyramidal symptoms (parkinsonian effects)
44 Zollinger-Ellison Syndrome Non-beta cell tumor of pancreatic islets. Produces gastrin in large quantities. Stimulates gastric acid secretion. PPI treatment is the therapy of choice.
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