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Drugs For Peptic Ulcer Emesis and Reflux Disorders PowerPoint Presentation

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Description : Check out this medical PowerPoint presentation titled "Drugs for peptic ulcer, emesis and reflux disorders” by Dr. Rishi Pal.

This medical PowerPoint presentation talks about types of drugs used for peptic ulcer, emesis, and reflux disorders.

Peptic ulcer, emesis, and reflux disorders are all related to the digestive system and can cause discomfort and pain for individuals who experience them.

A peptic ulcer is a sore that develops on the lining of the stomach or the duodenum, which is the first part of the small intestine. Peptic ulcers are usually caused by a bacterial infection or the use of nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin or ibuprofen. Symptoms of peptic ulcers can include abdominal pain, bloating, nausea, and vomiting.

Emesis, also known as vomiting, is the forceful expulsion of the contents of the stomach through the mouth. Emesis can be caused by a variety of factors including illness, motion sickness, pregnancy, and certain medications. Symptoms of emesis can include nausea, abdominal discomfort, and dehydration.

Reflux disorders, also known as gastroesophageal reflux disease (GERD), occur when stomach acid flows back into the esophagus, causing irritation and inflammation. Reflux disorders can cause symptoms such as heartburn, regurgitation, and difficulty swallowing.

Tags : peptic ulcer, emesis, reflux disorders, Gastroenterology, Gastroenterology PowerPoint presentation

Published on : Apr 26, 2023 | Views : 1600 | Downloads : 8

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Slide 1-

Drugs for peptic ulcer, emesis and reflux disorders Dr. Rishi Pal Assistant Professor
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Physiology of gastric secretion Stomach secretes 2-3 liters of gastric juice /day. Chief/peptic cells secrete pepsinogen. Parietal or oxyntic cells secrete acid and IF. Superficial epithelial cells secrete alkaline mucus and bicarbonates.
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Regulation of gastric acid secretion Ach Histamine Gastrin prostaglandin-E2 Phases of gastric acid secretion Basal, cephalic and hormonal Membrane bound proton pump (H+) K+ ATPase
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Peptic ulcer Damage to the mucosa and deeper tissue exposed to acid and pepsin is known as peptic ulcer. Causes of peptic ulcer :- H. pylori infection Use of NSAIDS Stress
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Classification of the drugs used in peptic ulcer Drugs that inhibit gastric acid secretion Proton pump inhibitors: omeprazole, esomeprazole, lansoprazole, pantoprazole, rabeprazole. H2-receptor antagonists: cimetidine, ranitidine, famotidine, roxatidine,nizatidine Antimuscarinic agents (anticholinergics): pirenzepine, telenzepine Prostaglandin analogs: misoprostol, enprostil.
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Anti-peptic ulcer drugs Ulcer protective sucralfate, and bismuth subcitrate (CBS) Drugs that neutralize gastric acid (antacids) a) Systemic antacids: sodium bicarbonate and sodium citrate. b) Non systemic antacids: magnesium hydroxide, magnesium trisilicate, aluminum hydroxide, and calcium carbonate.
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Anti-peptic ulcer drug Anti- H. pylori drugs Amoxicillin, tetracycline, clarithromycin, metronidazole, tinidazole, bismuth subsalicylate, H2-antagonists and PPIs.
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Proton pump inhibitors Proton pump, K+-ATPase membrane bound enzyme play an important role in the final step of gastric acid secretion (basal and stimulated). Omeprazole is the prototype drug: these are prodrugs and activated to sulfenamide at acidic pH. Activated form binds covalently with SH group of H+ pump and irreversibly inactivates it. PPIs administered orally 30 min. before meal. Half life short (1.5 hr), acid secretion suppressed for upto 24 hr.
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Enteric coated form or powder containing sodium bicarbonate. i.v. formulations available for esomeprazole, lansoprazole, pantoprazole and rabiprazole. They are highly bound to plasma proteins; extensively metabolized in liver and metabolites secreted in urine.
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Therapeutic uses of PPIs 1. Peptic ulcer disease Duodenal ulcer disease Gastric ulcer Acute bleeding ulcer H. pylori-associated ulcer Stress ulcers (curling ulcers) NSAIDs induced ulcers 2. Gastroesophegial reflux disease (GERD) 3. Zollinger’-Ellison syndrome.
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Adverse effects of PPIs Headache, diarrhoea and abdominal pain. Skin rashes and arthralgia. May decrease vit B12 absorption Increase rate of infection and fracture of bones. Drug interactions: omeprazole can inhibit metabolism of phenytoin, warfarin, diazepam. PPIs decreases bioavailability of itraconazole, iron salts, etc
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H2-Receptor antagonists Mechanism of action: Competitively block H2 receptors on parietal cells. Suppress all phases of acid secretion. Most effective in suppressing nocturnal acid secretion. Less potent than PPIs.
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Administered orally and well absorbed. Metabolized in liver. Cimetidine, ranitidine and famotidine available for i.v. administration Nizatidine has high bioavailability (100%)
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Therapeutic uses of H2 blockers Peptic ulcer disease Duodenal ulcer disease Gastric ulcer Acute bleeding ulcer H. pylori -associated ulcer Stress ulcers (curling ulcers) NSAIDs induced ulcers 2. Gastroesophegial reflux disease (GERD) 3. Zollinger’-Ellison syndrome.
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Anticholinergic agents Pirenzepine Telenzepine Selective M1-receptor blocker Inhibit acid secretion Not commonly used because of their low efficacy and anticholinergic effects.
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Prostaglandin analogues Misoprostol effective orally for prevention and treatment of NSAID-induced duodenal ulcers. Inhibit gastric acid secretion. Increase bicarbonate and mucus secretion. Common side effects: Diarrhoea and abdominal cramps. Containdicated in pregnancy
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Ulcer protective Sucralfate : it is complex aluminum hydroxide and sulphated sucrose. Polymerized to form sticky gel that adheres to the ulcer base and protects it. Form barrier against acid-pepsin.
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Increase mucus-bicarbonate secretion. Given orally empty stomach. Reduced absorption of digoxin, tetracyclines, ketoconazole, fluoroquinolones. etc. Concurrent use of PPIs, H2 blocker should be avoided.
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Bismuth containing preparation Bismuth salisylates and colloidal bismuth subcitrate. React with protein in the base of ulcer and protect it from peptic digestion. Stimulates secretion of PGE2, mucus and bicarbonate. Anti-microbial effects against H. pylori.
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Drugs that neutralized gastric acid Ideal antacids Insoluble and neutralize acid Should not liberate CO2 Non-absorbable Should not disturb acid-base balance
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Types of antacids Systemic: sodium bicarbonate and sodium citrate Non systemic: magnesium hydroxide, magnesium trisilicate, aluminum hydroxide gel and calcium carbonate.
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Antifoaming agents Methylpolysiloxane Oxethazaine Sodium alginate
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Anti H. pylori agents Gram negative, rod shaped bacteria associated with gastritis, duodenal ulcer, gastric ulcer and gastric carcinoma. Cause mucosal inflammation Ammonia produced by urease activity damage cells.
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Combination therapy To prevent or delay development of resistant organism. Prevent relapse Promote rapid ulcer healing Eradicate H. pylori infection Treatment for 1 or 2 weeks required
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Triple therapy x 14 days Lansoprazole 30 mg BD+ clarithromycin 500 mg BD + Amoxicillin 1 g BD Quadruple therapy x 14 days lansoprazole 30 mg BD + bismuth subsalicylate 525 mg QID + tetracycline 500 mg QID + Metronidazole 500 TDS After completion of above regimen, PPIs should be continued for six more weeks.
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Emetics and antiemetics pathways
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Emetics and antiemetics Mechanism of vomiting Pregnancy, infection, drugs, radiation, painful stimuli, motion sickness, metabolic and emotional disturbances. Neurotransmitters involved Ach, histamine,5HT and dopamine.
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Emetics Mustard Common salt Ipecac Apomorphine Used for certain poisoning cases
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Contraindications for emetics Emetics Children Unconscious patient Corrosive and caustic poisoning CNS Poisoning Kerosene poisoning
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Antiemetics Classification of antiemetics Anticholinergics: scopolamine, dicycloamine Antihistamines (H1-blockers): dimenhydrinate, diphenhydramine, cyclizine,meclizine, hydroxyzine,promethazine,doxylamine, cinnarizine 5HT3-receptor antagonists: ondansetron, granisetron, dolasetron, palonosetron
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Antiemetics Prokinetic agents: metoclopramide, domperidone Neuroleptics: chlorpromazine, fluphenazin, prochlorperazine, haloperidol Cannabinoids: dronabinol Adjuvant antiemetics: glucocorticoids, benzodiazepines
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Anticholinergics as antiemetic Scopolamine for motion sickness, it blocks afferent impulses from vestibular apparatus to the vomiting center by its anticholinergic action. Its sedative effects also contributes for its antiemetic effect. Scopolamine not effective in other types of vomiting.
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Antihistamine H1 blocker as antiemetic Motion sickness, morning sickness, post operative and other types of vomiting. Dimenhydrinate, diphenhydramine, doxylamine, promethazine, cyclizine, meclizine. Have sedative and anticholenergic action. Meclizine has longer duration of action.
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5HT3-receptor antagonist as antiemetic Ondensetron is prototype drug Granisetron, dolasetron,palanosetron. Blockade of 5HT3 receptor on vagal afferent in the gut also block 5HT3 receptors in CTZ & STN. Used for anticancer drug-induced nausea and vomiting, effective in hyperemesis of pregnancy, postoperative and post radiation vomiting but not effective in motion sickness.
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5HT3 receptor antagonist
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Prokinetic drugs Drugs promote coordinated movements of upper GIT and hasten gastric emptying are called prokinetic drugs. Metoclopramide: D2 receptor antagonist Have central and peripheral action. Enhance release of Ach from myentric neurons. Used in GERD
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Mechanisms
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Prokinetic effects
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Neuroleptics Prochlorperazine Used for vomiting due to systemic infection, drugs, uraemia. Cannabinoids: dronabinol used for cancer chemotherapy Adjuvant antiemetics: glucocorticoids, benzodiazepines.
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Anti emetics