1. GASTROINTESTINAL DRUGS

3. 1. Reduction of gastric acid secretion (a) H2 antihistamines : Cimetidine Ranitidine Famotidine Roxatidine (b) Proton pump inhibitors: Omeprazoie Lansoprazole Pantoprazole Rabeprazole Esomeprazole (c) Anticholinergics : Pirenzepine Propantheline Oxyphenonium (d) Prostaglandin analogue Misoprostol

4. 2. Neutralization of gastric acid (Antactids) (a)Systemic: Sodium bicarbonate Sod.citrate (b) Non Systemic: Magnesium hydroxide gel Mag. Trisilicate Aluminium hydroxide Magaldrate Calcium carbonate 3. Ulcer protectives: Sucralfate Colloidal bismuth subcitrate (CBS)

5. 4. Anti-H. pylori drugs: Amoxicillin Clarithromycin Metronidazole Tinidazole Tetracycline

6. Mechanisms of Action Suppress secretory responses to food stimulation and nocturnal secretion of gastric acid via their ability to decrease (indirectly) the activity of the proton pump. H2 blockers also partially antagonize HCl secretion caused by vagal stimulation or by gastrin. Clinical Uses Acid peptic disease (overall less effective than proton pump inhibitors) gastroesophageal reflux disease(GERD) Zollinger-Ellison syndrome

7. Adverse Effects GI distress, dizziness, somnolence; slurred speech and delirium possible in elderly. Cimetidine is a major inhibitor of Cyt.P450 isoforms Increase drug interaction via increasing effects of quinidine, phenytoin, tricyclic antidepressants and warfarin. Cimetidine decreases androgens gynecomastia

8. Mechanisms of Action Omeprazole and related "-prazoles" are irreversible, direct inhibitors of the proton pump(K+/H+ antiporter) in the gastric parietal cell Clinical Uses They are more effective than H2 blockers in peptic ulcer disease (PUD) and are also effective in GERD and Zollinger-Ellison syndrome. Adverse Effects May cause mild CNS and GI effects and decrease bioavailability of drugs that require acidity for oral absorption (e.g., fluoroquinolones, ketoconazole). Inhibit P450 decrease elimination of diazepam, phenytoin and warfarin

9. Mechanism of Action Anticholinergic drugs reduce the volume of gastric juice without raising its pH unless there is food in stomach to dilute the secreted acid

10. Mechanisms of Action PGE2 analog, which is cytoprotective increases mucus and bicarbonate secretion. Clinical Uses Selective use in NSAID-induced GI ulcers. Major problems in the use of misoprostol are- diarrhoea, abdominal cramps, uterine bleeding, abortion, and need for multiple daily doses.

11. Mechanisms of Action Ca, Mg, and Al hydroxides that neutralize protons in the gut lumen Adverse Effects May increase oral absorption of azoles, fluoroquinolones, and tetracyclines AntacidalkalosisAcid rebound diarrhoeaconstipationOther toxicity Al. hydroxide - - -++Hypophosphate mia, dementia Ca. carbonate +++ - hypercalcemia Mg. hydroxide_++ -Hypermagnese mia, resp. paralysis Na. bicarbonate++ __“Gas”

12. Mechanisms of Action Polymerizes on GI luminal surface to form a protective gel-like coating of ulcer beds Clinical Uses Increase healing and decrease ulcer recurrence. Sucralfate requires acid pH, antacids may interfere. Bismuth subsalicylate is also protective. Adverse effects Sucralfate: constipation hypophosphatemia Dry mouth and nausea are infrequent

13. CBS: diarrhoea, headache and dizziness. Prolonged use has the potential to cause osteodystrophy and encephalopathy

14. Two weeks regimes (mg) 1. Amoxicillin 750 + Tinidazole 500 + Omeprazole 20 all BD 2. Amoxicillin 750 + Tinidazole 500 +Lansoprazole 30 all BD 3. Clarithromycin 250 + Tinidazole 500 +Lansoprazole 30 all BD 4. Clarithromycin 500 + Amoxicillin 1000 +Lansoprazole 30 all BD 5. Clarithromycin 500 BD/Amoxicillin 750 BD + Omeprazole 20 BD 6 Amoxicillin 500 TDS/Tetracycline 500 QID + Metronidazole 400 QID/Tinidazole 500 BD + Bismuth 120 QID 7. Amoxicillin 750 TDS + Metronidazole 500 TDS + Ranitidine 300 OD 8. Amoxicillin 750 BD + Clarithromycin 250 BD + Lansoprazole 30 BD

16. 1.Anticholinergics Hyoscine, Dicyclomine 2. H1 antihistaminics Promethazine, Diphenhydramine, Dimenhydrinate, Doxylamine, Cyclizine, Meclozine, Cinnarizine 3. Neuroleptics Chlorpromazine, Prochlorperazine, Haloperidol, etc 4. Prokinetic drugs Metoclopramide Domperidone, Cisapride, Mosapride Tegaserod

17. 5. 5-HT3 antagonists Ondansetron, Granisetron 6. AdjuvantDexamethasone, antiemetics Benzodiazepines, Cannabinoids

18. Opioid analgesics (eg, morphine) have duality of action: decrease emesis by activating receptors that decrease pain transmission and increase emesis by activating receptors In the CTZ

19. Mechanisms of Action: It acts probably by blocking conduction of nerve impulses across cholinergic link in the pathway leading from the vestibular apparatus to the vomiting centre. Use: effective drug for motion sickness.. Adverse effect: brief duration of action Sedation Other anticholinergic actions

20. Mechanisms of Action It acts by inhibiting influx of Ca++ from endolymph into the vestibular sensory cells which mediates labyrinthine reflex. Uses: -mainly in motion sickness and -to a lesser extent in morning sickness -postoperative vomiting. Adverse effects: drowsiness, dry mouth, vertigo and abdominal upset

21. MOA Act by Blocking D2 receptors in the CTZ Antagonize apomorphine induced vomiting and Have additional antimuscarinic as well as H1 antihistaminic property. Uses (a)Drug induced and postanaesthetic nausea and vomiting. (b) Disease induced vomiting: gastroenteritis, uraemia, liver disease, migraine, etc. (c) Malignancy associated and cancer chemotherapy (mildly emetogenic) induced vomiting. (d) Radiation sickness vomiting (less effective). (e) Morning sickness: should not be used except in hyperemesis gravidarum

22. Adverse effect sedation. Acute muscle dystonia may occur after a single dose, especially in children and girls. The antiemetic dose is generally much lower than antipsychotic doses. These agents should not be administered until the cause of vomiting has been diagnosed; otherwise specific treatment of conditions like intestinal obstruction, appendicitis maybe delayed due to symptom relief.

23. These are drugs which promote gastrointestinal transit and speed gastric emptying by enhancing coordinated propulsive motility. METOCHLOPROMIDE MOA: (a)D2 antagonism (b)5-HT4 agonism (c)5-HT3 antagonism Uses 1.Antiemetic postoperative, Drug induced, disease associated (especially migraine), radiation sickness is less effective in motion sickness

24. 2. Gastrokinetic : To accelerate gastric emptying (a) When emergency general anaesthesia is to be given and the patient has taken food less than 4 hours before. (b) To relieve postvagotomy or diabetes associated gastric stasis. (c) To facilitate duodenal intubation 3. Dyspepsia and other functional g.i disorders. Metoclopramide may succede in stopping persistent hiccups 4. Gastroesophageal reflux disease(GERD) Metoclopramide may afford symptomatic relief in milder cases of GERD

25. Adverse effects Metoclopramide is generally well tolerated. Sedation, dizziness, loose stools, muscle dystonias (especially in children) are the main side effects. Long-term use can cause parkinsonism, galactorrhoea and gynaecomastia. It should not be used to augment lactation. Though the amount secreted in milk is small, but suckling infant may develop loose motions, dystonia, myoclonus.

26. MOA It blocks the depolarizing action of 5-HT through 5-HT3 receptors on vagal afferents in the g.i.t as well as NTS and CTZ. Uses: cancer chemotherapy/radiotherapy induced vomiting. Adverse effect the only common side effect is headache Mild constipation or diarrhoea and abdominal discomfort occur in few patients