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ANTI- ULCER AGENT

This document discusses anti-ulcer agents. It defines peptic ulcers as erosions in the stomach or duodenum lining caused by an imbalance between aggressive factors like acid and protective factors. Common causes of ulcers include H. pylori, NSAIDs, and stress. Treatment approaches aim to reduce acid secretion using H2 blockers, proton pump inhibitors, anticholinergics, and prostaglandins. Other approaches neutralize acid with antacids, protect the ulcer with sucralfate or bismuth, and eradicate H. pylori with antibiotic combinations.

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Peptic Ulcer•
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ANTI- ULCER AGENT Presented by: 1.Harshada R. khandewal B.Pharm 7th semester Presented by: 2.Anil Keshav Pawar B.Pharm 7th semister
Peptic ulcer: It is - • Erosion in the lining of the stomach or the first part of the small intestine, an area called the duodenum. • Ulcers damage the mucosa of the alimentary tract, which extends through the muscularis mucosa into the sub mucosa or deeper. • Ulcers that form in the stomach are called gastric ulcers; in the duodenum, they are called duodenal ulcers. Both types are referred to as peptic ulcers.
Peptic ulcer
•It results probably due to an imbalance between the two factors 1.Aggressive - (acid , pepsin, bile and H.pylori ) 2.Defensive - ( gastric mucus and bicarbonate secretions, PGs, innate resistance of the mucosal cells ). • In gastric ulcer generally acid secretion is normal or low. • In duodenal ulcer acid secretion is high in half of the patients but normal in the rest.
Pathogenesis of peptic ulcer : • Acid and Pepsine • Helicobacter pylori • NSAIDs • Motility disturbance • Stress • Ischemia • Hypergastrinemic Syndromes
Regulation of gastric acid secretion
• The terminal enzymes H+K+ATPase which secretes H+ ions in the parietal cells can be activated by histamine, Ach and gastrin acting via their own receptors located on the basolateral membrane of these cells. • Histamine acting through H2 receptors, plays the dominant role, because the other two, gastrin and Ach partly directly and to a greater extent indirectly by releasing histamine from ‘ histaminocytes’ located in the oxyntic glands. • While H2 receptors activate H+K+ATPase by generating cAMP, muscarinic and gastrin receptors appear to function through the phospholipase C IP3 – DAG pathway that mobilizes intracellular Ca+2.
• The cAMP mediated proton pump activation also involves ca+2. • The secretomotor response to gastrin and cholinergic agonists is expressed fully only in the presence of cAMP generated by H2 activation. • Histamine participates in the acid response to gastrin , ACh at more than one levels, and H2antagonists suppress not only histamine, but also Ach and in fact any other gastric secretion stimulus. • Gastrin is secreted from the antrum in response to rise in antral pH, food constituents and vagally mediated reflexes. The dominant muscarinic receptor mediating vagal responses is of The M1 subtype.
• Vagus releases Ach in close proximity to histaminocytes and gastrin secreting cells. • Prostaglandins have been a ‘cytoprotective’ role in the gastric mucosa by augmenting mucus and bicarbonate secretion, as well as other actions. • PGE2, produced by gastric mucosa, inhibits acid secretion by opposing cAMP generation ( in parietal cells ) and gastrin release ( from antral cells ).
Symptoms • Epigastric pain after meal or during meal • Upper dyspeptic syndrome – loss of appetite, nausea, vomiting. • Vomiting brings relief • Reduced nutrition • Loss of weight • Oral flatulence, bloating, distension and intolerance of fatty food • Heartburn • Pain radiating to the back
APPROACHES FOR THE REDUCTION OF PEPTIC ULCER 1. Reduction of gastric acid secretion 2. Neutralization of gastric acid ( antacids ) 3. Ulcer protectives 4. Anti- H.Pylori drugs
Reduction of gastric acid secretion 1. H2 Antihistamins : cimetidin, rantidine, famotidine, roxatidine. 2. Proton pump inhibitors : omeprazole, lansoprazole, pantoprazole, rabeprazole, esomeprazole. 3. Anticholinergics : pirenzepine, propantheline, oxyphenonium. 4. Prostaglandin analogue : misoprostol. Neutralization of gastric acid (antacids) 1. Systemic : sodium bicarbonate, sod. Citrate 2. Nonsystemic : magnesium hydroxide, mag.Trisilicate, aluminium hydroxide gel, calcium carbonate
Ulcer protectives Sucralfate , colloidal bismuth subcitrate (CBS) Anti H-pylori drugs Amoxicillin, clarithromycin, Metronidazole, trinidazole, tetracycline.
1. H2 Antagonist • Eg: Cimetidine ,ranitidine etc. • First class of highly effective drugs. Mechanisam of action: 1. H2 Blockade : Cimetidine and other H2 antagonists block histamine- induced gastric secretion, cardiac stimulaton ,uternine relaxation , bronchial realaxation. Attenuate Fall in BP due to histamine, especially the late phase response seen with high doses. 2. Gastric secretion : All phases of secretion are suppressed dose-dependently, but the basal nocturnal secretion is suppressed completely. Secretory responses to not only histamine but all other stimuli i.e Ach , gastrin, food, alcohol are seen.
Pharmacokinetics • Absorbed orally , bioavailibility is 60-80%. Absorption not interfered by presence of food in stomach. • Cross placenta and reaches milk • Dose reduction- in case of renal failure. Adverse effects • CNS effects like confusional state, restlessness, convulsions and coma have occurred infrequently in elderly persons with renal impairment with large doses infused i.v • Headach, dizziness, bowel upset, dry mouth, rashes. • Cemetidine - Anti androgenic action.Increases plasma prolactin and inhibit degradation of estradiol by liver. • High dose for long time - gynaecomastia, loss of libido, impotence and temporary decrease in sperm count
Use Used in conditions in which it is profitable to suppress gastric acid secretion. • 1. Duodenal ulcer • 2. Gastric ulcer • 3. Stress ulcers and gastritis • 4. Zollingers-Ellison syndrome • 5. Gastroesophagel reflux disease
PROTON PUMP INHIBITORS Mechanism of action :Proton pump inhibitors act by irreversibly blocking the hydrogen/potassium adenosine triphosphatase enzyme system of the gastric parietal cells. • The proton pump is the terminal stage in gastric acid secretion • Omeprazole: is inactive at neutral pH, but at pH<5 rearranges to two charged cationic forms that react covalently with SH groups of the H+ K+ ATPase enzyme and inactivate it irreversibly, especially when two molecules of omeprazole react with one molecule of the enzyme • SIDE EFFECTS: Stomach pain, Diarrhea,Constipation,Dizziness,Pain,Hives, Itching,seizures
Prostaglandin Analogs MISOPROSTOL Mechanism: Misoprostol acts upon gastric parietal cells, inhibiting the secretion of gastric acid via G-protein coupled receptor-mediated inhibition of adenylate cyclase, which leads to decreased intracellular cyclic AMP levels and decreased pump activity at the apical surface of the parietal cell Side effects: Diarrhea, abdominal ,pain, nausea, flatulence, headache, dyspepsia, vomiting, and constipation.
ANTACIDS a) SYSTEMIC ANTACIDS: Eg: SODIUM BICARBONATE : It is water soluble , acts instantaneously, but the duration of action is short. It is a potent neutralizer, pH may rise above 7. However it has several demerits a) Absorbed systemically , large doses will induce alkalosis. b) Produces carbon dioxide in stomach which creates discomfort, risk of ulcer perforation. c) Acid rebound
b)Nonsystemic antacids Eg:Magnesium hydroxide : Has low water solubility ; its aqueous suspension has low concentration of OH- ions and thus low alkalinity. However it reacts with HCL and is an efficacious antacid. • MILK OF MAGNESIA- 0.4 g / 5 ml suspension.
ULCER PROTECTIVES SUCRALFATE • Mechenism: Sucralfate is a locally acting substance that in an acidic environment (pH < 4), reacts with HCL in the stomach to form a crosslinking, viscous, paste-like material capable of acting as an acid buffer. It also attaches to proteins on the surface of ulcers, such as albumin and fibrinogen, to form stable insoluble complexes. These complexes serve as protective barriers at the ulcer surface, preventing further damage from acid, pepsin, and bile. • Side effects: constipation , nausea , headach, dry mouth.
ANTI H.PYLORI DRUGS • Anti microbials that have been found clinically effective against H.pylori are: amoxicillin, clarithromycin, tetracycline and metronidazole. • A combination regimen is preferred, using gastric acid inhibitors and antibiotics. Example: A proton pump inhibitor or H2 blocker + amoxicillin + clarithromycin or metronidazole .
ANTI- ULCER AGENT
ANTI- ULCER AGENT
ANTI- ULCER AGENT