This document discusses drugs used to treat hyperacidity and gastric ulcers. It begins with an introduction to hyperacidity and ulcers, then describes the regulation of gastric acid secretion and mechanisms of acid secretion. It classifies common drug treatments for ulcers such as H2 receptor antagonists, proton pump inhibitors, prostaglandins, and antimicrobials. It also discusses FDA-approved treatment regimens for Helicobacter pylori infections. In conclusion, it notes that while acid secretion plays a role in ulcers, other defensive and offensive factors are also involved, and current drug treatments aim to reduce acid secretion to provide relief while having various side effects.

1. PRESENTED BY
E. Madhan Mohan
Asst. Professor,
Department of
Pharmacology
School of Pharmacy,
NNRESGI.
HYD, TELANGANA, INDIA
DRUGS ACTING ON
HYPER ACIDITY AND
GASTRIC ULCERS
1

2. CONTENTS:
Introduction.
Regulation of gastric acid
secretion.
Mechanism of gastric acid
secretion.
Classification of drugs.
FDA-approved treatment
regimen.
Conclusion
References
2

3. INTRODUCTION:
 HYPER ACIDITY: It generally occurs when there is
excess secretion of acids from gastric glands of the
stomach.
 ULCER: It is defined as a local defect or erosion of the
surface of organ produced by inflammation of tissue.
Endoscopic image of gastric ulcer Benign gastric ulcer of antrum3

4. TYPES OF ULCERS:
 Peptic ulcer
 Duodenal ulcer
 Gastric Ulcer
 Zollinger –Ellison syndrome
CAUSATIVE FACTORS OF ULCER:
 Usage of NSAID drugs
 Helicobacter pylori (H.Pylori) infection
 Increased hydrochloric acid secretion
 Increased salt intake
 Inadequate mucosal defense against acid
 Stress
 Smoking & alcohol
4

5. Ulcer is an erosion in the stomach and is caused by the imbalance
between aggressive and protective factors in GIT and infection of
gastric mucosa with H.Pylori.
Aggressive Factors
 Acid (Hcl)
 Drugs (NSAIDs)
 H. pylori
Defensive Factors
 Mucus,
 bicarbonate layer
 Prostaglandins
5

6. REGULATION OF GASTRIC ACID SECRETION:
Gastric acid secretion is a complex, continuous process in
which multiple central and peripheral factors contribute to a
common endpoint: the secretion of H+ by parietal cells.
1. Neuronal control - Controlled enteric nervous system and
secretes Acetylcholine.
2. Hormonal control - Includes both endocrine and paracrine.
Hormones of gastrointestinal tract
Endocrine secretions – Gastrin.
Paracrine secretions - Histamine and Prostaglandin.
6

7. In parietal cells, the cyclic AMP and the Ca2+-dependent
pathways activate H+/K+-ATPase (the proton pump), which
exchanges hydrogen and potassium ions across the parietal
cell membrane.
7

8. ACh PGE2
Histamine Gastrin
Adenyl
cyclase
_
+
ATP cAMP
Protein Kinase
(Activated)
Ca++
+
Ca++
Proton pump
K
+
H+
Gastric acid
Parietal cell
Lumen of stomach
H2M3
+
PGE
receptor
+
+
Gastrin
receptor+
+
8

9. ACh PGE2
Histamine Gastrin
Adenyl
cyclase
_
+
ATP cAMP
Protein Kinase
(Activated)
Ca++
+
Ca++
Proton pump
K+ H+
Gastric acid
Parietal cell
Lumen of stomach
H2M3
+
PGE
receptor
+
+
Gastrin
receptor+
+
9

10. Classification of anti-ulcers:
Histamine H2 receptor antagonists
Proton Pump Inhibitors
Prostaglandins
Antimuscarinic agents
Antacids
Mucosal protective agents
Treatment for Helicobacter pylori infection (antimicrobials)
10

11. 11

12. Histamine H2 receptor antagonist:
Eg: Cimetidine,
Ranitidine,
Famotidine,
Nizatidine.
Mechanism of Action (MOA):
These agents inhibit gastric acid secretion by competitively blocking the
binding of histamine to H2 receptors. These agents reduce the intracellular
concentrations of cyclic adenosine monophosphate (cAMP) and thereby,
decreases gastric acid secretion.
Adverse effects:
Diarrhoea, dizziness, muscle pain, hypotention, gynaecomastia, impotence.12

13.  Proton Pump Inhibitors:
Eg: Esomeprazole
Lansoprazole,
Omeprazole,
Rabeprazole,
Pantoprazole.
MOA:
 Proton pump actively transports protons H+ into stomach lumen and K+
ions back to the parietal cells with hydrolysis of ATP.
 Proton pump inhibitors are the drugs which reduces the acid secretion of
the stomach.
 Drug binds irreversibly into proton pump and prevents active transport of
proton and this dramatically decreases acid secretion in stomach.
Adverse effects:
 Nausea, abdominal pain, constipation, flatulence, Subacute myopathy,
headaches, and skin rashes.13

14. Prostaglandins:
Eg: Misoprostol
MOA:
Prostaglandin E2 (PGE2) and prostacyclin (PGI2) are the major prostaglandins
synthesized by the gastric mucosa.
These bind to the EP3 receptor on parietal cell thereby decreasing intracellular
cyclic AMP and gastric acid secretion.
PGE2 also can prevent gastric injury by cytoprotective effects that include
stimulation of mucin and bicarbonate secretion.
Contraindications:
 It is contraindicated during pregnancy because it can increase uterine
contractility.
Adverse effects:
 Diarrhoea and nausea are the most common adverse effects .14

15. Antimuscarinic agents :
Eg : Dicyclomine,
Atropine.
MOA:
Muscarinic receptor antagonist can inhibit the gastrointestinal
motility and secretory activity.
Adverse effects: many side effects limits its use.
cardiac arrhythmias,
dry mouth,
constipation,
urinary retention.
15

16. Antacids:
Eg : NaHCO3, CaCO3.
Salts of aluminum [Al(OH)3] & Magnesium [Mg(OH)2],
MOA:
Antacids are weak bases that react with (neutralize) gastric acid to form water and
a salt, thereby diminishing gastric acidity. Because pepsin is inactive at a pH
greater than 4, antacids also reduce pepsin activity.
Adverse effects:
Salts of Mg, Al combinations are used because of Mg & Al itself produces
diarrhoea & constipation respectively, nausea and esophageal reflux are the
common side effects.
16

17. Mucosal protective agents:
Eg : Sucralfate,
Carbenoxolone,
Bismuth chelate.
MOA:
These compounds, known as cytoprotective compounds, have several actions
that enhance mucosal protection mechanisms, thereby preventing mucosal
injury, reducing inflammation, and healing existing ulcers.
Adverse effects:
Constipation, dryness of mouth, abdominal discomfort.
17

18. Treatment for Helicobacter Pylori
H. pylori is a spiral-shaped, pH-sensitive, gram-negative bacterium that
resides between the mucus layer and surface epithelial cells in the stomach.
Eg: Clarithromycin,
Amoxicillin
MOA:
The antimicrobial agents acts on bacterial cell wall synthesis and bacterial
protein synthesis.
Adverse effects:
Epigastric pain, Hypersensitivity reactions.
18

19. FDA-Approved Treatment Regimen for H. pylori
Infection
Omeprazole 20 mg BID + Clarithromycin 500 mg BID +
Amoxicillin 1 g BID for 10 days.
Lansoprazole 30 mg BID +Clarithromycin 500 mg BID +
Amoxicillin 1 g BID for 10 days.
Amoxicillin/Clarithromycin + Metronidazole + Omeprazole –
triple therapy.
Bismuth subsalicylate 525 mg QID + Metronidazole 250 mg
QID + Tetracycline 500 mg QID X 14 days + H2 receptor
antagonist – quadruple therapy.
19

20. Several kits are also available viz.., pylomax kit and HP kit.
One kit taken daily two doses.
HP kit consists of Omeprazole + Amoxicillin + Tinidazole, 2
tablets each.
Pylomax kit consists of Amoxicillin + Clarithromycin +
Metronidazole, 2 tablets each
20

21. CONCLUSION:
Ulcers were previously thought due to increase in
offensive factors namely acid and pepsin, but it has been
found that acid secretion is either normal or below normal
in gastric ulcer patients, and that 40 - 70 % cases of
duodenal ulcer patients show acidity within normal range.
suggesting that other factors are also involved in
ulcerogenesis.
Hence the interest then shifted to the defensive factors,
whose imbalance with the offensive factors may be the
cause of ulcers. Most of the anti-secretory drugs reduce
acid secretion, thus giving immediate symptomatic relief.
Although newer drugs are discovered, still every drugs has
its own side effects.21

22. REFERENCES
 Rang and Dale,Pharmacology, 6th edition, 2007, pg.385 – 390.
 Bertram G.Katzung, Basic & Clinical pharmacology, 11th
edition, 2009, pg.1070 – 1076.
 Goodman & Gilman's The Pharmacological Basis of
Therapeutics. 5th edition, pg 1008-1010.
 Lippincott's Illustrated Reviews Pharmacology, 4th Edition,
pg.329 – 335.
 K.D.Tripati, Essentials of Medical pharmacology, 6th
edition,2008, pg.627 – 638.
 Digestive Disorders. http://www.umm.edu/digest/ulcers.
University of Maryland medical center.2008.
22

23. 23