This document discusses drugs used to treat peptic ulcers and gastroesophageal reflux disease (GERD). It begins by defining peptic ulcers and their causes, including an imbalance between aggressive and defensive factors in the gastrointestinal tract. It then covers the different types of ulcers and regulators of gastric acid secretion. The document categorizes and describes the mechanisms and uses of several classes of drugs: H2 antagonists like cimetidine and ranitidine; proton pump inhibitors like omeprazole; prostaglandin analogues like misoprostol; antacids; and anti-H. pylori drugs. It discusses the interactions, adverse effects, and treatment of peptic ulcers, G

1. DRUGS USED FOR PEPTIC ULCER AND
GERD
PRESENTED BY- SAYANTAN DUTTA
ASSISTANT PROFESSOR
FACULTY OF PHARMACEUTICAL SCIENCES
RAMA UNIVERSITY
KANPUR, UTTAR PRADESH

2. WHAT IS PEPTIC ULCER
• Peptic ulcer - A sore of oesophagus, stomach,
intestine.
• It occurs in the part of gastrointestinal tract (g.i.t.)
which is exposed to gastric and pepsin.
• Etiology - imbalance between aggressive & defensive
factor.
.
AGGRESSIVE FACTORS DEFENSIVE FACTORS
Acid Gastric mucosa
Pepsin Bicarbonate
Bile Prostaglandins
H. pylori Nitric oxide

3. FORMS OF PEPTIC ULCER- 1. Duodenal 2. Gastric 3. Stress 4. NSAIDs
- Duodenal ulcer- Acid secretion is high in half of the patients.
- Gastric ulcer- Acid secretion is normal or low, but defense is low.
{Stomach secrete about 2.5 liter of gastric juice (parietal cells)}
Gastric acid secretion is regulated by-
a. Vagus pathway (Ach)
b. Gastric pathway
c. Local histamine
- They activate H+ K+ ATPase (proton
pump) on the parietal cells, which results
into secretion of H+ into gastric lumen,
where it combines with Cl- (drawn from the
plasma) and forms HCl
Causes-
1. H. Pylori
2. aspirin- NSIADs
3. stress
Risk-
1. alcohol abuse
2. Improper diet
3. Empty stomach

4. CLASSIFICATION OF DRUGS FOR PEPTIC ULCER

5. H2 ANTIHISTAMINES
• Cimetidine
• Ranitidine
• Famotidine
• Roxatidine
• Lafutidine
Physiology- Histamine H2 receptor on parietal cell HCl.
 H2 blockers are competitive antagonist (famotidine partially strong).
 They volume and acidity of basal , nocturnal and food induced gastric acid secretion.
 Inhibition is dose dependent.
 They also reduce gastrin induced HCl release and also reduce pepsin release.
 Effect on animal cells- 1. cardiac stimulation= isolated guinea pig
2. Uterine relaxation = rat
3. Bronchial relaxation = sheep

7. INTERACTIONS OF CIMETIDINE
1. Inhibitis several CYP450 isoenzymes and reduces hepatic blood flow.
2. Inhibits metabolism of many drugs --- accumulate to toxic level ( theophylline, phenytoin, warfarin, sulfonylurea,
metronidazole, etc.
3. Antacids reduce absorption of all H2 blockers.
4. Ketoconazole absorption by H2 blockers due to reduced gastric acidity.
Uses-
Promotes the healing of gastric and duodenal ulcer
• Gastric ulcer- 50 to 75%
• Duodenal ulcer- 70 to 90 % at 8 weeks
• Prophylaxis of aspiration pneumonia
• Peptic ulcer
• Urticaria
• Bleeding from stress ulcer
• Gastroesophageal reflux disease
• Nonulcer dyspepsia

8. ADVERSE EFFECTS
• Headache
• Dizziness
• Bowel upset Generally mild
• Dry mouth
• CNS: confusion, restlessness
• Rapid or high dose i.v. – bradycardia, cardiac arrhythmia, cardiac arrest
• Cimetidine has androgenic action.
• May cross placenta

9. PROTON PUMP INHIBITORS
DRUGS
• Omeprazole
• Esomeprazole
• Pantoprazole
• Lansoprazole
• Rabeprazole
• Dexrabeprazole
• Ilaprazole
OMEPRAZOLE
• Prototype of the class. Most effective in acid
• Parietal cells secrete H+ with the help of H+ K+ ATPase – proton pump.
• This is final step of acid secretion by any stimulus.
• PPI are inactive prodrugs.
• Accumulate in parietal cell  quickly activates in acidic environment
sulfenamide
• The active form firmly binds H+ K+ ATPase by covalent bond and inhibits
irreversibly the pump = gastric acid reduction
• They are enteric coated to prevent premature activation.
• PPI should be taken in empty stomach.

10. Mechanism of action
Omeprazole sulfenic acid sulfenamide H+ K+ ATPase gastric acid reduction.
Activ+ Covalent bond

11. PROTON PUMP INHIBITORS
ADVERSE EFFECTS
Generally well tolerated.
• Prolonged use  acid suppression =
bacterial growth increases.
• Nausea, loose stool, headache,
abdominal pain, joint pain.
• Accelerated osteoporosis among
elderly patients.
• Long term use- vitamin B12 deficiency
due to reduced absorption of acid.
DRUG INTERACTIONS
• Oxidation inhibits of diazepam,
warfarin, phenytoin.
• Inhibits CYP2C19.
• Reduced absorption of ketoconazole
and iron salts.
• Clarithromycin inhibits omeprazole
metabolism and increase its plasma
concentration

12. USES OF PROTON PUMP INHIBITORS
• Peptic ulcer- in patients who are not responding to H2 blockers.
• Drug induced ulcer- PPI drugs are required for NSAID usage.
• Stress ulcer- intravenous pantoprazole/ rabeprazole are effective for stress ulcer.
• Gastroesophageal reflux disease (GERD)- ulcer relieved fast and pain gets reduced.
• Zollinger Ellison syndrome- it is a gastric hypersecretory state due to gastrinoma, a rare
tumor secreting gastrin, which presents with difficult to heal ulcer.
• Aspiration pneumonia- for prophylaxis of aspiration pneumonia due to prolonged
anaesthia.

13. PROSTAGLANDIN ANALOGUE (MISOPROSTOL)
• PGE2 and PGI2 = produced in gastric mucosa.
• Protect ulcer by reducing acid secretion and increasing mucus + HCO3- secretion.
• Decrease gastrin release , increase mucosal blood flow and cytoprotective.
• Misoprostol is longer acting synthetic PGE1 derivative.
• food and antacid may reduced its absorption and bioavailability.
Adverse effects = diarrhoea and abdominal cramps.
• PG has stimulant effect and increase uterine contraction.
• Not suitable of used in pregnancy.

14. ANTACIDS
• Weak base that neutralize acid.
• Also inhibits formation of pepsin. ( as pepsinogen converted to pepsin at acidic
pH.)
• Duration of action is about 30 to 60 minutes.
Types =
1. systemic  which gets absorbed. = sodium bicarbonate
2. non- systemic acts only on stomach = Al / Mg hydroxide.

15. ANTACIDS.
SYSTEMIC
• Rapid but short acting.
• CO2 is released.
• NaHCO3 +HCl  NaCl + H20 + CO2
• Demerits: large dose induce alkalosis.
• Produce CO2 in stomach  distension,
discomfort.
• Short lasting acid rebound occurs.
NON- SYSTEMIC
• Insoluble compound.
• React with HCl form.
• CaCO3 + 2HCl  CaCl2 + H2O.
• No acid base disturbance occurs.
• However small amounts that are absorbed
have the same alkalinizing effects as
NaHCO3.

16. ANTACID COMBINATIONS:
• A combination of two or more antacid is frequently used.
• Superior effect.
• Fast ( Mag. Hydrox.) and slow (Alum. Hydrox.) acting components gives prompt as
well as sustained effect.
• Mag. Salts have laxative while alum salts are constipating  annul each others
action.
• Gastric emptying is least effected.
• Dose can be reduced = systemic toxicity is minimized.

17. DRUG INTERACTIONS:
Antacids reduce the absorption of many drugs: tetracyclines, iron salts, fluroquinone,
ketoconazole.
Uses
• Employed for only for intercurrent pain relief, dyspepsia and acidity.
• Nonulcer dyspepsia
• Heartburn.
• Faster symptom relief of GERD.

19. ANTI H. pylori DRUGS
 Gram negative bacteria. Survive in stomach.
 Attaches to the surface of the epithelium beneath
mucus.
 Secretes urease  convert urea to ammonia.
 Ammonia produce  neutral microenvironment
around the bacteria and promotes back diffusion
of H+ ions.
 For faster activity anti- H. pylori drugs + PPI are
used.

20. Lansoprazole 30mg + amoxicilline
1000mg + clarithromycin 500mg =
twice daily = 14 days
CBS 120mg QID + tetracycline 500 mg
QID + metronidazole 400mg TDS +
omeprazole 20mg BD
Quadruple therapy 
 US FDA approved regimen

21. DRUGS USED TO TREAT
GERD
• Reflux is very common
problem.
• Some cases have anatomical
defect but majority are
functional.
• Repeated reflux may lead to
esophagitis, erosion, ulcer,
pain on swallowing and
increases the risk of
esophageal carcinoma.

22. REFERENCES
Tripathi KD, Essentials of medicals pharmacology, JAYPEE Brothers medicalpublishers (P) Ltd., Drugs for
peptic ulcer and gastroesophageal reflux disease, 695-708.