Peptic ulcer

1. Peptic ulcer ( Duodenal ulcer + Gastric Ulcer)
• Peptic ulcer are the open sores that occurs in the lining of
the stomach or small intestine. It is the erosion of mucosal
layer and break in the lining of the stomach.
• Peptic ulcer results from imbalance of protective factors
(bicarbonate & mucus) and damaging factors (acid &
pepsin).
• Incidence of duodenal ulcer is more common than gastric
ulcer.
Risk Factors:
• Smoking
• Alcohol intake
• Spicy Food
• Prolong use of NSAIDS (e.g: Paracetamol, Ibuprofen, etc)
• H. Pylori
• Stress like major injuries, illness, tumor, etc

2. Symptoms
• Epigastric pain
• Nausea
• Vomiting
• Dyspepsia
• Bloating
• Belching
• Pain after food
intake
Diagnosis
• Endoscopy
• Barium swallow
• Lab test for H. pylori infection

3. DRUGS FOR PEPTIC ULCER
A. Reduction of gastric acid secretion
1. H2 antihistamines: Cimetidine, Ranitidine, Famotidine
2. Proton Pump Inhibitors (PPI): Pantoprazole, omeprazole,
rabeprazole, lansoprazole, esomeprazole
3. Anticholinergics: Pirenzepine, propantheline, oxyphenonium
4. Prostaglandin analogues: Misoprostol, enprostil, rioprostil
B. Antacids
1. Systemic: sodium bicarbonate, sodium citrate
2. Non-systemic: magnesium hydroxide, magnesium trisilicate,
aluminium hydroxide, magaldrate, calcium carbonate
C. Ulcer proctectives: sucralfate, colloidal bismuth subcitrate
D. Anti H. Pylori Drugs: Amoxicillin, Metronidazole,
Tetracycline, Clarithromycin

4. Mechanism of Gastric acid secretion

5. H2 ANTIHISTAMINES
• MOA: Drugs act on H2 receptors as antagonist &
blocks histamine mediated gastric release.
• Cimetidine
H2 receptor antagonist
Blocks histamine induced gastric secretion
Well absorbed orally, bioavailability 60-80%
• Ranitidine: 5 times more potent than cimetidine
• Famotidine: 5-8 times more potent than ranitidine
& longer duration of action
• Roxatidine: twice potent & longer acting than
ranitidine
• Nizatidine: high bioavailability

6. Indications
1. Duodenal ulcer
2. Gastric ulcer
3. Stress ulcer & Gastritis
4. Zollinger Ellision Syndrome (ZES): It is a gastric
hypersecretory state due to tumor secreting
gastrin.
5. Gastroesophageal reflux disease (GERD): It is a
recurrent reflex of gastric contents into the
esophagus that produces symptoms of heartburn
or causes esophageal injury.
6. Prophylaxis of aspiration pneumonia:
preanaesthetic medicine before surgery

7. Adverse effects
• reduced gastric acid production.
• headache, dizziness, diarrhoea, and muscular pain.
• confusion and hallucinations occur primarily in elderly
patients and after intravenous administration.
• gynecomastia and galactorrhea (continuous
release/discharge of milk).
• Reduce absorption of drugs such as ketoconazole
Contraindications
• Concurrent use with drugs like metronidazole,
phenytion will inhibit their metabolism
• Coadminstration with drugs like antacids will decrease
their absorption

8. PROTON PUMP INHIBITORS (PPI)
• MOA: Drug inactivates H+K+ATPase enzyme in parietal
cells & suppress the secretion of gastric acid. It is very
effective inhibition of gastric acid secretion.
• Omeprazole: Potent & prolong action PPI that irreversibly
inhibit H+K+ATPase enzyme & inhibit gastric acid secretion.
(Dose: 20-40 mg OD)
• Pantoprazole: high bioavailability & available as i.v.
(Dose: 40 mg OD)
• Rabeprazole: high Pka, fast suppression of gastric acid
secretion (Dose: 20-40 mg OD)
• Lansoprazole: more potent, higher bioavailability, faster
action (Dose: 30 mg OD)
• Esomeprazole : s-enantiomer of omeprazole, have higher
bioavailabilty (Dose: 20-40 mg OD)

9. Indications
1. Peptic ulcer
2. Bleeding peptic ulcer
3. Stress ulcer
4. Zollinger Ellision Syndrome (ZES): It is a gastric
hypersecretory state due to tumor secreting
gastrin.
5. Gastroesophageal reflux disease (GERD): It is a
recurrent reflex of gastric contents into the
esophagus that produces symptoms of heartburn
or causes esophageal injury.
6. Aspiration pneumonia: preanaesthetic medicine
before surgery to avoid aspiration of gastric
contents

10. Adverse effects
• nausea, loose stools, headache, abdominal pain,
muscle and joint pain, dizziness are complained by 3–
5%.
• rashes (1.5% incidence), leucopenia & hepatic
dysfunction
• atrophic gastritis, hypergastrinemia on prolonged use.
• gynaecomastia & erectile dysfunction in some patients
• accelerated osteoporosis among elderly patients
Contraindications
• PPI inhibits metabolism of diazepam, phenytoin and
warfarin.
• Reduced gastric acidity decreases absorption of
ketoconazole and iron salts.

11. ANTICHOLINERGICS
Drugs block the muscarinic receptor in parietal
cell that cause decreased intracellular ca++ level &
decreases gastric acid secretion.
• Pirenzepine: selective M1 anticholinergic with
fewer side effects (Dose 100-150 mg OD)
PROSTAGLANDIN ANALOGUES
Drugs stimulate secretion of mucus &
bicarbonate ion for protection of stomach lining
& inhibit secretion of gastric acid.
• Misoprostol: longer acting & inhibit acid output
dose dependently (Dose 200 µg QID)
• Contrainication: Pregnancy (may cause abortion)

13. ANTACIDS
• Drugs that neutralize gastric acid & raise pH of gastric
contents.
• e.g:-magnesium hydroxide, magnesium trisilicate,
aluminium hydroxide, magaldrate, calcium carbonate,
sodium bicarbonate, sodium citrate
• Acid Neutralizing Capacity: Number of mEq of 1N HCl that
are brought to pH 3.5 in 15 min by unit dose of antacid
(1g).
Functions of antacids:
• Neutralization of gastric acidity
• Inactivate pepsin due to increase pH (>4.0)
• Reduce peptic activity
• Reduction of helicobacter pylori
• Stimulation of PG synthesis

14. NEUTRALIZATION REACTION WITH ANTACIDS

15. Adverse effects
• Systemic alkalosis
• Distension, discomfort and belching
• Sodium overload (edema)
• Constipation & diarrhoea
Contraindications
• Antacids decrease the absorption of many drugs,
especially tetracyclines, iron salts, fluoroquinolones,
ketoconazole, H2 blockers, diazepam,
phenothiazines, indomethacin, phenytoin, isoniazid,
ethambutol and nitrofurantoin.

16. ULCER PROTECTIVES
• Drugs enhance mucosal protection and prevent mucosal
injury, reducing inflammation, and healing existing ulcers.
• Sucralfate: It binds to proteins of mucosa and forms
complex which creates a physical barrier between acid and
stomach. It also stimulates prostaglandin release as well as
mucus and bicarbonate output, and it inhibits peptic
digestion.
• Since it requires an acidic pH for activation, sucralfate
should not be administered with PPIs, H2 antagonists, or
antacids.
• Colloidal Bismuth subsitrate: CBS have anti H. Pylori
actions, inhibit the activity of pepsin, increase secretion of
mucus, and interact with glycoproteins in mucosal to coat
and protect the ulcer.

17. • H. pylori is a Gram negative bacteria associated with gastritis, gastric
& duodenal ulcers, gastric adenocarcinoma.
ANTI H. PYLORI DRUGS
• Triple therapy (3 drug regimen) for 1 or 2 weeks
• PPI, Amoxicillin, Clarithromycin, Metronidazole/Tinidazole
• Quadruple therapy (4 drug regimen)
• CBS 120 mg QID + Tetracycline 500 mg QID +
metronidazole 400 mg TDS + omeprazole 20 mg BD

18. • Miscellaneous Drugs
• Simethicone: antifoaming agent that reduces
surface tension, breaks bubble formation and
prevents reflux
• Alginates: Forms a layer of foam on top of
gastric contents & reduce reflux
• Oxethazaine: Surface anaesthetic