The document discusses anti-ulcer drugs. It begins by describing peptic ulcers and the imbalance between aggressive and defensive factors that can lead to their development. It then covers the classes of anti-ulcer drugs, including H2 blockers that reduce acid secretion, proton pump inhibitors, prostaglandin analogs, and antacids. Sucralfate and colloidal bismuth subcitrate are also covered as ulcer protective drugs. Diagnostic tests for ulcers like endoscopy and barium meal are mentioned. The goal of anti-ulcer treatment is outlined as relieving pain, promoting healing, preventing complications, and reducing relapse.

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ANTI-ULCER DRUGS
AMITY UNIVERSITY UTTAR PRADESH
AMITY INSTITUTE OF PHARMACY
LUCKNOW, INDIA
2018-20

2. Amity institute of pharmacyIntroduction
• Peptic ulcer/stomach ulcer is the condition in which imbalance
of aggressive factor and defensive factors.
• Pathogenesis of peptic ulcer disease:
• In the starting of 19th
century lot of reacher has been developed
the treatment for ulcer.
• After period of time it has been identified that bacteria can
cause the ulcer.
• Mainly Helicobacter pylori found to be recurrence of stomach
ulcer. 1
Aggressive factor Defensive factor
Gastric acid Prostaglandin
Pepsin Mucosa
Gastrin Epithelial junctions

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•The main goal of anti ulcer drug is to decrease the level of acidity
or enhancing mucosal protection.
•The goal of antiulcer therapy are:
 Relief of pain.
 Ulcer healing.
 Prevention of complications (bleeding, perforation).
 Prevention of relapse.
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4. Amity institute of pharmacyHelicobactor Pylori
• In 1981 Robin Warren, M.D. an Australian pathologist,
discovered numerous bacteria living in tissue taken during a
stomach biopsy(laboratory tests that examine stomach tissue).
• It is gram negative bacteria.
• Break down mucosal defense.
• Secretes urease → convert urea to
ammonia.
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• Symptoms of h. Pylori:
 Abdominal pain
 Feeling of Fullness
 Indigestion
 Feeling very hungry 1 to 3
hours
after eating.

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 Mild nausea
 Pain Starts 2/3 hours after meals, or in the middle of the night.
Test for diagnosing H.pylori
• Breath test: by measuring the amount of CO2 in exhaled
breath.
• Blood test: by identifying H.pylori antibodies by ELISA
test.
• Stool test: stool sample tested with H.pylori antigen.
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6. Amity institute of pharmacyClassification
Classes Drugs
1. Reduction of gastric acid secretion
a. H2 antihistamine Cimetidine,ranitidine,famotidine,roxatidine,
loxatidine
b. PPIs Omeprazole,lansoprazole,pantoprazole,
rabeprazole, esomeprazole
c. Anticholinegics Pirenzepine,propantheline,oxyphenonium
d. PG Analougues Misoprostol, enprostil, rioprostil
2. Neutralization of gastric acid
(Antacid)
a. Systemic
Sodiumbicarbonate,sodium citrate
b. Nonsystemic Mg. hydroxide, Mg. trisilicate, Al hydroxide,
calcium
3. Ulcer protective Sucralfate, CBS
4. Ulcer healing drugs Carbenoxolone sod.
5. Anti Hpylori drugs Amoxixillin, clarithromycin, metronidazole,
tinidazole, tetracycline 6

7. Amity institute of pharmacyH2 Antagonists
• These are first class of highly effective drugs, but have been surpassed
(less potent) by PPIs.
• Cimetidine was first H2 blocker introduce clinically and is describe as
prototype, though other h2 blocker are more commonly used.
Mode of action:
Blocks the H2 (histamine) receptor of
parietal cells to prevent transport of H+
ions out of the cell into the stomach
(acid formation)
Adverse effect:
 Headache
 Dizziness
 Bowel upset
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8. Amity institute of pharmacyPharmacokinetic
• Absorbed rapidly.
• Food and antacids may reduce absorption.
• Distributed widely throughout the body.
• Metabolized by the liver.
• Excreted primarily in the urine.
Therapeutic use
• Promote healing of duodenal and gastric ulcers.
• Provide long term treatment of pathological GI hyper secretory
conditions.
• Reduce gastric acid production and prevent stress ulcers.
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9. Amity institute of pharmacyProton pump inhibitor
• They are prodrugs that activate in acid environment.
• After absorption, the active metabolite diffuses into the parietal
cells.
• Clinically used PPIs are: Omeprazole, lansoprazole,
esomeprazole, pantoprazole, rabeprazole.
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Mode of action:
•Ach, histamine, gastrin the acid production
with the activity of proton pump.
•PPIs block the final step of acid
production.

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Therapeutic uses:
•Peptic ulcer
•Bleeding peptic ulcer
•Stress ulcers
•Zollinger-Ellison syndrome ( tumors cause the stomach to produce
too much acid, resulting in peptic ulcers)
Adverse effect:
•Headache
•Diarrhoea
•Constipation
•Rash
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11. Amity institute of pharmacyProstaglandin Analogs
• Prostaglandin analog are produce in gastric mucosa and appear to
serve a protective role by inhibiting acid secretion and promoting
mucus and bicarbonate secretion.
Moa:
• Misoprostol acts upon gastric parietal cell, inhibiting the
secretion of gastric acid via GPCR mediated inhibition of
adenylase cyclase, which lead to decreased intracellular cyclic
AMP levels and decreased pump activity at the surface of parietal
cell.
• PK: After oral administration it is rapidly absorbed and
metabolized, the half life is 30 min. and is excreted in urine.
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Antacid
MOA
•Neutralize gastric acid
•It shouldn’t be given with enteric coated tablet otherwise it will
dissolve in stomach because antacid increase the stomach Ph.
During acid neutralization foam formation occur
It will causes esophagus burn
So antifoaming agent(insoluble oils, polydimethylsiloxanes
and other silicones) or dispersing agent( urea, lyoprint G)
must be add.
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• Adverse Effect:
Nausea
Constipation
Diarrhoea
Headache
Loss of appetite
Black or tarry stool
Deep sleep
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• Non systemic antacid
These are in soluble and poorly absorbed basic compound.
React in stomach with acid to form respective chloride salts.
This again react bicarbonate is not allow for absorption,
hence no acid base disturbance.
• Aluminium hydroxide gel
They relaxes smooth muscle leads to delay in gastric
emptying.
This causes constipation.
Mucosal astringent reaction also leads to constipation.
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Ulcer protective
• Sucralfate
Aluminium salt of sulfated sucrose.
• MOA
In acidic environment (pH<4) it polymerises by cross
linking molecules to form sticky viscous gel that adheres to
ulcer crater– act as acid resistant physical barrier.
Dietary proteins get deposited on this layer forming another
coat.
May stimulate PGE2 synthesis & HCO3- secretion.
Bind epithelial & fibroblast growth factors which promotes
mucosal repair.
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• Uses
Prophylaxis of Stress ulcers.
Bile reflux gastritis.
Topically – burn, bedsore ulcers.
Colloidal Bismuth Subcitrate (CBS)
• MOA
CBS and mucous form glycoprotein bi complex which
coats ulcer crater.
↑ secretion of mucous and bicarbonate, through stimulation
of mucosal PGE production.
Detaches H.pylori from surface of mucosa and directly
kills them
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• Adverse effects:
 Blackening of tongue.
Stools.
Diarrhoea.
Headache.
Dizziness
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18. Amity institute of pharmacyDiagnosis
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Endoscopy:
•Flexible tube fitted with camera
is threaded down the esophagus
into stomach to see the ulcer by
physician.
Barium meal:
•Barium liquid is drunk making
ulcer visible on x-ray.

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Reference
1. KD Tripathi. Essential of medical pharmacology; 5th
edition,
2004,jaypee brothers publication, New Delhi: 587-598.
2. Prabha P, Karpagam T, Varalakshmi B, Packiavathy A
S.Indigenous anti-ulcer activity of Musa sapientum on peptic
ulcer. Pharmacognosy Res, 3(4):232-8, 2011.
3. Peptic ulcers [Online]. 2016 [Cited 2016 January 30];
Available from: URL: http://www.nhs.uk/Conditions/Peptic-
ulcer/Pages/clinical-trial.aspx.
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