ANTI-ULCER

AGENTS
Paper – Pharmacology III
Code – 618

Presented by ,

Name – Pritam Jana

University Roll No, - 18901920073
Year - 3rd
Section -B

Dr. B. C. Roy Collage of Pharmacy and Allied Health Sciences

 INTRODUCTION
The stomach secretes about 2.5 L of gastric juice daily.The production of acid is important for
promoting proteolytic digestion of foodstuffs, iron absorption and killing pathogens. Mucus
secreting cells also abound in the gastric mucosa. Bicarbonate ions are secreted and trapped in
the mucus, creating a gel-like protective barrier that maintains the mucosal surface at a pH of 6–
7 in the face of a much more acidic environment(pH 1–2) in the lumen. Alcohol and bile can
disrupt this protective layer. Locally produced ‘cytoprotective’ prostaglandin stimulate the
secretion of both mucus and bicarbonate. Disturbances in these secretory and protective
mechanisms are thought to be involved in the pathogenesis of peptic ulcer, and indeed in other
types of gastric damage such as gastro-oesophageal reflux disease (GORD1) and injury caused
by non-steroidal anti-inflammatory drugs (NSAIDs). The latter exchanges
across the basal membrane of the parietal cell for Cl−. The principal mediators that directly – or
indirectly control parietal cell acid output are:
• histamine (a stimulatory local hormone)
• gastrin (a stimulatory peptide hormone)
• acetylcholine (a stimulatory neurotransmitter)
• prostaglandins E2 and I2 (local hormones that inhibit
acid secretion)
• somatostatin (an inhibitory peptide hormone)
 ULCER
 A ulcer or more precisely peptic ulcer is an open sore in the upper digestive tract. There
are two types of peptic ulcers, a gastric ulcer, which forms in the lining of the stomach,
and a duodenal ulcer, which forms in the upper part of the small intestine.
Causes of Peptic Ulcer : The ulcer is caused due to imbalance between protective
factors/defensive factors(Mucus and bicarbonate secretion) and aggregative factors(HCL and
pepsin).and this is happened due to following reason –
 The bacterium named Helicobactor pylori, camphylobactor pylori.
 Decrease mucus and bicarbonate secretion.
 Increase protein diet.as well as for skipping of diet.
 Over intake of aspirin and NSAIDs.as well as coffee and tea.
 Alcohol and smoking, Radiation therapy.

 Signs and symptoms : Main symptoms are heart burn, stomach ulcer-blood in
vomiting, lower part bleeding ,black tarry stool.
Other symbols are abdominal pain, nausea, loss of appetite .,weight loss etc.

 Different kind of ulcer

 Anti ulcer drugs
 Anti ulcer drugs are categorized in five classes-
• Anti pyloric drugs /Antibiotics.
• Antacids.
• Drugs decrease HCL secretion.
• Ulcer protective.
• Ulcer healing drugs.

 This classes are describe below,

Anti pyloric drugs : Used when cause of ulcer are C. pylori and H. pylori.
 Macrolide Antibiotic( Clarithromycin)- MOA- Inhibit Protein synthesis.
 Beta lactum antibiotic (Amoxacillin)- MOA- Inhibit cell wall formation.
 Nitroimidazole dvt. (Tinidazole, Ornidazole)- MOA-cidal in nature
(reduction of their Nitro group and formation of metabolite that bind
with DNA and interferes its functions.)
 Antacid
MOA of antacid is to neutralize gastric HCL. Ideal antacid should not increase gastric pH not more than 5
(otherwise chances of rebound hyperacidity occurs) Antacids should not be given with enteric coated tablet.
Otherwise enteric coating will dissolve in stomach. Because antacid increase the stomach pH During acid
neutralization foam formation occurit will cause esophagus burn so it is must to add antifoaming agent or
dispersing agent (HLB value= 1-3 .these are the essential component of antacid. E.g. Polysiloxane (Simethicon,
Dimethicon)
There are basically two types of antacids.-

1.Systemic antacid : Absorbed systematically . E.g : NaHCO3.

2.Nonsystemic antacids : Poorly absorbable.

Examples are Al(OH)3,Mg(OH)2,and the most potent and fast acting CaCO3.
Nowadays combination antacid thertapy is very much common and it
decrease individual dose of antacid so least side effect come from individual
antacid. As example-Anti TB (Isoniazide)+Al(OH)3 gel = decrease the
absorption of Isoniazide.

Note- NSAIDs should be taken with antacid — It decrease the chances of ulcer. ACID NUTRALIZATION CAPACITY IS USED TO DETERMINE
THE STRENGTH OR ACTIVITY OF ANTACID
 Drugs decrease HCL secretion
Anticholinergic drugs : inhibit acetylcholine
action and decrease HCl secretion. E.g. Piperazine.
Decrease salivation, Dryness of mouth, skin eye.
Constipation and other anti cholinergic side effect
may occur.
H2 receptor blocker/H2 antihistaminic:
Inhibit Histamine action on H2 receptor .decrease
HCl secretion. E.g. Cimetidine , Ranitidine ,
Femotidine , Nizatidine etc. it use as pre anaesthetic
medication to decrease gastric secretion.
Prostaglandine analogue:increase mucus and
bicarbonate secretion; show cyto protective action by
increasing mucosal blood supply and decrease HCl
secretion. E.g. Misoprostel, Rioprostil ,Enprostil.
Contractions in intestinal smooth muscle – Abdominal
cramps-Diarrohea are some major side effects.
Proton pump inhibitors :these are inactivate
at normal pH but at lower pH these are rearrange in
cationic form (sulphenic acid, sulphonsamides).and
covalently bind with the –SH group of proton
pump ,inactivate proton pump and decrease HCl
secretion .E.g. are Omeprazole, Pantoprazole,
Rabeprazole, Esomeprazole. etc.
These are inhibit oxidation of some drugs e.g.
Warfarin , Diazepam.
Ulcer protective : Sucralfate is a
locally acting substance that in an
acidic environment (pH < 4),reacts
with hydrochloric acid in the
stomach to form a cross-linking,
viscous, paste-like material capable
of acting as an acid buffer for as long
as 6 to 8 hours after a single dose. It
also attaches to proteins on the
surface of ulcers, such as albumin
and fibrinogen, to form stable Ulcer healing drugs : these drugs act by
insoluble complexes. These increasing thick mucous secretion by
complexes serve as protective goblet cells. So make a thick protective
barriers at the ulcer surface, layer and increase life spam of gastric
preventing further damage from mucosal cell.
acid, pepsin, and bile. E.g. are Carbenoxolane sodium,
Deglycyrrhinized liquorice.
THANK YOU