1. United Institute Of Pharmacy, Prayagraj
Anti- ulcer agents
Presented By:- Vishal Kumar Yadav
M. Pharm 1st year
Pharmacology
Submitted to:- Dr. Sunil Kumar Singh
United Institute of Pharmacy,
Department of Pharmacology
2. Ulcerand Anti- Ulcer agents
Erosion in the layer of the gastrointestinal tract (G.I.T.) which is exposed to gastric
acid and pepsin.
It occurs due to imbalance between the –
i.) Aggressive- Acid, Pepsin, Bile and H. Pylori
ii.) and the defensive ( gastric Mucus and bicarbonate secretion)
iii.) H. Pylori
Means it occurs because of increase in acid secretion or decrease in gastric
mucus secretion.
Role of acid in stomach is to convert pepsin into pepsinogen for digestion of
food and destroy microbes.
In an empty stomach max. acidity is pH 1.0 – 1.5
• Potential tissue damage is prevented by epithelial regeneration every 6 day.
Protective mucin layer
Regulation of HCl secretion
5. The terminal enzyme H+K+ ATPase (Proton Pump) which secrete H+ ions
in the parietal cell.
Which can be activated by Histamine, acetylcholine, and Gastrin via receptor
located on the basolateral membrane.
H1 receptor activate H+K+ ATPase by generating cAMP
The Muscarinic and Gastrin cholecystokinin (CCK2) receptor appear to
function through the phospolipase C
IP3 – DAG pathway - Mobilize intracellular calcium
Proton pump activation, releasing of hydrogen ion, Thus increase in acid
secretion.
6. Prostaglandin have been ascribed a cytoprotective role in the gastric mucosa
by augmenting mucus and bicarbonate secretion from Gastric mucosal Epithelial cell
The gastric mucus Transform into adherent gel like film over the mucosa
Which trap the secreted bicarbonate ions and prevent their neutralization by creating
a barrier for H+ ions
PGE2 produced by astric mucosa inhibit acid secretion by opposing CAMP
genration.
7. ANTI – ULCER
The goals of Anti ulcer therapy are - Relief of pain
-ulcer healing
-prevention of complication bleeding
-prevention of relapse
8.
9. H2 ANTAGONIST
First class of highly effective drug for acid peptic disease suprassed by proton
pump inhibitors
They are compitative Antagonist of histamine H2 receptor and block the
histamine induce gastric secretion
H2 blocker can potentiate histamine induce bronchospasm
Fall in blood pressure
pharmacokinetics
Absorbed orally
Bioavailability 60-80%
Excreted via urine and bile
Half time 2-3 hours
Adverse Effect
• Cemtidine has anti-androgenicaction increase plaasma plasma prolactin and inhibit
degradation of estradiol by liver
•Gynaecomastia
•Loss of libido
•Hallucination confusion bradycardia,dry mouth bowl upset ,headache,diziness
10. PROTON PUMP IHIBITORS
PPIs irreversibly Inhibit the proton pump that is responsible for the
Final Gastric acid secretion from the parietal cell .
3 phases of activation
They are weak bases concentrated in the acid compartment of parietal
celll
The inactive prodrug is activated in the acid Environment
The reactive sulfahydryl grou then form a disulfide bond with residue on the
proton pimp inactivating the enzyme
Pharmacokinetics
Administrated orally
Enteric coated tablet
Bioavailability reduce with food becouse acidity decreases
Advere effect
Joint pain, hepatic dysfunction osteoporosis,
11. ANTACIDS
ANTACIDS are the basic substance which gastric acid and
raise pH f gastric content
Peptic ulcer activity is indirectly reduce if the PH rises above
Antacid donot decreases acid production rather agent that raises the
PH
ANC –acid neutralizing capacity
Systemic and non systemic antacid
12. ULCER PROTECTIVES
SUCRALFATE It is a basic aluminum salt of sulfated sucrose
It polymerizes at pH greater than 4
A sticky gel like consistency adhere to the ulcer based and remain there
for 6 hours.
It forms a physical barrier preventing acid, pepsin and bile from coming
contact with ulcer bases.
Sucralfate has no acid neutralizing capacity but delay gastric emptying .
It is absorbed orally, healing of both gastric and duodenal ulcer.
SIDE EFFECTS:- The side effects are
Dry mouth , Nausea and Constipation.