Peptic ulcer,Types of Ulcer,ANTI ULCER AGENTS

Peptic ulcer

Peptic ulcer is a areas of degree of degeneration of the tissue lining the stomach or the duodenum .(The first part of the small intestine).The lining of the stomach and duodenum normally has a barrier of mucus to protect it form acidic digestive juices. If this barrier is damaged, the acid may cause inflamation and erosion of the lining .The eroded areas are know as peptic ulcer.

Types of Ulcer

1 Acute peptic ulcer (stress ulcers).

2 Chronic peptic ulcer(gastric and duodenal ulcer).

1 Acute Peptic Ulcer

Acute peptic ulcer or stress ulcers are multiple small muscosal erosions seen most commpnly in the stomach.


a. Psychological stress

b. Physiological stress

Shock ,sever truma, septicaemia ,extensive burns,drug intake like aspirin ,steroids and local irritants like alcohol, smoking, coffee etc.

2 Chronic Peptic ulcers: (Gastric and Duodenal Ulcer)

Gastric ulcers are more common in people over the age of 50 .Duodenal ulcers are more common than gastric ulcers and usually occurs in people aged 20-45 particularly men.


The immediate cause of peptic ulcer diseae is disturbance in normal protective mucosal ‘barrier’ by acid pepsin,resulting in digestion of the mucosa.

1. Helicobacter pylori
H.pylori infection may lead to the development of gastritis, in which the stomach lining becomes inflamed or to
a peptic ulcer. The bacterium carried through feces and saliva and easily spread among people living in unsanitary conditions.

2. Acid-pepsin secretions
Some level of acid-pepsin secretion.

3. Mucus secretion
Any condition decreases the quantity or quality of normal protective mucus barrier leads to peptic ulcer.
4. Gastritis
Gastritis (inflammation of the lining of the stomach) present in the gastric ulcer, it is not clear, to the effect of ulcer.

5. Local irritants
Long-term use of aspirin, anti-inflammatory drugs ibuprofen may damage the lining of the stomach. Other factors may lead to peptic ulcer include smoking, alcohol and caffeine.

6. Dietary factors
Nutritional deficiencies may also be etiologic factors in peptic ulcer ase is acid-

7. Genetic factors
Genetic influences leads to duodenal ulcers.

8. Hormonal factors
Secretion of hormones associated with peptic ulceration. eg. Elaboration of gastrin by islet cell tumor in Zollinger- Ellison syndrome, endocrine secretions in hyperplasia.

Complications of Peptic Ulcer

The most common complication is bleeding
1. Minor bleeding leads to anemia such as pale skin, fatigue, feeling of faintness.
2. Bleeding from the digestive tract lead to vomiting of the blood.
3. Ulcer perforates all the layers of the stomach or duodenum, allowing gastric juices to enter the
abdomen causing sever pain.

1.  discomfort in the  abdomen.
2. Loss of appetite and weight loss.
3. Nausea and vomiting.


1. Endoscopy
To view stomach and duodenum, a sample of the stomach lining taken to check for H. Pylork

1. Antibiotic therapy: To eradicate H.pylori
a Pencillins
b. Cephalosporins.

2. Antacids
Act by neutralizing gastric and raising gastric pH.
a Magnesium hydroxide
b. Aluminium hydroxide

3. H, Receptor Antagonists

a Cimetidine
b Ranitidine
c Famotidine.

4. Proton Pump Inhibitors
a Block the intestinal H/K ATPase pump to inhibit gastric acid secretion
b. Omeprazal.

Peptic ulcer
Peptic ulcer is the disease related to the gastrointestinal tract (G.I.T.) which is exposed to gastric acid and pepsin (stomach & intestine). It produced due to imbalance between aggressive (acid, pepsin and H. pylori) and the defensive (gastric mucus and bicarbonate secretions) factors.


The peptic ulcer are of two types.
1. Gastric ulcer
2. Duodenal ulcer or intestinal ulcer.

Antiulcer agents
The agents or drugs used in the treatment of peptic ulcer is known as antiulcer agents,


A. Reduction of gastric acid secretion

1. H, antihistamines
a. Cimetidine
b. Ranitidine
c. Famotidine
d. Roxatidine
e. Loxatidine

2. Proton pump inhibitors
a Omeprazole
b. Lansoprazole
c Pantoprazole
d. Rabeprazole
e Esomeprazole

3. Anticholinergics
a Pirenzepine
b Propantheline
c Oxyphenonium
4. Prostaglandin analogues
a Misoprostol
b. Enprostil
c. Rioprostil

B. Neutralization of gastric acid (Antacids)
1. Systemic
a Sodium bicarbonate
b Sodium citrate

2. Nonsystemic

a Magnesium hydroxide
b. Mag. trisilicate
c Aluminium hydroxide gel
d. Calcium carbonate

C. Ulcer protectives
a Sucralfate
b. Colloidal bismuth subcitrate (CBS)

D. Ulcer healing drugs
a Carbenoxolone sodium

E. Anti-H. pylori drugs
a. Amoxicillin
b. Clarithromycin,
c. Metronidazole,
d. Tinidazole,
e Tetracycline.

A. Reduction of gastric acid secretion

1. H- receptor antagonists

These are the most popular drugs for the treatment of peptic ulcer. They bring about symptomatic relief and promote ulcer healing. Gastric acid secretion involves H2-receptors
which are blocked by H2-blockers.

Mechanism of action

There are four H-antagonist such as cimetidine, famotidine etc. have interaction with H, receptors and blocks the H, -receptors and allow the anti ulcer activity.


1. Headache, dizziness, bowel upset, dry mouth and rashes.
2. Mental confusions, restlessness, hallucinations, delirium convulsions and coma have occurred in elder patients.
3. Bolus 1.V. injection can release histamine and caused bradycardia, arrhythmias and anti androgenic action.
4. Fever and transient neutropenia occur rarely.

a. Cimetidine

It produceshealing in 60% of patients of duodenal ulcer and after 8 weeks this figure exceeds 80%. Following oral administration 80% is
absorbed and mostly excreted unchanged in urine, so caution should be exercised in renal failure.


200 mg thrice a day or 400 mg twice a day with meals and at bed time.

Adverse effects

The adverse effects include diarrhoea, drowsiness, itele and skin rashes

b. Ranitidine
It is a potent Hy antagonist having the same indications as cimetidine


150 mg twice a day or 300 mg at bed time.

2. Proton pump inhibitor

Parietal cells secrete H ions which is accomplished by an enzyme H,K-ATPase (serves as a proton pump, exchanging K for Hº ions). It is required for HCl secretion.

Mechanism of action

1. Omeprazole is a proton pump inhibitor which is inactive at neutral pH but at pH<5 rearranges to two charged cationic forms that resci covalently with SH groups of the HK Atpase enzyme and inactivate it irreversibly, specially when two molecules of omeprazole react with one molecule of the enzyme.

2.After diffusion of omeprazole into the parietal call from blood it gets concentrated in the acidic pH of the canaliculi and tightly bound to the enzyme thus protest
the peptic ulcer.


The proton pump inhibitors are able to produce nausesloose stools, headache, abdominal pain, muscles and joint

a. Omeprazole
It is the prototype member of substituted benzimidazoles which inhibit the final common step in gastric acid secretion and have overtaken H, blockers for acid-peptic disorders. The
only significant pharmacological action of omeprazole is dose dependent suppression of gastric acid secretion; without anticholinergic or H, blocking action. It is a powerful inhibitor of gastric acid: can totally abolish HCI secretion.

b. Pantoprazole
It is a newer H K ATPase inhibitor, similar in potency and clinical efficacy to omeprazole, but is more acid stable and less active at higher pH. It is the only PPI available for i.v. administration; particularly employed in bleeding peptic ulcer I for prophylaxis of acute stress ulcers. It has lower affinity for cytochrome Pse than omeprazole or lansoprazole: risk of drug interactions is minimal.

40 mg OD.

3. Anticholinergics

These drugs reduce the volume of gastric juice without raising its pH unless there is food in stomach to dilute the secreted acid. Stimulated gastric secretion is less completely inhibited. They also delay gastric emptying.

Mechanism of action
Atropine is a anticholinergic drug which reduce the volume of gastric juice without raising its pH and actions is performed by diluting the amount of secreted acid.

It may cause tachycardia restlessness, hallucinations respiratory depression and coma.

a. Pirenzepine
It is an anticholinergic which inhibits gastric acid secretion. It is more selective and more specific in inhibiting gastric acid secretion with fewer side effects.

50 mg twice a day for 4-6 weeks promotes duodenal ulcer healing

4. Prostaglandins
PGE .maintain gastroduodenal mucosal integrity.

Mechanism of action
1. There are two types of prostaglandins PGE and PGI, are produced in the gastric mucosa and appear to serve a protective role by inhibiting acid secretion and promoting HCO (bicarbonate) secretion in mucus.

2. PGs inhibit the gastric flow and causes cyto protective actions
3. The mucus layer covering gastric and duodenal mucosa and protects the epithelial layer of stomach and duodenum.


The major side effect is diarrhoea, abdominal cramps, uterine bleeding, abortion and patient acceptability is poor.

A Enprostil
It is a synthetic PGE, analogue claimed to have a healing rate more than 80% in a month in case of duodenal ulcer. The oral dose is 35 mcgtwice a day or 75 meg once a day.

Adverse effect
The adverse effects include diarrhoea which is the commonest side effect (20-50% patients), abdominal cramps, nausea, vomiting, flatulence,headache, backache, loss of appetite.

Leave a Comment

Your email address will not be published. Required fields are marked *