This presentation discusses the causes, symptoms, classification and treatment of peptic ulcers. It begins with an introduction defining ulcers and their locations in the stomach and duodenum. The main causes of ulcers are identified as alcohol, NSAIDs, smoking, stress and Zollinger-Ellison syndrome. Common symptoms include epigastric pain relieved by food or antacids. The presentation then classifies treatments for ulcers including anti-secretory agents like H2 receptor antagonists and proton pump inhibitors, anticholinergic drugs, prostaglandin analogues, antacids, and anti-H. pylori treatments. Sucralfate is also discussed as an ulcer protective agent.

1. Presentation By:
Mohd Taher Uddin
Dept. of Pharmacology.
170122887001
Under Guidance of:
Dr. R Padhmavati
Associate professor
Dept. of Pharmacology.
G. PULLA REDDY COLLEGE
OF PHARMACY, HYDERABAD

2. INTRODUCTION
• Ulcer: Formation of an erosion on the inner lining of
stomach (Peptic Ulcers)
• It is often characterized by a break in skin or
mucous membrane with loss of surface tissue,
disintegration and necrosis of epithelial tissue, and
often pus.
• Ulcers in stomach – Gastric Ulcers
• Ulcers in duodenum – Duodenal ulcers
Department of Pharmacology, GPRCP.

3. What can be the
causes of ulcer?
• Disruption of mucosal lining by the action of gastric acid and
pepsin is the main reason for formation of an peptic ulcer.
• Some of the common causes are:
• Drinking too much alcohol
• Regular use of aspirin, ibuprofen, naproxen, or other nonsteroidal
anti-inflammatory drugs (NSAIDs)
• Smoking cigarettes or chewing tobacco
• Radiation treatments
• Stress
• A rare condition, called Zollinger-Ellison syndrome, causes
stomach and duodenal ulcers.
• Ref// pennmedicine.org
Department of Pharmacology, GPRCP.

4. Expected symptoms
• Symptoms of peptic ulcer disease include epigastric
discomfort (specifically, pain relieved by food intake or
antacids and pain that causes awakening at night or that
occurs between meals), loss of appetite, and weight loss.
• Older patients and patients with alarm symptoms
indicating a complication or malignancy should have
prompt endoscopy.
• Intestinal bleeding: indication of surgery
• Ref// Peptic Ulcer Disease KALYANAKRISHNAN RAMAKRISHNAN, MD, FRCSE, and ROBERT C. SALINAS, MD University
of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma
Department of Pharmacology, GPRCP.

5. CLASSIFICATION
ANTI
SECRETORY
AGENTS
H-2
ANTAGONISTS:
CIMETIDINE,
RANITIDINE,
FAMOTIDIINE
PROTON PUMP
INHIBITORS:
OMEPRAZOLE,
PANTOPRAZOLE,
LANSO PRAZOLE,
RABEPRAZOLE
ANTI
CHOLINERGICS
: PIREZEPINE,
TELENZIPINE
PROSTAGLANDIN
ANALOGUES:
MISOPROSTOL,RIOPROSTIL
ANTACIDS
SYSTEMIC:
NAHBO3, SOD
CITRATE
NON
SYSTEMIC:
MGOH2, CACO3 ULCER
PROTECTIVES
SUCRALFATE, COLLOIDAL
BISMUTH SUBCITRATE
CBS
ANTI- H.
PYLORI
DRUGS
AMOXICILLIN,
CLARITHROMYCIN
METRONIDAZOLE,
TETRACYCLINE
Department of Pharmacology, GPRCP.

6. Anti Secretory agents
These are the agents which act upon receptors ad suppresses or reduces
the gastric acid secretion
Gastric acid regulation->
Department of Pharmacology, GPRCP.

7. H2 – Receptor antagonists
• Examples: Ranitidine, Cimetidine, Famotidine, etc.
• These agents blocks the action of histamine at the H2
receptors by competing with histamine for H2 receptors.
• H2 receptors are located on the basolateral membrane
of the parietal cells of GIT, and are responsible for
increased gastric acid secretion
• H2 receptor antagonists bind to H2 receptors and reduce
gastric acid secretion thereby used in prophylaxis of
peptic ulcers.
Department of Pharmacology, GPRCP.

8. CIMETIDINE (prototype)
• Pharmacological actions:
1) H2 blockade – Blocks histamine induced gastric acid
secretion, cardiac stimulation and uterine relaxation.
2) Gastric secretion - Marked inhibition of gastric secretion,
the volume, pepsin content and intrinsic factor secretion
are reduced
• Pharmacokinetics:
• Well absorbed orally, absorption is not interfered by
present of food in stomach.
• About 2/3 of dose is excreted unchanged in urine and bile
• Elimination T ½ is 2-3 hours
Department of Pharmacology, GPRCP.

9. • Adverse effects:
1. Anti-androgenic action
2. Inhibits degradation of estradiol by liver
3. High doses – Gynecomastia
4. Loss of Libido, Impotence
5. Temporary decrease in sperm count
• Therapeutic uses:
1. Duodenal and gastric ulcers
2. Stress induced ulcers and gastritis
3. Zollinger- Ellison syndrome
4. GERD
Department of Pharmacology, GPRCP.

10. Proton pump inhibitors
(PPIs)
• Examples: Omeprazole, Pantoprazole, Rabeprazole, etc.
• These agents inhibits the gastric acid secretion by blocking the proton pump(H+K+
ATPase Pump)
• General MOA:
Department of Pharmacology, GPRCP.
• Prodrugs
• Gets activated (after absorption)
• Ionization (results in formation of sulphenic acid and
sulphenamide)
• Suphenamide reacts with sulfhydryl group present in proton pump
• Inactivation of proton pump
• Suppression of gastric acid secretion

11. Department of Pharmacology, GPRCP.

12. Department of Pharmacology, GPRCP.
All PPIs are
administered
enteric coated
Oral
bioavailability is
50% due to acid
instability
Food interferes
with absorption
Should be taken
1 hour prior to
meal
Plasma t1/2 is1
hour
Metabolites are
excreted in urine
Nausea, loose
stools, headache,
abdominal pain,
muscle and joint
pains and rashes
Leucopenia
Hepatic dysfunction
Gynecomastia and
erectile dysfunction
(lately observed)
Pharmacokinetics: Adverse effects:

13. Peptic ulcer
Stress ulcer
GERD
Zollinger Ellison syndrome
Aspiration pneumonia
Bleeding peptic ulcer
Department of Pharmacology, GPRCP.
THERAPEUTIC USES

14. Anti Cholinergic agents
• Examples: Pirenzepine, Telenzepine.
• These agents blocks the action of Acetylcholine on
autonomic effectors exerted through muscarinic
receptors.
• Pirenzepine is a selective M1 blocker and inhibits
gastric action
• These receptors are present in Autonomic ganglia
and gastric glands
• Pirenzepine and telenzepine works through G
Protein coupled receptors
Department of Pharmacology, GPRCP.

15. Ph’Col actions Pharmaco
kinetics
Adverse effects Uses
Similar to
Atropine
Rapidly
absorbed
from GIT
General:
Dry mouth, difficulty in
swallowing,
micturition
Duodenal ulcers
Decreases
secretion of:
50%
metabolize
d in liver
and rest is
excreted in
urine
CNS:
Excitement, psychotic
behavior and
hallucinations
Stomach ulcers
Gastric acid T1/2 = 3-4
hours
Eyes:
Dilated pupil,
photophobia, blurred
near vision and
palpitation
Used along with
antacids for
treatment of
peptic ulcers
Pepsin CVS:
Hypotension, weak
and rapid pulse
Also used to
prevent nausea,
vomiting, and
motion sickness.
Department of Pharmacology, GPRCP.

16. Prostaglandin
analogues
• These are the agents that enhance mucosal
defense
• Prostaglandins are produced in the gastric mucosa
and appear to serve a protective role by inhibiting
acid secretion and promoting mucus and
bicarbonate secretion.
• In addition, PGs inhibits gastrin production, increase
mucosal blood flow and probably have an ill defined
cytoprotective action.
• DRUGS: Misoprostol, Rioprostil
Department of Pharmacology, GPRCP.

17. • MECHANISM:
• Misoprostol acts upon gastric parietal cells, inhibiting the
secretion of gastric acid via G-protein coupled receptor-
mediated inhibition of adenylate cyclase, which leads to
decreased intracellular cyclic AMP levels and decreased
pump activity at the apical surface of the parietal cell
• Adverse effects:
• Diarrhea
• Other common side effects include: abdominal pain,
nausea,
• flatulence, headache, dyspepsia, vomiting, and
constipation.
Department of Pharmacology, GPRCP.

18. Department of Pharmacology, GPRCP.

19. Antacids
• These are basic substances which neutralize gastric
acid and raise pH of gastric contents.
• Antacids does not decrease acid production rather,
these are the agents that raise anthral pH to more
than 4.
• Peptic activity is indirectly reduced if the pH rises
above 4
• The potency of an antacid is generally expressed in
terms of its acid neutralizing capacity (ANC)
Department of Pharmacology, GPRCP.

20. • Systemic Antacids
• Sodium bicarbonate and Sodium citrate
• It is water soluble, acts instantaneously, but the duration of
action is short.
• It is a potent neutralizer (1 g → 12 mEq HCI), pH may rise
above 7. However, it has several demerits:
• (a) Absorbed systemically.
• (b) Produces CO2 in stomach.
• (c) Acid rebound.
Department of Pharmacology, GPRCP.

21. • Non systemic antacids
• Insoluble and poorly absorbed basic substance react in
stomach to form corresponding chloride salts
• The chloride salts reacts with intestinal bicarbonate so that
HCO3 in spread for absorption- no acid basic disturbances
occurs
• Magnesium hydroxide (milk of magnesia) with 30mEq HCI
• Magnesium trisilicate: mg salts are having laxative action
generation osmotically active MgCl2 induced cholecystokinin
hormone
Department of Pharmacology, GPRCP.

22. • Aluminum hydroxide:
• It ANC depends upon storage, it activity decline as
storage time increases
• Aluminum hydroxide binds phosphate in the intestine and
prevents its absorption-hypophosphatemia occurs on
regular use. This may: (a) cause osteomalacia (b)used
therapeutically in hyperphosphatemia and phosphate
stones.
• Small amount of Al3+ that is absorbed is excreted by
kidney. This is impaired in renal failure-aluminium
toxicity(encephalopathy, osteoporosis) can occur.
Department of Pharmacology, GPRCP.

23. Anti - H. pylori drugs
• Helicobacter pylori is a gram negative bacteria which breaks
down mucosal defense.
• It is known as an important contributor in causing gastritis,
dyspepsia, peptic ulcer, gastric carcinoma, etc.
• Up to 90% patients of duodenal and gastric ulcer have tested
positive for H. pylori.
• Antimicrobials that have been found clinically effective against
H. pylori are:
• Amoxicillin, clarithromycin, tetracycline, and
metronidazole/tinidazole.
Department of Pharmacology, GPRCP.

24. Department of Pharmacology, GPRCP.
Treatment of H. pylori infection

25. Ulcer protectives
• Ulcer protectives or mucosal protective agents
are medications that protect the mucosal lining of
the stomach from gastric acid, and are used to treat
conditions like peptic ulcers, NSAID-induced ulcers,
and gastroesophageal reflux disorder or GERD.
• Example: Sucralfate
Department of Pharmacology, GPRCP.

26. 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 insoluble complexes.
These complexes serve as protective barriers at the ulcer surface,
preventing further damage from acid, pepsin, and bile.
Department of Pharmacology, GPRCP.
MECHANISM

27. • ADR:
• It is not absorbed → virtually devoid of systemic ADR
• Inducing hypophosphatemia by binding phosphate ions in
the intestine
• Constipation (2%) due to aluminum salt
• Long term uses → may cause aluminum toxicity
• Contraindication :Avoid kidney patients prolonged use
Department of Pharmacology, GPRCP.

28. • Interaction:
• May bind to Tetracycline, Digoxin, Cimetidine & Phenytoin
impairing their absorption
• It should not be given with antacids → neutralize gastric acid &
raises pH → At pH > 4, Sucralfate cannot polymerize & thus
not able to protect ulcer
• Uses:
• Ulcer protective in peptic ulcer
• Stress ulcer → prophylaxis
• Bleeding in critically ill patient
• Gastritis
• Bile reflux
Department of Pharmacology, GPRCP.

29. References
• 
• Pennmedicine.org
• Review article: Peptic ulcer disease Kalyanakrishnan Ramakrishnan,
MD, FRCSE, and Robert C. Salinas, MD university of Oklahoma
health sciences center, Oklahoma
• Essentials of Medical Pharmacology, 7th Edt., K D Tripathi
• Lippincott Illustrated Reviews Pharmacology, 6th Edit., Richard A.
Harvey
• Exam Preparatory Manual for Undergraduates Pharmacology, 1st
Edt., Gobind Rai Garg & Sparsh Gupta
• Pharmacology for MBBS, 1st Edt., S.K. Srivastava
• Medical Pharmacology, 5th Edt., Padmaja Udaykumar.
Department of Pharmacology, GPRCP.

30. THANK YOU
Department of Pharmacology, GPRCP.