peptic ulcer

1. ANTI-ULCER
DRUGS
BY
CH.DEEPTHI(10T21S0116)
UNDER THE GUIDANCE OF
MR.J.ANUP
M.Pharm
(Asst.Professor)

2. PEPTIC ULCER
An Ulcer is …
 Erosion in the lining of the stomach or the first
part of the small intestine, an area called the
duodenum.
Ulcers damage the mucosa of the alimentary tract,
which extends through the muscularis mucosa into
the sub mucosa or deeper.

3. Ulcers that form in the stomach are called gastric ulcers;
in the duodenum, they are called duodenal ulcers. Both
types are referred to as peptic ulcers.

4. PEPTIC ULCERPEPTIC ULCER

5. PATHOGENESIS OF PEPTIC ULCER
DISEASE
IMBALANCE:
Acid
Pepsin
Helicobacter pylori
NSAIDS
Prostaglandins
Mucosal blood flow
Mucous gel layer
HCO
3
Epithelial junctions
Regeneration of the
epithelial layer
Epidermal growth
factor
AGGRESSIVE FACTORS DEFENSIVE FACTORS

6. HELICOBACTER PYLORI
1981 - Robin
Warren, M.D., an
Australian
pathologist,
discovered numerous
bacteria living in
tissue taken during a
stomach biopsy.
Spiral urease-
producing, Gram-
negative bacteria
always accompanied
changes in the
stomach lining

7. HELICOBACTER PYLORI
Gram negative, Spiral bacilli
Spirochetes
Do not invade cells – only mucous
Breakdown urea - ammonia
Break down mucosal defense
Chronic Superficial inflammation

8. SYMPTOMS OF H. PYLORI
Abdominal pain
Feeling of Fullness
Indigestion
Feeling very hungry 1 to 3 hours after eating
Mild nausea
Pain Starts 2/3 hours after meals, or in the
middle of the night

9. PHYSIOLOGY OF GASTRIC ACID
SECRETION
Gastric acid secretion is a complex, continuous
process in which multiple central and peripheral
factors contribute to a common endpoint
secretion of H⁺ by parietal cells.
Neuronal(acetylcholine,Ach),paracrine(histamine),
and endocrine (gastrin) factors all regulate acid
secretion.
Their specific receptors (M
3,H
2,and CCK
2
receptors, respectively)are on the basolateral
membrane of parietal cells in the body and
fundus of the stomach.

10. The H
2
receptor is a GPCR that activates the Gs-
adenyl cyclase –cyclic AMP-PKA pathway.
Ach and gastrin signal through GPCRs that
couple to the G
q
-PLC-IP
3
-Ca
2+
pathway in parietal
cells .
In parietal cells , the cyclic AMP and the Ca
2+
dependant pathways activate H
+
,K
+
-ATPase (the
proton pump), which exchanges hydrogen and
potassium ions across the parietal cell membrane

11. PATHOPHYSIOLOGY

12. SYMPTOMS
Burning abdominal pain
Haematemesis
Melena
Nausea or vomiting
Unexplained weight loss
Anorexia
Abdominal fullness

13. DIAGNOSIS
Endoscopy:
Flexible tube fitted with
camera is threaded down the
esophagus in to stomach to
see the ulcer by physician
Barium meal:
Barium liquid is drunk
making ulcer visible on X-
ray

14. Test for diagnosing H.pylori
Breath test :by measuring the amount of co
2
in
exhaled breath.
Blood test: by identifying H.pylori antibodies by
ELISA test.
Stool test :stool sample tested with H.pylori
antigen.

15. LIFE-STYLE MODIFICATION IN
PUD
Doubtful efficacy
REST
RELAXATION
GOOD SLEEP
DIET INDICATION
Balanced diet
Frequent small meal
fiber
vitamin E and dietary fatty acids
fat diet
CONTRAINDICATION
caffeine-containing beverages
spices
Alcohol

16. ANTI ULCER DRUGS
REDUCTION OF GASTRIC ACID
SECRETION
Histamine antagonist: Cimetidine, ranitidine
Proton pump inhibitors: omeprazole,
pantaprazole
Acetyl choline antagonist: pirenzepine,
propantheline
Prostaglandin analogue: misoprostol

17. ANTIULCER DRUGS
 Neutralization of gastric acid(antacids)
Systemic : Sodium bicarbonate, Sodium
citrate
Nonsystemic : Magnesium hydroxide ,
Aluminium hydroxides
Ulcer protectives : Sucralfate
Anti helicobacter pylori: amoxicillin,
clarithromycin etc

18. HISTAMINE ANTAGONIST
Cimetidine
.Histamine
antagonists inhibit
the action of
histamine on the acid-
producing cells of the
stomach and reduce
stomach acid

19. CIMETIDINE
SIDE EFFECTS ; it include constipation,
diarrhea, fatigue, headache, insomnia, muscle
pain, and vomiting. Major side effects include
confusion and hallucinations, gynacomastia
(enlargement of the breasts); impotence.
USES: it is used in treatment of duodenal ulcer,
Gastric ulcer, stress ulcer, GERD, zollinger
ellison syndrome

20. PROTON PUMP INHIBITORS
 
 Proton pump inhibitors act by irreversibly
blocking the hydrogen/potassium adenosine
triphosphatase enzyme system of the
gastric parietal cells.
The proton pump is the terminal stage in gastric
acid secretion

21. PROTON PUMP INHIBITORS
OMEPRAZOLE
Omeprazole is inactive at neutral pH, but at
pH<5 rearranges to two charged cationic forms(a
sulphenic acid and a sulphenamide
configurations)that react covalently with SH
groups of the H
+
K
+
ATPase enzyme and
inactivate it irreversibly, especially when two
molecules of omeprazole react with one molecule
of the enzyme
SIDE EFFECTS Stomach pain,
Diarrhea,Constipation,Dizziness,Pain,Hives,
Itching,seizures

22. ACETYL CHOLINE ANTAGONIST
PIRENZEPINE
 MECHANISM:

 It selectively block M1 muscaranic recptors and
inhibits gastric secretion.
 Because of their relatively poor efficacy, side
effects, and risk of blood disorders, they are
rarely used today

23. AGENTS THAT ENHANCE MUCOSAL
DEFENSE
Prostaglandin Analogs:
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

24. MISOPROSTOL
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
Side effects
Diarrhea.
Other common side effects include: abdominal
pain, nausea, flatulence, headache, dyspepsia,
vomiting, and constipation.

25. ULCER PROTECTIVES
SUCRALFATE
MECHANISM:
 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.

26. Side effects
The most common side effects seen are
constipation. Less commonly reported include
flatulence, cephalalgia (headache), xerostomia
(dry mouth).
USES:
It is used in treatment of
Gastritis,
Stress ulcers.

27. SODIUM BICARBONATE (ANTACID)
It is water soluble, acts instantaneously,
but duration of action is short. It is a
potent neutralizer, pH may raises above 7.
Adverse reactions
It causes systemic alkalosis, gastric
distention, rebound acidity and milk-
alkali syndrome
Uses
It is restricted to casual treatment of
heartburn and to treat acidosis

28. ANTI H.PYLORI DRUGS
 Anti microbials that have been found clinically
effective against H.pylori are: amoxicillin,
clarithromycin, tetracycline and metronidazole.
A combination regimen is preferred, using gastric
acid inhibitors and antibiotics.
Example:
A proton pump inhibitor or H2 blocker +
amoxicillin + clarithromycin or metronidazole

29. CONCLUSION

30. Avoid stress
Avoid contamination