Introduction Etiology Causes Various factors Treatment Further aspect

1. Peptic Ulcer
A Gastrointestinal Diseases
Presented By :Sonali Hiranwar
MPharm 1st year
JLC College of Pharmacy

2. Index
• Introduction
• Etiology
• Type of ulcer
• Pathogenesis Of Peptic Ulcer
• Symptoms
• Diagnosis Test
• Classification Of Anti Ulcer Drugs

3. Introduction:
• 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 muscular is
mucosa into the sub mucosa or deeper.
• 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. It can be teamed as the
areas of degeneration and Necrosis of gastrointestinal mucosa exposed to acid-peptic
secretions.

4. • Etiology
• Etiology of peptic ulcer disease is multifactorial.
• Infection with the bacteria Helicobacter pylori occurs in 80 to 95% of patients with
peptic ulcer disease.
• H. pylori infection impairs the protective mechanisms of the G.I. tract against low pH
and digestive enzymes and leads to ulceration of the mucosa.
• Stress — Emotional, trauma, surgical.
• Injury or death of mucus-producing cells. Chronic use of NSAIDs Smoking Alcohol and
diet ,Hyperkalemia (↑gastric secretion)
• Excess acid production in the stomach. The old hypothesis that ulceration is caused
simply by hyperacidity is not tenable. About 70% of gastric ulcers and 50% of
duodenal ulcers are not associated with abnormally high acid production
• . Genetic factor: The lifetime prevalence of developing ulcer disease in first-degree
relatives of ulcer patients is about three times greater than the general population.
20-50% of duodenal ulcer reported a positive family history.

5. • Types of Ulcer
• Oesophageal ulcers.
• Gastric Ulcers.
• Duodenal Ulcers.
• Stress-induced Ulcers.
• Drug or NSAID-induced Ulcers

6. • Pathogenesis Of Peptic Ulcer
Aggressive Factors
• Acid
• Pepsin
• H.Pyrolis
• NSAIDS
Defensive Factor
• Prostaglandins
• Mucosal blood flow
• Mucous gel layer
• HCO 3
• Epithelial junctions
• Regeneration of the epithelial
layer
• Epidermal growth factor

7. • Symptoms
• 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

8. • 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(acetyl-choline , Ach),paracrine(histamine), and endocrine
(gastrin) factors all regulate acid secretion.
• Their specific receptors (M 3 ,H 2 ,and CCK 2receptors,
respectively)are on the baso-lateral membrane of parietal cells in the
body and fundus of the stomach.

9. • The H 2receptor 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+dependantpathwaysactivate H + ,K + -ATPase (the proton pump),
which exchanges hydrogen and potassium ions across the parietal cell
membrane

11. • Ulcer formation due to H.Pylori Bacteria
H. pylori secretes urease (generates ammonia), protease (breaks down glycoprotein in the
gastric mucus) and phospholipases.
Bacterial lipopolysaccharide attracts inflammatory cells to the mucosa. Chronically
inflamed mucosa are susceptible to injury.
A bacterial platelet-activating factor promotes thrombotic occlusion of surface capillaries.
That damages the surface and causes formation of Ulcer

12. • DIAGNOSIS
• Endoscopy: Flexible tube fitted with camera is threaded down the
oesophagus in to stomach to see the ulcer by physician.
• Barium meal: Barium liquid is drunk making ulcer visible on X-ray
• Test for diagnosing H.pylori
• Breath test: by measuring the amount of co 2in exhaled breath.
• Blood test : by identifying H.pylori antibodies by ELISA test.
• Stool test: stool sample tested with H.pylori antigen

13. • Anti Ulcer Drugs

14. • Gastric Acid secretion Inhibitor
1. Histamine Antagonist
Cimetidine:
It is an histamine antagonists inhibit the action of histamine on the
acid-producing cells of the stomach and reduce stomach acid
• Side Effects: It include constipation ,diarrhoea ,fatigue , headache,
insomnia, muscle pain and vomiting. Major side effects include
confusion and hallucinations, Gynacomastia (enlargement of the
breasts); impotence.
• Uses: Duodenal ulcer, Gastric ulcer, stress ulcer, GERD, zollinger-
Ellison syndrome

15. • PROTON PUMP INHIBITORS
• Proton pump inhibitors act by irreversibly blocking
the hydrogen/potassium adenosine tri-phosphatase enzyme system
of the gastric parietal cells.
• The proton pump is the terminal stage in gastric acid secretion.
• Eg Omeprazole, Pantoprazole Rabeprazole

16.  Pantoprazole
1. Pantoprazole is a proton pump inhibitor (PPI) that suppresses the
final step in gastric acid production by covalently binding to the (H+,
K+)-ATPase enzyme system at the secretory surface of the gastric
parietal cell.
2. This effect leads to inhibition of both basal and stimulated gastric
acid secretion, irrespective of the stimulus.
3. The binding of pantoprazole to H+/K+-ATPase is irreversible in
nature, and effectively inhibits acid secretion until new enzyme is
synthesized.
• Side effect: Stomach pain, Diarrhea, Constipation, Dizziness, Pain ,
Hives, Itching , seizures

17. • Agents That Enhance Mucosal Defence
• Prostaglandin Analogs :
MISOPROSTOL:
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 ,abdominal pain, nausea, flatulence,
headache, dyspepsia, vomiting, and constipation.

18. • Ulcer Protective
• 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.
• Side effects: constipation flatulence cephalalgia (headache), dry mouth
• USES: Gastritis, Stress ulcers.

19. • Anti H.Pylori Drugs
Anti microbial 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

20. • Life-style Modification In Pud
• Rest
• Relaxation
• Good Sleep
• Balanced Diet
• Frequent Small Meal
• Fiber
• Vitamin E And Dietary Fatty Acids
• Fat Diet

21. Thank you