DEFINITION,HSTORY,ETIOLOGY,EPIDEMIOLOGY,PATHOGENESIS,PHARMACOLOGICAL & NON -PHARMACOLOGICAL TREATMENT OF PEPTIC ULCER DISEASE.

2. PEPTIC ULCER DISEASE
The term ‘peptic ulcer’ describes a condition in which there is a
discontinuity in the entire thickness of the gastric or duodenal
mucosa that persists as a result of acid and pepsin in the gastric juice.

3. HISTORY
Helicobacter pylori was identified in 1982 by
two Australian scientists,
Robin Warren and Barry J. Marshall, as a causative
factor for ulcers.
Barry J. Marshall Robin Warren

4. ETIOLOGY
Upper abdominal pain.
• Anorexia,
• Weight loss,
• Nausea and vomiting,
• Heartburn
• Eructation/BURPING/BELCHING
• Patients with predominant symptoms of heartburn are likely to have
GORD.
• Haemorrhage,
• Chronic iron-deficiency anaemia,
• Pyloric stenosis and perforation.

5. EPIDEMIOLOGY
About 10% of the population in developed countries is likely to be
affected at some time by peptic ulcer, with the prevalence for active
ulcer disease being about 1% at any particular point in time.
Infection by H. pylori, a spiral bacterium of the stomach,remains an
important epidemiological factor in causing peptic ulcer.
• The most important risk factors for H. pylori infection are low social
class, overcrowding and home environment during childhood, for
example, bed sharing.
• There may be other genetic, environmental or cultural factors
influencing peptic ulcer disease.

6. Helicobacter pylori. The Gram-
negative spiral
bacterium H. pylori, formerly
known as Campylobacter pylori,
was isolated serendipitously from
patients with gastritis by Barry
Marshall and Robin Warren in
1982. Seven years later, it was
conceded that H. pylori is
responsible for most cases of
gastric and
duodenal ulcer.

7. Pathogenesis
There are 2 common forms of peptic ulcer disease: with the organism H.
pylori & with the use of aspirin and NSAIDs.
Less common is ulcer disease associated with massive hypersecretion of
acid which occurs in the rare gastrinoma (Zollinger–Ellison)
syndrome.
The underlying pathophysiology
associated with H. pylori infection
involves the production of cytotoxin-
associated gene A (CagA) proteins and
vacuolating cytotoxins, such as vac A,
which activate the inflammatory cascade.
A number of enzymes produced by H.
pylori may be involved in causing tissue
damage and include urease,
haemolysins, neuraminidase and
fucosidase.
High acid content in the proximal
duodenum leads to metaplastic gastric-
type mucosa, which provides a niche for
H. pylori infection followed by
inflammation and ulcer formation.

8. Three patterns of mucosal damage are caused by NSAIDs. These include
superficial erosions and haemorrhages, silent ulcers detected at
endoscopy and ulcers.
• Weak acid NSAIDs, such as acetylsalicylic acid, are concentrated from
the acidic gastric juice into mucosal cells,& may produce acute
superficial erosions via inhibition of COX and by mediating the
adherence of leucocytes to mucosal endothelial cells.
• Enteric coating may prevent this superficial damage but does not
demonstrate any clinical benefit in terms of reduction of gastro-
intestinal bleeding or ulceration.
• The presence of NSAID-induced ulcers does not correlate with
abdominal pain and NSAIDs themselves often mask ulcer pain.
• Smoking leads to Atherosclerosis & vascular spasms– causes vascular
insufficiency & promote Ulcer development.

11. Diagnosis

12. Non-Pharmacological treatment

13. s

14. MECHANISM OF ACTION OF DRUGS