2. Definition:
• It is inflammation of the gastric mucosa.
• It might be acute or chronic.
Causes:
a. H. pylori gastritis (commonest cause)
b. Erosive and hemorrhagic gastritis (NSAIDs)
c. Autoimmune gastritis
d. Viral infection (CMV & herpes simplex)
e. Crohn's disease
Gastritis
5. •Drugs: as aspirin and NSAIDs.
• Aspirin inhibits the synthesis of PGE2 and F2a ↑↑↑ acid secretion &
↓↓↓ protective mucosal layer gastritis and acute mucosal erosions.
• Chronic: chronic or recurrent use of these drugs e.g. in patients with
osteoarthritis.
•Alcohol ( damage of the mucosal protective layer gastric
erosions).
•Stress gastritis (stressful situations e.g. acute myocardial
infarction and cerebrovascular strokes).
Erosive & Hemorrhagic Gastritis
6. • It is a spiral-shaped Gram-negative urease-
producing bacterium.
• H. pylori may be transmitted from person
to person through contaminated food and
water
• It is found in the gastric antrum and in
areas of gastric metaplasia in the
duodenum.
• The organism’s motility allows it to localise
& live deep beneath the mucus layer closely
adherent to the epithelial surface.
H. Pylori Gastritis
7. H. Pylori Prevalence
76%
5 million
s
41%
37 million
66%
21 million
14006
Peer reviewed study
From 1970 to 2016
184
Study implemented
8. The most common human infection
worldwide.
Over 3.5 billion are known to be infected with
H.pylori.
Hundreds of millions develop PU during their
lifetime.
Tens of millions might progress to gastric
cancer.
Most infected subjects continue
their life with superficial chronic
gastritis.
17% will
develop
peptic
ulcers
4.2%
will
develop
complicate
d peptic
ulcers
1% Gastric
Cancer
H. Pylori infection
9. Of Duodenal
ulcers
caused by H. pylori
Of Gastric
Cancers
caused by H. pylori
Of Gastric ulcers
caused by H. pylori
H. Pylori infection
10. Colonization occurs despite of the acid environment of the gastric
mucosa because:
• Sheathed flagella allow the organisms to move quickly from the acidic lumen of
the stomach through the mucus layer where the PH is higher.
• H. pylori produces urease enzyme which convert urea to ammonia which is very
toxic to the gastric mucosa, leaving CO2 to form bicarbonate to raises the pH
around the bacterium.
H. Pylori infection
11. How does H. pylori cause gastritis and ulcers?
11
H. pylori penetrate the mucus layer and adhere the surface
of gastric epithelial cells.
12. How does H. pylori cause gastritis and ulcers?
12
Produce ammonia (from urea by the urease), and the
ammonia neutralize the gastric acid
13. How does H. pylori cause gastritis and ulcers?
13
Proliferate, migrate, and finally form the infectious focus.
14. How does H. pylori cause gastritis and ulcers?
14
The gastric ulcer is developed by destruction of mucosa,
inflammation and mucosal cell
16. • Although it is non-invasive, the bacterium
stimulates chronic gastritis by provoking local
inflammatory response in the underlying
epithelium due to release of a range of cytotoxins.
•The mucosa appears reddened endoscopically and
there is epithelial cell damage;.
• This leads to activation of an Inflammatory
Infiltrate such as PNL, eosinophils, lymphocytes
and monocytes.
17.
18. Carbon13-Urea Breath
Testing
• Used to detect H. pylori
• Client swallows a carbon-enriched urea capsule
• Exhaled carbon dioxide is then measured
20. Endoscopic Biopsy
• Determines atrophic gastric mucosa and infiltration by H pylori.
• Antibiogram (Antibiotic Susceptibility Test)
21. Rapid Urease Test
• With endoscopy Biopsy
• From the gastric body and the antrum
• Sensitivity in diagnosing infection is greater than 90%, and
specificity is 95% to 100%
• Sensitivity of the test is lowered in patients who are taking PPIs,
H2 antagonists, or antibiotics
25. •Eradication therapy: All patients with
duodenal and gastric ulcers should have H.
pylori eradication therapy.
•There are several protocols for eradication: PPI
+ 2 Antibiotics.
NB: However recurrence is common.
Therapeutic Options