1. Gastritis

2. Gastritis is a histological diagnosis, although it cab sometimes be recognized at endoscopy
Acute gastritis
Chronic non-specific
Chronic Specific
Gastritis (rare)

3. Acute Gastritis It is often erosive & hemorrhagic Causes:
Aspirin, NSAIDs
H pylori (initial infection)
Alcohol
Other drugs e.g. iron preparations
Severe physiologic stress e.g. burns, multi-organ failure, CNS trauma
Bile reflux e.g. following gastric surgery
Viral infections e.g. CMV, Herpes simplex in AIDS
Symptoms (often produces no symptoms):
Dyspepsia
Anorexia
Nausea or vomiting
Hematemesis or melena

4. Hemorrhagic gastritis

5. Gastric erosion in combination with punctuate hemorrhages

6. Macroscopic appearance of multiple gastric erosions

7. Acute Gastritis Diagnosis: Treatment:
Many cases resolve quickly & do not merit investigations
Endoscopy & biopsy may be indicated in some patients to exclude:
Peptic ulcer
Malignancy
Treatment:
Treat the underlying cause
Short term symptomatic therapy with;
Antacids
Acid suppression e.g. H2 receptor antagonists
Anti-emetics e.g. metochlopromide

8. Chronic Non-specific Gastritis
Causes:
H pylori infection
Autoimmune (pernicious anemia)
Postgastrectomy

9. H. pylori Infection In the developed world:
Prevalence of infection increase steadily with age
In UK 50% of those over 50 years old are infected
In the underdeveloped world:
Infection is much more common
It is often acquired during childhood
Up to 90% of the population are infected by adult life
The vast majority of colonized people remain healthy and asymptomatic
90% of duodenal ulcer & 70% of gastric ulcer patients are infected

10. H. pylori Infection Pathogenesis & pathophysiology:
The organism’s motility (flagellum) allows it to localize and live deep beneath the mucous layer closely adherent to the epithelial surface.
Enzyme urease produced by the organism produces ammonia and raises the pH around the bacterium.
Because of the release of range of cytokines, H pylori stimulates chronic gastritis by provoking local inflammatory response in the underlying epithelium.
H pylori exclusively colonizes gastric type epithelium and is only found in duodenum in association with patches of gastric metaplasia.

11. Some factors which may influence virulence of H. pylori

13. H. pylori Infection
The role of H pylori in the pathogenesis of gastric ulcer is less clear
It might act by reducing gastric mucosal resistance to attack from acid and pepsin.
In 1% of infected people, H pylori causes pangastritis leading to:
gastric atrophy
Hypochlohydria
Proliferation of the organism within the stomach produce mutagenic nitrites from dietary nitrates, predisposing to gastric cancer

14. Duodenal Ulcer Gastric Cancer
Host
Factors
H. pylori
Other
Environmental
Pangastritis
Antral gastritis
Duodenal
Ulcer
Gastric
Cancer

15. H. pylori Infection-Diagnosis
1- Non-invasive Tests:
Disadvantages
Advantages
Test
Lacks sensitivity & specificity
Cannot differentiate current from past infection
Rapid office kits available
Good for population studies
Serology
14C uses radioactivity
13C requires expensive mass spectrometer
High sensitivity & specificity
Urea breath tests

16. H. pylori Infection-Diagnosis
2- Invasive tests (antral biopsy):
Disadvantages
Advantages
Test
False negatives occur
Takes several days to process
Sensitivity & specificity
Histology
Lack sensitivity
Cheap, quick
Specificity
Rapid urease tests
Slow & laborious culture
Lacks sensitivity
“Gold Standard”
Defines antibiotic sensitivity
Micorbiolo-gical culture

17. Antral gastritis related to H pylori infection

18. Toluidine blue sections of duodenal mucosa showing H pylori only in areas of gastric metaplasia

19. Transmission electron micrograph showing duodenal gastric metaplasia, H pylori are adhering to the mucosa via attachment pedestals

20. Detection of H pylori by urease activity in antral biopsy
Detection of H pylori by urease activity in antral biopsy. The upper one is negative while the lower slide shows positive result

21. non-radioactive 13C urea breath test

22. Chronic gastritis due to H. pylori infection:
H. pylori is the most common cause of chronic gastritis
The predominant inflammatory cells are lymphocytes & plasma cells
Poor correlation between symptoms & endoscopic or pathologic findings
Most patients are asymptomatic and do not require any treatment
Patients with dyspepsia & H. pylori associated gastritis may benefit from H. pylori eradication.

23. Autoimmune chronic gastritis
This involves the body of the stomach, spares the antrum, & results from autoimmune activity against parietal cells.
Histological features are:
Diffuse chronic inflammation
Atrophy
Loss of fundic glands
Intestinal metaplasia
Sometimes hyperplasia of enterochromaffin-like (ECL) cells.
Circulating antibodies to parietal cells and intrinsic factor may be present.
In some patients the degree of atrophy is severe and loss of intrinsic factor secretion lead to pernicious anemia
The gastritis itself is usually asymptomatic but some patients have evidence of other autoimmune diseases like thyroid disorders.
There is FOUR fold increase in the risk of gastric cancer