Gastritis

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* Gastritis

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

* 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

* Hemorrhagic gastritis

* Gastric erosion in combination with punctuate hemorrhages

* Macroscopic appearance of multiple gastric erosions

* Diagnosis: 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

* Causes: H pylori infection Autoimmune (pernicious anemia) Postgastrectomy

* 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

* 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.

* Some factors which may influence virulence of H. pylori

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* 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

* Host Factors

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

* 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
1- Non-invasive Tests:

* 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
2- Invasive tests (antral biopsy):

* Antral gastritis related to H pylori infection

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


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


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

* non-radioactive 13C urea breath test

* 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.

* 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