Acute gastritis by Dr. Evelyn Mbugua

GASTRITIS

DR. EVELYN MBUGUA

GASTRIC SECRETIONS

• HCl and Pepsinogen

• Acid secretion occurs under Basal, and Stimulated conditions.

Basal gastric acid production

• Basal acid production occurs in a circadian pattern, with highest levels occurring during the night and lowest levels during the morning hours.

• Cholinergic input via the vagus nerve and histaminergic input from local gastric sources are the principal contributors to basal acid secretion.

Stimulated gastric acid production

• Stimulated gastric acid secretion occurs primarily in three phases based on the site where the signal originates :- – cephalic, – gastric, – intestinal.

• Cephalic phase - Sight, smell, and taste of food stimulates gastric secretion via the vagus nerve.

• Gastric phase - Activated once food enters the stomach. Driven by nutrients (esp amino acids and amines) that directly stimulate the G cell to release gastrin, which in turn activates the parietal cell via direct and indirect mechanisms. Distention of the stomach wall also leads to gastrin release and acid production.

• Luminal phase - The last phase of gastric acid secretion is initiated as food enters the intestine and is mediated by luminal distention and nutrient assimilation.

GASTRODUODENAL MUCOSAL DEFENCE SYSTEMS

• Exposure to noxious stimuli :- HCl acid, bile acids, ?pepsin, ?pancreatic enzymes, bacteria, drugs

• Mucosal integrity is maintained by a highly intricate system that provides mucosal defense and repair.

• The mucosal defense system can be envisioned as a three-level barrier:-– preepithelial, – epithelial, – subepithelial elements

Gastritis

• Acute gastritis often due to chemical injury (alcohol drugs)

• Chronic gastritis:– Helicobacter pylori infection– Chemical damage (bile reflux, drugs)– Autoimmune (associated with vitamin B12

malabsorption (pernicious anaemia)

Acute gastritis

• Drugs:– NSAIDs– Alcohol cause acute

erosion – Severe

haemorrhage• Acute Helicobacter

infection:– Prominent

neutrophil infiltrate

Chronic gastritis ABC

• A – autoimmune• B – bacterial (helicobacter)• C - chemical

Autoimmune chronic gastritis

• Autoantibodies to gastric parietal cells• Hypochlorhydria/achlorhydria• Loss of gastric intrinsic factor leads to

malabsorption of vitamin B12 with macrocytic,megaloblastic anaemia

Cag A

• Cytotoxin associated gene A — Histopathologic changes in H. pylori gastritis correlate with the presence of an H. pylori-derived cytotoxic protein encoded for by a gene called cytotoxin associated gene A (Cag A).

• Approximately 60 percent of H. pylori isolates possess the Cag A gene and express the toxin .

• Cag A toxin correlates with a number of features that suggest a more severe form of infection, including :

– A larger number of H. pylori organisms – A greater degree of acute and chronic inflammation – More severe epithelial injury – A higher likelihood of associated peptic ulceration (duodenal and gastric) – An increased risk for developing gastric gland atrophy, intestinal

metaplasia – Gastric adenocarcinoma

Treatment of H. Pylori

• PPI, amoxicillin 1 gm, clarithromycin 500 mg all twice daily for 7-14 days 1st line treatment regimen of choice

• Bismuth 525 mg, metronidazole 500 mg, tetracycline 500 mg all four times daily with a PPI twice daily for 7-14 days

• PPI, amoxicillin 1 gm, metronidazole 500 mg all twice daily for 14 days

RESCUE THERAPY

• PPI, levofloxacin 250 mg, amoxicillin 1 gm all twice daily for 14 days "Rescue" therapy for those failing two course of above treatments

• PPI, rifabutin 150 mg, amoxicillin 1 gm all twice daily for 14 days Alternative "rescue" therapy

• PPI twice daily plus amoxicillin 1 three times daily for 14 days Alternative "rescue" therapy

CONFIRMATION OF ERRADICATION

• Confirmation of eradication has been recommended by a European consensus panel.

• A 2007 guideline from the American College of Gastroenterology recommends confirming eradication in the following settings :

– Any patient with an H. pylori-associated ulcer Individuals with persistent dyspeptic symptoms despite the test-and-treat strategy

– Those with H. pylori-associated MALT lymphoma– Individuals who have undergone resection of early gastric cancer

The Tests…• Urea breath testing performed at least four weeks after treatment has been

promoted as the test of choice to confirm eradication of infection. Stool antigen testing is a more widely available alternative, but it may be less accurate.

• Until further data are available, the stool antigen test should not be performed sooner than four to six weeks after completion of treatment because of both false-positive and false-negative results in this time period

• Antibiotics and bismuth should be discontinued for at least four weeks and PPIs at least one week if possible prior to testing done to confirm H. pylori cure (with urea breath test, stool antigen testing, or endoscopic testing) to reduce the chance of false-negative results.

• Serologic testing is not useful for follow-up since many patients continue to have antibodies for months or even years after eradication therapy.

TAKE HOME POINTS

THE END

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