Overview
Gastritis
1. Clinical Overview
Summary
Gastritis is inflammation of the gastric mucosa. It can be acute (NSAIDs, alcohol, stress) or chronic (autoimmune Type A, or bacterial Type B due to H. pylori). Chronic gastritis can lead to complications including peptic ulcer disease, atrophic gastritis, and gastric cancer.
Key Facts
| Aspect | Detail |
|---|---|
| Acute Causes | NSAIDs, alcohol, stress, H. pylori |
| Type A (Autoimmune) | Parietal cell antibodies, body of stomach, pernicious anaemia |
| Type B (Bacterial) | H. pylori, antrum predominantly, most common |
| Key Complication | Peptic ulcer disease, gastric cancer (chronic atrophic) |
Clinical Pearls
- Type A = Autoimmune = Body = B12 deficiency (mnemonic)
- Type B = Bacterial = Base (antrum) = H. pylori (mnemonic)
- Achlorhydria in Type A: Increased gastric pH → iron malabsorption + B12 deficiency
- H. pylori: Causes 80-90% of gastric ulcers and 70-80% of duodenal ulcers
2. Epidemiology
Prevalence
| Type | Prevalence |
|---|---|
| H. pylori-associated | 50% of world population infected |
| Autoimmune gastritis | 2-5% of population |
| NSAID-induced | Common in chronic NSAID users |
Risk Factors
| Risk Factor | Association |
|---|---|
| H. pylori infection | Type B gastritis |
| NSAIDs/Aspirin | Erosive gastritis |
| Alcohol excess | Acute erosive gastritis |
| Autoimmune diseases | Type A (thyroiditis, vitiligo) |
| Critical illness | Stress-related mucosal disease |
3. Pathophysiology
Type A (Autoimmune)
Parietal Cell Antibodies + Intrinsic Factor Antibodies
↓
Destruction of Parietal Cells (Body/Fundus)
↓
↓ Acid Production (Achlorhydria)
↓ Intrinsic Factor
↓
┌──────────┴──────────┐
↓ ↓
Iron Malabsorption B12 Malabsorption
(needs acid) (needs IF)
↓ ↓
Iron Deficiency Pernicious Anaemia
Anaemia
Type B (H. pylori)
H. pylori Colonisation (Antrum predominantly)
↓
Urease → Ammonia (neutralises acid)
↓
Inflammatory Response + Cytotoxins
↓
Mucosal Damage → Gastritis
↓
┌────────────────┼────────────────┐
↓ ↓ ↓
Peptic Ulcers Atrophic Intestinal
Gastritis Metaplasia
↓ ↓
Gastric Cancer (Adenocarcinoma)
4. Clinical Presentation
Symptoms
| Symptom | Notes |
|---|---|
| Epigastric pain | Burning, gnawing |
| Nausea/vomiting | May be prominent |
| Early satiety | Fullness after small meals |
| Bloating | Upper abdominal |
| Anorexia | Reduced appetite |
| Haematemesis/melaena | If erosive/complicated |
Asymptomatic Presentation
Many patients with chronic gastritis, especially H. pylori, are asymptomatic
Common presentation.
5. Clinical Examination
Findings
| Finding | Significance |
|---|---|
| Often unremarkable | Common finding |
| Epigastric tenderness | Non-specific |
| Pallor | If anaemic (B12, iron, or blood loss) |
| Glossitis | B12 deficiency |
| Signs of malignancy | Weight loss, Virchow's node |
6. Investigations
First-Line Tests
| Test | Purpose |
|---|---|
| Full blood count | Anaemia (B12, iron, blood loss) |
| H. pylori testing | Urea breath test (first-line), stool antigen, serology |
| B12, folate, ferritin | If anaemia or Type A suspected |
Invasive Tests
| Test | Indication |
|---|---|
| OGD (Endoscopy) | Age ≥55 + dyspepsia, red flag symptoms, failed empirical treatment |
| Biopsy | Confirm diagnosis, H. pylori CLO test, exclude malignancy |
Notes
- Stop PPI 2 weeks before urea breath test / stool antigen (false negatives)
7. Management
General Measures
- Stop NSAIDs if possible
- Reduce alcohol
- Smoking cessation
H. pylori Eradication
| Regimen | Components | Duration |
|---|---|---|
| First-line Triple | PPI + Amoxicillin + Clarithromycin | 7 days |
| Alternative | PPI + Amoxicillin + Metronidazole | 7 days |
| Quadruple (penicillin allergy) | PPI + Bismuth + Tetracycline + Metronidazole | 10-14 days |
Acid Suppression
| Drug | Notes |
|---|---|
| PPIs | Omeprazole, lansoprazole - mainstay |
| H2RAs | Ranitidine (less effective than PPI) |
Type A (Autoimmune) Specific
- Lifelong B12 replacement (IM hydroxocobalamin)
- Iron supplementation if deficient
- Surveillance OGD (increased gastric cancer risk)
8. Complications
| Complication | Notes |
|---|---|
| Peptic ulcer disease | H. pylori and NSAIDs |
| GI bleeding | Erosive gastritis, ulcer |
| Atrophic gastritis | Chronic inflammation |
| Gastric adenocarcinoma | Chronic atrophic, intestinal metaplasia |
| MALT lymphoma | H. pylori-associated |
| Pernicious anaemia | Type A |
| B12/iron deficiency | Type A |
9. Prognosis & Outcomes
| Factor | Outcome |
|---|---|
| H. pylori eradication | Excellent - ulcers heal, cancer risk reduced |
| NSAID cessation | Rapid healing |
| Autoimmune gastritis | Chronic, requires lifelong B12 |
| Atrophic gastritis | Surveillance for dysplasia/cancer |
10. Evidence & Guidelines
| Organisation | Key Points |
|---|---|
| NICE Dyspepsia | Test & treat H. pylori in under-55s without red flags |
| BSG | Triple therapy 7 days, re-test after eradication |
| Maastricht VI | Updated H. pylori management consensus |
11. Patient / Layperson Explanation
What is gastritis? Gastritis is inflammation of the stomach lining. It can be short-term (acute) or long-lasting (chronic).
What causes it?
- Infection with a bacteria called H. pylori (very common)
- Painkillers like ibuprofen or aspirin
- Drinking too much alcohol
- An autoimmune condition affecting the stomach
What are the symptoms?
- Burning or gnawing pain in the upper tummy
- Feeling sick or being sick
- Bloating and discomfort
- Sometimes no symptoms at all
How is it treated?
- Stopping painkillers and reducing alcohol
- Tablets to reduce stomach acid (PPIs)
- Antibiotics if H. pylori is found
- B12 injections if autoimmune gastritis
12. References
- Malfertheiner P, et al. Maastricht VI Consensus. Gut. 2022.
- NICE NG183. Gastro-oesophageal reflux and dyspepsia. 2019.
- BSG Guidelines on H. pylori management. 2021.