Acute and chronic gastritis

Gastritis: Acute and Chronic 
Definition and General Overview

Gastritis refers to inflammation of the gastric mucosa, which may present as either an acute or chronic process depending on duration, etiology, and histological features. The condition develops when there is an imbalance between aggressive factors, such as gastric acid and pepsin, and protective mechanisms including mucus secretion, bicarbonate production, epithelial integrity, prostaglandins, and adequate mucosal blood flow.

Core Concept

• Gastritis = inflammation of gastric mucosa
• Caused by imbalance:
  • Aggressive factors > Defensive mechanisms

Aggressive factors

• HCl (acid)
• Pepsin
• NSAIDs
• Helicobacter pylori
• Alcohol, bile

Defensive factors

• Mucus-bicarbonate barrier
• Tight epithelial junctions
• Prostaglandins
• Mucosal blood flow

Acute Gastritis
Definition and Characteristics

Acute gastritis is a transient inflammatory condition characterized by rapid onset and predominantly neutrophilic infiltration of the gastric mucosa. It is usually reversible if the causative factor is promptly removed.

Etiology

Acute gastritis most commonly results from exposure to irritants such as NSAIDs and alcohol. It may also occur in critically ill patients due to stress-related mucosal disease, as well as from infections or chemical injury.

Causes of Acute Gastritis

• NSAIDs → ↓ prostaglandins
• Alcohol → direct mucosal damage
• Stress (burns, trauma, sepsis)
• Infections (e.g., H. pylori)
• Bile reflux
• Corrosive substances

Pathophysiology

The pathogenesis involves disruption of the mucosal barrier, allowing hydrogen ions to diffuse into epithelial cells. This leads to cellular injury, inflammatory mediator release, and neutrophil recruitment. In severe cases, mucosal erosions and hemorrhage may occur.

Pathogenesis

1. Mucosal barrier disruption
2. Back-diffusion of H+ ions
3. Epithelial injury
4. Inflammatory mediator release
5. Neutrophil infiltration
6. Erosion ± bleeding

Clinical Presentation

Patients typically present with epigastric pain, nausea, vomiting, and anorexia. In severe cases, gastrointestinal bleeding may manifest as hematemesis or melena.

Symptoms

• Epigastric pain (burning)
• Nausea, vomiting
• Loss of appetite
• Hematemesis (severe)
• Melena (severe)

Diagnosis

Diagnosis is primarily clinical but is confirmed by endoscopy, which may reveal mucosal erythema, edema, or erosions. Laboratory findings may indicate anemia if bleeding is present.

Management

Treatment focuses on removing the offending agent and reducing gastric acidity using proton pump inhibitors or H2 receptor blockers.

Treatment

• Remove causative factor
• Proton pump inhibitors (PPIs)
• H2 receptor blockers
• Antacids
• IV fluids (if severe)

Chronic Gastritis

Definition and Characteristics Chronic gastritis is a long-standing inflammatory condition characterized by infiltration of lymphocytes and plasma cells. Over time, it may lead to glandular atrophy, intestinal metaplasia, and an increased risk of gastric carcinoma.

Etiology and Classification

Chronic gastritis is classified into autoimmune (Type A), Helicobacter pylori–associated (Type B), and chemical (Type C) gastritis.

Classification of Chronic Gastritis

Type	Cause	Location	Key Feature
Type A	Autoimmune	Fundus/body	Achlorhydria, B12 deficiency
Type B	H. pylori	Antrum	Most common
Type C	Chemical	Antrum	Bile/NSAIDs

Pathophysiology

Autoimmune Gastritis Autoimmune gastritis involves antibodies directed against parietal cells and intrinsic factor. This results in reduced gastric acid secretion and impaired vitamin B12 absorption, leading to pernicious anemia.

Autoimmune Gastritis

• Autoantibodies against:
  • Parietal cells
  • Intrinsic factor
• ↓ HCl (achlorhydria)
• ↓ Vitamin B12 absorption
• ↑ Gastrin

Helicobacter pylori–Associated Gastritis Helicobacter pylori is a gram-negative bacterium that colonizes the gastric mucosa. It produces urease, allowing it to survive in an acidic environment, and induces chronic inflammation through toxin release.

H. pylori Gastritis

• Urease production → neutralizes acid
• Toxins (CagA, VacA)
• Chronic inflammation
• Mucosal damage → atrophy → metaplasia

Chemical (Reactive) Gastritis Chemical gastritis results from chronic irritation due to bile reflux or long-term NSAID use and is associated with minimal inflammation and epithelial hyperplasia.

Clinical Presentation

Chronic gastritis is often asymptomatic in early stages. When symptoms occur, they include mild epigastric discomfort, bloating, and early satiety. In autoimmune gastritis, vitamin B12 deficiency may lead to anemia and neurological symptoms.

Symptoms

• Mild epigastric discomfort
• Bloating
• Early satiety
• B12 deficiency:
  • Fatigue
  • Neuropathy

Complications

Chronic gastritis may lead to serious complications, particularly when associated with long-term inflammation and mucosal damage.

Complications

• Peptic ulcer disease
• Gastric adenocarcinoma
• MALT lymphoma
• Pernicious anemia

Diagnosis

Diagnosis requires endoscopy with biopsy for histological confirmation. Helicobacter pylori infection can be detected using non-invasive tests such as the urea breath test or stool antigen test.

Diagnosis

• Endoscopy + biopsy (gold standard)
• Urea breath test
• Stool antigen test
• Autoantibodies (Type A)
• Vitamin B12 levels

Management Treatment depends on the underlying cause. Helicobacter pylori infection requires eradication therapy, while autoimmune gastritis requires lifelong vitamin B12 supplementation.

Treatment

H. pylori eradication

• PPI + 2 antibiotics

Autoimmune gastritis

• Vitamin B12 supplementation

Comparison of Acute and Chronic Gastritis

Acute gastritis presents with rapid onset and is typically reversible, whereas chronic gastritis develops gradually and may lead to irreversible mucosal damage and increased cancer risk.

Acute vs Chronic Gastritis

Feature	Acute	Chronic
Onset	Sudden	Gradual
Duration	Short	Long-term
Cells	Neutrophils	Lymphocytes
Damage	Erosions	Atrophy/metaplasia
Symptoms	Prominent	Mild/absent
Cancer risk	Low	High

Disease Progression

Chronic gastritis, particularly due to Helicobacter pylori, may progress through a sequence known as the Correa cascade, ultimately leading to gastric adenocarcinoma.

Correa Cascade

• Normal mucosa

→ Chronic gastritis → Atrophic gastritis → Intestinal metaplasia → Dysplasia → Gastric adenocarcinoma