Gastritis and Peptic Ulcer Disease

Gastritis Overview - Stomach Lining Storms

• Inflammation of gastric mucosa; imbalance between mucosal protective & aggressive factors.
• Acute Gastritis: Sudden onset, often transient. Causes: NSAIDs, alcohol, H. pylori, stress (burns, trauma).
• Chronic Gastritis: Persistent inflammation. Main types:
  • Type A (Autoimmune): Fundus/body; anti-parietal cell Abs; pernicious anemia. 📌 Autoimmune = Achlorhydria, Anemia.
  • Type B (Bacterial): Antrum; H. pylori infection (most common).
  • Type C (Chemical): NSAIDs, bile reflux.

⭐ H. pylori is the most common cause of chronic gastritis and is strongly associated with peptic ulcer disease, gastric adenocarcinoma, and MALT lymphoma.

Acute Gastritis & Erosions - Sudden Mucosal Mayhem

• Acute inflammation of gastric mucosa, often transient, due to breakdown of protective barriers.
• Key Causes:
  • NSAIDs (↓ prostaglandins 📌), alcohol, bile reflux, chemotherapy.
  • Severe stress: Curling's ulcer (extensive burns), Cushing's ulcer (CNS trauma/surgery).
  • H. pylori (initial infection phase).
• Pathology: Neutrophilic infiltrate in lamina propria, edema, hyperemia. Erosions (superficial defects not breaching muscularis mucosae), potential hemorrhage.
• Clinical: Epigastric pain, nausea, vomiting. Hematemesis ("coffee-ground"), melena. Often self-limiting.

⭐ NSAID-induced gastritis is a leading cause of acute gastric erosions and upper GI bleeding.

Chronic Gastritis Deep Dive - Persistent Parietal Pain

• Persistent gastric mucosal inflammation. Main types:
  • Type B (H. pylori): Most common; antrum. Patho: Urease, CagA, VacA → inflammation. Risks: Peptic Ulcer Disease (PUD), MALT Lymphoma, AdenoCa.
  • Type A (Autoimmune): Corpus/fundus. Patho: Anti-parietal cell/IF Abs → achlorhydria, ↓Intrinsic Factor (B12 def.), ↑gastrin. Risks: Pernicious anemia, carcinoid tumors, AdenoCa.
• Others: NSAIDs, bile reflux, Crohn's disease, eosinophilic gastritis.
• Clinical: Often asymptomatic; dyspepsia, epigastric pain. Weight loss or alarm symptoms warrant investigation.
• Dx: Endoscopy + Biopsy (gold standard). H. pylori tests (UBT, SAT). Serum gastrin/Abs for Type A.
• Progression: Atrophy → Intestinal Metaplasia → Dysplasia → Gastric Cancer.

⭐ H. pylori is a WHO Class I carcinogen for gastric adenocarcinoma.

Peptic Ulcer Disease - Ulcer Underpinnings Unveiled

• Def: Mucosal breach >0.5 cm, through muscularis mucosae.
• Sites: Duodenum (1st part, anterior) > Stomach (lesser curve, antrum).
• Etiology: Imbalance: Aggressive (acid, pepsin, H. pylori) vs. Protective (mucus, PGs).
  • H. pylori (major cause).
  • NSAIDs (↓PGs).
  • Zollinger-Ellison syndrome.
  • Stress: Cushing's (↑ICP), Curling's (burns).
• Types & Symptoms:
  • Duodenal (DU): Pain ↓ with food. 📌 "DUde, give me food".
  • Gastric (GU): Pain ↑ with food.
• Complications: Bleeding (most common), perforation, penetration, GOO.
• Diagnosis: Endoscopy + biopsy (GU for malignancy, H. pylori).

  ⭐ Duodenal ulcers are almost never malignant; gastric ulcers always need biopsy. Awaited by planner

High‑Yield Points - ⚡ Biggest Takeaways

• H. pylori is the primary cause of chronic gastritis, PUD, and gastric MALT lymphoma.
• Autoimmune gastritis targets parietal cells, leading to achlorhydria and pernicious anemia.
• NSAIDs induce acute gastritis and PUD by inhibiting protective prostaglandins.
• Duodenal ulcers are more common and typically benign; gastric ulcers can harbor malignancy.
• Zollinger-Ellison syndrome (gastrinoma) causes multiple, severe, and often distal duodenal ulcers.
• Key PUD complications: hemorrhage, perforation (free air), gastric outlet obstruction.