04.1 Stomach anatomy and function

Stomach Anatomy and Function

• The stomach regulates motility and secretion through hormonal, neural, and paracrine control.
• Its function includes food storage, digestion, and self-protection.
• Gastrin, somatostatin, and secretin are key gastrointestinal hormones.
• Distension influences gastric acid secretion.
• The stomach protects itself with a thick mucus and bicarbonate layer.
• Oblique muscle layer facilitates food grinding and mixing.
• Enteroendocrine cells (G cells, D cells, S cells) regulate digestive processes.
• Parietal cells secrete hydrochloric acid (HCl) and intrinsic factor.
• Chief cells secrete pepsinogen, the precursor to pepsin for protein digestion.
• Gastrin stimulates HCl secretion and enhances motility.
• Somatostatin inhibits gastrin and acid production (important pH control).
• Secretin stimulates bicarbonate secretion from the pancreas and inhibits gastric acid secretion.
• Stomach blood and lymphatic supply, vitamin B12 absorption, and iron metabolism are crucial functions.
• Gastritis, ulcers, and Zollinger-Ellison syndrome are conditions affecting stomach function.

Key Concepts

• Enteroendocrine Cells: Specialized cells releasing hormones regulating stomach functions.
• G cells: Located in the antrum, secreting gastrin (increases gastric acid and motility).
• D cells: Located in the antrum, secreting somatostatin (inhibits gastrin and acid production).
• Parietal Cells: Located in the fundus and body, secreting HCl and intrinsic factor.
• Chief Cells: Located in the fundus and body, secreting pepsinogen.

Clinical Applications

• Zollinger-Ellison Syndrome: Caused by gastrin-secreting tumors (gastrinomas) leading to hypergastrinemia and recurrent peptic ulcers.
• Diagnosis uses fasting gastrin levels and imaging studies (endoscopy, CT scans).
• Proton pump inhibitors (PPIs) reduce gastric acid production for ulcer treatment.
• Treatment of Zollinger-Ellison Syndrome often includes surgical resection.

Pathophysiology

• Acid Secretion Pathway: Gastrin, histamine, and acetylcholine stimulate HCl secretion by parietal cells.
• Regulation: Somatostatin inhibits acid production when pH drops too low. This feedback loop is critical.
• Motility: Three muscle layers (longitudinal, circular, oblique) enable mixing and grinding movements, converting food into chyme.

Pharmacology

• Proton Pump Inhibitors (PPIs): Inhibit H+/K+ ATPase, reducing acid production important for GERD, peptic ulcers, and Zollinger-Ellison syndrome.
• H2 Receptor Antagonists: Block histamine H2 receptors on parietal cells, reducing acid secretion.
• Antacids: Neutralize stomach acid for quick symptom relief (heartburn, indigestion)

Differential Diagnosis

• Peptic Ulcer Disease (PUD): Epigastric pain, possibly improving or worsening with food. Common causes are H. pylori infection and NSAID use. Diagnosis is typically confirmed through endoscopy, treatment involves acid suppression, and, in some cases, H.pylori eradication.
• Gastritis: Inflammation of the stomach lining, common causes include H.pylori infection, chronic alcohol use, or NSAIDS, symptoms include nausea, bloating, and epigastric pain.
• Hiatal Hernia: Part of the stomach pushes into the chest cavity. A contributing factor to GERD, leading to acid reflux, heartburn.
• Barrett's Oesophagus: Chronic GERD causes changes in the esophageal lining, increasing risk for esophageal cancer.

Investigations

• Endoscopy: Gold standard for diagnosing peptic ulcers, gastritis, malignancies. Allows visualization and biopsy.
• Gastrin Level Test: Used to diagnose conditions with excessive gastrin production like Zollinger-Ellison syndrome.
• H. pylori: Testing helps diagnose gastritis and peptic ulcer disease.
• pH Monitoring: Measures acid exposure in the esophagus and confirms GERD diagnosis.