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Gastrointestinal | Gastric Secretion: The Cephalic & Gastric Phase

Ninja Nerd・2 minutes read

Gastric secretions involve three phases: cephalic, gastric, and intestinal, with varying stimuli and mechanisms for hydrochloric acid and pepsin production. Different receptors and cells are responsible for regulating the digestive process, including inhibitory factors like somatostatin and the sympathetic nervous system.

Insights

  • The three phases of gastric secretions are cephalic, gastric, and intestinal, with the cephalic phase contributing one-third of the total gastric juice secretion, triggered by stimuli like sight, thought, smell, and taste of food before it even reaches the stomach.
  • Gastric juice production in the cephalic phase is driven by the vagus nerve, activating parietal and chief cells to produce hydrochloric acid and pepsin, while inhibitory events in the sympathetic nervous system can decrease acid and enzyme production, showcasing the intricate balance of factors influencing digestive processes.

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Recent questions

  • What are the three phases of gastric secretions?

    Cephalic, gastric, intestinal phases.

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Summary

00:00

Phases of Gastric Secretions: Cephalic and Gastric

  • Gastric secretions involve three phases: cephalic, gastric, and intestinal.
  • The cephalic phase accounts for one-third of gastric juice secretion.
  • Stimuli for the cephalic phase include sight, thought, smell, and taste of food.
  • Gastric juice production in the cephalic phase occurs before food enters the stomach.
  • Stimuli for the cephalic phase involve the cerebral cortex, hypothalamus, and medulla.
  • The vagus nerve is crucial in stimulating parietal and chief cells to produce hydrochloric acid and pepsin.
  • Inhibitory events for gastric secretion involve activation of the sympathetic nervous system.
  • The sympathetic nervous system inhibits vagal nerve stimulation, reducing hydrochloric acid and pepsin production.
  • The gastric phase, accounting for two-thirds of gastric juice secretion, is stimulated by distension.
  • Stretch receptors in the stomach walls trigger the vagus nerve to stimulate hydrochloric acid and pepsin secretion.

15:56

"Gastrin and Acid Secretion in Digestion"

  • Gastrin binds to CCK2 receptors, activating an intracellular mechanism via GQ to increase calcium levels and activate a pump on parietal cells.
  • The pump on parietal cells pushes potassium out into the stomach lumen, creating hydrochloric acid.
  • Antral G cells are stimulated by partially digested proteins, leading to the secretion of gastrin.
  • Gastrin acts on CCK2 receptors on parietal cells, stimulating the proton pump to concentrate protons, forming hydrochloric acid.
  • Chief cells contain vesicles with enzyme molecules activated by gastrin binding to CCK1 receptors, converting pepsinogen to pepsin.
  • Pepsinogen is converted to pepsin in the presence of a proper concentration of protons within an optimal pH range of 1.8 to 3.5.
  • Proteins act as buffers, tying up protons and affecting pH, crucial for pepsin activation.
  • The sympathetic nervous system inhibits the release of hydrochloric acid and pepsinogen, affecting the digestive process.
  • Somatostatin is a strong inhibitor stimulated by low pH/high proton concentration, inhibiting gastrin release and subsequent acid secretion.
  • Parietal cells produce hydrochloric acid by combining CO2 with water via carbonic anhydrase, disassociating into protons and bicarbonate, with chloride ions aiding in hydrochloric acid formation.

32:53

Regulation of Gastric Acid Secretion in Stomach

  • Stimulation of M3 receptors leads to increased pepsin and hydrochloric acid secretion.
  • Gastrin acts on CCk receptors on D cells, controlling antral D and G cells.
  • Somatostatin inhibits proton pumps through G inhibitory pathway.
  • Acetylcholine stimulates proton pump via muscarinic type 3 receptors.
  • Histamines stimulate hydrochloric acid secretion through H2 receptors.
  • Mucosal barrier, formed by mucus neck cells and fo ve Oller cells, protects against corrosive damage from hydrochloric acid and pepsin.
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