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sections
secretion and enzymatic breakdown
effect of gastrin
secretion and regulation
gastric mucosal barrier
secretion and enzymatic breakdown
The stomach produces 2–3 L of gastric juice daily, containing water, HCl, mucus, and enzymes.
Gastric juice mixes with food to aid digestion.
Mucous cells secrete mucus to protect the stomach lining from acid and enzymes.
Parietal cells secrete HCl (kills bacteria) and intrinsic factor (needed for vitamin B12 absorption).
Chief cells secrete pepsinogen (inactive form of pepsin) and gastric lipase.
Pepsin (activated by HCl) breaks down proteins.
Gastric lipase helps digest fats.
Pepsinogen is secreted in inactive form to prevent damage to chief cells.
Release of hormone gastrin into the bloodstream in response to many stimuli, such as signals from the vagus nerve
Glandular stimulation by gastrin leads to increased secretion of gastric juice to increase digestion.
Stimulation of smooth muscles by gastrin leads to stronger contractions of the stomach and the opening of the pyloric sphincter to move food into the duodenum.
Gastrin binds to receptor cells in the pancreas and gallbladder →increases the secretion of pancreatic juice and bile.
effect of gastrin
Release of hormone gastrin into the bloodstream in response to many stimuli, such as signals from the vagus nerve
Glandular stimulation by gastrin leads to increased secretion of gastric juice to increase digestion.
Stimulation of smooth muscles by gastrin leads to stronger contractions of the stomach and the opening of the pyloric sphincter to move food into the duodenum.
Gastrin binds to receptor cells in the pancreas and gallbladder →increases the secretion of pancreatic juice and bile.
secretion and regulation
WATER is absorbed by the stomach, drugs eg, aspirin, about 20% of alocohol, some amino acids
Phases of Gastric Acid Secretion
Cephalic Phase (≈30%)
Triggered by the sight, smell, taste, or thought of food (anticipation of eating).
Mediated by the vagus nerve (parasympathetic response).
Vagal stimulation activates:
Parietal cells → secrete HCl
Enterochromaffin-like (ECL) cells → release histamine
G cells → stimulated by gastrin-releasing peptide (GRP) → release gastrin, which further stimulates acid secretion.
The vagus nerve also inhibits somatostatin release, removing its inhibitory effect on acid production.
Gastric Phase (≈50%)
Initiated by food entering the stomach.
Stimuli include:
Stomach distension (activates stretch receptors and mechanoreceptors)
Presence of peptides and amino acids in the stomach contents.
These factors further stimulate G cells, ECL cells, and parietal cells, enhancing acid secretion.
Intestinal Phase (≈10%)
Begins when chyme enters the small intestine.
Triggered by intestinal distension and nutrients (especially amino acids) in the chyme.
Provides a minor stimulation of gastric acid production compared to earlier phases.
Regulation of Gastric Acid Secretion
Stimulated by:
Parasympathetic nervous system (via the vagus nerve)
Gastrin (from G cells)
Histamine (from ECL cells)
Inhibited by:
Somatostatin (from D cells)
VIP (vasoactive intestinal peptide)
CCK (cholecystokinin)
Secretin
gastric mucosal barrier
Barrier has 3 protective components which provide resistance for mucosal surface of the stomach
Bicarbonate ions, secreted by the surface epithelial cells. -neutralize acids.
compact epithelial cell lining
insoluble mucous covering- protective
Factors that can damage the barrier:
Bacterial Infection by Helicobacter pylori
Alcohol
NSAID
ASPIRIN