Gastric Secretion Flashcards
Describe the structure and various functions of the stomach.
Fundus;
- Storage
Body;
- Storage
- Mucus
- HCl
- Pepsinogen
- Intrinsic factor
Antrum;
- Mixing/grinding
- Gastrin
Explain the essential role of intrinsic factor in vitamin B12 absorption.
- Only essential (non-compensated) function of stomach
- Produced by parietal cells
- Required for vitamin B12 absorption
- Intrinsic factor/B12 complex absorbed from ileum
- Defect results in pernicious anaemia
Explain the functions of gastric mucus.
- Produced by surface epithelial cells and mucus neck cells
- Cytoprotective role: protects mucosal surface from mechanical injury
- Neutral pH (HCO3) protects against gastric acid corrosion and pepsin digestion
Describe the basic physiology of gastric acid secretion.
- CO2 enters cell from blood.
- In cytoplasm, sped up by carbonic anhydrase: CO2 + H2O –> H2CO3 (highly unstable)
- H2CO3 –> HCO3- + H+
- ATP hydrolysis drives H+ out of cell into stomach lumen and K+ into cell
- HCO3- moves out of cell in exchange for Cl-
- Cl channel opens and allows Cl into stomach lumen
- H+ + Cl- = HCl
Describe the cellular composition of gastric glands.
- Mucus neck cells (mature into surface mucus neck cells): mucus
- Chief cells: pepsinogens
- Parietal cells: HCl, intrinsic factor
Describe hormonal (endocrine) control of gastric acid secretion.
Gastrin –> receptors on parietal cells –> rise in intracellular Ca –> affects protein kinases –> rise in activity of proton pump –> rise in acid secretion.
Describe the mechanisms inhibiting gastric acid secretion in the cephalic phase.
Stop eating –> decrease in vagal activity.
What are enterogastrones? Give examples.
Hormones released from gland cells in duodenal mucosa e.g. secretin, cholecystokinin (CCK), GIP.
Describe pepsinogen secretion.
- Pepsinogen (zymogen = inactive precursor) secreted by chief cells
- Low pH (<3) –> pepsinogen (undergoes acid hydrolysis) –> pepsin
- Zymogen storage prevents cellular digestion
- Pepsins inactivated at neutral pH
- Mechanisms for pepsin control of pepsin secretion parallel HCl secretion
Describe hormonal (paracrine) control of gastric acid secretion.
Histamine –> binds to Gs and adenolase cyclase (unique type II histamine receptor) –> turns ATP into cAMP –> affects protein kinases –> rise in activity of proton pump –> rise in acid secretion.
Prostaglandins –> binds to Gi and INHIBITS adenolase cyclase –> stops production of cAMP –> fall in activity of proton pump –> fall in acid secretion.
Describe neural control of gastric acid secretion.
Vagus nerve/local ENS nerves –> acetylcholine –> cholinergic receptor –> rise in Ca –> affects protein kinases –> rise in activity of proton pump.
Describe the mechanisms stimulating acid secretion in the cephalic phase.
Sight, smell, taste of food –> Increase in vagus nerve –> ACh –> parietal cells.
Sight, smell, taste of food –> Increase in vagus nerve –> G cells –> gastrin –> parietal cells.
Gastrin/ACh –> ECL cells –> histamine –> parietal cells.
Describe the mechanisms stimulating acid secretion in the gastric phase.
Distension of stomach (arrival of food) –> vagal/enteric reflexes –> ACh –> parietal cells.
Peptides in lumen –> G cells –> gastrin –> parietal cells.
Gastrin/ACh –> ECL cells –> histamine –> parietal cells.
Describe the mechanisms inhibiting gastric acid secretion in the gastric phase.
Decrease in pH (rise in [HCl]) –> decrease in gastrin.
Describe the mechanisms inhibiting gastric acid secretion in the intestinal phase.
Acid in duodenum –> enterogastric reflex/secretin release –> decrease in gastrin secretion/gastrin stimulation of parietal cells.
Fat/CHO in duodenum –> GIP release –> decrease in gastrin secretion/parietal cell HCl secretion.
