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.
Enterogastrones are release in response to what?
Released in response to acid, hypertonic solution, fatty acids or monoglycerides in duodenum.
What do enterogastrones do and how do they do it?
Act collectively to prevent further acid build-up in duodenum.
Two strategies;
- Inhibit gastric acid secretion
- Reduce gastric emptying (inhibit motility/contract pyloric sphincter)
