Gastric secretions Flashcards
Major components of gastric juice
water
organic compounds: intrinsic factor, pepsinogen, lipase, mucus
Ions: Na, H, K, Cl, HCO3
Oxyntic/gastric glands
Parietal
Chief (Peptic)
Mucous Neck
Paracrine
Products of parietal glands
HCl IF
Products of chief/peptic glands
pepsinogen, lipase
Products of mucous neck glands
mucin
Products of paracrine glands
histamine (ECL), somatostatin (D)
Pyloric glands
Mucous
Endocrine
Paracrine
Products of mucous glands
mucous/HCO3-
Products of endocrine glands (pyloric)
gastrin (G)
Products of paracrine glands (pyloric)
somatostatin (D)
Major functions of stomach acid
bacteriostatic agent
activate pepsinogen
denature protein
facilitate absorption of vitamin B12, calcium
Mechanism of acid secretion by the parietal cell
- K+ dependent H+ ATPase transports H+ out of the cell in exchange for K+ at the secretory membrane
- OH- remaining in cytoplasm is converted to HCO3- by carbonic anhydrase
- HCO3- exchanged for Cl- at basolateral membrane surface, passes into bloodstream. HCO3- makes blood slightly alkaline
Tubulovascular system
contain H/K ATPase and glycoprotein intrinsic factor
large amounts of tubulovesicles close to the cell membrane in parietal cells
Stimuli –> vesicles fuse with canaliculus, increase surface area for pumping out acid
Conversion of pepsinogen –> pepsin
Pepsinogen secreted by chief cells into gastric lumen
Pepsinogen activated by acid –> pepsin
Pepsin can activate pepsinogen (autocatalysis)
Components of the gastric mucosal barrier
mucus
surface active phospholipids
Function of the gastric mucosal barrier
mucus: lubricant, acid neutralization, trapping alkaline epithelial cell secretions, prevents back diffusion of H+ across the mucosa
Surface active phospholipids: binds to mucus and repels protons
PGs: inhibits acid secretion, prevents surface epithelial cell exfoliation, increases mucosal blood flow, stimulates mucus and bicarbonate secretion, enhances synthesis of surface-active phospholipids that line the gastric mucosa
Gastrin
originates in G cells (pyloric gland)
receptor on parietal cell, stimulate acid secretion
stimulate histamine release
Histamine (gastric)
origin: ECL cells, (oxyntic gland), mast cells, neurons
H2 receptor on parietal cells –> acid secretion
ACh (gastric)
origin: intrinsic neurons
M3 receptors on parietal cells –> acid secretion
stimulates histamine release
Characteristics of H. pylori
High mutation rate motility ability to attach to epithelial cells virulence factors urease evasion of immune response
Stimulatory phases of gastric secretion
- Cephalic
- Gastric
- Intestinal
Cephalic phase - stimulatory
Prior to food being swallowed
Conscious thoughts/stimulation of olfactory, gustatory and mechanoreceptors
- Sensory input stimulates hypothalamus
- Parasympathetic motor output via vagus nerve –> stimulates parietal and chief cells (via ACh) and G cells (GRP) due to neurotransmitter release from enteric neuron
Gastric phase - stimulatory
- Food enters the stomach and activates stretch/mechanoreceptor-based reflex, both local and via the vago-vagal loop that stimulates secretion (neuronal component)
- Food buffers gastric juice –> feeds back to activate parietal cells and the products of protein breakdown (peptones) directly stimulate G cells to produce gastrin (non-neuronal component)
Intestinal phase - stimulatory
- Food reaches proximal part of the small intestine
- Peptone in the chyme stimulates G cells located in duodenal mucosa to produce more gastrin –> acts on parietal & chief cells in the gastric glands (via gastrin)