Gastric Secretions Flashcards
Oxyntic (gastric) glands
- mucous neck cells that secrete mucus and some pepsinogen
- peptic (chief) cells that secrete pepsinogen
- parietal (oxyntic) cells: HCl and intrinsic factor
Pyloric glands
- primarily mucus
- small amounts of pepsinogen and large amounts of thin mucus
- gastrin
*Actions of gastrin
Secreted by G cells in response to proteins in the gastric lumen
- stimulates secretion of histamine by enterochromaffin-like cells
- histamine then acts on parietal cells stimulating acid secretion
- gastrin also has trophic effects on enterochromaffin and parietal cells
*Increased gastrin =
Increased gastric acid
Pepsinogen secretion
Secreted pepsinogen is an inactive precursor
- activated by HCl to form pepsin
- catalyzed by presence of pepsin
- HCl is required for proteolytic activity of pepsin
Regulation of pepsinogen secretion
Release from peptic cells is stimulated by Ach release or presence of acid
- rate of release strongly influenced by amount of acid in the stomach
Acid secretion
Stimulated parietal cells secrete acid solution
- isotonic to body fluids
- pH: 0.8
- requires 1500 calories per liter of gastric juice
Mechanisms of acid secretion: process 1
Chloride is actively transported from cytoplasm to lumen, while Na is actively transported in the opposite direction
- causes negative potential in lumen = K diffuses out of cell into lumen
Mechanisms of acid secretion: process 2
H2O dissociated via carbonic anhydrase
- H ions actively secreted into lumen in exchange for potassium
- catalyzed by H K ATPase pump
- remaining Na in lumen is actively absorbed, allowing H to take its place
Mechanisms of acid secretions: process 3
CO2 combines with hydroxyl ions in cytoplasm to form bicarb
- bicarb diffuses out of cell into ECF in exchange for chloride ions
Mechanisms of acid secretions: process 4
Water passes into lumen by osmosis following ions
Final secretion contains
- HCl
- KCl
- small amount of NaCl
*Hydrogen-potassium ATPase
Unique to parietal cell
- pumps H against an enormous concentration gradient (3 million to one)
- exists, preformed in cytoplasm of cell until needed
- transported to cell membrane upon stimulation of the parietal cell
Neural and hormonal control
- Ach: acts on all cell types in gastric glands
- gastrin: secreted by G cells in pyloric glands and acts on parietal cells in gastric glands
- histamine: acts on parietal cells, secreted by enterochromaffin-like cells
Control of acid secretion
Parietal cells are only source of HCl, closely associated with enterochromaffin-like cells which lie adjacent to parietal cells in gastric glands
- rate of acid secretion is related to the rate of histamine secretion
Enterochromaffin-like cells are stimulated by ____
- gastrin secreted by pyloric glands in response to proteins
- acetylcholine released from vagus nerve
Activation of what receptors leads to production of gastric acid?
- acetylcholine (M3)
- histamine (H2)
- gastrin (G)
What contributes to complete blockade of acid secretion?
H-K pump (proton pump) blockade
- drug of choice for reduction of acid secretion
Delayed effect
Complete pump inhibition may take up to 4 days
- include histamine blockers for first few days of therapy
When pH drops below 3.0
- gastrin secreted by G cells is stopped
- gastrin mediated HCl release is reduced
- reduction in acid (raising pH) slows pepsinogen release
If acid production is blocked?
- feedback inhibition is lost
- gastrin release continues
- may lead to hypertrophy of parietal and enterochromaffin-like cells
*Cephalic phase (neural stimulation)
- release of HCl by parietal cells
- release of gastrin by G cells
- gastrin subsequently acts on parietal cells increasing acid secretion
*Cephalic phase is the ______ response to food
Brain
- sight, smell, thought, taste, intensity increases with appetite
- mediated by neural signals: transmitted via vagus nerve, responsible for 20% of gastric secretion
Gastric phase
Presence of food in the stomach
- stimulates vagovagal and enteric reflexes
- stimulates gastrin mechanism
- accounts for 70% of gastric secretion
Intestinal phase
Presence of food in proximal SI
- releases small amounts of gastrin from duodenum
- leads to a weak stimulus for secretion
*Inhibition of gastric secretion intestinal factors
Following the weak intestinal phase the intestines often inhibit gastric secretion
- presence of chyme may lead to an inhibitory enterogastric reflex
*Enterogastric reflex
- distention of small bowel
- presence of acid in duodenum
- presence of protein breakdown products
- mucosal irritation
Presence of acid, fat, protein breakdown products, hyper/hypo osomolar fluids, or any irritation leads to release of
Secretin: opposes gastric secretion
- gastric inhibitory peptide
- vasoactive intestinal polypeptide
- somatostatin