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Flashcards in Gastric Secretions Deck (28)
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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

- 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