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Gastric acid secretion Questions and Answers

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Gastric acid secretion Questions and Answers Gastric acid secretion multiple central and peripheral mechanisms with the common end point of secretion of H by H/K ATPase pump located in parietal cells. the 3 mechanisms of gastric acid secretion neuronal (ACh, M3) paracrine (histamine, H2)...

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  • September 28, 2024
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Gastric acid secretion Questions and
Answers
Gastric acid secretion - answer multiple central and peripheral mechanisms with the
common end point of secretion of H by H/K ATPase pump located in parietal cells.

the 3 mechanisms of gastric acid secretion - answer neuronal (ACh, M3)
paracrine (histamine, H2)
endocrine (gastrin, CCK2)

Parietal cell - answer are the epithelial cells that secrete hydrochloric acid (HCl) and
intrinsic factor. These cells are located in the gastric glands found in the lining of the
fundus and in the body of the stomach. H/K ATPase or proton pump is located on apical
cell membrane allowing the exchange of H and K across the cell membrane.

chief cells - answer produce pepsinogen - which is converted into pepsin when in
contact with acid produced by the parietal cells

Goblet cells - answer produce mucin which is mucus

Modulation of gastric acid secretion - phase 1 cephalic - answer CNS or cephalic
phase of acid secretion is stimulated by sight, smell, taste, or anticipation of food. it
starts the parasympathetic nervous system. efferent fibres from dorsal motor nuclei
descend to stomach via vagal nerve and synapse with ganglion cells of enteric nervous
system.
ACh (direct neural) from postganglionic vagal fibres directly stimulates muscarinic M3
receptors.
ACh also indirectly stimulates release of histamine from ECL cells in the fundus and
gastrin from G cells in antrum

Modulation of gastric acid secretion - phase 2 gastric - answer food stretches the
walls of the stomach this is sensed by mechanoreceptors activating a neural reflex to
stimulate acid secretion. Peptides and amino acids in food stimulate G cells to release
gastrin (which also releases more histamine). Food also acts as a buffer raising the pH
and thus removing the stimulus for somatostatin (inhibits the negative feedback loop of
the stomach to allow the food to be broken down)

Modulation of gastric acid secretion - phase 3 intestinal - answer once chyme enters
the duodenum, intestinal phase stimuli activates the negative feedback mechanisms to
reduce acid secretion and prevent the chyme from becoming too acidic.
Somatostatin (SST) released from antral D cells when gastric acid <3 inhibits gastric
acid release in -ve feedback loop

, How does histamine work - answer diffuses from site of release to parietal cells
stimulating the H2 receptors which activates GPCR (H2 = Gs -> adenylyl cyclase ->
cAMP -> PKA
so is a cAMP dependent pathway
cAMP activates H/K ATPase pump

How does gastrin and ACh work - answer both activate GPCR (M3 = Gq -> PLC ->
IP3 and Ca
so is a Ca2+ dependent pathway
Ca2+ activates H/K ATPase pump

Gastric defences against acid - answer primary defence is lower oesophageal
sphincter - prevents reflux of gastric acid contents
stomach requires good mucosal BF
key stomach defence - secretion of mucous layer - slows ion diffusion, prevents
damage by pepsin
Prostaglandins PGE2 and PGI2 stimulate mucous production and inhibits H secretion
by parietal cells
Secretion of bicarbonate by superficial gastric epithelial (or goblet) cells -> increases pH
and prevents acid related damage

Aggressive factors that can cause gastric mucosal injury - answer gastric acid
pepsin
NSAIDs
stress
alcohol
H. pylori
free radicals

Antacids - answer act locally to buffer gastric and oesophageal contents. provide
rapid but short term relief
useful for very mild cases of GERD
does not prevent over production of acid
combinations of Al, Mg, Ca, and Na salts
excessive use can cause kidney stones (Ca salts) or metabolic alkalosis (sodium
bicarbonate)

Antacids the cause constipation - answer Al and Ca

Antacids that cause diarrhoea - answer Mg

Antacids that cause gas and belching - answer Calcium carbonate

H2 receptor antagonist - answer block the H2 receptor to stop histamine from
binding and causing the cAMP dependent pathway resulting in acid production. thus it
stops acid production

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