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24 Cards in this Set
- Front
- Back
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stomach - what layer do our cells of interest not extend beyond?
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muscularis mucosa: all our interesting cells are more toward the lumen from that.
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what are our cells of interest in the stomach, just generally?
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mucous cells.
chief cells: pepsinogen parietal cells (in gastric pits): they make HCl. They're pretty large. argentaffin cells |
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what are argentaffin cells? which ones do we care about
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it's named after a stain - they're all endocrine cells.
G cells - make gastrin I cells - make CCK ECL cell - makes histamine D cells: somatostatin S cell: secretin D-1: Vip K: Gip |
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what's interesting about the stomach and b12 absorption?
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parietal cells, in addition to making HCl, also makes Intrinsic Factor - this is required for absorbing B12 later in the intestines. It removes the R-protein and forms a complex with B12.
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a parietal cell getting ready to secrete acid. what's different about it?
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there are 2 distinct morphologies for the parietal cell: one of resting, one of active.
In the resting state, the secreting business end (with an H/K ATP-ase) is mostly tubovesicular. When its stimulated to release, it transforms: get INTRACELLULAR CANALICULI. |
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what's pepsin and how does it work?
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secreted as pepsinogen from chief cells. activated by low pH into pepsin (likes it 1.8 to 3.5). it eats peptides.
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gastric secretions and the electrolytes therein: what changes over time? Why is vomiting interesting here?
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H+ and Cl- are, of course, the things of greatest concentration and go up over time.
Also worthy of note: K+ is higher than in saliva and is higher than plasma. Not hugely significant, 'cept that when vomiting, high potential for hypokalemia from loss of that high K+ concentration. Also worthy of note: [Na+] decreases hugely as secretion time goes on. |
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acid secretion, stomach content volume: what's up? why are GERD patients often in the ER really late at night? what happens post meal, and when?
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pH of stomach between meals is very LOW (acidic) - this is because food buffers the stomach acids.
eat meal: volume goes up immediately, then secretion of acid reaches peak within 1-2 hours. the pH rises immediately (buffered by the food), then steadily declines back down to very, very low level within 3-4 hours. So, late at night, long time after meal, pH is very low and can cause GERD. |
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Parietal Cell Apical Transporters: what's going on in acid release?
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Big guy: there's a K+ in/ H+ out, ATP-ase.
To keep this working, need a K+ channel out into the lumen. Also, because it's HCl, need a Cl- channel to let Cl- out into the lumen. |
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Parietal Cell B/L transporters: go
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As always, have our Na+/K+ ATPase.
also, think about the ALKALINE TIDE: so, there's an HCO3- out (into ICS), Cl- in (to cell) antiporter. Also, there's a random K+ out channel. |
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what phenomenon drives the production of H+ ions in the parietal cell?
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this is related to alkaline tide: metabolism makes Co2, carbonic anhydrase makes H2co3, loose an H+ and make bicarb. H+ goes out into lumen, bicarb goes back into the blood and is carried back up to the surface of the stomach.
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what does a proton pump inhibitor, and what does it target?
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Amaprosol: it targets the H+/K+ ATPase that releases hydrogen ions into the stomach.
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what are our four phases of digestion?
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interdigestive (between meals, pH is very very low)
cephalic (thinking about eating, which can actually release a little acid). gastric (stomach churning out acid) intestinal |
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talk about the gastric phase: what factors are released, what cells do they work on, and what do they initiate?
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Big divisions: distension (releasing ACh) vs. protein digestion (releasing gastrin).
so: distension activates the ENS, releasing ACh. Vasovagal response releases ACh. ACh acts on everything: G-cells (make gastrin), ECL (to make histamine), and work directly on parietal cells. Both gastrin and histamine turn on parietal cells. GRP from the vasovagal response acts on G-cells to make gastrin. Peptide digestion: AA's work on the G-cells to make gastrin. Gastrin works on ECL cells to make histamine and works on parietal cells to make acid. So, in the end, all the responses work on G-cells, all work on ECL cells, and all cause parietal cells to up their H+ secretion. |
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so, what receptors do parietal cells have? which are they specifically, and what pathway do they work through?
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gastrin receptors, histamine receptors, and ACh receptors.
ACh works through an M3 (muscarinic) receptor. Gastrin works through the CCKb receptor (remember, gastrin looks a lot like CCK). Both ACh and gastrin work through PIP/Ca++ opening Histamine binds an H2 receptor and works like sympathetics (cAMP/pKA) |
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what's potentiation? what's the effect of an H2 blocker?
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h2 blockers will stop histamine release, stopping the cAMP-mediated release of acid by the parietal cells.
because parietal cells experience potentiation, there's a synergistic effect of the cAMP and Ca++ mediated pathways. Blocking one lowers secretion significantly, but still get above basal level. Better off blocking protons at the source - at the parietal cells. |
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what's the intestinal phase all about?
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This is protein sampling in the dudenum.
Absorbed amino acids and proteins can turn off H+ secretion by either directly acting on parietal cells or through an intermediate, "entero oxytin" also, intestinal G-cells can repsond to proteins by making more gastrin, to up secretion of H+ by parietal cells. either way, this is all about how the intestines communicate back to the parietal cells in the stomach. 2 effects stop H+, one turns it on (gastrin) |
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released GI peptides - what are the 3 big categories?
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neurocrine, endocrine, and paracrine.
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what are our endocrine peptides?
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gastrin,
CCK (made by the duodenum, signals pancreas to make enzymatic secretions) secretin (from the duodenum, release bicarb and lots of it from pancreas) GIP (gastric inhibitory peptide) - stops motility and acid secretion. NOTE: made by INTESTINAL mucosal epithelial cells |
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paracrines?
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histamine and somatostatin.
somatostatin - big stopper of H+ release. NOTE: from D-cells in the antrum and body of the stomach. Stops motility and H+ secretion |
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neurocrine?
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VIP (vasoactive intestinal polypeptide), made by D-1 cells. Not really limited to GI system, made all over the place. Increases watery secretions of the pancreas and stops H+ secretion by the stomach.
GRP (gastrin releasing protein enkephalins. small, in vagus, like morphine. |
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what hormones are inhibitory on the stomach?
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prostiglandins
somatostatin. note: somatostatin comes from D cells in response to low pH |
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why is acid bad for the stomach?
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it decreases mucous secretion AND blocks prostiglandins (which turn off acid) : so you get a two hit on your stomach.
no mucous, and more acid secretion = bad news. |
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what transporters are important for alkaline secretion?
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the H/K antiporter.,
Also, a K+ channel out and a Cl- out. |
