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39 Cards in this Set
- Front
- Back
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Cardia
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where the esoph and stomach join.
begins at the z line. transition from squamous to columnar. protects esoph from corrosive gastric contents. |
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pylorus
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controls what empties out of the stomach.
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5 layers of the stomach
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mucosa, deep mucosa/lamina propria, submucosa, muscularis propria, serosa.
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Pits of the stomach
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in all areas of the stomach. gives more surface area and represents entrance to deep gastric glands.
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Fundus and body
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gastric acid secretion
deep gastric pits - surface and neck mucus cells, parietal cells, chief cells, endocrine cells (ECL and D cells) |
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Antrum
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Mixing and grinding of particles here.
Gastrin and somatostatin. Intermediate gastric pits that has surface and neck mucus cells and endocrine cells (G and D cells) |
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parietal cells
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make acid and intrinsic factor.
acid is mainly to to protect from bacteria and also convert pepsinogen to pepsin (protein digestion) |
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Chief cells
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makes pepsinogen and gastric lipase.
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Surface and neck cells
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make mucus, HCO3- and trefoil peptides
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endocrine cells (3)
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G cells - gastrin
ECL cells - histamine D cells somatostatin |
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Parietal cell (resting)
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gastric-acid pump in tubules (inactive) and canaliculus is collapsed (acid secreted through this).
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parietal cell (stimulated)
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gastric acid pump (H+/K+-ATPase) in tubulovesicles is incorp into the canaliculus and becomes active.
It exchanges H for K and creates HCl which is released into the lumen. |
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Stimulators of the parietal cell
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ACh, gastrin, histamine.
histamine is the most important one. |
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PPI mech of action
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inhibits H/K ATPase to block gastric acid secretion.
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Things that turn off the parietal cell from making acid and intrinsic factor
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Somatostatin and PGE2 (via G protein to reduce cAMP)
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Mech of gastric acid secretion
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CO2 made by mitochon to eventually be hydrated to make acid and bicarb.
H+ then secreted by proton pump and bicarb secreted into plasma for chloride into the cell. Then Cl- is secreted (to make HCl) along with K+ |
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Gastric juice changes with secretory rate
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Early the gastric juice is high in Na+ and chloride. Later it is high in chloride and H+ and not high in sodium.
"Someone vomiting for many days is hypokalemic and hypochloremic (lots of gastric loss) and alkalotic" So at peak rates of secretion, it is mainly HCl. In early secretion, mainly NaCl. |
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Clinical presentation of hypokalemic, hypochloremic, alkalosis and dehydration.
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lethargy, musc weakness, cramps, nausea.
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Mucus made by neck cells and surface cells.
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Neck cells - soluble.
Surface - insol. Vagal nerve stim and ach increase soluble mucus from neck cells. |
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What two things protect the gastric mucosa?
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mucus and bicarb.
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Things that disrupt mucosal barrier
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aspirin, ethanol, ibuprofen, bile salts.
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3 mechanisms of communication in the GI tract
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endocrine - gastrin
neurocrine - ACh paracrine - histamine |
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Gastrin
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G-cell makes it.
Secreted in resp to AAs, stomach distention, vagal stimulation by gastrin releasing peptide Actions of gastrin - stim ECL cells, stim parietal cells, gastric mucosal growth, pepsinogen secretion. Inhib by H+ in stomach and somatostatin. |
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Cholecystokinin
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from I cell in duodenum.
Secreted in resp to AAs and FAs. Stimulates H+ secretion by parietal cell and inhibits gastric emptying |
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secretin
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From S cell in duodenum in response to H+ and FAs in duodenum
It inhibits H+ secretion by gastric parietal cells. |
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Glucose-dependent insulinotropic peptide (GIP)
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inhibits H+ secretion by gastric parietal cells.
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Hormones inv in gastric acid sec
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gastrin, CCK, secretin, GIP
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somatostatin
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paracrine.
From D cell. secreted with H+ in the lumen. Inhibits acid secretion by parietal cell and inhibits release of all GI hormones. Inhibited by vagal stimulation. (it slows the gut down) |
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histamine
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paracrine
from ECL cell (fundus and body) Responds to ach/vagal stim and gastrin. It directly stim parietal cell and potentiates effects of gastrin and vagal stim to increase H+ secretion. Inhib by somatostatin and histamine |
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Gastrin-releasing peptide
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Neurocrine.
From vagus nerve that innervates G-cells. In resp to vagal action potential and it stimulates G cell to release gastrin. |
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3 phases of acid secretion in resp to a meal
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cephalic phaes - intion response to sight of thought etc of food.
gastric phase - response to food in the lumen. intestinal phase - response to movement of food out of the stomach and to low pH. this phase slows gastric secretions down. |
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slide 55
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good slide.
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Gastric phase
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Food causes an increase in the pH so gastrin release is upregulated and somatostatin is downreg.
AAs stimulates G cells to release gastrin. Fundal distention increasess parietal cell secretion. |
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High H+ stimulates....
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somatostatin which inhibits G-cells.
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slide 58 and 60 and 64
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also good
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why do ulcer pts have relief of pain after meals but then return 2 hours after meals?
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food bring up the pH initially but then the high amt of gastrin a couple hours later brings more H+ back into the stomach.
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Chyme effects on the upper intestine
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Inhibits gastric acid secretion possible via secretin and GIP.
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summary of response to a meal
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Acid secretion occurs in 3 phases:
Cephalic phase- initial response to sight, smell, taste or thought of food- Vagally mediated via direct stimulation of parietal cells, ECL cells (histamine) and indirect stimulation of G-cells Gastric phase- Distention Buffering of gastric acid pH AA stimulation of the parietal cell and G-cell Intestinal phase- response to movement of food out of the stomach/low pH chyme components in duodenum with release of secretin/GIP |
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slide 66
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another good summary...
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