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17 Cards in this Set
- Front
- Back
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What are the 4 things that control H+ secretion in the stomach's parietal cells? Does each act in an endocrine, paracrine, or neuronal fashion?
Do they upreg or downreg? Name their receptors on the parietal cell. Which uses a Ca++ dependent pathway? cAMP dependent? Which transporter to all of these pathways affect? |
Gastrin- endocrine (CCK2)
Histamine- paracrine (H2) Acetylcholine (ACh)- neuronal (M3) Prostaglandins-paracrine and autocrine (EP3) All but prostaglandin upreg. - prostaglandin downregs cAMP M3 and CCK H2 and EP3 H/K ATPase. |
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What does the enterochromaffin cell do in the stomach?
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responds to gastrin and ACh with the production and secretion of histamine
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How is gastrin production in antral G cells regulated? (3)
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CNS activation
Local distention Gastric content composition, i.e., something fatty, etc. |
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What does the superficial epithelial cell do? Stimulators (2)?
What is the function of this action? |
secretes mucus and HCO3-
Prostaglandin (EP3) and ACh (M?) cytoprotective function |
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Is ACh from dorsal motor nucleus of the vagal nerve (DMNV) a therapeutic target?
What is the primary regulator of the "cephalic phase" of H+ secretion (anticipatory): sight, smell, taste? |
No, side effects would be a bitch.
ACh |
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Are -azole's proton pump inhibitors or H2R antagonists?
What are the other ones? |
proton pump inhibitors:
Prilosec (omeprazole) Prevacid (lansoprazole) Aciphex (rebeprazole) Protonix (pantoprazole) Nexium (esomeprazole) -tidines (H2R antag): Tagamet (cimetidine) Zantac (ranitidine) Pepcid (famotidine) Axid (nizatidine) |
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What to proton pump inhibitors do?
In which form are pp-inhibs given? Is this stable in the stomach? Solution? How do p.p.-inhibs enter the parietal cell? Do they bind the intracellular or extracellular domain of the ATPase? |
irreversibly inhibit the H+/K+ ATPase i/ parietal cells
prodrug; no. encapsulated as gelatin shells. from the bloodstream extracellular |
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What is the only thing that can "reverse" p.p.-inhibition of the H/K ATPase?
How are PPI's metabolized? |
synth of new proton pump proteins.
cP450 i/liver. |
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Should PPI's be given with H2 antagonists? Why or why not?
When should PPI's be taken? |
No, because acid in the parietal cell canliculi is needed for prodrug activation.
Before or with meals. |
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How do H2r antag's work?
Do they have more of an effect on basal H+ secretion or on stimulated (eating, vagal, etc.) H+ secretion? What does this mean re: tx? |
REVERSIBLY, competitively antagonize the H2 receptor.
basal. very effective in inhibiting nocturnal H+ secretion. |
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Which drug class is indicated for:
Promoting healing of gastric and duodenal ulcers Treatment of uncomplicated GERD Prophylaxis of stress ulcers |
H2r antags
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What is Misoprostol? What does it do?
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Prostaglandin analog
i/parietal cell: \cAMP --> \acid production i/epithelial cell: ^mucus, ^HCO3- |
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______ is octasulfate of sucrose plus aluminum hydoxide.
in acid environment undergoes crosslinking to produce a viscous gel that adheres to the cellular lining of the stomach- functions to protect the mucosal lining of the stomach. |
Sucralfate
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___% of ulcers may be associated with H.pylori infections of the stomach. What might it cause re: gastrin?
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80-90%
^gastrin production --> ^^H+ --> \HCO3- |
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What are the common tx's for h.pylori infection?
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Treatment generally involves the use of a pH-dependent antibiotic
such as amoxicillin, clarithromycin or metronidazole for two weeks, in combination with a proton pump inhibitor or histamine receptor antagonist. Combination therapies: PPI + clarithromycin + amoxicillin or metronidazole 1-2 weeks PPI + bismuth compound + metronidazole + tetracycline 1-2 weeks |
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How to we tx NSAID related ulcers?
ZE syndrome? |
PPIs
PPIs |
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Are ulcer drugs linked to pneumonia?
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they might be, in pts with asthma and other chronic lung aliments.
- could be more of a risk as more drugs become over-the-counter --> abuse --> unwanted SEs |
