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27 Cards in this Set
- Front
- Back
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What structures are placed next to each other for the cannalicular membrane to work? 2) What cell structures are they dependent on? 3) What ion?
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Tubulovesicular membrane ahs the H/K ATPase that is placed next to the K/Cl channels on the plasmalemma membrane.
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How does ACh from vagus affect parietal cells? 2) ECL cells? 3) Chief cells. 4) Antral G cells.
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1) Through Ma muscarinic receptors to activate IP3/DAG (inc Ca). 2) M1 muscarinic receptors to induce histamine release (affects parietal cells). 3) Release pepsinogen. 4) Release gastrin, but via GRP release
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Gastrin release from G-Cells via (2)? 2) Affect on parietal cells? 3) On ECL cells?
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Protein containing food and during cephalic phase from GRP. 2) Gastrin receptors that activate H/K ATPase via IP3 pathway. 3) Histamine release (which affects parietal cells)
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Histamine acts on what receptors? Result? Secretagogue status?
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H2 on parietal cells. 2) G-protein coupled with adenylyl cylase that inc cAMP, protein kinase, that opens Cl channels and activates H/K ATPase. 3) It is the most important gastic secretagogue
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4 inhibitors of Gastric acid secretion in respect to pH? 2) D cells? 3) Prostaglandins (esp oxyntic cells). 4) Enterogastrones
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1) < 3 pH inhibits. 2) somatostatin inhibits. 3) PGE2 his oxyntic cells which are negatively coupled to adenyl cylase and effects histamine secretion. 4) inhibitory effect (secretin, GIP, PYV, neurotensin)
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Info! Gastroduodenal mucosal barrier: Mucus, HCO3, transcellular resistance to back diffusion of protons, Reconsitution, maintenance of local blood flow, pancreatic HCO3, and prostaglandins of the E series stimulate secretion of mucus
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Ya damn straight
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Peptic ulcer from what 3 things? Causation of GERD?
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1) H. pylori 2) chronic aspirin or NSAID. 3) Zollinger-Ellison Syndrome. 4) transient inappropriate relaxation of LES
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3 strategies to protect the gastic mucosa from acid
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1) inhibit it. 2) prevent contact with it. 3) neutralize it.
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Name the contraindication for the following antacids. 1) Sodium Bicarbonate. 2) Calcium Carbonate (2). 3) Magnesium Hydroxide. 4) Aluminum hydroxide (3).
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1) HTN. 2) renal impairment and can have acid rebound. 3) Laxative. 4) produce constipation, deplete phosphate, resorption of bone
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Antacid effects are additive. 1) what is added for GERD? 2) Al and Mg antacids reduce bioavailability of what two things? 3) Chelate what two drugs?
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1) alginic acid. 2) weak acids and H2 blockers. 3) tetracycline and digoxin
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Atropine, propantheline, Isopropamid, and pirenzepine are what? 2) What 2 things do they do?
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Antimuscarinics. 2) Block motility and secretions throughout GI tract.
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H2 blockers result in what? What is common side effect that causes relapse?
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decreased acid secretion after all known stimuli. 2) acid rebound
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Cimetidine is a what? 2) 3 side effects?
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H2 blocker. 1) elderly, debilitated and renal impairment very susceptible to mental confusion (seizures), elevated serum creatinine, and hematologic disturbances. 2) Anti-androgen effects (gynecomastia, impotence, galactorrhea). 3) inhibits P450….
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Ranitidine is a what? 2) what two side effects are greatly reduced compared to others in same class?
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1) H2 blocker. 2) does NOT bind androgen receptor. Inhibits drug metabolism but less so.
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Famotidine is a what? 2) two advantages to Ranitidine? 3) 2 big advantages in class?
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1) H2 blocker. 2) more potent and longer duration. 3) does NOT inhibit hepatic drug metabolism, does NOT bind androgen receptor
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Nizatidine is a what? 1) Rare side effect? 2) 2 advantages in class?
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H2 blocker. 1) hepatic toxicity. 2) no drug interaction or androgen receptor binding
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Misoprostol is a derivative of what and resistant to what? 2) Effect on parietal cell? 3) gastic mucosa? 4) Mucosal blood flow?
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PGE1 and resistant to principle catabolizing enzyme. 2) inhibits acid secretion by opposing histamine. 3) stimulates. 4) increases
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Omeprazole, lansoprazole, rabeprazole, and esomeprazole are what? 2) MOA, discuss location too. 3) duration of effect
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1) proton pump inhibitors (PPI). 2) they are weak bases and are trapped and activated in the secretory canaliculi. At low pH, stable covalent bond with critical site (K+ transport) and H/K ATPase loses activity. 3) prolonged effect
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PPIs have what two AEs? 2) Contraindicated for what? 3) unusual tissue effect?
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1) Inc incidence of GI/Respiratory infection and osteoporosis due to calcium malabsorption. 2) Clopidogrel! 3) hypergastrinemia with gastic ECL clustering
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How do contact agents work?
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primarily by stimulating mucus secretion
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What is Sulcrafate? What is it made of? 3) What happens at acidic pH? 4) what does it bind to?
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Contact protective agent. 2) sulfated sucrose and aluminum hydroxide. 3) undergoes extensive polymerization and crosslinking. 4) exposed protein in ulcer and creates persistent barrier
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Sulcrafate has what suppressive activity? 2) stimulates mucosal production of what? 3) Inhibits what? 4) Systemic effects? 5) AE?
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1) H. pylori. 2) PGEs 3) Pepsin activity. 4) not absorbed systemically! 5) constipation
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What two things does Rebamipide do?
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Stimulate mucus secretion and scavange free radicals
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Carbenoxylone does what?
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Stimulate mucus secretion
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Bismuth compounds do what 3 things
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1) mucus secretion. 2) adherence. 3) antibacterial
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How do you Tx H. pylori?
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Triple therapy: PPI / amoxicillin / calrythromycin (substituting metronidazole if allergic to amoxicillin). Also: Antimicrobial (metronidazole) + antibacterial (amoxicillin) + bismuth salt
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stopped on p. 174
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