Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
67 Cards in this Set
- Front
- Back
Where in the brain does acid secretion signal begin and how does it travel
|
begins with a cephalic response, via vagus nerve
|
|
What does the ECLs secrete and what does it support
|
-histamine
-long term acid secretion |
|
Gastrin is secreted by what and stimulates what
|
-G cells in antrum of stomach
-parietal and ECL cells |
|
How do prostaglandins promote stomach protection
|
-activate Gi GPCRs
-decrease cAMP --> decreases acid -increase mucus and bicarbonate protection |
|
Proton pump inhibitors:
-MOA -all require what -acid stabile/labil |
-covalently modify active site of H/K ATPase
-acid activation - prodrugs -acid labile |
|
how are proton pump inhibitors dosed vs. how long are they active
|
-dosed daily
-active for 2 hours, therapy relies on slow turnover of ATPase at the apical surface |
|
what type of drug is the firstline treatment of hyperacidity and ulcers
|
-proton pump inhibitors
|
|
What 2 proton pump inhibitors can be given parenterally?
**ON EXAM** |
-pantoprazole
-lansoprazole |
|
How can proton pump inhibitors can be given how?
|
-gelatin capsules
-enteric coated tablets -mixed with bicarbonate |
|
How much do proton pump inhibitors lower acid secretion by
|
-90%
|
|
6 uses of proton pump inhibitors
|
-GERD, erosive esophagitis, peptic ulcers, zolinger-ellison syndrome, NSAID induced ulcers, part of H. pylori treatment
|
|
T/F - all proton pumps are active all the time
|
-false, only some are active
-so only those that are active are reacted with these drugs |
|
how long does treatment with proton pump inhibitors take
|
-2 to 5 days because not all proton pumps are active at any one time
|
|
proton pump inhibitors are cleared where
|
-thru the liver
|
|
adverse reactions of proton pump inhibitors
|
-if in hepatic failure clearance will be reduced
-nausea, pain, constipation, flatulence, diarrhea, -rare = myopathy, arthralgia, headaches, skin rashes |
|
Which proton pump inhibitors interact with warfarin, diazepam and cyclosporine
|
-esomeprazole, lansoprazole, omeprazole, rabeprazole
(ROLE) |
|
What can occur with sudden withdrawl
|
-hyper gastrinemia and gastritis
|
|
How do H2 receptor antagonists work
|
-block the base level of acid secretion maintained by ECL cells
|
|
What are H2 receptor antagonists useful for
|
-acid secretion at night and duodenal ulcers
|
|
Which are more potent, proton pump inhibitors or H2 receptor antagonists
|
-proton pump inhibitors
-H2 antagonists decrease acid secretion 70% for 24 hours with daily dosing |
|
Cimetidine, ranitidine, famotidine, nizatidine are all what type of drug?
|
-H2 receptor antagonists
|
|
Adverse reactions of H2 receptor antagonists
|
-diarrhea, headache, drowsiness, fatigue, muscle pain
-CNS effects in parenteral administration in the elderly |
|
What does long term use of cimetidine at high doses cause
|
-decreases testosterone binding to androgen receptor and hydroxlyation of estradiol causing galactorrhea in women and decreased sperm count, impotence and gynecomastia in men
-need a high dose (not seen w/OTC) |
|
T/F - tolerance to H2 receptor antagonists develops quickly
|
-true - w/in 3 days
|
|
what problem is caused if you discontinue H2 receptor antagonists suddenly
|
-rebound (esophagitis)
|
|
What is sucralfate and how does it work
|
-octasulfate of sucrose with aluminum
-forms sticky polymer coating that coverd epithelium -acid activated, avoid other GI drugs that lower acid -prefers to bind to ulcers over normal tissue |
|
Sucralfate most common side effect
|
-constipation
-will also block absorption of other drugs through the stomach |
|
Antacids:
-MOA |
-neutralize pH of gastric contents
|
|
Which is faster acting - Mg or Al
|
-Mg is faster, Al is slower
(30 sec vs. 5 min) |
|
T/F - using Mg is combination with Al is better than each alone
|
true
-Mg stimulates emptying while Al delays emptying and slows motility |
|
What is treatment of H. Pylori consist of
|
-acid neutralization, cytoprotection and antibacterial agents
(proton pump inhibitor, antibiotics, bismuth) |
|
Stimulation of enterochromaffin cells releases what?
|
-serotonin
|
|
Serotonin causes what to be activated
|
-primary afferent neuron inside the gut
|
|
How does GI motility happen
|
local reflex pathways contract orally and relax anally
|
|
T/F - activating muscarinic receptors activates coordinated motility so this is an approach
|
-false - will not activate coordinated movement
|
|
What are cholingergic derivatives used for (bethanechol)?
-MOA -side effects |
-help in urination post-surgery
-selectively activate M2 and M3 receptors -bradycardia, flushing, diarrhea, cramps, salivation, blurred vision |
|
Neostigmine methylsulfate (acetylcholinesterase inhibitor) can be used to treat what GI ailment
|
-ileus (bowel obstruction)
|
|
Dopamine receptor antagonists:
-MOA |
-dopamine antagonizes Ach release so receptor antagonists enhance the normal ACh response
|
|
metoclopramide -
|
-a dopamine receptor antagonist
-used for N&V, laxative |
|
tegaserod
-MOA -useage |
-partial serotonin 5-HT4 agonist
-improves lower bowel motility, used for IBS |
|
Cisapride
-MOA -use |
-5-HT4 receptor and adenylate cyclase stimulant
-used for GERD |
|
mycin antibiotics are all what?
-MOA -effect |
-motilin agonists
-peptide hormone that increases motility (secreted by ECF cells) -gastric dumping |
|
Definition of consipation
|
-<3 stools/week
|
|
Osmotic laxatives:
-MOA -examples |
-cause water retention, may stimulate CCK receptors and increase motility
-cathartics - cause bowel emptying with watery stool -go-litely, milk of magnesia, magnesia products |
|
lactulose, sorbitol, mannitol
-MOA -use |
-draw water into gut, drop pH by bacterial fermentation
-constipation with opioid use and vincristine |
|
Docusate salts:
-MOA -category |
-surfactants that allow mixing of fatty substances and water in stool
-stool wetting agents (stool softeners) |
|
T'/F - docusate saltes increase frequency of defacation
|
-false
|
|
bisacodyl
-moa -what would you warn patients of |
-irritant laxatives - make bowel release serotonin = more peristalsis
-not to chew tablets or mix with milk or antacids to ensure tablet reaches site of action in small intestine and avoid gastric irritation |
|
castor oil
-MOA -uses |
-smooth muscle stimulant
-laxative, cathartic, induce labor -from castor bean - oil and rincin (poison) |
|
glycerin
|
-suppository that acts as a hydroscopic agent and lubricant
|
|
bulk forming agents
|
-based on colloids or polymers such as carboxymethylcellulose
|
|
diphenoxylate diphenoxin piperidine derivatives, loperamide:
-MOA -potency -why they don't work as normal opioids |
-mu opioid receptor agonists that stop bowel mobility
-40-50x more potent than morphine -do not enter CNS |
|
somatostatin/octreotide parenterals
-used for -side effect |
-combat diarrhea of hormone secreting tumors
-post-surgical dumping syndrome -diarrhea w/chemo -rest pancreas with pancreatitis -long term may cause gallstones |
|
bismuth:
|
-peptobismol = magnesium aluminum silicate and oil of wintergreen
-salicylate is released into the stomach and absorbed systemically |
|
What can all play a role in emesis:
|
-CNS, memory, environmental inputs, sensors of toxins, gut sensations, movement sensations
|
|
What controls emesis centrally:
|
the chemoreceptor trigger zone - at the bottom of the 4th ventricle
-transverses BBB so senses spinal fluid and blood for toxins -AND the solitary tract nucleus of the vagus nerve |
|
What controls emesis peripherally:
|
-senses
-inner ear -small intestine -pharynx (gaggin) |
|
How do serotonin receptor antagonists help with nausea
|
-act centrall at the CTZ and STN, peripherally at small intestine
-serotonin promotes gut motility, so antagonize it's receptor |
|
ondansetron
|
-a serotonin receptor antagonist used to help with emesis/nausea with chemo
|
|
palonosetron
-delivery |
-5-HT2 antagonist
-highest affinity for receptor in its class -parenteral only |
|
ondasetron, granistron, doasetron
|
5-HT2 antagonists given in chemo for anti-emesis
|
|
metoclopramide:
MOA Useage |
-dopamine receptor antagonist that strongly affects CTZ and increases forward motility
-preferred agent for chemo nausea |
|
phenothiazines:
MOA -useage |
-primary targets D2 receptors in CTZ (dopamine receptor antagonist)
-motion sickness, NOT for chemo |
|
major side effect of dopamine receptor antagonists
|
-parkinsons-like symptoms
-will make parkinsons worse |
|
antihistamines for anti-emesis:
-MOA -useage |
-H1 receptor antagonists, act primarily on brainstem and vestibular apparatus
-motion sickness and post-op emesis |
|
cyclizine, promeethazine, hydroxyzine, diphenhydramine
|
-antiemetic antihistamines
|
|
cyclizine has what other effect than antiemesis
|
-anticholinergic
-given to pts with abdominal cancer |