Week 11 - GI Flashcards
Antacids MOA
neutralize gastric acidity
Antacids magnesium AE
diarrhea
Antacids aluminum and calcium AE
constipation
Antacids AE
effervescent (fizzy) have high sodium, DDI bc of altered pH, alter elctrolyte absorption in GI
When should you avoid antacids with other oral meds?
within 2 hours of taking other oral meds
H2 receptor antagonists MOA
reduce secretion of stimulated acid
H2 receptor antagonists AE
diarrhea, muscle pain, rashes
H2 receptor antagonists on drug list
famotidine (Pepsid) and ranitidine (Zantac)
PPI MOA
irreversibly inhibis H+/K+ ATPase pump which blocks secretion of acid into stomach
PPI AE
well-tolerated, long term use associated w/ gastric polyps, altered calcium metabolism, some CV issues
PPI on drug list
-azole, omeprazole (Prilosec) and esomeprazole (Nexium)
7 drug classes for nausea
anticholinergics, antihistamines, neuroleptics, prokinetic, serotonin blockers, neurokinin-1 receptor blockers, cannabinoids
Anticholinergics MOA
binds to ACh receptor on vestibular nuclei to block communication
Anticholinergics AE
dizziness, drowsiness, dry mouth, blurred vision, dilated pupils, difficult urination
Antihistamines MOA
inhibit vestibular input to the CTZ (chemoreceptor trigger zone)
Antihistamines AE
dizziness and sedation
What antiemetics are used for motion sickness?
antihistamines
Neuroleptic MOA
block dopamine receptors in CTZ
Neuroleptic AE
OH, tachycardia, blurred vision, dry eyes, urinary retention - long term use causes extrapyramidal symptoms
Prokinetic MOA
block dopamine in CTZ
Prokinetic AE
sedation, diarrhea, weakness - prolong use causes extrapyramidal symptoms
Serotonin blockers MOA
block serotonin receptors in GI, CTZ, and vomiting center
Serotonin blockers AE
headache, dizziness, diarrhea
Neurokinin 1 receptor blockers MOA
block supstance P from binding to neurokinin 1 receptors - prevents central and peripheral stimulation of vomiting centers
Neurokinin 1 receptor blockers AE
sedation, GI issues, Stevens-Johnson
Cannabinoids MOA
unclear
Cannabinoids AE
ataxia, light-headedness, blurred vision, dry mouth, CNS symptoms
scopolamine (Transderm Scop) is in what class?
anticholinergic antiemetic
meclizine is in what class?
antihistamines antiemetic
metoclopramide is in what class?
prokinetic antiemetic
ondansetron (Zofran) is in what class?
serotonin blockers antiemetic
what are the 4 antidiarrheal agents?
absorbents, anticholinergics, intestinal flora modifiers, and opiates
Absorbents MOA
binds bacteria causing diarrhea to carry them out with feces
Absorbents AE
aspirin product so avoid with flu children, increase bleeding, GI bleed, tinnitus
Anticholinergics antidiarrheal MOA
inhibit parasympathetic to reduce peristalsis of GI tract
Anticholinergics antidiarrheal AE
stop PNS, decrease secretions (atropine AE), etc
intestinal flora modifiers MOA
restore natural balance of bacteria - great to take with antibiotic
Opiates MOA
decrease GI motility
Opiates AE
sedation, dizziness, constipation, nausea, vomiting, bradycardia, hypotension, urinary retention
5 laxatives classes
bulk-forming, hyperosmotic, saline, emollient, and stimulant
stimulant MOA
stimulate peristalsis through enteric nervous system
stimulant AE
long term use can lead to dependence and loss of cell/colon function
emollient MOA
facilitate water and fab absorption into stool (fecal softeners)
emollient AE
well–tolerated, skin rash, decrease vitamin absorption, electrolyte imbalance
hyperosmotic MOA
draws fluid into colon by creating gradient
hyperosmotic AE
abdominal bloating, rectal irritation, electrolyte imbalance
saline MOA
osmotic pressure pushes water into intestines
saline AE
salts may cause issues with individual with diminished cardiac or renal function
bulk forming MOA
increase water absorption to soften and increase bulk of feces
bulk forming AE
relatively safe, not for individuals with abdominal pain, nausea, vomiting