segers meds Flashcards
antacids antiulcer N/V IBD Diarrhea, Abd pain, Constipation
indications for antacids
SHORT term use, temporary relief of PUD and GERD
low systemic antacids
aluminum based agents
Ca based agents
Mg based agents
high systemic antacids
Na based agents
how do antacids work
combine chemically with H+ to make H2O, CO2, Cl- salts
–>increease LES tone in high doses
not any reduction in acid production, in fact rebound increase in acid production can happen
which antacids work fastest and longest, and have the best neutralizing ability
Ca based agents
Mg based agents
what is the clinical use of simethicone
= an antacid
= pro-fart+burp to get rid of gas thats already been made in the body
side effects of Al based antacids
constipation, HYPOphosphatamia
side effects of Mg based antacids
dose related diarrhea, increased Mg
side effects of Ca based antacids
constipation, increase Ca (leading to stones), nephropathy, met alk, HYPOphosphatemia
side effects of Mg based antacids
dose related diarrhea, increased Mg
side effects of Na based antacids
bicarb burps, increased Na, met alk
what important considerations should be taken when considering prescribing antacids
dosage
hx of renal/heart ds
electrolyte status
hx of diarrhea/constipation
lots of drug interactions- take all antacids 1-2 hours before, or 2-4 hours after any other med
which drugs work on the H+ leaving parietal cells into the extracellular gastric content
antacids
which drugs inhibit the luminal H/K+ ATPase on parietal cells membranes
PPIs
which drugs inhibit H2 receptors on the basolateral membrane of parietal cells
H2 receptor antagonists
which drug is a PGE1 analog, working on EP3 receptors on the basolateral membrane of parietal cells and superficial epithelial cells
misprostol
which drugs directly inhibits H Pylori
bismuth clonthromycin metronidazole tetracycline amoxicillin
what drug enhances mucus and bicarb transport on the luminal membrane of superficial epithelial cells
sucralfate
“__-tidine”
group special drug notes method of action side effect contraindications
h2 receptor antagonist= antiulcer
cimetidine= decreased T binding= gynecomastia/galactorrhea, neutropenia, thrombocytopenia, DRUG INTERACTIONS SO REPLACE WITH RANITIDINE
partially inhibits acid production –> ulcer will heal in 4-8 weeks if H pylori is not present
side effects= mild and transient if at all, GI and HA
PREGNANCY= use ranitidine or famotidine
rate the speed of action of dif antiulcer+antacids
antacids > H2 block > PPI
drugs that have a lot of drug drug interactions usually affect what pathway
CYP450
with what anti-ulcer drug classes do you need to use an NSAID
PPI and PGE1 analog
“__-prazole”
group special drug notes method of action side effect contraindications
PPIs= antiulcer
takes days to create a new steady state by binding sulfhydryl group of H/K ATPase
short have life but effect lasts days, ulcers heal in 4-8 weeks if H Pylori not present
omeprazole= increased drug interactions
sideeffects= dyspepsia, myalgia, life threatening C. Dif fiarrhea (CDAD)= watery and smelly
pregnancy= only if necessary, use lansoprazole
sucralfate
group method of action indications side effect contraindications
surface acting =antiulcer
=sucrose + Al(OH)3 create viscous polymer when adheres to epithelial cells around ulcer –> stimulate PGE + mucus production
NO effect on pH
can also use for mucositis, enema, bile acid reflex
side effect= constipation
relative contra= severe renal failure
possible drug interactions->take 2 hours after any other male
misprostol
group method of action indications side effect contraindications
PGE1 analog = antiulcer
protect prostoglandin + decreased gastric acid release from parietal cell
+increased mucous+bicarb production
used to prevent NSAID-induced ulceration in pts who can’t stop taking NSAIDs
also for pregnancy termination, cervical ripening, post partum hemorrhage
side effects= diarrhea, HA, dizzy
contra= pregnancy, IBD (r)
“bismuth”, peptobismol, kaopectate
group method of action indications side effect contraindications
bismuth compounds, anti-ulcer
prevent attachment to mucosa, disrupt cell wall
use for heartburn, diarrhea
antidiarrheal and antimicrobial = can work against H Pylori (in combo w abx+acid suppressant)
side effect= constipation, black stool (norm shape)
drug interactions, take 2 hrs after other meds
relative CI= anticoag use, severe renal failure
abs CI= GI bleed, hypersensitivity to salicytes
trx for H pylori
at least 2 abs + PPI
- clorythromycin/amoxicillin
- if can’t use PPI, give H2 blocker
if failed regimen, then do triple therapy:
BID PPI+ clarythromycin + amoxicillin/metronidazole
if failed then do quadriple
BID PPI+ QID metronidazole +tetracycline + bismuth
receptors responsible for N/V
5-HT3 (seratonin) HI (histamine) MI (muscurinic) D2 (dopamine) NKI (neurokinin/substance P)
what is the vomiting center of the brain and what receptors are there
nucleus of tractus solitaris
5HT3
HI
NK1
what is the chemoreceptor trigger zone in the brain and what receptors are there
area postrema
5HT3
D2