GERD treatment Flashcards
Pathways with gastric acid secretion
Sight of food- vagus nerve signal Ach release
Ach binds to receptors in parietal cells, stimulates H/K ATPase
H+ react with Cl in blood to form HCl
Prostaglandins
Cytoprotective effect on yhr GI tract
Acid Neutralization w antacids
Ca Carbonate
MgOH
Efficacy
SE
OTC antacids
Effective, but can cause belching
combined with AlOH and CaCarbonate to mediate gastric emptying
Similar
Diarrhea, constipation, renal, altered absorption (daizepam)
Histadine synthesis
from AA Histidine by histidine decarboxylase
Diphenhydramine
Works best when
Duration
SE
1st gen H1 inhibitor
Inverse agonist of H1 receptor (does not inhibit release)
Admin prior to histamine release, effective orally/topically
4-6 hrs
Crosses BBB, so sedation, antimuscarinic
Minimal GI SE
Cetirizine
SE
1/2 life
Duration
2nd gen H1 blocker
Cant penetrate BBB (no sedation)
Drowsiness (dose related)
8 hrs
12-24 hrs
H1 receptor location
mechanism
effect
Nonvascular SM, Vasc SM, brain
inc DAG/IP3
inc vasc permeability and VD, constrict Vasc SM
H2 receptor location
Mech
Effect
Gastric mucosa, cardiac, mast cells brain, Vasc SM
Inc cAMP
Inc gastric acid and VD, cardiac stimulation
H3/H4 location
mech
Effect
H3- CNS, inc cAMP, dec histamine release, inc NT release
H3- immune cells, inc cAMP, mediate immune cell recruitment
Selective H2 receptor antagonists
Use
Mech
Cimetidine/ranitidine- dec GA sec
Effective against basal acid sec, esp nocturnal (primary factor for duodenal ulcer healing), also stimulated acid production
Competitive, reversible inhibitors of H2 receptor (similar in structure to histamine)
Nocturnal acid breakthrough
Give _____ to suppress NAB
> 60 min of intragastric pH <4 between 10/6 for pts taking PPI twice daily
H2 antihistamine
H2 antihistamine pharmacokinetics
SE
Oral/IV (rapid absorption)
Rare
Cimetidine inhibits p450 metab in liver (interferes with warfarin, phenytoin, cafeinne)
Gastric pump inhibitors
Mech
Ex
most effective acid suppressing agents
Selective, irreversible H/K ATPase inhibitors (gastric parietal cells)
Bind to H/K APTase, inhibit reease of acid into GI tract
Omeprazole/pantoprazole
Omep/Panto use
Structure
Primary tx for GERD, PUD, NSAID/stress ulcers, combo to treat H pylori
Omep= mix of R/S isomers
Esomeprazole (S isomer)
Omep/panto mech
PPI travel to parietal cells and acumulte in acidic secretory canaliculi
Form covalent bonds with cysteine residues of H/K pump
Omep/panto uptake
activation
Do not give with
Duration
unstable at low pH- omep given in alkali soluble capulse to prevent degradation in stoamch
require acid environment to be active- given with food to stimulate acid secretion
acid suppressors (H2 antag)
90 min in blood
Omep/panto pharm
Effective
PPI metabolized in liver by p450
24-48 hrs (due to irreversible nature)
Typical course of treatment
Omep SE
potential cause of
PPI for 8 weeks, disc/maintained at low dose
hypochlorhydria (dec HCl) hypergastremia (inc gastrin prod)
Gastric bacterial overgrowth ( C diff) can occur
CKD
PPI and azoles
Omep inhibits
Inc risk of
inc pH can alter uptake of azoles
hepatic metabolizing drug enzymes (infl metab of benzos, warfarin, phenytoin)
gastric cancer
Esomeprazole
extremely similar to Omep
Bismuth
Sucralfate
promotes mucosal healing, no GA neutralization (soothe, coat)
AlOH and sulfated sucrose
Binds/protects mucosa- promotes PG synthesis
H pylori tx
Ab include
Beware
double/triple regimen with PPI and 2/3 ab for 2 weeks
metronidazole/clarithromycin\
resistance
