acid/pepsin txt Flashcards
what are the two major groups of drugs for acid/pepsin disorders?
- decrease acid from gastric lumen
2. promote mucosal defense (promote HCO3- secretion)
what are the 3 groups of drugs that decrease acid from gastric lumen?
anatacids, H2 blockers, PPIs
what are the 3 drugs that promote mucosal defense?
prostoglandin analogs (Misoprostol aka Cytotec)
Bismuth (aka Pepto Bismol)
Sucaralfate (aka Carafate)
MOA of antacids
they are all weak bases that react w/ gastric acid to produce H2O and salt.
This raises the pH (decreasing acid effects)
DOA or antacids
2 hours (cover post-mealtime)
how to use antacids: what do they treat? when do you take them? how many times a week can you use them?
treat heartburn/dyspepsia,
take after meals for symptoms
use < 2 days/week
antacids can combine ___ and ___ to decrease ADRs
Al (ADR is constipation)
Mg (ADR is diarrhea)
- antacids may combine these to counteract the ADRs of each
ADRs for antacids: Na+ Al Mg Ca
Na+: burping (which may provide relief), Na+ retention, metabolic alkalosis (rare)
Al: CONSTIPATION, hypophosphatemia
Mg:DIARRHEA, high Mg+
Ca: high Ca++
Antacids: A ffect _____, ______ or _____ of other drugs by altering gastric and urinary pH or by delaying gastric emptying
Affect absorption, bioavailability or urinary excretion of other drugs by altering gastric and urinary pH or by delaying gastric emptying
contraindications for Antacids:
Sodium bicarb
Al and Mg
CHF (for sodium bicarb) renal impairment (Al and Mg ones will accumulate b/c youre not excreting them)
Abx like fluroquinolones, tetracyclines and ketoconazoles are given before or after antacids?
before, they need acidic enviornment for them to work!
what are the four H2 blockers (antagonists) ?
"tidines" Cimetidine (Tagamet) Famotidine (Pepcid) Ranitidine (Zantac) Nizatidine (Axid)
Which H2 blocker has the most ADRs?
Cimetidine (tagamet)
- lots of drug/drug- (warfarin for example)
- imbalance of androgen - prolactin produced =gynecomastia
MOA of H2 blockers
Reversible H2 block on parietal cells
Decreases cAMP = decreased H+ secretion into gastric lumen
PKs of H2 blockers (maybe weeds): Abs, metabolism, 1/2 life, onset, excretion
Absorption-rapid Metabolism-hepatic ½ life – 2 hours; prolonged with renal impairment Onset – 45 min-2 hours Excretion – primarily renal
4 ADRs of H2 blockers (weeds)
- May reduce efficacy of drugs that require an acidic environment for absorption
- CIMETIDINE: DRUG/DRUG, GYNECOMASTIA
- Elderly- confusion after IV administration (dont really know why)
- B-12 deficiency with long term use (although mostly with PPIs)
what do we use H2 blockers for?
mild esophageal reflux (best use for them)
Peptic ulcer
gastritis
which drugs do we use for pregnant pts?
Antacids, then H2, then PPIs
what are the PPI drugs?
"prazoles" Esomeprazole (Nexium) Omeprazole (Prilosec) Lansoprazole (Prevacid) Pantoprazole (Protonix) Rabeprazole (Aciphex) Dexlansoprazole (Dexilant)
MOA of the PPIs, why is this so effective?
Irreversibly binds to H+/K+ ATPase enzyme of parietal cell preventing H+ secretion into gastric lumen
(stop acid secretion at its source! = very effective)
Also, Effective because it take 18 hours for enzyme to be resynthesized
All PPIs are ____, what does this mean?
ALL are Prodrugs: have acid resistant enteric coatings to prevent degradation by gastric acid
Coating removed in alkaline duodenum, prodrug is weak base an is absorbed/taken to parietal cell
PKs of PPIs : abs, onset, 1/2life (weeds)
Rapid absorption
Onset 30 min – 2 hours
½ life – 1-2 hours
why is there a long DOA of PPIs?
Long DOA due to irreversible binding with enzyme
metabolism and excretion for PPIs
Hepatic metabolism
Excretion: urine, feces, bile