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1

what are the two major groups of drugs for acid/pepsin disorders?

1. decrease acid from gastric lumen
2. promote mucosal defense (promote HCO3- secretion)

2

what are the 3 groups of drugs that decrease acid from gastric lumen?

anatacids, H2 blockers, PPIs

3

what are the 3 drugs that promote mucosal defense?

prostoglandin analogs (Misoprostol aka Cytotec)
Bismuth (aka Pepto Bismol)
Sucaralfate (aka Carafate)

4

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)

5

DOA or antacids

2 hours (cover post-mealtime)

6

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

7

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

8

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++

9

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

10

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)

11

Abx like fluroquinolones, tetracyclines and ketoconazoles are given before or after antacids?

before, they need acidic enviornment for them to work!

12

what are the four H2 blockers (antagonists) ?

"tidines"
Cimetidine (Tagamet)
Famotidine (Pepcid)
Ranitidine (Zantac)
Nizatidine (Axid)

13

Which H2 blocker has the most ADRs?

Cimetidine (tagamet)
-lots of drug/drug- (warfarin for example)
-imbalance of androgen - prolactin produced =gynecomastia

14

MOA of H2 blockers

Reversible H2 block on parietal cells
Decreases cAMP = decreased H+ secretion into gastric lumen

15

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

16

4 ADRs of H2 blockers (weeds)

1. May reduce efficacy of drugs that require an acidic environment for absorption
2. CIMETIDINE: DRUG/DRUG, GYNECOMASTIA
3. Elderly- confusion after IV administration (dont really know why)
4. B-12 deficiency with long term use (although mostly with PPIs)

17

what do we use H2 blockers for?

mild esophageal reflux (best use for them)
Peptic ulcer
gastritis

18

which drugs do we use for pregnant pts?

Antacids, then H2, then PPIs

19

what are the PPI drugs?

"prazoles"
Esomeprazole (Nexium)
Omeprazole (Prilosec)
Lansoprazole (Prevacid)
Pantoprazole (Protonix)
Rabeprazole (Aciphex)
Dexlansoprazole (Dexilant)

20

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

21

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

22

PKs of PPIs : abs, onset, 1/2life (weeds)

Rapid absorption
Onset 30 min – 2 hours
½ life – 1-2 hours

23

why is there a long DOA of PPIs?

Long DOA due to irreversible binding with enzyme

24

metabolism and excretion for PPIs

Hepatic metabolism
Excretion: urine, feces, bile

25

3 ADRs of PPIs

1. Increased risk of C difficile infection (acidic env. is there to kill Cdiff and we are taking that away)
2. hypomagnesemia (increased excretion through GI)
3. B-12 deficiency, iron and calcium malabsorption (fracture risk)

26

what do we use PPIs for?

Peptic ulcer, gastritis, esophageal reflux, H pylori (in combination), stress ulcer prophylaxis, NSAID associated ulcer

27

when do we take PPIs? why do we take them at this time? (maybe weeds)

Administration: 30-60 minutes before meal
Greatest amount of H+/K+ ATPase enzyme is present after prolonged fast

28

PPIs for pregnancy? (keep in mind, antacids are class A - aka first choice for pregnant)

omeprazole/esomeprazole class C; all others class B

29

why do we use PPIs for H pylori?

if we dont irradicate Hpylori, pt is more at risk for certain cancers : we use PPI b/c H pylori in acidic env is dormant (we want it to start replicate so that the abx can target the replicating cyle of the Hpylori)

(wake the monster and kill it !)

30

what is the controversy of using PPIs on someone taking clopidegrel?

both Omeprazole + Esomeprazole and Clopidegrel are prodrugs- CYP C19 converts both into their active forms -some think if you take them together, the PPI is inhibiting the Clopidegrel but pt may just be poor metabolizers of Clopidegrel!