Antacid Pharm/ H. Pylori Eradication Flashcards Preview

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Flashcards in Antacid Pharm/ H. Pylori Eradication Deck (32):

What are antacids?

Weak bases that work to neutralzie gastric acid most commonly for tx of heartburn (rapid onset, and short DOA)

These wouldnt really be used for chronic things like GERD but more for the occasional heartburn


What are the kinds of antacids?

Non-absorbables that work via Mg, Al, and Ca mostly and

absorbables that work via HCO3- (do not use longterm)


Note that overloading on Na+ isnt going to be so good for the chronic renal failure pt.


What is the role of H2-receptor binding?

promotion of gastric acid secretion by stomach parietal cells


What are the H2-receptor antagonists?

-Cimetidine (Tagamet)

Ranitidin (Zantac)

Famotidine (Pepcid)



How effective are H2 antagonists?

They are much more effective for tx of acid secretion overnight/in fasting states than compared to food-stimulated acid secretion. So these are best taken before bedtime and pts should not eat afterwards

Tolerance will develop if used chronically


 The use of H2 receptor antagonists to treat peptic ulcers

Single nocturnal doses healed 80% of duodenal ulcers within 4 weeks and 80% of gastric ulcers within 8 weeks, with smokers doing worse and GERD pts. requiring more doses and they are unlikely to work in most pts (PPIs tend to work better for someone having heartburn very often like in GERD). 

NOTE: These are no longer indicated for tx. of peptic ulcers


What is the most important factor in treating peptic ulcer disease?

determine the H. pylori status. If the pt. is +, tx the infection, and if they are negative, PPIs are superior to H2 blockers


Cimetidine is a CYP inhibitor. What drugs increase in bioavailabilty when used concurrently with cimetidine?






Erosive esophagitis pts. need a PPI


You really want to try to get the pH up to around 4 to inhibit pepsin activity and H2 blockers dont go that high



Describe the pharmacokinetics of PPIs?

They must be given as PO enteric-coated granules (in capsules or tablets) to prevent denaturation from gastric acid. As the gelatin capsule is broken down by the gastric acid in the stomach, the enteric-coated granules are dispersed and make it to the duodenum where the higher pH degrades the coating and the granules are absorbed. Once in the blood these granules act in the parietal cell H/K ATPase and then are metabolized by the liver (CYP2C19/3A4)


What is the half-life of PPIs?

1-2 hrs. But they act longer than this 


T or F. PPIs block basal AND food-stimulated acid production

T. But they dont 100% suppress acid secretion (aka produce achlorhydria) due to H/KATPase constantly being re-synthesized

Which expains their superiority in GERD over H2 blockers


Do PPIs increase the risk of infection in the GI tract?

Yes, dose-dependent


Does tolerance develop against PPIs?

No- they are not competitive inhibitors


Its gonna take 30-60 minutes for the granules to reach their target! The pt. should then eat because ***you need to have active parietal cells for uptake of the drug from circulation***

So, PPIs should be followed by eating!



PPIs should be used in Erosive esophagitis! Much better than H2 blockers


If a pt. is taking clopidogrel and needs a PPI DONT give Omeprazole because clopidogrel has to be activated via CYPs so there will be less clopidogrel available in blood



PO PPIs are indicated for minor ulcer bleeding if there isnt an identifable vessel at the base of the clot, and if there is-- tx directly through the endoscope and keep the pt. on IV PPI for up to 72 hrs


Other POTENTIAL AEs of chronic PPI use

-chronic kidney disease

-dementia (OR: 1.33)

-bone fractures


these are not set in stone


What is sucralfate?

A macromolecule composed of sucros aluminum tat adheres to proteins in the GI tract and forms insoluble coagulum over ulcers 

This works best at an acidic pH (so dont give with a PPI) and will also bind bile acids


Main use now is biliary reflux 


causes cramps and diarrhea



T or F. H. pylori ONLY lives on gastric mucosa

T. And that includes ectopic stomach tissue


Causes about 60-70% of peptic ulcers and is the #1 cause of gastric cancer


Only use metronidazole is allergic to penicillins


Note about clarithromycin tx of HP

If a pt. has taken clarithromycin for ANY reason in the past, DONT give to tx HP because it is probably resistant now (and probably metronidazole)

BUT it hardly ever becomes resistant to amoxicillin or tetracycline