Antacid Pharm/ H. Pylori Eradication Flashcards
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)
Nizatidine
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?
- phenytoin
- warfarin
- theophylline
- diazepam
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
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
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
