PUD Flashcards
4 drug classes used in PUD/GERD? Major goal of treatment?
Regulation of HCl Secretion!
1) Antacids (Ca and Mg)
2) H2 blockers (–idines)
3) PPIs (-prazoles)
4) +/- antibiotics for H Pylori (metronidazole, vancomycin, etc)
**Major goal: eliminate extrinsic / intrinsic sources of inflammation!
3 substances that stimulate H+ secretion in stomach?
1) ACh (vasovagal/ENS reflexes)
2) Gastrin (GRP / peptides and AAs –> CCK)
3) Histamine (ECL cells – potentiated by ACh and gastrin)
3 main goals of PUD treatment?
1) eradication of H pylori! (metranidazole, tetracycline, clarithromycin) 2) Symptom relief (antacids, PPIs/H2 blockers) 3) heal ulcers (PG Agonists, bismuth, sucrasulfate)
Calcium Carbonate (TUMS)
Simethicon
Gaviscon
Ca Carbonate –> xgas and acid reflux
Simethicon –> surfactant / anti-flatulant / non systemic
Gaviscon –> anti reflux antacid
Antacids: Aluminum hydroxides vs. Mg hydroxides
When do you use antacids?
Al –> xConstipation
Mg –> xDiarrhea
- *combos are popular
- *used for simple dyspepsia or adjuvently w/ H2 blockers/PPIs
Problem w/ systemic/absorbable antacids?
Hypercalcemia and metabolic/systemic alkalosis
(ex) NaHCO3
Cimetidine, Ranitidine, Famotidine, Nizatidine
MOA: H2 blockers –> block basal > food stimulated, and nocturnal gastric acid secretion (take before bed - no snacks)
**~1 log pH change –> 90% dec in gastric acid, need pH >4 to have effect!
**similarly efficacious, but differ in potency:
Famotidine 20-50x potency –> Cimetidine 1x
Why aren’t H2 blockers used as much now?
- Multiple daily doses needed to tx GERD – only used for mild GERD
- less effective w/ smokers (dec pancreatic HCO3)
- now mixed PPIs w/ NaHCO3= inc absorption / dec degredation
Side effect of cimetidine? Drug interactions most worried about?
Inhibits Cyp3A4!
Most relevant w/:
Warfarin, Phenytoin, Theophylline
narrow therapeutic window
Omeprazole, Esomeprazole, Lansoprazole, Pantoprazole, Rabeprazole
MOA, 3 uses, AEs
MOA: Irreversible xH+/K+ ATPase –> dec gastric HCl secretion/Achlorhydria
Uses: short term/heal DU/GUs, GERD/NERD, Erosive esophagitis, anti-H pylori regimen, Stress related upper GI bleed (ICU pts), during endoscopic tx of bleeding ulcer, manage ZE syndrome
Do PPIs act directly in the stomach?
NO, enteric coating = prodrug released in intestine –> absorbed into blood stream –> carried to parietal cells and diffuse into secretory canaliculi (acidic pH traps drug near proton pump)
Which PPIs are most effective orally? which is less effective in servere esophagitis? which is minimally metabolized by CYP3A4?
Orally: Omeprazole, Esomeprazole
Not good w/ esophagitis: lansoprazole
Least Cyp3A4 metabolism: Rabeprazole
When do you take PPIs? when do you take H2 blockers?
PPIs – First thing in the MORNING, empty stomach = increased uptake, “prophylaxis for the day”
H2 blockers – at night, when you are done eating for the night (xbasal acid secretion > food stimulated)
Bismuth Subsalicylate
MOA:
- increases secretion of Mucus and HCO3-,
- inhibits pepsin activity,
- chelates proteins at base of ulcer/forms protective barrier against acid and pepsin
- xH Pylori
**adjunct therapy for DU/GU, GERD, diarrhea treatment
Sucralfate
**special use??
MOA: forms sticky/viscous gel that adheres to gastric epithelial cells – protects against acid/pepsin
**REQUIRES ACIDIC pH for MAX ACTIVITY – only one
**used in H2block/PPI induced pneumonia bc it doesn’t alkalinize stomach (increases harmful bacteria)
