PUD, GERD, IBD Flashcards
antacids
Mg-Al hydroxide (Maalox)
Mg-Al hydroxide/alginic acid
Calcium carbonate (Tums)
MOA of antacids
neutralize gastric acid in stomach (aluminum causes constipation, magnesium causes diarrhea -opposing effect) (alginic acid prevents regurgitation)
DDI of antacids
significant interaction in absorption of other drugs, do not take within 1-2 hours
dose timing of antacids
1 & 3 hr after meal & @ bedtime
H2 receptor antagonists used for PUD
cimetidine, ranitidine, nizatidine, famotidine
MOA of H2 receptor antagonists & effects
MOA: bind and block H2 receptor and inhibit basal, food stimulated & nocturnal gastric acid secretion
effects: decrease volume & H+ concentration of gastric acid
H2 receptor antagonists AE
infrequent and mild…
rank the H2 antagonists in order of potency
Famotidine 20-50x > ranitidine/nizatidine 4-10x > cimetidine 1x
which H2 antagonists inhibits CYP450
cimetidine
PPI’s for PUD
omeprazole, esomeprazole, lansoprazole, rebeprazole
MOA of PPI
enteric coating to get through stomach, absorbed to bloodstream and brought to parietal cells where acid protonates drug and traps near proton pump causing IRREVERSIBLE binding to H/K ATPase
PPI AE
single dose is safe & effective for > 2 yrs
PK of omeprazole & esomeprazole
effective orally, long duration & more powerful than H2 blockers
PK of lansoprazole
similar to omeprazole but LESS effective in severe esophagitis
PK of Rebeprazole
metabolized to much lower extent by CYP450
4 uses for the PPIs
- short term for active PUD
- zollinger-ellison
- refractory ulcers
- GERD
cytoprotective agents (2)
bismuth subsalicylate (pepto) sucralfate
MOA of bismuth subsalicylate
- enhances secretion of mucous & HCO3-
- inhibits pepsin activity
- chelates proteins and forms barrier against acid
- inhibits h pylori
clinical use for pepto
- adjuct tx for ulcers, GERD, diarrhea
2. traveler’s diarrhea
sucralfate MOA
forms sticky, viscous gel that adheres to gastric epithelial cells protecting them from acid and pepsis
PK for sucralfate
requires acidic pH for max activity
clinical use of sucralfate
value in H2 blocker or PPI induced pneumonia because alkaline environment promotes bacteria
antibiotics for H pylori eradication
clarithromycin, metronidazole, amoxicillin, ampicillin, furazolidine
clarithromycin MOA
macrolide - inhibits protein synthesis
metronidazole MOA
synthetic antibiotic active against obligate anaerobes
penicillin class drugs used for h pylori
amoxicillin & ampicillin
furazolidine MOA
nitrofuran antibacterial and antiprotozoal
which antibiotic has the highest primary resistance to h pylori
metronidazole (43%)
clarithromycin (8%)
general treatment regimen for h pylori
2 (abx) + 1 (ppi)
dopamine receptor blocker to treat GERD?
metoclopramide
metroclopromide MOA and effects
GI: block D2-R and increase Ach via 5HT4 - stimulates GI smooth muscle and increases amplitude of esophageal contractions, increase gastric emptying time and increase LES pressure
BBW for metoclopramide
Tardive dyskinesia - so only give for 2 weeks
what other non-pharm tx is there for GERD
- dec gastric contents
- dec size of meal
- dec weight
- dec fat in diet
- bed elevation
- avoid coffee & peppermint
treatment goals for IBD (4)
- control inflammation
- reduce morbidity
- prevent complications
- maintain nutritional state
sulfasalazine MOA
metabolized to 2 metabolites:
- 5-aminosalicylic acid - anti-inflammatory
- sulfapyridine - causes AE
sulfasalazine AE
anemia, rash, impotence
infliximab MOA
monoclonal ab that is a fusion against TNF-a
etanercept MOA
fusion protein of TNFa receptor linked to Fc portion of human IgG1 - binds TNFa and prevents its interaction
lactulose MOA
semisynthetic disaccharide and is a fecal acidifier (forms lactic, formic and acetic acid)
lactulose AE
not absorbed so causes osmotic diarrhea
lactulose PK
metabolized by enteric bacteria to its organic acid
neomycin MOA
antibacterial given as an enema to reduce bacteria in colon
2 drugs for tx of portal encephalopathy
lactulose, neomycin
