GI Meds Flashcards
(48 cards)
Antibiotic choices to treat H. Pylori
- Amoxicillin
- Clarithromycin
- Metronidazole
- Tetracycline
**must be used in some form of combo
Bismuth for treatment of H. Pylori MoA
- disrupts cell wall
- inhibits urease activity
- likely creates protective later in stomach, bicarb/mucus secretion
- decreases stool liquidity
1st choice drug class to treat ulcers
Histamine2 receptor antagonists –> suppress secretion of gastric acid
Histamine 2 receptor antagonist drugs (H2RAs)
- Cimetidine
- Famotidine
- Nizatidine
Cimetidine MoA
- blocks H2 receptors, decreasing volume of gastric juice and [H+ ion]; reversible process
- effective specifically against nocturnal acid secretion; suppresses basal acid secretion
- cross BBB –> CNS effects
Cimetidine uses
- GERD
- gastric/duodenal ulcers
- Zollinger-Ellison syndrome
- aspiration pneumonitis
- heartburn
Cimetidine AEs
Binds to androgen receptors producing blockade
- gynecomastia, reduced libido, impotence
- CNS: confusion, hallucinations, depression, or excitation
- IV hypotension and dysrhythmias
*CYP inhibitor
opioids and antacids
- inhibitory property of antacids leads to better high in opiate use
- increasing stomach pH allows for better opiate absorption/longer high
Famotidine & Nizatidine differences from Cimetidine
- more potent and fewer drug interactions than Cimetidine
- no effect on H1 receptors; absorbed w/ or w/o food
- less CNS effects, no androgen binding
- weak CYP inhibition
Famotidine & COVID 19
- in adults with mild-mod covid-19, tx with high dose famotidine led to early resolution of symptoms and inflammation
long term H2RA safety issues
- cognitive impairment –> linked to dementia
Most effective class of drugs to suppress gastric acid secretion
- PPIs/proton pump inhibitors
*End in -prazole
Proton pump inhibitor (PPIs) drugs
- Omeprazole
- Esomeprazole
- Lansoprazole
- Rabeprazole
- Pantoprazole
Omeprazole moa
- prodrug converted to active form inside parietal cell
- causes irreversible inhibition of H+, K+, ATPase and lasts until new one is synthesized
- inhibits basal and stimulated acid release
omeprazole uses
- ulcers
- GERD
- hypersecretory conditions
omeprazole AEs
HA, diarrhea, N/V, long term risk of CA
omeprazole d-d interactions
- affects absorption of atazanacir, ketoconazole, itraconazole due to increased gastric pH
Long term PPI safety (endocrine/nutritional/Hip fx)
- Endo: elevated serum gastric levels
- Nutrition: can lower B12 absorption
- Hip Fx: higher dose = higher risk; presumed that cid inhibition interferes with Ca2+ absorption in small intestine
Long term PPI safety (C. Diff, Plavix, CKD)
- CA-C. diff: theorized that decrease in gastric acidity may be “permissive” to enteric infection
- Plavix: omeprazole reduces efficacy; pantoprazole less likely to do so
- CKD: significantly higher incidence of CKD in PPI users
Long term PPI safety (Cognition & pediatric use)
- Cognition: long term use linked to dementia
- Peds: use of lansoprazole in poorly controlled asthma showed no improvement; increased respiratory symptoms and community acquired pneumonia
H. Pylori newest tx regimen (2)
- Quadruple therapy (PBMT)
–> PPI, Bismuth, Metronidazole & Tetracycline
OR - Concomitant therapy (PAMC)
—> PPI, Amoxicillin, Metronidazole, Clarithromycin
Sucralfate use
- mucosal protective agent
- other ulcer tx drug
- binds to actual ulcer, MoA unknown
Misoprostol moa/use/AEs
- prostaglandin analog
- other ulcer tx drug
- moa: inhibits acid and protects mucosal lining; short half life, freq. dosing needed
- use: NSAID induced ulcers
- AE: stimulates uterine contractions, abd pain, diarrhea (often using in L&D!)
Antacids effects
- neutralize stomach acid; different capacities depending on the compound
- enhances mucosal protection by stimulating PG production, used for ulcers
- symptomatic relief, doesnt accelerate healing