GI Drugs Flashcards
what do acid peptic diseases compose of
peptic ulcer (duodenal and gastric), gastroesophageal reflux, zollinger ellison syndrome (ZES)
pathologies that causes peptic ulcers
- gastric acid
- decreased mucosal resistance to acid
- H pylori infection
- NSAIDs
- concurrent use of warfarin and corticosteroids
- stress esp if older than 65
- lifestyle
- gastrinoma - gastrin secreting tumor
what do peptic disease do to the surface of GI tract
erodes and ulcerates the mucosal lining
therapeutic choices for peptic ulcer diseases and their functions
A HAM
- Antacids: neutralizes acid
- H2 antagonist and Proton Pump Inhibitor - reduces gastric acid secretion
- Antimicrobial treatments - eradicate H pylori infection
- Mucosal protective agents - augment mucosal surface defense
mechanism of gastric antacids
they are weak bases that react with gastric HCl to form water and salt –> increase in pH –> quick relief of symptoms
name the antacids
CAM
Calcium Carbonate
Aluminum Hydroxide
Magnesium Hydroxide
adverse effects of each antacids
- Calcium Carbonate –> Hypercalcemia which leads to nephrolithiasis and constipation –> fecal compaction
- Aluminum Hydroxide –> form aluMINIMUM chloride that is insoluble –> MINIMUM amount of feces –> constipation and Hypophosphatemia
- Magnesium Hydroxide –> for Mg salt which is poorly absorbed and causes diarrhea (Mg – Must go to the bathroom)
clinical correlates of antacids and drug absorption
- increases oral absorption of weak bases (quinidine)
- decreases oral absorption of weak acids (warfarin)
- decreases oral absorption of Ca, Mg, and Al molecules –> chelate tetracycline
what are some factors that enhance gastric acid secretion and via what mechanism
Histamine, Acetylcholine, and Gastrin via H+/K+ ATPase pump
what are the H2 receptor blockers
FRaNC
Famotidine
Ranitidine
Nizatidine
Cimetidine
how effective are H2 receptor blockers/mechanism
they are effective at decreasing gastric acid secretion but have no effect on gastric emptying time
of all the H2 receptor blockers, which ones are longer acting/more potent
all but cimetidine
clinical uses of H2 receptor blockers
- promote healing of duodenal and gastric ulcers
- relieve gastro esophageal reflux
- given preoperatively to prevent aspiration pneumonia
adverse effects of H2 blockers excluding cimetidine
nausea, headache, dizziness
adverse of H2 blocker cimetidine
- inhibitor of CYP450 enzymes
- antiandrogenic effects - gynecomastia, elevated prolactin levels, decreased libido
- confusion in older people
- decrease renal excretion of creatinine
since Cimetidine is a CYP450 inhibitor, what drugs does it affect
- warfarin
- procainamide
- phenytoin
- benzos
- theophylline
- imipramine
- quinidine
what are the proton pump inhibitors
PROLE PRAZOLES
- Pantoprazole
- Rabeprazole
- Omeprazole
- Lansoprazole
- Esomeprazole
mechanism of proton pump inhibitors
in parietal cells, they are converted to their active form –> reacts with cysteine on H+/K+ ATPase –> form stable covalent bond –> irreversible inactivation of enyzme
clinical uses of proton pump inhibitors
- GERD, duodenal and gastric ulcers, multiple endocrine neoplasia 1 (MEN-1), Zollinger Ellison
- together with antibiotics help with H pylori infection
- NSAIDs induced ulcers: not only inhibit proton release but also they support platelet aggregation and maintain clot integrity (hemorrhagic ulcers usage)
adverse effects of proton pump inhibitors
- omeprazole inhibits metabolism of warfarin, clopidogrel, phenytoin, diazepam, cyclosporine
- decrease bioavailability of vit B12
- acid needed for absorption of digoxin and ketocanozole so decreased absorption of them
- long term use of omeprazole –> gastric carcinoid tumor
how do you diagnose H pylori infection
- endoscopic biopsy of ulcer margin
- serology test
- urea breath test
first line antimicrobials for H pylori eradication
CAMT Clarithromycin Amoxicillin Metronidazole Tetracycline
what are the mucosal protective agents
Mucosal MoBS
Misoprostol
Bismuth Subsalicylate
Sucralfate
mechanism of sucralfate
- binds to necrotic tissue and acts as a barrier to acid
- stimulates prostacyclin synthesis
