GI Drugs Flashcards
Antacid examples
Calcium carbonate (TUMS)
Aluminum hydroxide
Magnesium hydroxide (MoM)
Maalox contains aluminum and magnesium
Antacids MOA
React locally in stomach with H+ to increase pH
Route of administration of antacids
Suspension more effective than tablets and powders
Antacids indications
Hyperacidity
reflux
Indigestion
Antacids CIs
Poor renal function
Antacids S/E
Magnesium —> diarrhea
Calcium —> Hypercalcemia, renal calculi, bloating, flatulence, belching, nausea, constipation
Aluminum —> hypophosphatemia, constipation
Antacids drug interactions
Bind to tetracycline resulting in decreased bioavailability
Which antacids are often combined
Aluminum and magnesium
Mg is rapid onset/Al is slower onset
Mg causes diarrhea/aluminum causes constipation
What is added to antacids to reduce bloating
Simethicone
H2 antagonist examples
Ranitidine / Zantac
Famotidine / Pepcid
H2 antagonist MOA
Inhibit histamine at H2 receptors of the gastric parietal cells, which reduces gastric acid secretion
H2 antagonist indications
GERD
PUD
Dyspepsia
Gastritis
H2 antagonist CIs
Caution in patients with renal impairment
Liver failure or liver disease
H2 antagonist S/E
Generally well tolerated
Common - diarrhea, headache, drowsiness, fatigue, muscle pain, constipation
Rare - CNS side effects (confusion, delirium, hallucinations, slurred speech), thrombocytopenia
disadvantages of H2 antagonists
less effective than PPIs
tolerance can develop
lots of drug interactions with Cimetidine
PPI Examples
- omeprazole / prilosec
- pantoprazole / protonix
- esomeprazole / nexium
PPI MOA
act within gastric parietal cell, inactivate the acid pump and inhibit secretion of hydrochloric acid into stomach
PPI Indications
- gastric and duodenal ulcers
- GERD
- Upper GI bleeding (Mallory Weiss)
- Zollinger-Ellison Syndrome
- H. pylori infection
PPI CIs
co-administration of other drugs
all interfere with absorption of drugs given orally that depend on gastric acid pH to be effective - vit B12, ampicillin, ketoconazole
formulation of PPIs
all have enteric coating to protect them from acidic environment until they reach small intestine for absorption - don’t break up the tablets
when to take PPIs
take 30-60 min prior to meals
PPI metabolism
liver
PPI S/E
generally well tolerated
Common: nausea, abdominal pain, constipation, diarrhea, flatulence
Less Common: hypergastrinemia –> rebound hypersecretion of gastrin if PPI stopped
Long term use: increased risk of fractures of the wrist, hip, spine (over 1 year of daily use)
benefits of PPIs
most effective for GERD - reduce acid by 85-90%
GI cytoprotectant examples
Misoprostol / Cytotec (prostaglandin analog)
Sucralfate / carafate (coating agent)
bismuch / pepto bismol (coating agent)
GI cytoprotectant MOA
protect cells in lining of stomach - either increase gastric pH or enhance mucosal barrier
sulcralfate selectively binds to necrotic tissue, covers ulcer site, acts as barrier to acid, pepsin, bile salts