Upper GI drugs Flashcards
what are the drugs that make up the Bismuth quadruple therapy for uclers
Bismuth subsalicylate,
Metronidazole,
Tetracycline,
PPI
what are the drugs that make up the concomitant quadruple therapy for uclers
Clarithromycin,
Metronidazole,
Amoxicillin,
PPI
Omeprazole and Lansoprazole are what class of drugs?
Proton Pump Inhibitors [PPIs]
what is the mode of action for PPI’s
Covalent linkage of sulfenamide form to sulfhydryl groups of H+-K+-ATPase irreversibly inactivates enzyme.
what are the clinical uses of Proton Pump Inhibitors [PPI]
GERD. Most effective agent for nonerosive and erosive reflux disease and complications
Peptic ulcer disease. More rapid symptom relief and faster healing than H2 antagonists
NSAID-induced ulcers. Effective for treatment (healing impaired if NSAID not stopped) or prevention of ulcers and ulcer-related complications.
Prevention of stress gastritis. Increasing use in critically ill patients to reduce mucosal bleeding.
Zollinger-Ellison syndrome. Higher doses provide complete symptomatic relief and ulcer healing
what are the Drug-drug interactions of PPI
due to actions on CYP450 enzymes: omeprazole may inhibit conversion of antiplatelet agent clopidogrel to active form
Chronic use (> 1 year) of PPI have been associated with ______
reductions in oral absorption and levels of cyanocobalamin (B12),
fractures,
pneumonia,
C. difficile infections.
Name the 4 H2 receptor antahonists
Ranitidine
Cimetidine
Famotidine
Nizatidine
what is the Mechanism of action of Ranitidine, Cimetidine, Famotidine, and Nizatidine
reversible, competitive block at parietal cell H2 receptors on basolateral membrane
H2 antagonist are Better at blocking \_\_\_\_\_\_\_\_\_\_\_\_ acid secretion (90%) than meal-stimulated (ACh- and gastrin-mediated, 60-80%) secretion
nocturnal (basal, H2-mediated)
what are the clinical uses of H2 antagonists
GERD. Infrequent heartburn can be managed with OTC antacids (more rapid onset) or intermittent H2 antagonists. Frequent heartburn generally requires BID H2 antagonists. Proton pump inhibitors (PPIs) preferred in severe erosive esophagitis.
Peptic ulcer disease. H2 antagonists largely replaced by PPIs. Still useful in suppressing nocturnal acid secretion (given at bedtime) for acute uncomplicated ulcers (6-8 week duration, 80-90% healing rate).
Stress-related gastritis. Reduced bleeding when given IV.
what are the Endocrine side effects with cimetidine (> 8 weeks and in high doses):
Gynecomastia,
galactorrhea (excessive or inappropriate production of milk),
decreased sperm count
_______ inhibits cytochrome P450 oxidative metabolism (CYP1A2, 2C9, 2D6, 3A4) that can increase the effects or toxicity of number of drugs (theophylline, warfarin, phenytoin, carbamazepine, ketoconazole, itraconazole, benzodiazepines).
Cimetidine
what kind of drug is Sucralfate
Mucosal Protective Agent
why shouldn’t Sucralfate be administered simultaneously with antacids, H2 blockers?
because Sucralfate is only Activated by acid pH < 4,
best on empty stomach, 1 hour before meals
what is Misoprostol
Prostaglandin (PGE1) analog
what is the method of action of Misoprostol
Prostaglandins (analog) have physiological action in gastric parietal cells to inhibit cAMP formation that results in decreased H+ secretion ; they also stimulate acid neutralizing HCO3 formation and cytoprotective mucus formation.
what is the Major indication for Misoprostol use
alleviation of NSAID-induced GI ulceration
what are the side effects of Misoprostrol
Diarrhea (promote fluid secretion), uterine stimulation (cramping) in up to 30% of patients. Contraindicated during pregnancy
what is the Primary use of Gastric Antacids?
pain relief (healing?) due to peptic ulceration and acute gastritis. Largely replaced by more effective and more conveniently administered and dosed drugs.
For treatment of ulcers, when should antacids be taken?
1 and 3 hours after meals and at bedtime.
what are the side effects of antacids?
constipation (Ca++ and Al+++ antacids).
diarrhea (Mg++ antacids)
What are Prokinetic Agents.
Utilized as empiric and symptoms-based treatment for various disorders of bowel motility [achalasia of esophagus, gastroparesis] and symptom relief of esophagitis associated with gastroesophageal reflux disease (GERD).
what are Mechanisms of Promotility Drugs.
These agents directly or indirectly increase agonist activity at smooth muscle M3-receptors.
name the 5 promotility drugs
- Erythromycin
- Cisapride
- Metoclopramide
- Neostigmine
- Bethanechol
what is the MOA of Cisapride
an agonist (+) at excitatory (+) neural 5-HT4 receptors on enteric nervous system cholinergic motor neurons
what is the MOA of Erythromycin
(+) is an agonist at excitatory (+) at neural and smooth muscle motilin receptors
What is the MOA of Metoclopramide
is an antagonist (-) at presynaptic dopamine (DA) receptors (D2) that inhibit the release of acetycholine
what is the MOA of Neostigmine
inhibits (-) hydrolysis of acetylcholine by acetylcholinesterase (AChE)
what is the MOA of Bethanechol
acts directly as an agonist (+) at excitatory (+) M3 smooth muscle receptors
Describe The mechanism of action common to most prokinetic agents
They act to increase gastric motility by increasing release of acetylcholine from cholinergic neurons in the enteric nervous system
what are the clinical uses of promotility drugs
Diabetic gastroparesis (increase GI motility), gastroesophageal reflux disease (Increase lower esophageal sphincter [LES] pressures),
________ may cause life-threatening arrhythmias from prolongation of QT interval (especially if its metabolism by cytochrome P450 is inhibited).
Cisapride
________ may cause somnolence, dystonic reactions, and tardive dyskinesia.
Metoclopramide
