GI Drugs Flashcards
Name the H2 blockers
“-tidine”
cimetidine, ranitidine, famotidine, nizatidine
Mechanism of H2 blockers
reversible block of the histamine H2 receptors –> decrease H+ secretion by parietal cells
Use of H2 blockers
peptic ulcer, gastritis, mild GERD
Toxicity of cimetidine specifically
inhibits cytochrome p450 (multiple drug interactions) antiandrogenic effects (prolactin release, gynecomastia, impotence, decreased libido in males) can cross BBB (cause confusion, dizziness, headaches) and can cross placenta
Toxicity of cimetidine and ranitidine
decrease renal excretion of creatinine
Name the proton pump inhibitors
“-prazole”
omeprazole, lansoprazole, esmeprazole, pantoprazole, dexlansoprazole
Mech of PPIs
irreversibly inhibit H+/K+ ATPase in stomach parietal cells
Use of PPIs
peptic ulcer, gastritis, esophageal reflux, Zollinger-Ellison syndrome
Toxicity of PPIs
increased risk of C. difficile infection, pneumonia
decreased serum Mg2+ with long-term use
Mechanism of bismuth and sucralfate
bind to ulcer base, providing physical protection and allowing HCO3- secretion to reestablish pH gradient in the mucous layer
Use of bismuth and sucralfate
increase ulcer healing, travelers diarrhea
Mechanism of misoprostol
a PGE1 analog
increases production and secretion of gastric mucous barrier, decreases acid production
Use of misoprostol
prevention of NSAID-induced peptic ulcers (NSAIDs block PGE1 production); maintenance of a PDA
also off label for induction of labor (ripens cervix)
Toxicity of misoprostol
diarrhea
contraindicated in women of childbearing potential (abortifactant)
Mechanism of octreotide
long-acting somatostatin analog; inhibits actions of many splanchnic vasodilatory hormones
Use of octreotide
acute variceal bleeds, acromegaly, VIPoma, carcinoid tumor
Toxicity of octreotide
nausea, cramps, steatorrhea
Concern with use of antacids
can affect absorption, bioavailability, or urinary excretion of other drugs by altering gastric and urinary pH or by delaying gastric emptying
cause hypokalemia
Toxicity of aluminum hydroxide
constipation and hypophosphatemia
proximal muscle weakness
osteodystrophy
seizures
Toxicity of calcium carbonate
hypercalcemia
rebound acid
Toxicity of magnesium hydroxide
diarrhea
hyporeflexia
hypotension
cardiac arrest
Name the osmotic laxatives
Magnesium hydroxide, magnesium citrate, polyethylene glycol, lactulose
Mechanism of osmotic laxatives
provide osmotic load to draw water into the GI lumen
Use of osmotic laxatives
constipation
Toxicity of osmotic laxatives
diarrhea, dehydration; may be abused by bulimics
Specific use of lactulose
treats hepatic encephalopathy since gut flora degrade it into metabolites (lactic acid and acetic acid) that promote nitrogen excretion as NH4+
Mechanism of sulfasalazine
combination of sulfapyridine (antibacterial) and 5-aminosalicylic acid (anti-inflammatory)
activated by colonic bacteria
Use of sulfasalazine
ulcerative colitis, Crohn disease (colitis component)
Toxicity of sulfasalazine
malaise, nausea, sulfonamide toxicity, reversible oligospermia
Mechanism of ondansetron
5-HT3 antagonist
decreases vagal stimulation
powerful central-acting antiemetic
Use of ondansetron
control vomiting postoperatively and in pts receiving cancer chemotherapy
Toxicity of ondansetron
headache, constipation, QT interval prolongation
Mechanism of metoclopramide
D2 receptor antagonist
increases resting tone, contractility, LES tone, motility
does NOT influence colon transport time
Use of metoclopramide
diabetic and postsurgery gastroparesis, antiemetic
Toxicity of metoclopramide
increased parkinsonian effects, tardive dyskinesia
restlessness, drowsiness, fatigue, depression, diarrhea
Drug interaction of metoclopramide
with digoxin and diabetic agents
Contraindication of metoclopramide use
in patients with small bowel obstruction or Parkinson disease (due to D1 receptor blockade)
Mechanism of orlistat
inhibits gastric and pancreatic lipase –> decreased breakdown and absorption of dietary fats
Use of orlistat
weight loss
Toxicity of orlistat
steatorrhea, decreased absorption of fat soluble vitamins