GI Drugs Flashcards
H2 blockers
Cimetidine, ranitidine, famotidine, nizatidine
Mechanism: Reversible block of H2 receptors-> decreased H+ secretion by parietal cells
Clinical use: Peptic ulcer, gastritis, mild esophageal reflux
Toxicity:
*Cimetidine: inhibitor of P450, antiandrogenic effects (prolactin release, gynecomastia, decreased libido in males); crosses BBB (neuro symptoms) and placenta
Cimetidine and rantidine: decrease renal excretion of creatinine
Other H2 blockers relatively free of effects
Proton pump inhibitors
Omeprazole, lansoprazole, esomeprazole, pantoprazole, dexlansoprazole
Mechanism: Irreversible inhibition of H/K ATPase in parietal cells -> decreased H+ secretion
Clinical use: Peptic ulcer, gastritis, esophageal reflux, Zollinger-Ellison syndrome
Toxicity: Increased risk of C.diff infection, pneumonia. Risk of fractures and decreased serum Mg2+ with long-term use
Bismuth, sucralfate
Mechanism: Binds to ulcer base -> physical protection and allows bicarb secretion to reestablish pH gradient
Clinical use: increase ulcer healing, traveler’s diarrhea
Misoprostol
Mechanism: PGE1 analog. Increases production and secretion of gastric mucous barrier and decreases H+ production
Clinical use: Prevent NSAID-induced peptic ulcers (NSAIDs block PGE1 production); Maintenance of PDA; Induction of labor (excited myometrium); Used with mifepristone to terminate pregnancy
Toxicity: Diarrhea. Abortifacient
Octreotide
Mechanism: Long-acting somatostatin analog; inhibits many splanchnic vasoconstriction hormones, decrease GI motility, decreased gallbladder contraction, decreased GH secretion..etc
Clinical use: Acute variceal bleeds, acromegaly, VIPoma, carcinoid tumors
Toxicity: GI distress, steatorrhea, hypothyroidism
Antacids
Mechanism: Affect absorption, bioavailability or urinary excretion of other drugs by altered gastric and urinary pH or delaying gastric emptying
Clinical use: gastric ulcers etc
Toxicity:
All- hypokalemia
Aluminum hydroxide- constipation and hypophosphatemia; prox. muscle weakness, osteodystrophy, seizures
Calcium carbonate- hypercalcemia, rebound acid increase
Magnesium hydroxide- diarrhea, hyporeflexia, hypotension, cardiac arrest
Oxmotic laxatives
Magnesium hydroxide, magnesium citrate, polyethylene glycol, lactulose
Mechanism: osmotic load draws water into GI lumen
Clinical use: Constipation;
Lactulose treats hepatic encephalopathy since gut flora degrades it into metabolites (lactic acid and acetic acid) that promote nitrogen excretion in feces as NH4+
Toxicity: Diarrhea, dehydration; can be abused by bulimics
Sulfasalazine
Mechanism: Combo of sulfapyridine (antibacterial) and 5-ASA (inflammatory). Activated by colonic bacteria to provide tropical anti-inflammatory relief
Clinical use: UC, Crohn disease, RA
Toxicity: Malaise, nausea, sulfa toxicity, reversible oligospermia
Infliximab
Mechanism: monoclonal antibody against TNFalpha (major inflammatory cytokine) -> decreased inflammation (administered via IV)
Clinical use: IBD, RA
Toxicity: increased risk of respiratory infection, TB reactivation (PPD needs to be checked), fever, hypotension
Ondansetron
Mechanism: 5HT3 antagonist -> decreases vagal stimulation. Powerful central-acting antiemetic
Clinical use: Control vomiting post-op and in chemo
Toxicity: HA, constipation, QT prolongation
Metolopramide
Mechanism: D2 receptor antagonist -> increases resting tone, contractility, LES tone and motility. Does not influence colon transport time
Clinical use: Diabetic and post-op gastroparesis, antiemetic
Toxicity:
*Same mech of action as typical antipsychotics -> EPS side effects- parkinsonian effects, tardive dyskinesia
Restlessness, drowsiness, fatigue, depression, diarrhea. Drug interaction with digoxin and diabetic agents
Contraindicated in: small bowel obstruction or Parkinson disease
Orlistat
Mechanism: Inhibits gastric and pancreatic lipase -> decreased breakdown and absorption of dietary fats
Clinical use: Weight loss
Toxicity: Steatorrhea, decreased fat soluble vitamin absorption
