Gastrointestinal Flashcards
Cemetidine, ranitidine, famotidine, nizatidine
MOA: reversible block of histamine H2 receptors leadign to decreased H+ secretion by parietal cells
Clinical: peptic ulcer, gastritis, mild esophageal reflux
Toxicity: cimetidine potent inhibitor of cytochrome p450 and antiadrogenic effects (prolactin release, gynecomastia, impotence, decreased libido),
can cross BBB leading to confusion, dizziness, headaches
Crosses placenta
Cimetidine and ranitidine decrease renal excretion of craetinine
Omeprazole, lansoprazole, esomeprazole, pantoprazole, dexlansoprazole
MOA: irreversibly inhibit H+/K+ ATPase in stomach and parietal cells (decreases HCl in gastrin lumen)
Clinical: peptic ulcer, gastritis, esophageal reflux, Zollinger-Ellsion syndrome
Toxicity: increased risk of C. difficile infection, pneumonia, Hip fractures (decreased Ca absorption), decreased serum Mg2+ with long term use
Bismuth, sucralfate
MOA: bind to ulcer base, providing physical protection and allowing HCO3- secretion to reestablish pH gradient in mucous layer
Clinical: increased ulcer healing, travelers diarrhea
Misoprostol
MOA: PGE1 analog. Increased production and secretion of gastric mucosa barrier. Decrease acid production
Clinical: prevention of NSAID induced peptic ulcers (NSAIDS block PGE production). Maitenance of a PDA, Induces labor
Toxicity: diarrhea
CI: women of childbearing potential
Octreotide
MOA: long acting somatostatin analog
Spinachnic vasoconstriction and reduces portal pressure
Clinical: acute variceal bleeds, acromegaly, VIPoma, and carcinoid tumors
Toxicity: nausea, cramps, steatorrhea
Aluminum hydroxide
Antacid
Toxicity: hypokalemia, constipation, hypophosphatemia, proximal muscle weakness, osteodystrophy, seizures
Calcium corbonate
antacid
Toxicity: hypokalemia, hypercalcemia, rebound acid increase
Can chelate and decreased effectiveness of other drugs (tetracycline)
Magnesium hydroxide
antacid
Toxicity: hypokalmeia, diarrhea, hyporeflexia, hypotension, cardiac arrest
Magnesium hydroxide, magnesium citrate, polyethethylene glycol, lactulose
MOA: osmotic laxatives
Clinical: constipation
Lactulose: hepatic encephalopathy because metabolites (lactic acid and acetic acid) promote nitrogen excretion as NH4+
Toxicity: diarrhea, dehydration, may be abused by bulimics
Infliximab
MOA: monoclonal Ab to TNF-a
Clinical: crohn disease, ulcerative colitis, rheumatoid arthritis, ankylosing spodylitis, psoriasis
Toxicity: infection (reactivation of latent Tb), fever, hypotension
Sulfasalazine
MOA: combo of sulfapyridine (antibacterial) and 5-aminosalicylic acid (anti-inflammatory)
Activated by colonic bacteria
Clinical: ulcerative colitis, crohn disease
Toxicity: malaise, nausea, sulfonamide toxicity, reversible oligospermia, acute pancreatitis
Ondansetron
MOA: 5HT3 antagonist, decrease vagal stimulation
Powerful central acting antiemetic
Clinical: control vomiting postoperatively and in patients undergoing cancer chemotherapy or GI irritation
Toxicity: headache, constipation
Metoclopramide
MOA: D2 receptor antagonist
increase resting tone, contracitility, LES tone, motility
Does not influence colon transport time
Clinical: diabetic and post surgery gastroparesis, antiemetic (acute migraine)
Toxicity: increase parkinosonian effects
Restlessness, drowsiness, fatigue, depression, nausea, diarrhea
Drug interaction with digoxin and diabetic agents
CI: patients with small bowel obstruction of parkinson disease
Diphenoxylate
Binds mu opiate receptors in GI tract slowing motility
Low therapeutic doses don’t have euphoria or physical dependence
High doses do have euphoria and dependence therefore given with atropine that produces dry mouth, blurry vision and nausea discouraging abuse
SE: bloating and mild sedation
Lactulose
Increases NH4 production
Used for hepatic encephalopathy
