Gastrointestinal Pharmacology Flashcards
Examples of H2 blockers
-dine
Cimetidine
ranitidine
famotidine
nizatidine
“Take H2 blockers before you dine. Think ‘table for 2’ to remember H2.”
H2 blockers: MOA
Reversible block of histamine H2 receptors –> DECREASE H+ secretion by parietal cells
H2 blockers: INDICATIONS
- peptic ulcer
- gastritis
- mild esophageal reflux
Cimetidine--TOXICITY
(H2 blocker)
- potent inhibitor of cytochrome P-450
- antiandrogenic effects - prolactin release, gynecomastia, impotence, dec libido in males
- can cross BBB –> confusion, dizziness, headaches
- can cross the placenta - Contraindicated in pregnancy and breastfeeding?
name the proton pump inhibitors
Examples of PPIs
-praZOLE
omeprazole
lansoprazole
esomeprazole
pantoprazole
dexlansoprazole
PPIs: MOA
Irreversibly inhibit H+/K+ ATPase in stomach parietal cells
(unlike H2 blocker which is a reversible block of histamine H2 receptor and indirectly affect the parietal cells)
PPIs: INDICATIONS
- PUD
- gastritis
- esophageal reflux / GERD
- Zollinger-Ellison syndrome
PPIs - toxicity
- INCREASE risk of C. difficile infection, pneumonia (short term?)
- DECREASE serum Mg2+ with long term use
How does antacid usage affect other drugs?
Antacids: Drug Interactions
Affect absorption, bioavailability, or urinary excretion of other drugs by
- altering gastric and urinary pH or
- by delaying gastric emptying
name 3 types of antacids
- aluminum hydroxide
- calcium carbonate
- magnesium hydroxide
what can all antacids cause?
HYPOKALEMIA
aluminum hydroxide–toxicity
- contipation
- hypophosphatemia
- proximal muscle weakness
- osteodystrophy
- seizures
“Aluminimum amount of feces”
calcium carbonate–toxicity
- hypercalcemia–milk alkali syndrome
- rebound acid increases
- can chelate and decrease effectiveness of other drugs (ie. tetracycline)
magnesium hydroxide–toxicity
diarrhea
hyporeflexia
hypotension
cardiac arrest
“Mg2+ = Must go to the bathroom”
bismuth, sucralfate–mechanism
bind to ulcer base which protects it and allows HCO3- secretion to reestablish pH gradient in the mucous layer
bismuth, sucralfate–use
inc ulcer healing
travelers’ diarrhea
misoprostol–mechanism
a PGE1 analog
inc production and secretion of gastric mucous barrier
dec acid production
misoprostol–use
prevention of NSAID induced peptic ulcers (NSAIDs block PGE1 production)
maintenance of a patent ductus arteriosis
also used off label for induction of labor–ripens cervix
misoprostol–toxicity
diarrhea
contraindication for misoprostol
women of childbearing potential (abortifacient)
name the stimulant laxatives
Bisacodyl (DULCOLAX)
Senna (SENOKOT)
Castor Oil
Examples of saline laxatives
Magnesium hydroxide (MILK OF MAGNESIA)
Magnesium sulfate (EPSOM SALTS)
Magnesium citrate
Sodium phosphate (FLEET’S PHOSPHOSODA)
Saline laxative MOA
draw water into the intestinal lumen
name the osmotic laxatives
magnesium hydroxide
magnesium citrate
polyethylene glycol
lactulose
osmotic laxatives–mechanism
provide osmotic load to draw water into the GI lumen
osmotic laxatives–use
constipation
lactulose–use and specific mechanism
(osmotic laxative)
helps treat hepatic encephalopathy since gut flora degrade it into metabolites (lactic acid and acetic acid) that promote nitrogen excretion as NH4+
osmotic laxatives–toxicity
diarrhea
dehydration
may be abused by bulimics
sulfasalazine–mechanism
combination of sulfapyridine (antibacterial) and 5-aminosalicyclic acid (anti-inflammatory)
activated by colonic bacteria
sulfasalazine–use
ulcerative colitis
Crohn disease (colitis component)
sulfasalazine–toxicity
malaise
nausea
sulfonamide toxicity
reversible oligospermia
loperamide–mechanism
agonist at mu-opioid receptors
slows gut motility
poor CNS penetration (low addictive potential)
loperamide–use
diarrhea
loperamide–toxicity
constipation
nausea
ondansetron–mechanism
5-HT3 antagonist
decrease vagal stimulation
powerful central acting antiemetic
ondansetron–use
control vomiting postop and in patients undergoing cancer chemotherapy
“at a party but feeling queasy? Keep on dancing with ondansetron”
ondansetron–toxicity
headache
constipation
QT interval prolongation
metoclopramide–mechanism
D2 receptor antagonist
inc resting tone, contractility, LES tone, motility
does not influence colon transport time
metoclopramide–use
diabetic and postsurgery gastroparesis
antiemetic
metoclopramide–toxicity
inc Parkinsonian effects, tardive dyskinesia
restlessness
drowsiness
fatigue
depression
diarrhea
what is a possible drug interaction with metoclopramide?
digoxin
diabetic agents
what is a contraindication for metoclopramide?
patients with small bowerl obstruction or Parkison disease (due to D2 receptor blockade)
What drugs/classes of drugs can lower lower esophageal sphingter tone increasing risk of reflux?
Anticholinergics
Benzodiazepines
Caffeine
CCB (dihydropyridines)
Estrogen/progesterone
Nicotine
Nitrates
Theophylline
TCAs
What is important patient teaching when prescribing a PPI?
uDo not crush or chew capsules
uTake before meals – preferably breakfast
uLong term users (>6 months) need to taper off
uRebound gastric hypersecretion is common
which class of anti-emetics is most frequently prescribed for motion sickness?
anticholingerics/antihistamines
ursodiol (ursodeoxycholic acid)–mechanism
non toxic bile acid
inc bile secretion
dec cholesterol secretion and reabsorption
ursodiol (ursodeoxycholic acid)–use
primary biliary cirrhosis
gallstone prevention or dissolution
Common side effects of phenothiazines (compazine and phenergan)
Blurred vision, Dry mouth, Dizziness, Restlessness, Seizures, Extrapyramidal effects - Tardive dyskinesia (long term treatment)
