GI Pharm from FA Flashcards
what class?
Cimetidine
Ranitidine
Famotidine
Nizatidine
H2 blockers
Take H2 blockers before you dine: “Table for 2”
H2 blockers: mech?
Reversible block of histamine H2 receptors
-> decr H+ secr by parietal cells
H2 blockers: use?
peptic ulcers, gastritis, mild esophageal reflux
Which H2 blockers have the most toxicity?
what is that tox?
Cimetidine: inhibits cytochrome P-450 -> multiple drug interactions.
Also is an anti-androgen -> prolactin release, gynecomastia, impotence, decr libido in males
Crosses BBB -> confusion, dizziness, headaches
crosses placenta.
Both Cimetidine and Ranitidine decrease renal excr of creatinine (could be a reason for elevated creatinine without another cause)
Name the H2 blockers that have no toxic effects listed in FA? (2)
Famotidine
Nizatidine
(Ranitidine has only one tox effect: decr renal excr of creatinine. Cimetidine has a boatload.)
What class?
Omeprazole, Lansoprazole, Esomeprazole, Pantoprazole, Dexlansoprazole
Proton Pump Inhibitors
Mechanism?
Omeprazole, Lansoprazole, Esomeprazole, Pantoprazole, Dexlansoprazole
Irreversibly inhibit H/K ATPase in stomach parietal cells
(receptors on LUMEN side of the stomach)
(Proton Pump Inhibitors: inhibit “primary active transport”)
Clinical Use?
Omeprazole, Lansoprazole, Esomeprazole, Pantoprazole, Dexlansoprazole
Peptic ulcer, gastritis, esophageal reflux, Zollinger-Ellison syndrome
Toxocity?
Omeprazole, Lansoprazole, Esomeprazole, Pantoprazole, Dexlansoprazole
Incr risk of C Diff infection
Pneumonia
With long term use: hip fractures, decr serum Mg2+
(I’m sure this all has something to do with acid.)
Bismuth, Sucralfate: Mech?
Binds to ulcer base –> physical protection, allows Bicarb secretion to re-establish pH gradient in the mucous layer.
Bismuth, Sucralfate: Use?
Allows ulcer healing
Traveler’s diarrhea
Misoprostol
Mech?
PGE1 analog
- Incr production/secretion of gastric mucous barrier
- Decr acid production
Misoprostol
Use?
- Prevents peptic ulcers from NSAID use (NSAIDs block PGE1 production)
- Maintains PDA
- Ripens cervix -> induces labor
(miso soup steams things open (PDA, cervix). Also is Jen’s hangover cure: aspirin + miso soup)
Octreotide
Mech?
Long-acting somatostatin analog
Acts on ECL cell, not parietal cell
(Endocrine connection: somatostatin from hypothal decr GH and TSH release. If hypothalamus is destroyed, Octreotide can replace somatostatin)
Octreotide
Use?
- Acute variceal bleeds
- Acromegaly (blocks GH release from pituitary)
- VIPoma
- carcinoid tumors
- helpful for ‘secretory’ diarrhea
Octreotide
Tox?
nausea, cramps, steatorrhea
What class?
Aluminum hydroxide
Calcium carbonate
Magnesium hydroxide
Antacids
Antacids: general tox?
- affect absorption, bioavailability, or urinary excr of other drugs by altering gastric and urinary pH or by delaying gastric emptying
- Hypokalemia
Aluminum hydroxide: tox?
Antacid general tox = alter gastric/urinary pH or delay gastric emptying -> affect other drugs; hypokalemia
Specific to Al hydroxide: constipation, hypophosphatemia, prox muscle weakness, osteodystrophy, seizures
“Aluminimum amount of feces”
Calcium carbonate: tox?
Antacid general tox = alter gastric/urinary pH or delay gastric emptying -> affect other drugs; hypokalemia
Specific to Ca carbonate: hypercalcemia, rebound acid increase.
Can chelate and decr effectiveness of other drugs (ex tetracycline)
Magnesium hydroxide: tox?
Antacid general tox = alter gastric/urinary pH or delay gastric emptying -> affect other drugs; hypokalemia
Specific to Mg hydroxide: diarrhea, hyporeflexia, hypotension, cardiac arrest
“Mg = Must Go to the bathroom”
Class?
Magnesium hydroxide
Magnesium citrate
Polyethylene glycol
Lactulose
Osmotic laxatives
Osmotic laxatives: mech?
(Magnesium hydroxide
Magnesium citrate
Polyethylene glycol
Lactulose)
Provide osmotic load to drive water out
Lactulose treats hepatic encephalophy (gut flora degrade it into lactic acide and acetic acid -> promotes nitrogen excretion as NH4+
Osmotic laxatives: use?
(Magnesium hydroxide
Magnesium citrate
Polyethylene glycol
Lactulose)
Constipation
Lactulose: hepatic encephalopathy
Osmotic laxatives: tox?
(Magnesium hydroxide
Magnesium citrate
Polyethylene glycol
Lactulose)
diarrhea
dehydration
abuse by bulimics
Infliximab: mech?
Monoclonal antibody to TNF-a
Infliximab: use?
Crohn’s
Ulcerative colitis
rheumatoid arthritis
ank spondylitis
psoriasis
Infliximab: tox?
Infection (possible reactivation of latent TB)
fever
hypotension
sulfazalazine: mech?
combination of sulfapyridine (antibacterial) + 5-aminosalicylic acid (anti-inflammatory)
Activated by colonic bacteria
Sulfasalazine: use?
Ulcerative colitis
Crohn’s
Sulfasalazine: tox?
Malaise
nausea
sulfonamide tox
decr sperm count (reversible)
metoclopramide: mech?
D2 receptor antagonist.
decr resting tone, contractility, LES tone, motility
does not change colon transport time
metoclopramide: use?
diabetic and post-surg gastroparesis (paralysis)
Anti-emetic
metoclopramide: tox?
incr parkinsonian effects
restlessness, drowsiness, fatigue, depression, nausea, diarrhea.
Interacts with digoxin and diabetic agents
metoclopramide: CI in what patients?
pts with small bowel obstruction
Parkinson dz patients (D1-receptor blockade)
Odansetron: mech?
5-HT3 antagonist; decr vagal stimulation
Powerful central-acting antiemetic
“Keep on dancing with odansetron!”
Odansetron: use?
control vomiting post-op
patients undergoing cancer chemo
Odansetron: tox?
headache
constipation
Diphenoxylate: mech?
binds mu receptors in GI; slows motility
Diphenoxylate: use?
opiate anti-diarrheal (similar to meperidine - opioid agonist)
in low doses, can slow gut motility with no euphoric effects
packaged with atropine to discourage abuse!
Treatment for Crohn’s disease? (5)
Corticosteroids
Azathioprine
Methotrexate
Infliximab
Adalimumab
Treatment for Ulcerative Colitis? (4)
ASA preparations (sulfasalazine)
6-mercaptopurine
infliximab
Colectomy
Treatment for hepatic encephalopathy?
Lactulose (bacterial action -> acid produced -> NH3 becomes NH4, ammonium trap)
Low protein diet (less nitrogen intake)
Rifaximin (kills intestinal bacteria)
Treatment for Crigler-Najjar syndrome?
(type I, Type II)
Type I: plasmapheresis, phototherapy
Type II (less severe): phenobarbital (incr liver enzyme synthesis)
Treatment for Wilson disease?
Penicillamine or Trientine
Treatment of hereditary hemochromatosis?
- repeated phlebotomy
- Iron chelation (deferasirox, deferoxamine)
