GIT - drugs Flashcards
H2 blockers
“___TIDINE”
[adine = H1G2]
Cemetidine, Ranitidine, famotidine, nizatidine
H2 blocker mechanism
[Cemetidine, Ranitidine, famotidine, nizatidine]
REVERSIBLY block H2 receptors of ECL cells
H2 blocker use
[Cemetidine, Ranitidine, famotidine, nizatidine]
peptic ulcers, gastritis, mild esophageal reflux
H2 blocker toxicity
[Cemetidine, Ranitidine, famotidine, nizatidine]
Cemetidine:
- inhibits p450
- anti-androgen (prolactin, gynecomastia, impotence, libido)
- cross BBB (HA, dizzy, confusion)
- cross placenta
- decrease renal creatinine excretion
Ranitidine:
- decrease renal creatinine excretion
Cemetidine
H2 reversible blocker
Ranitidine
H2 reversible blocker
Famotidine
H2 reversible blocker
Nizatidine
H2 reversible blocker
PPIs
“___prazole”
[Omeprazole, lansoprazole, esomeprazole, pantoprazole, dexlansoprazole]
PPI mechanism
[Omeprazole, lansoprazole, esomeprazole, pantoprazole, dexlansoprazole]
IRREVERSIBLY inhibit H/K ATPase in stomach parietal cells
better than H2 blockers because blocks the final step
PPI use
[Omeprazole, lansoprazole, esomeprazole, pantoprazole, dexlansoprazole]
PUD, gastritis, esophageal reflux, ZE
PPI toxicity
[Omeprazole, lansoprazole, esomeprazole, pantoprazole, dexlansoprazole]
c. DIFF!, pneumonia, low Mg++ with extended use
Omeprazole
PPI
Lansoprazole
PPI
Esomeprazole
PPI
Pantoprazole
PPI
Dexlansoprazole
PPI
Bismuth mechanism
Binds ulcer base providing physical protection while bicarb is secreted to fix pH in mucus layer
Bismuth use
increase ulcer healing
travellers diarrhea
Sucralfate mechanism
Binds ulcer base providing physical protection while bicarb is secreted to fix pH in mucus layer
needs acidic pH .: can’t use with PPIs or H2 blockers
Sucralfate use
increase ulcer healing
travellers diarrhea
Drugs that promote ulcer healing and treat travellers diarrhea
Bismuth and sucralfate
Misoprostol MOA
PGE1 analog, binds Gi
GIT: increases production and secretions gastric mucosal barrier and decreases acid production
Repro: given with Mifepristone (RU-486) to sensitize the receptors to it
Misoprostol use
Prevent NSAID-induced ulcers (NSAIDs block PGE1 production, so this replaces it).
MAINTAIN PDA.
Induces labour/ripens cervix + abortions [off-label]
Misoprostol AE
Diarrhea
Contraindicated in child-baring age women (abortifacient)
Octerotide MOA
Somatostatin analog; mimics splanchnic vasoconstriction hormones
Octerotide use
Acute variceal bleeds (VC) Acromegaly VIPoma Carcinoid Insulinoma
Octerotide AE
Steatorrhea
Cramps
Nausea
Antacids GENERAL AE:
- Altered absorption, bioavailability, or urinary extortion of other drugs via altered gastric and urinary pH or gastric emptying
- Hypokalemia
- Specific overuse problems
Antacids:
Aluminum hydroxide
Calcium carbonate
Magnesium hydroxide
Aluminum hydroxide specific overuse AE:
Constipation Hypophosphatemia Proximal muscle weakness Renal Osteodystrophy Seizures
Calcium carbonate specific overuse AE:
Hypercalcemia
Rebound increase in acid
Chealates and decreases effectiveness of other drugs i.e. tetracyclin
Magnesium hydroxide specific overuse AE:
Diarrhea
Hyporeflexia
Hypotension
Cardiac arrest
Osmotic laxatives
MgOH, MgCitrate, polyethylene glycol (PEG), lactulose
Osmotic laxative use
[MgOH, MgCitrate, polyethylene glycol (PEG), lactulose]
Constipation
*Lactulose for hepatic encephalopathy: gut flora degrade it to lactic acid and acetic acid, donates H+ to NH3 which increases NH4+ excretion
Osmotic laxative toxicity
[MgOH, MgCitrate, polyethylene glycol (PEG), lactulose]
Diarrhea
Dehydration
Abused by bulimics
Sulfasalazine MOA
= sulfapyridine (antibacterial) + 5-ASA (anti-inflammatory)
Activated by colonic bacteria
Sulfasalazine use
Ulcerative colitis
Chrons
Sulfasalazine toxicity
malaise
nausea
sulfonamide toxicity (G6PD; lupus-like)
reversible oligospermia
Ondansetron mechanism
5-HT3 antagonist; decreases vagal stimulation
Ondansetron use:
powerful central anti-emetic - post-op and chemo
Ondansetron AE
HA
Constipation
QT prolongation
Metochlopromide mechanism
D2 antagonist
increases resting tone, contractility, LES tone, and motility = PROKINETIC
[does NOT influence colon transport time]
Metochlopromide use
Diabetic and post-surgical gastroparesis
Antiemetic
Metochlopromide AE
Increased parkinsonian effects (D2 antagonism)
Interacts with digoxin and diabetic drugs
Contraindicated with small bowel obstructions and parkinsons
Orlistat mechanism
inhibits gastric and pancreatic lipases to decrease fat breakdown and thus absorption
Orlistat use
weight loss
Orlistat AE:
Steatorhea
Decreased absorption of fat-soluble vitamins
