GI Drugs Flashcards
- tidine drugs mechanism
reversible block of H2 receptors –> decreased H+ secretion by parietal cells (no translocation of K+/H+ exchange pump to apical membrane)
- tidine drugs clinical use
- peptic ulcers
- gastritis
- mild GERD
- tidine drugs SEs
- antiandrogenic - prolactin release, gynecomastia, impotence, decreased libido
- crosses BBB (confusion, dizziness, HA) and placenta
- decrease renal excretion of creatinine
-prazole drugs mechanism
irreversible inhibitor of H+/K+ ATPase on apical membrane of stomach parietal cells
-prazole drugs clinical use
- peptic ulcers
- gastritis
- GERD
- Zollinger-Ellison syndrome
-prazole drugs SEs
- increased risk of C. difficile, pneumonia (bugs don’t have low pH to kill them)
- decreased GI absorption of Ca 2+, Mg 2+ due to higher gastric pH –> osteoporosis
In terms of onset of action and efficacy, _____ are faster and more efficacious to treat GERD.
PPIs (-prazole)
Bi, sucralfate mechanism
- insoluble salt that binds to ulcerated sites or breaks in mucosa to provide physical protection and allow HCO3- secretion to reestablish pH gradient in the mucous layer
- enhances mucosal defense/repair
Bi, sucralfate clinical use
- ulcer healing
- traveler’s diarrhea
Bi, sucralfate SEs
- due to binding of GI mucosa, may decrease absorption of other drugs –> avoid this by timing meds properly and taking Bi, sucralfate by itself
- hyperpigmented stool
misoprostol mechanism
PGE1 analogue - increases production/secretion of gastric mucous and decreases gastric acid production
misoprostol clinical use
- to prevent NSAID-induced peptic ulcers (NSAIDs block endogenous PGE1 production)
- to keep patent ductus arteriosus open
- to induce labor
misoprostol SEs
- diarrhea
- abortifacient
- ab. cramps
antacids mechanism
- neutralize gastric acid, but has no role in prevention or healing
antacids SEs
- can affect absorption, bioavailability, or urinary excretion of other drugs by altering gastric and urinary pH
- delayed gastric emptying
- hypokalemia
Al(OH)3 SEs
constipation
Ca3(CO3)2 SEs
hypercalcemia
Mg(OH2) SEs
- diarrhea
- avoid in CKD to prevent hypermagnesemia
Maalox
Al + Mg hydroxide - SEs cancel each other out!
MgOH, Mg-citrate, polyethylene glycol, and lactulose are all:
osmotic laxatives - draw water into GI lumen from intravascular and interstitial compartments of ECF
clinical use of osmotic laxatives
- constipation
- lactulose used for hepatic encephalopathy since gut flora degrade it into metabolites that promote NH4+ excretion
SEs of osmotic laxatives
- diarrhea
- dehydration
- metabolic acidosis
mechanism of sulfasalazine
- combo of sulfapyridine (antibacterial) and 5-aminosalicylic acid (anti-inflammatory)
- cleaved to release 5-ASA by colonic bacteria
clinical use of sulfasalazine
ulcerative colitis, Crohn’s disease colitis
SEs sulfasalazine
- malaise, nausea, sulfonamide toxicity (hemolytic anemia, agranulocytosis), oligospermia (from sulfapyridine portion)
- nephritis (from 5-ASA portion)
mechanism of rifamixin
gut-directed antibiotic that simply wipes out gut flora non-specifically
clinical use of rifamixin
- used before probiotics to repopulate gut flora (any dz in which gut flora is out of whack like symptomatic IBS)
lubiprostone
fatty acid derived from PGE1 that activates and opens luminal Cl- channels causing GI luminal secretion (laxative)
methylnaltrexone
blocks opiate receptors in GI tract, so good for opiate-induced constipation
linaclotide
peptide agonist of guanalyl cyclase that reduces activation of colonic sensory neurons and activates colonic motor neurons (used in IBS)
budesonide
corticosteroid effective for short-term IBD managemenT
mechanism of azathioprine/6-MP
- aza –> 6-MP
- purine analogue that via pseudofeedback prevents purine synth and also disrupts DNA/RNA synthesis
clinical use of azathioprine/6-MP
maintenance of IBD
SEs of azathioprine/6-MP
- GI disturbances
- hepatotoxicity
- infxns
- pancreatitis
- BM suppression
- malignancy (lymphoma)
mechanism of methotrexate
folic acid analogue that competitively inhibits dihydrofolate reductase –> decreased DNA synthesis
clinical use of methotrexate
maintenance of Crohn’s dz
mechanism of infliximab
anti-TNF monoclonal ab
clinical use of infliximab
treats IBD flairs and fulminant dz
SEs of infliximab
- autoimmunogenicity
- CHF
- hepatotoxicity
- malignancy (lymphoma)
- demyelinating dz
- infxn
- DM suppression
