Drugs For Inflammatory Bowel Disease Flashcards
Pathogenesis of IBD
More pathogenic vs beneficial microbes Is present. Also inappropriate immune responses are present as well.
TH1/TH17 pathways predominant in CD
- TNFa is the most present cytokine
TH2/TH17 pathways predominant in UC
- IL-4 is the most present cytokine
Goals of IBD therapy
Induction of clincial remission and maintain remission
Avoid surgery unless needed
Treatment choices = depends on disease severity
What are special formulations of 5-aminosalycilates that can be used for IBD?
Depositories
Enemas
PH dependent release capsules
Delayed released capsules
these are used since the bioavailability is 20% off normal oral doses
Azo compounds of 5-ASA
Decrease absorption of the drug within the small intestine
However, normal terminal ileum and colon flora have high levels of azoreductase enzymes which cleave the 5-ASA off this drug and activate function
- is more active in colon regions of the bowel
Sulfasalazine = 5-ASA + sulfapyridine
Olsalazine = 2 5-ASA bound together
Balsalazide = 5-ASA bound to 4-aminobenzoyl-B-alanine
What is the purpose of using corticoids with high glucocorticoid potency vs mineralcorticoid potency?
Glucocorticoid = actual anti inflammatory actions
Mineralcorticoid = salt/water imbalances
- *goal is to have high glucocorticoid potency vs mineralcorticoid potency**
- this is why hydrocortisone can be used for treatment of IBD, but is almost never really used
What enzyme breaks down 6-mercaptopurine into its active form (6-methyl-mercaptopurine)
TPMT