pharm - immune modifiers.txt

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tallone4830
ID:
164478
Filename:
pharm - immune modifiers.txt
Updated:
2012-07-30 19:03:46
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pharm immune modifiers
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pharm - immune modifiers.txt
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  1. systemic steroids MOA
    mimic the action of cortisol, an endogenous clucocorticoid (turns immune activity/inflammation down). catabolic effects (hyperglycemia, hypercalcemia, muscle breakdown), inflammatory effects (incr neutrophil counts but decr their migration into tissue, decr all other counts)
  2. systemic steroids other SE
    weight/water gain (moon face), skin (thin skin, violaceous striae/stretch marks, ulcers), avascular necrosis of the hips, Cushing's, adrenal suppression
  3. mineralcorticoids v glucocorticoids
    dexamethasone only antiinflammatory (glucocorticoid), no mineralcorticoid. prednisone is a glucocorticoid with minimal mineralcorticoid activity.
  4. B-cell biologics
    destroy or interfere with B cell's ability to mount an immune response. CD20 induces apoptosis and is found in 90% of B-cell neoplasms.
  5. B-cell biologics kinetics
    T1/2 dependant on how many CD20 receptors available to bind and take drug out of circulation. takes 9-12 months for counts to recover.
  6. B-cell biologics SE
    infusion rxns, progressive multifocal leukoencephalopathy (due to infection)
  7. T-cell biologics targets
    CD3, CD25, CD11a, LFA-3 (aka CD58), CD28
  8. T-cell biologics SE
    strong inflammatory reaction (cytokine-release syndrome) often occurs with the first dose of OKT3 (newer drugs have been designed to be nonactivating so as to avoid this problem).
  9. mixed biologic targets
    CD52, IL6
  10. mixed biologic indications
    alemtuzumab CA, transplant. tocilizumab doesn't destroy lymphocytes, so only use is RA.
  11. mixed biologic SE
    alemtuzumab pancytopenia. tocilizumab hypercholesterolemia, elevated LFTs, neutropenia.
  12. tumor necrosis factor-alpha inhibitors MOA
    TNFa is produced by macrophages/inflammatory cells, promotes inflammation, apoptosis. inhibitors blunt this effect. high TNFa levels are often in autoimmune diseases.
  13. tumor necrosis factor-alpha inhibitors kinetics
    injected every 2-4 wks
  14. amtimetabolites MOA
    azathioprine mimics nucleotides, gets incorporated and inhibits further synthesis of DNA/RNA. mycophenolate inhibits enzymes that create nucleotides, inhibiting DNA/RNA synthesis.
  15. antimetabolites kinetics
    metabolism linked to TPMT activity (thiopurine methyltransferase)
  16. antimetabolites contraindications
    mycophenolate pregnancy (azathioprine is OK)
  17. antimetabolites interactions
    azathioprine metabolized to mercaptopurine, which is metabolized by xanthine oxidase (an enzyme important in gout) -- therefore allopurinol, a xanthine oxidase inhibitor, is a significant interaction
  18. antimetabolites SE
    messes with systems that have high cell turnover
  19. calcineurin inhibitors MOA
    binds and inhibits the actions of calcineurin (the upregulation of IL-2 receptors, activators of T-cells)
  20. calcineurin inhibitors kinetics
    cyclosporine narrow therapeutic index (100-400ng/mL), monitor trough levels. metabolized by CYP3A4.
  21. calcineurin inhibitors SE
    nephrotoxicity/HTN (especially cyclosporine), CNS problems (especially tacrolimus). cyclosporine hirsutism, gum hyperplasia. tacrolimus hyperglycemia, alopecia.
  22. target of rapamycin (mTOR) inhibitors MOA
    binds and inhibits mTOR, stopping cell cycle progression. immunosuppressant/antineoplastic effects include inhibition of VEGF, proliferation, activation, and possibly more.
  23. target of rapamycin (mTOR) inhibitors indication
    transplant medicine
  24. target of rapamycin (mTOR) inhibitors interactions
    mTOR inhibitors + calcineurin inhibitors = greater risk of nephrotoxicity
  25. target of rapamycin (mTOR) inhibitors SE
    messes with systems that have high cell turnover. also interstitial pneumonitis, metabolic effects (hyperglycemia, hyperlipidemia)
  26. glatramoids MOA
    competes for binding to MHC II molecules on antigen presenting cells, and induces Th suppressor cells. these antiinflammatory factors may facilitate remyelination and provide a protective effect for axons.
  27. glatiramer indication
    MS

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