Therapeutics - MS 1

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kyleannkelsey
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298410
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Therapeutics - MS 1
Updated:
2015-03-14 21:38:55
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Therapeutics MS
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Therapeutics - MS
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Therapeutics - MS
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  1. What MS drugs can be used for RRMS?
    All
  2. Which MS drugs can be used for CIS?
    • Interferons
    • Glatiramer Acetate (Copaxone)
  3. What MS drugs are indicated for SPMS or PRMS?
    Mitoxantrone (Novantrone®)
  4. What are the predictors of worse outcomes with MS?
    • Bladder or bowel symptoms at onset
    • Incomplete recovery from first attack
    • Short interval between first and second attack
    • Early accumulation of disability
    • African American
    • Male?
    • Older age at onset?
  5. What is the DOC for acute relapse in MS?
    Methylprednisolone 1 gram IV QD x 3-5 days
  6. What are the alternative treatments for Acute MS relapse?
    • Plasmapheresis
    • Intravenous Immune Globulin (IVIG) – Not FDA approved
  7. What drug is approved for improving walking speed in MS patients?
    Dalfampridine (Ampyra®)
  8. What is the MOA for Dalfampridine (Ampyra®)?
    Increase conduction of action potentials in demyelinated neurons by inhibiting potassium channels
  9. What are the SE/CIs of Dalfampridine (Ampyra®)?
    • Seizures – risk increases with dose so don’t double dose if one is missed
    • CI with history of seizures
  10. What is the MOA of Mitoxantrone (Novantrone®)?
    • Suppresses proliferation of T-cells, B-cells and macrophages
    • Enhances T-cell suppressor function
    • Decreases secretion or pro-inflammatory cytokines
  11. What are the SE/CIs of Mitoxantrone (Novantrone®)?
    • CI liver disease
    • CI pregnancy
    • Causes Systolic dysfunction – limit lifetime dose to 140 mg/m^2
    • Secondary acute myelogenous leukemia
    • Nausea, Alopecia and Amenorrhea
  12. What should you monitor in a patient taking Mitoxantrone (Novantrone®)?
    • LVF at baseline and before every dose (CI <50%)
    • Pregnancy prior to each dose
    • LFTs (Liver disease = CI)
    • CBC (AML)
  13. How often is Mitoxantrone (Novantrone®) dosed?
    Q3Months
  14. What is the MOA for Alemtuzumab (Lemtrada®)?
    • Targets CD52 (glycoprotein expressed on T and B cells during differentiation)
    • Targets cells for lysis
    • Decreases the number of new lesions
    • Stabilizes the BBB
  15. What are eth SE/CI for Alemtuzumab (Lemtrada®)?
    • Potentially fatal infusion reactions, 2-24 hours after injection
    • Autoimmune thyroid disorders (Graves)
    • Immune Thrombocytopenia
    • Antiglomerular basement membrane disease (goodpasture’s)
    • Malignancies (Thyroid, Melanoma and Lymphoma)
    • Clinical infections
  16. You should prophylax for herpes during and for a minimum of 2 months after the end of the infusion period OR until the CD4 count > 200 (whichever is LATER) with the use of what drug?
    Alemtuzumab
  17. What is the MOA for Dimethyl Fumarate (Tecfidera®)?
    • Activates nuclear factor [erythroid-derived 2]-like 2 (Nrf2)
    • Nrf2 is normally upregulated in response to oxidative stress
  18. What are the SE/Ci for Fumarate (Tecfidera®)?
    • Decreased lymphocytes
    • PML?
    • Flushing – antihistamine or ASA premedicate, resolve with time
  19. What is the MOA of Teriflunomide (Aubagio®)?
    • Blocks dihydroorotate dehydrogenase (DHODH)
    • Enzyme necessary for mitochonidrial pyrimidine synthesis
    • Cytostatic effect on activated lymphocytes in periphery decreasing overreactive immune responses
    • Resting lymphocytes are unaffected
  20. What are the SE/CI of Teriflunomide (Aubagio®)?
    • Teratogenicity (men and women)
    • Hepatotoxicity
    • Peripheral neuropathy
    • Acute renal failure
    • Interstitial lung disease
    • Increased infections
  21. What drug requires a rapid elimination procedure if pregnancy occurs?
    Teriflunomide (Aubagio®)
  22. What is the MOA of Fingolimod (Gilenya®)?
    • Metabolized by sphingosine kinase to the active metabolite, fingolimod-phosphate
    • Blocks capacity to egress from lymph nodes and reducing the number of lymphocytes in the peripheral blood
    • Decreases lymphocyte count by 20-30%
  23. What are the SE/CI of Fingolimod (Gilenya®)?
    • Bradyarrhythmias and Atrioventricular block
    • Infection
    • CI = MI, HF, unstable angina, stroke, TIA, Hreat block, QTc > or = to 500 msec, live vaccines
    • DDI/Ci w/ quinidine, procainamide, amiodarone, sotalol and dofetilide
    • Macular edema, Hepatic injury or PML
  24. What drug causes Bradyarrhythmias and Atrioventricular block, Infection and is CI in MI, HF, unstable angina, stroke, TIA, Hreat block, QTc > or = to 500 msec, live vaccines, has DDIs w/ quinidine, procainamide, amiodarone, sotalol and dofetilide and can cause Macular edema, Hepatic injury or PML?
    Fingolimod (Gilenya®)
  25. What is the MOA of Natalizumab (Tysabri®)?
    • Blocks α4-integrin (adhesion molecules on the lymphocyte surface) preventing linkage to VCAM-1 (vascular cell adhesion molecules found on vessel surfaces) ultimately preventing the lymphocyte from stopping to be recruited across the BBB
    • Increases the number of lymphocytes in circulation
  26. What are the SE/Ci for Natalizumab (Tysabri®)?
    • PML – screen for JCV
    • Increased infection, Hepatotoxicity
  27. What drug causes PML – screen for JCV, Increased infection, Hepatotoxicity
    Natalizumab (Tysabri®)
  28. What is the MOA of Glatiramer Acetate (Copaxone)
    Glatiramer cells secrete anti-Inflammatory IL-10 cytokines in CNS
  29. What are the SE/Ci for Glatiramer Acetate (Copaxone)?
    • Immediate post-injection reaction
    • Lipoatrophy
  30. What drug has the following MOA: Blocks α4-integrin (adhesion molecules on the lymphocyte surface) preventing linkage to VCAM-1 (vascular cell adhesion molecules found on vessel surfaces) ultimately preventing the lymphocyte from stopping to be recruited across the BBB. Increases the number of lymphocytes in circulation
    Natalizumab (Tysabri®)
  31. What drug causes: Immediate post-injection reaction and Lipoatrophy?
    Glatiramer Acetate (Copaxone)

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