pharm - oncology.txt

  1. alkylators MOA
    trasfer alkyl (chemical) groups to DNA, leading to strand breakage and the death of the cell. nitrosoureas (ie. bendamustine) also carbamoylate proteins, limiting the ability of cells to repair their DNA.
  2. alkylators kinetics
    cyclophosphamide PO, bendamustine IV. nitrosureas lipophilic so good CNS penetration.
  3. alkylators contraindications
    cyclophosphamide leukopenia, thrombocytopenia.
  4. alkylators SE
    toxicities (pulmonary, kidney, bladder), hemorrhagic cystitis, leukemia.
  5. anthracyclines MOA
    prevent the resealing of DNA by topoisomerase II, resulting in a large number of DNA fragments that eventually prompt apoptosis. also produce free radicals, damaging membranes/proteins/lipids. also intercalate, inhibiting transcription/replication.
  6. anthracyclines kinetics
    doxorubicin is a prodrug, converted to idarubicin. doxorubicin sequested in liposomes (avoids cardiotoxicity).
  7. anthracyclines contraindications
    severe cardiac disease
  8. anthracyclines interactions
    anthracyclines + trastuzumab = bad for heart
  9. anthracyclines SE
    cardiotoxicity, mucositis/stomatitis, soft tissue necrosis.
  10. antimetabolites MOA
    folate antagonists inhibit DHFR, which is required for purine synthesis.
  11. antimetabolites MOA
    interfere with one or more enzymes or reactions needed for DNA synthesis
  12. antimetabolites kinetics
    methotrexate doesn't cross the BBB, so interthecal administration if needed there
  13. antimetabolites interactions
    folate analogues + other drugs secreted in the proximal tubule (ie. aspirin) = reduced clearance
  14. antimetabolites SE
    GI (epithelial damage, stomatitis), pneumonitis, nephro/hepatotoxicity, dermatitis, defective oogenesis/spermatogenesis. mercaptopurine hepatotoxicity. fludarabine altered mental status, seizures.
  15. bleomycin MOA
    intercalates into DNA
  16. bleomycin SE
    cutaneous (hyperpigmentation, hyperkeratosis, erythema, ulceration). interstitial pneumonitis/fibrosis.
  17. bleomycin bonus
    unlike most agents, bleomycin causes minimal bone marrow suppression so it is often included in many regimens.
  18. platinum compounds MOA
    the platinum ions cross-link DNA strands, inhibiting synthesis/function. if damaged enough, cell will undergo apoptosis.
  19. platinum compounds SE
    tinnitus, hearing loss, peripheral neuropathy. nephrotoxicity (especially cisplatin).
  20. platinum compounds bonus
    myelosuppression less severe with platinum compounds than with other conventional drugs. pre/post infusion with calcium and magnesium used to help prevent neuropathy.
  21. taxanes MOA
    microtubule inhibitors (specifically, binds to b-tubulin, stabilizing it so it can't dissolve like it is supposed to). tubules are key to chromosome segregation during mitosis.
  22. taxanes indications
    prevention of restenosis after angioplasty
  23. taxanes contraindications
    severe hepatic impairment
  24. taxanes SE
    neurotoxicity, resistant fluid retention (pretreat c dexamethasone), (hypersensitivity to solvent, not drug)
  25. topoisomerase inhibitors MOA
    camptothecins inhibit topoisomerase I (single stranded DNA), while polophyllotoxins inhibit topoisomerase II (double stranded DNA), blocking the resealing of breaks in the DNA (fragmented DNA leads to cell death).
  26. topoisomerase inhibitors kinetics
    IV. etoposide also PO.
  27. topoisomerase inhibitors contraindications
    topotecan severe bone marrow suppression, severe renal impairment. ironotecan concomitant use with potent CYP3A4 inhibitors (ketoconazole).
  28. topoisomerase inhibitors SE
    interstitial lung disease. ironotecan severe diarrhea (tx early onset = atropine, severe late onset = loperamide). etoposide hypersensitivity, transient hypotension.
  29. topoisomerase inhibitors bonus
    pts with UGT1A1*28 polymorphism will have reduced metabolism of irinotecan (10% of the population).
  30. vinca alkaloids MOA
    microtubule inhibitors (inhibits b-tubulin polymerization), preventing chromosomes from aligning normally.
  31. vinca alkaloids kinetics
    IV but long T1/2 (1-2 days)
  32. vinca alkaloids contraindications
    neurologic diseases, intrathecal administration, severe bone marrow suppression.
  33. vinca alkaloids SE
    peripheral neuropathy. vinblastine has least neurotoxicity.
  34. vinca alkaloids bonus
    vincristine least likely to suppress bone marrow, so more likely in hematologic cancer regimens.
  35. GnRH analogues kinetics
    goserelin/leuprolide both long-acting (1+ month) injections. buserelin can be a nasal spray.
  36. GnRH analogues contraindications
    undiagnosed vaginal bleeding
  37. GnRH SE
    related to either androgen deprivation or estrogen deprivation. agonists ovarian hyperstimulation syndrome. antagonists allergic reactions.
  38. angiogenesis inhibitors MOA
    bind to VEGF-A, preventing it from binding to its receptors and promoting angiogenesis.
  39. angiogenesis inhibitors SE
    GI perforation, hemorrhage, HTN, thrombosis, decreased wound healing.
  40. tyrosine kinase inhibitor targets
    HER2, EGFR, BCR-ABL, multiple
  41. tyrosine kinase inhibitor MOA
    bind to growth receptors (tyrosine kinases) that regulate cell division, prevents them from signaling to divide (often permanently "on" in cancers)
  42. tyrosine kinase inhibitor kinetics.
    all PO, reduced absorption c high fat meals.
  43. tyrosine kinase inhibitor SE
    left ventricular dysfunction, fluid retention, QT prolongation, hemorrhage, interstitial lung disease, toxicities (heart, lungs, liver).
Card Set
pharm - oncology.txt
pharm - oncology.txt