Pharmacology: Antineoplastics II - 3

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Pharmacology: Antineoplastics II - 3
2014-04-18 13:00:30
Pharmacology Antineoplastics II

Pharmacology: Antineoplastics II - 3
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  1. What is the con to using Nanoparticle albumin-bound  paclitaxel (Abraxane) over normal paclitaxel?
    More expensive
  2. What is the MOA of Paclitaxel?
    Causes the buildup of the microtubules rather than allowing free tubulin dimers to form
  3. What are the side effects of paclitaxel?
    • Myelosuppression (neutropenia, less with nano-particle form)
    • Peripheral neuropathy
    • Hypersensitivity (unless pretreated with corticosteroid and antihistamines or using nano-particle form)
    • Radiation recall
    • Cardiotoxic (bradychardia)
  4. What are the side effects of docetaxel?
    • Myelosuppression
    • Less peripheral neuropathy than paclitaxel
    • Less severe hypersensitivity than paclitaxel
    • More fluid retention than paclitaxel
  5. Are taxanes used to treat Leukemia?
    No, mostly solid tumors
  6. Which can cause cardiac arrhythmias, paclitaxel or doxetaxel?
  7. What are the Topioisomerse II inhibitors?
    Epidophyllotoxins = Etoposide (Ve Pesid)
  8. What is Etoposide (Ve Pesid) derived from?
    Mandrake or May apple tree
  9. What is the MOA for Etoposide?
    Inhibits topoisomerase II DNA repair enzymes and thus the resealing of DNA strand breaks 
  10. What are the indications for etoposide?
    Solid tumors
  11. What are the side effects for etoposide?
    Bone marrow, GI, vesicants, secondary leukemias, radiation recall
  12. What drugs might you give with Etoposide to lower the amount needed and reduce bone marrow effects?
    Cisplatin or Bleomycin
  13. What are the Topoisomerase I inhibitors?
    • Camptothecins:
    • Topotecan
    • Irinotecan
  14. What is the MOA of Topoisomerase I inhibitors?
    • 1)Drugs bind to DNA-topoisomerase I complex ( which relieves torsional strain in DNA during DNA replication by creating reversible single-strand breaks)
    • 2)Prevents repair of the strand breaks 
    • 3)Impairs DNA replication
  15. topotecan (Hycamtin) is given by what route?
  16. What are the indications for topotecan (Hycamtin)?
    Solid tumors
  17. What are the side effects for topotecan (Hycamtin)?
    Bone marrow suppression
  18. Irinotecan (Camptosar) is given by what route?
  19. Which Topoisomerase I is a prodrug?
  20. What are the indications for Irinotecan?
    • Very specific:
    • Metastatic cancer of the colon or rectum
  21. What are the side effects of Irinotecan?
    Severe diarrhea and myelosuppression
  22. What are the antibiotic groups that are used as antineoplastics?
    • Anthracenes/Anthracyclines
    • Bleomycin
    • L-Aspariginase
    • Pegasparagase
  23. What are the Anthracenes and Anthracyclines?
    • Doxorubicin (Adriamycin or Hydroxydaunorubicin)
    • Doxorubicin-liposomal (Doxil)
    • Daunorubicin (Cerubidine) 
    • Idarubicin (Idamycin)
    • Epirubicin (Ellence)
  24. What stage of the cell cycle do  Anthracenes and Anthracyclines inhibit?
    Non-stage specific
  25. What regimen does Doxorubicin fit into, CHOP or ABVD?
  26. What is the ending for a Anthracycline?
  27. Why would you give doxorubicin in a liposomal formulation?
    Increases the surface area and increases absorption
  28. What is the MOA of anthracyclines?
    • Intercalates  DNA
    • Distorts the structure 
    • RNA polymerase cannot use DNA as a template.
    • Also binds to topoisomerase II (inhibiting DNA repair)
  29. How are anthracyclines administered?
  30. Do anthracyclines have vesicant properties?
  31. What effects do anthracylclines have on the urine?
    Turns it red
  32. Anthracyclines can cause a cardiotoxic reaction, what is this reaction dependant on?
  33. What is the antidote for the cardiotoxic reaction caused by anthracyclines?
    • Dexrazoxane is a maybe ( iron chelator)
    • May inhibit Doxorubicin’s ability to operate
  34. What are the side affects of Doxorubicin and other anthracyclines?
    • Cardiac toxicity (irreversible):  arrhythmias, congestive heart failure
    • Myelosuppression
    • GI
    • radiation recall
  35. What is the mechanism for cardiac toxicity caused by doxorubine and other anthrocyclines?
    • CYP P450 system forms a superoxide anion causing free radical reactions in the presence of iron. 
    • Heart has little peroxidase enzymes to remove toxic products
  36. Doxorubicin and Anthrocyclines are used to treate what?
    Solid tumors and Leukemias
  37. What are the routes of administration for Bleomycins?
    IM and IV
  38. What type of molecule is bleomycin?
  39. What is the MOA for Bleomycin?
    Binds to DNA forming a bleomycin-iron-oxygen complex which breaks DNA
  40. What are the side effects of Bleomycin?
    • Pulmonary fibrosis and toxicity (potentially fatal)
    • Anaphylactic reactions
    • Fever
    • Hyperkeratosis – blistering 
    • G.I.
    • (very little bone marrow toxicity)  Important for combination therapy.
  41. What are the indications for Bleomycin?
    Testicular cancer
  42. What is the route of administration for L-aspariginase?
    IV or IM
  43. What is the MOA of L-asparaginase (Elspar) and pegasparagase (Oncaspar)?
    • Breaks down Asparagine to ammonia and aspartic acid
    • Limits protein synthesis in cancer cells requiring large amount of Asparagine for growth (ALL/Leukemia)
  44. What are the indications for L-asparaginase (Elspar) and pegasparagase (Oncaspar)? 
    Acute lymphocytic leukemia (require L-asparagine)
  45. What are the side effects of L-aspariginase?
    • Hypersensitivity (E. coli derived)
    • CNS neurotoxicity
    • Fever
    • Liver and kidney damage pancreatitis (excess NH3)
    • Coagulation deficiencies (reduces synthesis of coagulation factors)
  46. Is L-asparaginase cytotoxic?
    No, does not cause toxicity to bone marrow, gastrointestinal tract, and hair follicles
  47. Arsenic Trioxide (As2O3)—(Trisenox) is used for what type of cancer?
    • Differentiating Agents for Acute Promyelocytic Leukemia (APL)
    • APL in patients refractory to first line therapy of tretinoin or anthracycline based therapy
  48. What is the route of administration for Arsenic Trioxide (As2O3)—(Trisenox) 
  49. What is the mechanism of Action for Arsenic Trioxide (As2O3)—(Trisenox)?
    • Induces differentiation of promyelocytic leukemia cells and induces apoptosis:
    • Translocation produces the fusion protein PMS-RARα
    • Arsenic binds to PML-RARα in a region containing zinc fingers (arsenic binds instead of zinc) 
    • Stimulates SUMOylation , ubiquitination, and degradation of the PML-RARα protein
    • Allows partial differentiation of leukemic promyelocytes and eliminates leukemia-initiating cells
  50. What are the side effects of Arsenic Trioxide (As2O3)—(Trisenox)?
    Rash, nausea, vomiting, tachycardia, QT prolongation (EKG) leading to ventricular
  51. Would you expect bone marrow suppression with Arsenic Trioxide (As2O3)—(Trisenox)?
  52. What is the route of trentoin administration?
  53. What is the mechanism of action for Trentoin?
    • Induces differentiation of acute promyelocytic cells to normal myelocytic cells
    • It acts by binding to a nuclear receptor and affects transcription
  54. What is the indication for Trentoin?
    APL in patient’s refractory to first line anthracycline based therapy
  55. What are the side effects of Trentoin?
    Vit A toxicity, fever, skin dryness and rash, CNS toxicities, teratogenic
  56. Should you be taking a multivitamin when using Trentoin?
    Not if it has Vitamin A in it