AI NOVA V Review.txt

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scottrbowen
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240534
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AI NOVA V Review.txt
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2013-10-14 14:26:51
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AI NOVA 5
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  1. AI NOVA V Review
  2. Difference immunocompromised pt and imunosuppressed?
    IC: Having an impaired immune system, IS: Your immune system is suppressed by drug or radiation
  3. What’s the standard of tx for a hematologic cancer?
    HSCT
  4. Where do they harvest stem cells?
    Marrow, peripheral blood, cord blood p60
  5. 2 types of marrow transplant?
    Autologous and allogenic, auto = automatic, stem cells are exact match, usually from pt. Allo as close as possible to find. P.63
  6. Most common type of HSCT?
    Auto p.63
  7. Nephrotoxicity?
    Poisonous effect or destruction of kidney cells, serum creatinin. P.
  8. Importance of nephrotoxicity to patient?
    Can reduce body’s ability to clear blood of toxins, make have to DC AmB-d or Abelcet,limiting or complicating other med regimens, dialysis if severe
  9. Drugs can be metabolized by?
    Kidney or liver
  10. Inducer?
    Reduces blood levels of other drug
  11. Inhibitor?
    Increases blood level of other drug
  12. Importance of inducers/inhibitors?
    Because immunosuppressant drugs have narrow therapeutic threshold.
  13. Risk fx’s for invasive fungal inf?
    AB’s, steroids, ICU stay, neutropenia, diseases (leukemia, lymphpoma, AIDS), central or peripheral intravenous catheters, immunosuppressants, surgery, extensive burns, chemotherapy, p101
  14. Most common strand of yeast in humans?
    Candida Albicans p103
  15. Is cryptococcus a yeast or mold?
    Yeast
  16. Zygomycetes and aspergillus, yeast or mold?
    Mold p104
  17. Most common entry point for aspergillus?
    Lungs
  18. What is empiric therapy?
    Broad spectrum therapy without knowing species
  19. Ind for myca?
    Must have identified candida inf. – pts w/ candidemia, acute disseminated candidiasis, candida peritonitis and abscesses; esophageal candidiasis; prophylaxis for candida inf in pts undergoing HSCT P 133
  20. How many echinos?
    3, myca, cancidas, eraxis
  21. What is the philosophy of antifungal stewardship?
    Right drug, right pt, right dose, right time. P.8
  22. Where do the echinos target activity?
    Fungal cell wall.
  23. Why important that echinos target that area?
    Humans don’t have cell walls, lower ae’s.
  24. Are echinos fungicidal or static?
    Cidal, except Cancidas w/ aspergillus is static
  25. Cidal?
    Kills.
  26. Static?
    stops growth p12
  27. Panel questions….
  28. State what makes each drug different
  29. Features and benefits?
  30. Caspo messaging?
    H2H data, no loading, no refrig, Pyxis reduce hang time, minibagplus.
  31. Eraxis messaging?
    No loading dose, refrig, Pyxis, no head to head, no ped ind, drug interaction studies p13.
  32. Indications, Caspo vs Myca?
    Caspo has empiric, myca is treatment.
  33. Aspergillus indication with Caspo?
    Ambisome, static activity with echinocandins. Cancidas refractory only. P14.
  34. #1 studied echino?
    Myca
  35. Why no loading dose w/ Myca?
    Reaches therapeutic levels w/i 2hrs and maintains for 24 hour dosing cycle
  36. Why is the d2d w/ cyclosporine an important issue?
    Immunosuppressed, changes drug levels. Ask about who makes those changes when pt leaves hosp setting.Who makes sure dose is readjusted when pt clear? Can lead to rejection. P15.
  37. Eraxis…no data doesn’t mean no d2d interactions?
  38. Is there renal adj with Eraxis?
    No
  39. Loading dose w/ Eraxis?
    Yes
  40. Infusion time for Eraxis?
    • 3hrs loading, 90 minutes daily dose p17
    • Tie value into panel questions…what does it mean to hcp, pt, hosp?
    • More time on pump, can’t run another drug at the same time, requires dedicated line, timing of medication important, may delay other drugs dosed. P19
  41. Why is Pyxis important? p20
    Hang time, Refrig space, Pt movement/discharge
  42. Azoles cidal or static candida?
    Static
  43. 3 azoles?
    Fluconazole, Voriconazole, Posiconazole
  44. Largest challenge with Posi?
    Oral suspension w/ high fat meal
  45. Where do azoles target?
    Cytoplasm
  46. Most common azole?
    Fluconazole
  47. Why azoles?
    Safe, cheap, effective
  48. Md using fluconazole. What would you say?
    Shifting etiology, Lack of coverage for non-albicans p24 and 25
  49. Vori: Formulations?
    Oral and IV, susp
  50. Is it an advantage that Vori has a broader spectrum of activity than Myca?
    • Could be, but risk of those species is low, could lead to cross resistance. IDSA says don’t use azole if prior azole exposure. IDSA says must switch classes, not just meds. IDSA doesn’t define “recent” P27
    • Could tie in readmittance and Medicare not paying.
    • If on fluconazole for prophylaxis, must change
  51. Max does of Myca?
    896mg, did not see increase in toxicity
  52. Posi advantage?
    Zygomycetes p30
  53. Where do the polynes target activities on the fungal cell?
    Membranes, more toxic to human cells because can target human cells
  54. Ampho B advantages?
    No resistance, Cidal/effective, Cheap
  55. Ampho B Disadvantages?
    Nephrotoxicity, Toxic to human cells, cell membrane p36
  56. 2 major saftety challenges with deoxy?
    • Nephrotoxcitity
    • Inf related rxs
  57. Abelcet – same amount of data as Ambisome?
    Not even close
  58. What does data between Abelcet and AmBisome show?
    Less nephrotoxicity, Less irr, Lead to less dc’s
  59. Perceived advantage of Abelcet over deoxy
    Less nephrotox
  60. MOA of Ambisome?
  61. Is there h2h data deoxy v Ambisome?
    Safety and efficacy data showed less nephrotoxicity, comparable efficacy
  62. What drug is killing fungus in AmBisome?
    Amphotericin B p40/41

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