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PHM 703: Crit Care/Heme/Onc > Onco 1: Leukemia > Flashcards

Onco 1: Leukemia Flashcards

1
Q

Anthracycline (class) ADR

A
  • myelosuppression - drop blood count (kind of what we want it to do in treatment of leukemia)
  • cardiac tox (life time dose to reduce risk of HF)
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2
Q

cytarabine HiDAC ADR

hidac - high dose

A
  • neurotox (cerebellar/motor area)-> neuro check prior to each dose
  • conjunctivitis -> give dexamethasoe eye drops Q6H (or artificial tears Q1-2H) during and 3 days after HiDAC is compelte
  • hand-foot syndrome (palmar rash)
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3
Q

gemtuzumab ozogamicin ADR

A
  • infusion related reaction -> premedicate with APAP, benadryl, methylprednisolone
  • hepatotox: including fatal veno-occlusive disease
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4
Q

azacitidine ADR

HMA

A
  • constipation -> standing bowel regimen
  • low-moderate emetogenicity -> pre medicate with ondansetron
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5
Q

secondary AML

A
  • ## secondary prior to chemo; much poorer outcomes

  • anthracyclines
  • alkylators
  • topoisomerase inhibitors
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6
Q

cytogenetics and AML

A
  • predict ability to obtain remission with induction chemo, risk of relapse, and overall survival
  • looks at chromosomal abnormalities in leukemia cells
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7
Q

FMS-like tyrosine kinase (FLT3) mutation

AML

A
  • targetable proliferative mutation
  • has subtypes

  • internal tadem duplication (ITD) - worse prognosis
  • tyrosine kinase domain (TKD)
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8
Q

isocitrate dehydrogenase (IDH) mutation

AML

A

IDH 1 and 2 are targetable mutations

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9
Q

risk stratification in AML

A
  • based on cytogenetics and mutatiosn
  • idnetifies prognosis relative to relapse (risk of relapse after remission)
  • poor and intermediate risk likely to relapse without stem cell transplant
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10
Q

“clogged pipe”

AML

A
  • hypercellular bone marrow: immature cells otugrow all other cells - crowding out -> cytopenia
  • goal of AML treatment is hypocelllular to allow for normal hematopoeisis
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11
Q

hyperleukocytosis

A
  • onco emergency
  • can present with hyperviscosity syndrome (“blood sludging”)
  • can present with
    - SOB
    - vision change
    - stroke
    - retinal hemorrhage
    - resp failure
    - cardiac ischemia
    - renal failure
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12
Q

management of hyperleukocytosis

A

hydroxyurea: “count control”, it suppresses it until we can acutely treat - use until pt clinally stable and ready to start chemo

dose is whatever works tbh

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13
Q

hydroxyurea MOA

A

ribonucleotide reductase inhibitor

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14
Q

hydroxyurea ADR

A
  • N/V/D
  • TLS
  • long term tox: unlikely to occur in the treatment of hyperleukcytosis dt short duration
    - cutaneous vasculitic ulcerations
    - mucositis
    - alopecia
    - hyperpigmentation
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15
Q

AML: who qualifies for aggressive induction chemo

A
  • <60
  • > 60 with NO signficiant comorbidites
  • aggressvie dsiease
  • canditiate for transplant
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16
Q

aggressive inductio chemo treatment pathway for AML

A
  1. cytarabine 7 days+ anthracyline 3 days (daunorubicin or idarubacin)
  2. bone marrow biopsy at day 14
  3. if pt leukemia free at bone biopsy: wait for count recovery and re-biopsy for documentation of complete remission; if NOT, reinduction or salvage therapy
  4. after complete remission: consolidation and consderation for bone marrow transplant

in step 1 can use lipossomal daunorubicin/cytarbine if pt qualifies

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17
Q

what is considered leukemia free at day 14 in AML?

A

bone biopsy
- 5-10% blasts
- hypocellular
- < 10-20% cells

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18
Q

what is cosidered complete remission in AML?

A
  • <5% blasts
  • ANC > 1000
  • plts > 100,000
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19
Q

what to do if pt fails reinduciton or salvage therapy in AML?

A

switch over to supportive care/comfort measures

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20
Q

treatment for pts who did NOT qualify for aggressive induction chem in AML

A
  • low-intensity chemo
    • azacitidine + venetoclax
    • if pt has IDH1: ivosidenib+venetoclax
    • if pt qualifies: gemtuzumab ozogamicin
  • if pt progresses, switch to supportive care/comfort measures

pts who go down this route do NOT receive curative treatment

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21
Q

venetoclax DDI

A

azole antifungals -> dose reduce

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22
Q

relapse AML treatment

A
  • venetoclax if pt has NOT received it in the past
  • targeted relapse treatment
    - gilteritinib: FLT - ITD or TKD
    - ivosidenib: IDH1
    - enasidenib: IDH2
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23
Q

AML consolidation treatment

A
  • pts with favorable outcomes:high dose cytarabine (HiDAC)
    - give with growth factor (do NOT give growth facotrs to plts with active AML)
  • pt who have intermediate/high risk: can get stem cell trasplant
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24
Q

growth factor ADR

A

bone pain (treat with claritin)

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25
Q

AML inductio chemo: 7+3

A
  • day 1-7: chemo admin (ADR: N/V, GI, fatigue)
  • day 8-24: cell count nadir, plt transfusion, recovery (ADR: fatigue, fever, infection, high RBC)
  • day 25+: complete cell count recovery - dcc from hospital once ANC > 500 and pt no longer transfusion dependent
26
Q

AML additive agents to induction 7+3

A
  • FLT3-ITD: quizartinib o days 8-21 of induciton and 6-19 of consolidation
  • FLT3-TKD (and technically ITD): midostaurin BID with food on days 8-21 of induction and consolidation
  • favorable/intermediate cytogenetics: gemtuzumab ozogamicin on days 1, 4, 7 of induction and day 1 of consoldiaiton
27
Q

quizartinib ADR

A

cardiac (QT prolongation)

28
Q

midostaurin ADR

A

smell so bad pts throw up

29
Q

when to use liposomal daunorubicin/cytarabine instead of 7+3 in aggressive AML induction therapy

A

in pts with t-AML or AML with myelodysplatic related changes (AML-MRC)

better outcomes than 7+3 in secondary AML

30
Q

mutation of interest in CML

A

9;22 translocation (philadelphia chromosome)

test for prior to treatment, if pt doesn’t have, it’s likely not CML

31
Q

CML presentation

A
  • mostly asymp
  • splenomegaly
  • WBC > 25 x 10^9
32
Q

chronic phase CML

A
  • <10% blasts
  • treatment: TKI
  • treatment goal: delayed progression, eradicate Ph chromosome
33
Q

accelerated phase CML

A
  • blasts 10-19%
  • treatment: TKI (at probs a higher dose than chronic phase)
  • treatment goal: control WBC, go back to chronic phase and avoid progression
34
Q

blast phase CML

A
  • blasts > 20%
  • treatment: treat like AML and slap on a TKI
  • treatment goal: suvivie iduciton, bridge to allogenic stem cell transplant
35
Q

TKI class ADR

A
  • myelosuppresision
  • transaminitis
  • electrolyte changes
36
Q

TKI agents by generation

A
  • 1st gen: imatinib
  • 2nd gen: dasatinib, nilotiib
  • 3rd: bosatinib, polatinib
  • other; asciminib (binds ot Myristoyl pocket instead of ATP pocket)
37
Q

which TKIs need to be dose adjusted in hepatic impairment

A
  • imitinib
  • nilotinib
  • bosutinib
  • ponatinib
38
Q

whcih TKIs need to be dose adjusted in renal impairment

A

imitanib

39
Q

T315I mutation

A
  • the “gatekeeping mutation”
  • mutation that prevents most TKIs from working
  • treat the CML with ascimiib (preferred) or ponatinib
40
Q

CML treatment monitoring

A

molecular response: look at transcript level of fusion protein (which leads ot proliferation) -> quantifiy amount of that protein in your blood

41
Q

CML treatment: BCR-ABL goal

A
  • @ 3 months: BCR-ABL < 10%
  • @ 6 months: < 1%
  • @ 12 months: < 0.1%

if not meeting goal, look into reaosns why

42
Q

picking a TKI

A

low/intermediate risk: dasatinib preferred dt tolerability
- can also just do
- bosutinib
- nilotinib
- imatinib (not preferred in intermedate)

43
Q

CML remssion treatmetn

A

can actually dc a TKI if pt is completely in remssion and meets other strict requirements

44
Q

imatinib off target effect

A

inhibits
- PDGFR
- c-KIT

45
Q

imatinib ADR

A

fluid build up: peripheral edema

46
Q

imatinib: DDI

A

CYP 3A4 substrate and nihibitor

47
Q

dasatinib off target effects

A

inhibits
- PDGFR
- c-KIT
- Src family kinases

results in edema

48
Q

dasatinib ADR

A

fluid build up: pleural effusions

49
Q

dasatinib DDI

A

CYP3A4 substrate

50
Q

dasatinib admi

A

needs acidic environment to absorb -> no H2RA or PPI

51
Q

nilotinib ADR

A

cardio (Qt porlongation, arrhythmias)

52
Q

nilotinib admin

A

BID on ann empty stomach

53
Q

nilotinib DDI

A
  • CYP3A4 substrate and inhibitor
  • CYP 2C8, 2C9, 2D6 action
54
Q

bosutinib off target effects

A

ihibits
- Src kinases
- Lyn kiases
- Hck kinases

in terms of on-target effects has activity against a lot of mutations that early drugs don’t, however, does NOT cover T315I or V299L

55
Q

bosutinib ADR

A

diarrhea for first 2 weeks

56
Q

bosutinib DDI

A

CYP3A4 substrate

57
Q

poatinib off targe effects

A

inhibits
- VEGFR
- PDGFR
- Src kinases
- FGFR
- FLT3
- RTK
- TIE2

active agaist all mutaitons

58
Q

ponatinib ADR

A
  • vascular occlusion - ppx asa
  • HF
  • hepatotox

it’s very poorly tolerated

58
Q

ponatinib DDI

A

CYP 3A4 substrate

59
Q

indication for asciminib

A
  • if pt has T315I mutaiton or
  • if pt has received 2+ TKi in past

CML

60
Q

asciminib admi

A

empty stomach

PHM 703: Crit Care/Heme/Onc (16 decks)

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