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PHRM 864 > leukemia > Flashcards

leukemia Flashcards

1
Q

chronic myeloid leukemia survual

A

70%

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2
Q

how common is leukemia

A

3%

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3
Q

philidelphia chromosome in what disease state

A

chronic myeloid leukemia

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4
Q

what is the philidelphia chromosome

A

BcrABL - constitutively active tyrosine kinase oncogene
9 and 22

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5
Q

CML risk factors

A

atomic bomb
ionizing radiation

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6
Q

is CML familial

A

no

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7
Q

CML presentation

A

leukostasis - medical emergency
thick blood
- confusion
- stroke

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8
Q

what is leukostasis

A

white blood cell count can be in millions

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9
Q

tests we can do to find CML

A

FISH - fluorescence in situ
PCR - measures pos genes

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10
Q

90% of patients will be in what phase CML

A

chronic phase
<10% blasts

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11
Q

phases of CML

A

chronic
accelerated
blast crisis

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12
Q

CML treatment for cure

A

allogenic hematopoetic stem cell transplant

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13
Q

what is allogenic stem cell transplant

A

cells from a donor

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14
Q

CML common treatment

A

tyrosine kinase inhibitors
1st gen: imatinib
2nd gen: nilotinib, dasatinib, bosutinib
3rd gen: ponatinib
T315I: ascitinib, ponatinib

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15
Q

CML treatment monitoring for molecular response done how and with what responses

A

early BCR-ABL <10% at 3 and 6 month
major: <0.1%
deep: <0.01% - best

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16
Q

imatinib side effect

A

nausea

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17
Q

dasatinib side effect

A

fluid retention
pleural effusion

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18
Q

nilotinib side effect

A

QTC prolongation
metabolic syndrome

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19
Q

bosutinib side effect

A

diarrhea

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20
Q

ponatinib side effect

A

HTN
ischemic reactions
vascular occlusion

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21
Q

dasatinib consideration

A

avoid acid reducers

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22
Q

nilotinib consideration

A

BID

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23
Q

which drug used for T135I mutation

A

ponatinib, ascitinib

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24
Q

when can CML patients take a drug holiday

A

deep molecular response for 2 years (<0.01%)
must be on TKI for 3 years

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25
Q

chronic lymphoid leukemia in who and how common

A

old white men
more common than CML

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26
Q

CLL risk factors

A

first degree relative (3 times)
old white men

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27
Q

when do we treat CLL

A

when we get constiutional symptoms like lymphadenopathy

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28
Q

genetics for CLL linked with worse outcomes

A

Del 11q
Del 17p

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29
Q

what is Del17p

A

loss of p53 - worst outcome

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30
Q

Del 17 p happens where

A

G2 checkpoint

31
Q

CLL diagnosis

A

> 5 x 10^9 monoclonal B lymphocytes in peripheral blood

32
Q

who do we treat in CLL

A

stage III-IV
symptoms
end organ dysfunction

33
Q

if pt has super high white count in CLL what do we do

A

we dont treat a number, they not sick or symptoms

34
Q

first line CLL if no Del 17p mutation

A

BTK inhibitors + anti CD20
venetoclax + obinutuzumab
chemo

35
Q

first line CLL if del 17p

A

no chemo
BTK + CD20
venetoclax + obinutuzumab

36
Q

BTK inhibitors

A

acalabrutinib
zanubrutinib

37
Q

which BTK not recommended anymore

A

ibrutinib - lots toxicities like afib

38
Q

venetoclax class

A

bcl 2 inhibitor

39
Q

venetoclax drug interactions

A

CYP3A4 and PGP

40
Q

PGP drugs

A

heart drugs: carvedilol, amio, verapamil
phenytoin / rifampin
carbemazepine

41
Q

venetoclax side effect/toxicity

A

tumor lysis syndrome (ramp up dosing)

42
Q

what can happen when we give BTK inhibitros

A

peak in white / lymphocyte count
transient lymphocytosis
does not signify disease progression
watch after 3 weeks

43
Q

transient lymphocytosis occurs with what

A

BTK inhibitors

44
Q

AML death rate

A

poor prognosis
5 yr 30%

45
Q

AML arises from what

A

arise from single leukemic cell

46
Q

AMl risk factors

A

alkylating agents
topo II inhibitors
most causes unknown

47
Q

AML presentatiomn

A

anemia
neutropenia
thrombocytopenia
bone pain
gum hypertrophy

48
Q

AML diagnosis

A

> 20% blasts from bone marrow

49
Q

gentic factor in AML that would be poor prognosis

A

FTL3-ITD mutation

50
Q

drugs that target FTL31

A

midostaurin
quizartinib

51
Q

how does AML treatment work

A

induction and consolidation phase
biopsy then induction and remission (counts go back up)
biopsy again to confirm remission or do consolidation

52
Q

what is consolidation in AML

A

if favorable: chemo
unfavorabel: stem cell

53
Q

AML treatment analogy

A

spray the weeds and flowers, wait to see what grows back
if only flowers - complete remission
if weeds too - need to do something else

54
Q

induction therapy eligible AML

A

cytarbaine (7 day) + anthracycline (3 day)

55
Q

induction therapy ineligible (cant tolerate chemo)

A

venetoclax + azicitibine

56
Q

what is 7+ 3

A

7 days cytarbine
3 days rubicin

57
Q

cytarabine toxicity

A

myelosupression
neutropenia

58
Q

AML consolitadtion treatment

A

high dose cytarabine

59
Q

high dose cytarbine side effects

A

cerebellar toxicities
(check handwriting)
chemical conjunctivitis`

60
Q

acute promyelocytic leukemia is what gene

A

10% of AMLs
t(15,17) = PML: RARA

61
Q

acute promyelocytic leukeia treatment

A

trans retinoic acid
arsenic trioxide

62
Q

differentiation syndrome happens from waht

A

APL treatment

63
Q

ALL most common leukemia in whatq

A

children

64
Q

risk factors for ALL

A

predisposition gene
EBV
HIV

65
Q

ALL presentation

A

anemia
thrombocytopenia
neutropenia

66
Q

ALL diagnosis

A

> 20 % blasts

67
Q

ALL is what type of cell cancer

A

B cell mostly

68
Q

ALL patients can have what gnetic

A

philidelphia chromosome
TKI added to chemo

69
Q

ALL treatment layout

A

induction
consolidation
maintenance

70
Q

ALL can hide where>?

A

brain and testes
give CNS prophylaxis

71
Q

how can we do CNS prophylaxis for ALL

A

intrathecal chemo

72
Q

ALL chemo treatment

A

CVAD
hyperfractioned cyclophos
vincristine
doxorubicin
dexamethasone
THEN
methylpred
methotrex
cytarabine

73
Q

ALL low risk 5 year survuval
ALL high risk 5 year survival

A

low -62%
high - 5%

74
Q

ALL treatment non chemo

A

blinatumumab
asparaginase

PHRM 864 (23 decks)

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