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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
chronic lymphoid leukemia in who and how common
old white men more common than CML
26
CLL risk factors
first degree relative (3 times) old white men
27
when do we treat CLL
when we get constiutional symptoms like lymphadenopathy
28
genetics for CLL linked with worse outcomes
Del 11q Del 17p
29
what is Del17p
loss of p53 - worst outcome
30
Del 17 p happens where
G2 checkpoint
31
CLL diagnosis
> 5 x 10^9 monoclonal B lymphocytes in peripheral blood
32
who do we treat in CLL
stage III-IV symptoms end organ dysfunction
33
if pt has super high white count in CLL what do we do
we dont treat a number, they not sick or symptoms
34
first line CLL if no Del 17p mutation
BTK inhibitors + anti CD20 venetoclax + obinutuzumab chemo
35
first line CLL if del 17p
no chemo BTK + CD20 venetoclax + obinutuzumab
36
BTK inhibitors
acalabrutinib zanubrutinib
37
which BTK not recommended anymore
ibrutinib - lots toxicities like afib
38
venetoclax class
bcl 2 inhibitor
39
venetoclax drug interactions
CYP3A4 and PGP
40
PGP drugs
heart drugs: carvedilol, amio, verapamil phenytoin / rifampin carbemazepine
41
venetoclax side effect/toxicity
tumor lysis syndrome (ramp up dosing)
42
what can happen when we give BTK inhibitros
peak in white / lymphocyte count transient lymphocytosis does not signify disease progression watch after 3 weeks
43
transient lymphocytosis occurs with what
BTK inhibitors
44
AML death rate
poor prognosis 5 yr 30%
45
AML arises from what
arise from single leukemic cell
46
AMl risk factors
alkylating agents topo II inhibitors most causes unknown
47
AML presentatiomn
anemia neutropenia thrombocytopenia bone pain gum hypertrophy
48
AML diagnosis
>20% blasts from bone marrow
49
gentic factor in AML that would be poor prognosis
FTL3-ITD mutation
50
drugs that target FTL31
midostaurin quizartinib
51
how does AML treatment work
induction and consolidation phase biopsy then induction and remission (counts go back up) biopsy again to confirm remission or do consolidation
52
what is consolidation in AML
if favorable: chemo unfavorabel: stem cell
53
AML treatment analogy
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
induction therapy eligible AML
cytarbaine (7 day) + anthracycline (3 day)
55
induction therapy ineligible (cant tolerate chemo)
venetoclax + azicitibine
56
what is 7+ 3
7 days cytarbine 3 days rubicin
57
cytarabine toxicity
myelosupression neutropenia
58
AML consolitadtion treatment
high dose cytarabine
59
high dose cytarbine side effects
cerebellar toxicities (check handwriting) chemical conjunctivitis`
60
acute promyelocytic leukemia is what gene
10% of AMLs t(15,17) = PML: RARA
61
acute promyelocytic leukeia treatment
trans retinoic acid arsenic trioxide
62
differentiation syndrome happens from waht
APL treatment
63
ALL most common leukemia in whatq
children
64
risk factors for ALL
predisposition gene EBV HIV
65
ALL presentation
anemia thrombocytopenia neutropenia
66
ALL diagnosis
>20 % blasts
67
ALL is what type of cell cancer
B cell mostly
68
ALL patients can have what gnetic
philidelphia chromosome TKI added to chemo
69
ALL treatment layout
induction consolidation maintenance
70
ALL can hide where>?
brain and testes give CNS prophylaxis
71
how can we do CNS prophylaxis for ALL
intrathecal chemo
72
ALL chemo treatment
CVAD hyperfractioned cyclophos vincristine doxorubicin dexamethasone THEN methylpred methotrex cytarabine
73
ALL low risk 5 year survuval ALL high risk 5 year survival
low -62% high - 5%
74
ALL treatment non chemo
blinatumumab asparaginase

PHRM 864 (28 decks)

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