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PHRM 864 Therapeutics > Exam 2 - HM 2 Leukemias Grove > Flashcards

Exam 2 - HM 2 Leukemias Grove Flashcards

1
Q

what genetic abnormality is associated with CML (~95% of pts)? How does it work?

A

Philadelphia chromosome (chromosome 22; BCR-ABL fusion gene causes constitutively active TK -> uncontrolled WBC growth)

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2
Q

what presentation of CML can be a medical emergency?

A

leukocytosis (very high WBC count) can lead to leukostasis (includes organ dysfunction)

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3
Q

T or F: PCR or FISH can be used to see if something is causing dysregulation of WBCs

A

T

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4
Q

CML 3 phases

A

chronic phase (CP) - 90% of pts at diagnosis
accelerated phase (AP)
blast crisis (BC)

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5
Q

what is the only way to cure CML?

A

allogenic hematopoietic stem cell transplant (HSCT)

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6
Q

which of the following drugs are approved first line for CML?

a. imatinib
b. dasatinib
c. nilotinib
d. bosutinib
e. all of the above

A

e. all of the above

(imatinib prob most used, then others could be 2nd line as well)

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7
Q

TKI SE: nausea

a. imatinib
b. dasatinib
c. nilotinib
d. bosutinib
e. ponatinib

A

a. imatinib

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8
Q

TKI SE: fluid retention (pleural effusion)

a. imatinib
b. dasatinib
c. nilotinib
d. bosutinib
e. ponatinib

A

b. dasatinib

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9
Q

TKI SE:
-QTc prolongation
-metabolic syndrome

a. imatinib
b. dasatinib
c. nilotinib
d. bosutinib
e. ponatinib

A

c. nilotinib

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10
Q

TKI SE: diarrhea

a. imatinib
b. dasatinib
c. nilotinib
d. bosutinib
e. ponatinib

A

d. bosutinib

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11
Q

TKI SE:
-ischemic rxn
-vascular occlusion
-HTN

a. imatinib
b. dasatinib
c. nilotinib
d. bosutinib
e. ponatinib

A

e. ponatinib

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12
Q

with which TKI for CML should we avoid acid reducers?

a. imatinib
b. dasatinib
c. nilotinib
d. bosutinib
e. ponatinib

A

b. dasatinib

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13
Q

which CML drugs work in T315l mutations? SELECT ALL THAT APPLY

a. imatinib
b. bosutinib
c. asciminib
d. omacetaxine
e. dasatinib
f. ponatinib

A

c, d, e

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14
Q

what is the “deep molecular response” for CML?

A

BCR-ABL of 0.01% or less; means reduction in leukemia cells and pt might be able to discontinue

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15
Q

how long must a pt be on a TKI for CML?

A

3 years

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16
Q

CLL is a cancer of which cells?

A

B lymphocytes (B cells)

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17
Q

constitutional sx of CLL (5 of them; slide 38)

A

-lymphadenopathy
-hepatosplenomegaly
-peripheral lymphocyte doubling time < 6 months
-anemia (Hgb < 10)
-thrombocytopenia (plt < 100,000)

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18
Q

is CLL a slow or fast progressing disease?

A

slow (indolent)

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19
Q

two CLL cytogenetics (slide 39)

A

Del(11q), Del(17p)

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20
Q

which chromosomal deletion in CLL is associated with extensive lymphadenopathy, disease progression, and shorter median survival time?

a. del(11q)
b. del(17p)

A

a. del(11q)

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21
Q

which chromosomal deletion in CLL is associated with the loss of the TP53 gene and a poorer response to chemotherapy?

a. del(11q)
b. del(17p)

A

b. del(17p)

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22
Q

CLL diagnosis criteria needs monoclonal B lymphocytes > what value?

A

5 x 10^9 in peripheral blood

23
Q

first line oral drugs for CLL (4 of them)

A

-ibrutinib
-zanabrutinib
-acalabrutinib
-venetoclax

24
Q

what is the preferred tx for the following CLL pt?

-no deletions
-IGVH-mutated disease

a. BTK inhibitor
b. venetoclax
c. venetoclax + obinutuzumab
d. chemo-immunotherapy

A

d. chemo-immunotherapy

25
Q

look at venetoclax drug interactions (slide 52)

A

sure

26
Q

which CLL drug has the highest risk of A fib and bleeding?

a. acalabrutinib
b. ibrutinib
c. zanubrutinib
d. venetoclax

A

b. ibrutinib

27
Q

which CLL drug can cause tumor lysis syndrome?

a. acalabrutinib
b. ibrutinib
c. zanubrutinib
d. venetoclax

A

d. venetoclax

(use a ramp-up dosing schedule to lower risk)

28
Q

what is transient lymphocytosis? what drug class can cause this?

A

Transient inc in lymphocyte count. Caused by TKI inhibitors for CLL (peaks early in tx and resolves by week 12)

29
Q

AML is due to defect in the pluripotent stem cell or a myeloid _______ stem cell

A

precursor

30
Q

AML presentation (3 things; slide 62)

A

-signs of pancytopenia (anemia, neutropenia, thrombocytopenia)
-bone pain
-gum hypertrophy

31
Q

what is used for AML diagnosis?

A

bone marrow biopsy: greater than 20% blasts

32
Q

mutation important for AML

a. T315l
b. BRAFV790E
c. FLT3
d. del(17q)

A

c. FLT3

33
Q

two steps of AML tx

A

-induction (goal: remission)
-consolidation (goal: prevent relapse)

34
Q

intensive induction tx for AML (2 drugs)

A

cytarabine + anthracyline (7+3 regimen)

35
Q

consolidation therapy for AML (3 options)

A

-3-4 cycles of high dose cytarabine
-venetoclax + azacitidine
-allogenic stem cell transplant

36
Q

important SE of high dose cytarabine

A

cerebellar SE

37
Q

drug added to induction chemo on day 8 in newly diagnosed FLT3+ AML pt

a. acalabrutinib
b. midostaurin
c. imatinib
d. carboplatin

A

b. midostaurin

38
Q

2nd line therapy for AML FLT3+ disease

a. ibrutinib
b. venetoclax
c. imatinib
d. gilteritinib

A

d. gilteritinib

39
Q

subclass of AML to know

A

APL (acute promyelocytic leukemia) ~10% of AML

40
Q

APL genetic abnormality

A

t(15;17) = PML:RARA

transolocation between chromosome 15 and 17, leads to PML-RARA fusion gene, which produces abnormal protein that leads to accum of promyelocytes

41
Q

APL tx (2 drugs)

A

ATRA (all trans retinoic acid)
ATO (arsenic)

42
Q

ATRA side effect

a. differentiation syndrome
b. QT prolongation

A

a. differentiation syndrome

43
Q

differentiation syndrome: what drugs can be used for prophylaxis? what drug is used for tx?

A

prophylaxis -> steroids
tx -> hydroxyurea

44
Q

T or F: ALL is most common in pts 65+

A

F (median age at diagnosis is 17)

45
Q

ALL is caused by a defect in the lymphopoietic stem cell or an early _______ precursor

A

lymphoid

46
Q

what drug class can we add-on to multi-agent chemo in pts with Philadelphia Positive ALL?

A

tyrosine kinase inhibitor (TKI)

47
Q

which disease presentation includes painless testicular enlargement, lymphadenopathy, gum hypertrophy, and bone pain?

a. CML
b. CLL
c. AML
d. ALL

A

d. ALL

48
Q

-ALL can hide in sanctuary sites such as the _____ and _____
-all pt should receive ____ prophylaxis or tx
-most protocols include __________ __________

A

brain, testes
CNS
intrathecal chemotherapy

49
Q

ALL Ph+ maintenance tx (3 drugs)

A

TKI + vincristine + prednisone

50
Q

ALL Ph- maintenance tx (3 drugs)

A

methotrexate + 6MP + vincristine

51
Q

what are the two parts of the HyperCVAD regimen for ALL?

A

Hyper-fractionated Cyclophosphamide
Vincristine
Doxorubycin (Adriamycin)
Dexamethasone

Methotrexate + cytarabine + methylprednisolone

52
Q

what is pegasparagase?

A

drug used for ALL; breaks down asparagine, which cancer cells cannot make their own so they undergo cell death

53
Q

which of the following is FALSE about blinatumomab?

a. binds CD19 and CD3
b. first FDA approved T-cell engager
c. CRS and ICANS toxicities
d. used for CML refractory/relapsed disease

A

d. used for CML refractory/relapsed disease

(used for ALL)

54
Q

2 frequently used protocols for ALL

A

HyperCVAD or ECOG1910

PHRM 864 Therapeutics (28 decks)

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