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444-Oncology and Neurology > Leukemias > Flashcards

Leukemias Flashcards

1
Q

CML rseults from

A

acquired mutations + proliferation of myeloblasts

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2
Q

what is characterized by the philadelphia chromosome

A

CML

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3
Q

what is the philadelphia chromosome

A

Translocation between long arms of chromosomes 9 and 22 = joining of ABL gene of chromosome 9 and BCR gene of chromosome 22 = formation of BCR-ABL fusion oncogene
Results in super long chromosome 9 and shorter chromosome 22 (philadelphia chromosome, Ph+)

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4
Q

joining of ABL gene of chromosome ___ and BCR gene of chromosome ___= formation of BCR-ABL fusion oncogene

A

9, 22

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5
Q

what does the BCR-ABL gen cause

A

production of BCR-ABL protein = abnormal TK that has an ATP bindng site that can transfer phosphate groups to protein substrate, causing CML cells proliferate and avoid apoptosis

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6
Q

CML S/S

A

splenomegaly
suppression of hematopoiesis
leukocytosis or leukostasis
up to 50% asumptomatic due to initial indolent phase of disease

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7
Q

what is leukocytosis

A

WBC >25

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8
Q

what is leukostasis

A

WBC >100

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9
Q

dx of CML requires

A

cytogenetics for philadephia chromosome
molecular testing of QPCR
staging

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10
Q

describe the 3 stages of CML and the amount of myeloblasts

A

chronic phase <10%
accelerated phase 10-20% or persistent leukocytosis, thrombocytosis, thrombocytopenia, splenomegaly unresponsive to tx
blast crisis >20%

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11
Q

leukostasis in CML requires

A

asap hydroxyurea to rapidly lower WBCs + allopurinol to prevent tumor lysis syndrome

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12
Q

MOA of BCR-ABL TKis

A

competitively binds to ATP binding site on BCR-ABL kinase = inhibits phosphorylation of proteins involved with signal transduction for CMl clone proliferation

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13
Q

name the 3 TKis for CML

A

imatinib, dasatinib, nilotinib

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14
Q

which TKis should be taken with food

A

imatinib, dasatinib

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15
Q

which TKis should be taken without food? why

A

nilotinib - increases bioavailability

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16
Q

which TKi is acid dependent absorption

A

dasatinib

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17
Q

AEs of BCR-ABL TKis

A

myelosuppression
fluid retention
N/V
QT interval prolongation
hepatotoxicity
drug rash
diarrhea

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18
Q

which TKis has a black box warning for QT prolongation

A

nilotinib and dasatinib- baseline ECG rec

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19
Q

which TKi is most associated with fluid retention

A

dasatinib

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20
Q

reasons for Tki failure

A

compliance
drug interactions
resistance- point mutation in ABL kinase domain that activates it

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21
Q

what is the only cure for CML

A

allogenic stem cell transplant

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22
Q

can CML pts ever d/c TKis

A

yes if they’ve been on BCR-ABL TKi for at least 5yrs + undetectable disease for 2yrs consecutively (monitor QPCR q1mth)
- may result in 50% relapse rate

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23
Q

why are allogenic stem cell transplants rarely done in CML

A

cause TKis work fine
not everyone has a donor + transplant has many toxicities

24
Q

ALL sx

A

B sx like weight loss, night sweats, fever
pain in joints/ bones
CNS manifestations
cytopenias

25
Q

what is required for an ALL diagnosis

A

20% lymphoblasts

26
Q

chemo for ALL is usually the ______ protocol

A

modified Dana-Farber

27
Q

in addition to chemo, ALL usually adds

A

BCR-ABL TKi therapy (gene is present in 25% cases)

28
Q

drugs for LL

A

asparaginase
methotrexate
chemo

29
Q

asparaginase MOA in ALL

A

asparaginase hydrolyses all L-asparagine to L-aspartic acid and ammonia so the ALL cells have nothing to use to repro as they can’t make themselves

30
Q

asparaginase AEs

A

severe hypersensitivity rxns- asparaginase from E coli has the highest incidence
Prior intradermal test dose is recommended

31
Q

methotrexate is used with _________ intrathecally as ______in ALL

A

chemo
CNS prophylaxis

32
Q

methotrexate MOA

A

folate antagonist- inhibits dihydrofolate reductase required to convert folic acid to tetrahydrofolate (required for purine and thymidylate synthesis)

33
Q

what is an important factor to make sure methotrexate is safe

A

keep urine alkaline with sodium bicarb so it doesn’t precipitate and cause kidney damage
- start sodium bicarb PO/IV day before infusion

34
Q

methotrexate therapy usually requires ____ rescue

A

leucovorin

35
Q

how is leucovorin rescue used with methotrexate

A

Must receive doses of leucovorin q6h until lvls undetectable to rescue pt from life threatening myelosuppression and other toxicities

36
Q

methotrexate AEs

A

myelosuppression, organ toxicities (nephrotoxicity, hepatotoxicity, neurotoxicity)- pts require rescue leucovorin

37
Q

TLS results in what chem anomalies

A

hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia

38
Q

RFs for TLS

A

large bulky tumor, high LDH or WBCs, higher baseline SCr or uric acid
high chemo
aggressive lymphoma or leukemia

39
Q

sx of TLS

A

N/V, acute kidney injury (↑SCr), ↓urine output, edema, lethargy, HPTN, ECH changes (arrhythmias), muscle twitching, cramping, numbness, weakness, tetany, confusion and seizures

40
Q

drugs for TLS prevention

A

allopurinol
rasburicase

41
Q

how does allopurinol treat TLS

A

inhibits xanthine oxidase (enzyme responsible for formation of uric acid)

42
Q

how does rasburicase treat TLS

A

recomb urate-oxidase enzyme that converts uric acid to allantoin + degrades uric acid already formed

43
Q

how to treat asymptomatic hyperkalemia from TLS

A

oral or rectal sodium polystyrene sulphonate

44
Q

how to treat symptomatic hyperkalemia from TLS

A

rapid acting insulin and 25% dextrose infusion

45
Q

what is the most common form of acute leukemia

A

AML

46
Q

sx of AMl

A

Rapidly fatal if not treated
Cytopenias- drop in other cell lines (pancytopenia)
Anemia: fatigue, malaise, weakness
Thrombocytopenia: easy bruising, petechiae, ecchymosis, heavy and/ or long menses, bleeding like epistaxis, gingival bleed, conjunctival hemorrhage
Neutropenia: infection, s/s may be absent due to nonfunctioning malignant WBC clones
High myeloblast count

47
Q

diganosis of AML is

A

> 20% myeloid blasts

48
Q

what are some predictors of outcome in adult ML

A

redictors of outcomes in adult AML
Age: Outcomes better in <60yrs
Performance status: fitter pts do better
Duration of first remission
Cytogenetics and molecular abnormalities- MOST IMPORTANT

49
Q

treatment plan for AML

A

Induction chemo → consolidation chemo → allogeneic stem cell transplant

50
Q

what is usually induction chemo for AML

A

7+3
7 days of continuous infusion cytarabine (rash common)
3 days of IV push anthracycline (idarubicin or daunorubicin)
+ midostaurin for FLT3 positive AML

51
Q

T or F: AML pts undergoing 7+3 still require allopurinol to prevent TLS

A

T- though TLS not as common as in ALL

52
Q

consolidation therapy in AAML is done with

A

HIDAC- high dose ARA-C (cytarabine)

53
Q

HIDAC AEs

A

ocular toxicity (Excessive tearing, pain, photophobia, sensation of foreign body)
cerebellar toxicity

54
Q

how to treat ocular toxicity caused by HIDAC for AML

A

steroid eyedrops (dexamethasone or prednisolone) for duration of HIDAC therapy + 48hrs after last dose

55
Q

list some purposes of an allogenic HSCT

A

Rescue recipient from myeloablative therapy
Replace abnormal hematopoietic component
Establish graft vs leukemia (tumor) effect where donor cells destroy residual malignant cells in host - advantage over autologous HSCT

56
Q

stem cell sources for allogenic HSCT

A

boen marrow
peripheral blood
ubilical cord blood

444-Oncology and Neurology (22 decks)

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