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Haematology > Sweatman Hematologic Malignancies > Flashcards

Sweatman Hematologic Malignancies Flashcards

1
Q

What are we trying to achieve with Heme. Malignancy drugs

A

myelosuppresson–> an unwanted side effect usually but here it is the desired effect

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2
Q

Consequence of myelosupression

A

opportunistic infection risk goes up considerable

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3
Q

Induction

A

high dose: intolerable chronically

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4
Q

Consolidation

A

repetition of induction therapy during remission: intolerable chronically–>increases chance of eradication

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5
Q

Maintainence

A

long term tolerable, lower dose therapy during remission

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6
Q

Adjuvant

A

after sx/ radiotherapy

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7
Q

neo-adjuvant

A

before sx/ radiotherapy

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8
Q

Metronomic dosing used for

A

multiple myeloma, recurrent NHL, malignant glioma, glioblastoma, SCC, breat, ovarian, and hormone resistant prostate cancer
*but not all tumor types in all pt.’s

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9
Q

Metronimic therapy work by

A

direct and indirect effect on the tumor cells and their
microenvironment
–>takes into account darwinian selection (chemotherapy we are applying)

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10
Q

how can metronomic dosing affect a tumor

A

> inhibit angiogenesis
stimulate anti cancer immune response
create a drug-driven dependency/deprivation effect

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11
Q

explains phenotypic divergence arising from applied chemo and the coinciding resistance

A

adaptive therapy

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12
Q

explain adaptive chemotherapy treatment

control vs eradication

A

takes into account resistant vs non-resistance clones and tries to maintain an acceptable amount of these (retain the correct ration)–> overall goal is to control the tumor, maintain some level of resistant/non-resistance–>bring the number down chronically rather than acutely

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13
Q

most common toxc effects of metronomic dosing

A

N/V, Grade 1 and anemia, neutropenia, leukopenia, and pymphopenia

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14
Q

more than half the leukemias present

A

acutely

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15
Q

Most common in children 3-7

A

ALL

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16
Q

Most commonly seen in elderly

A

CLL

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17
Q

Ph1 chromosome most commonly seen in (3)

A

CML (210)> ALL(190)>AML

*detectable by FISH or PCR

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18
Q

AML tx regimine

INDUCTION

A

CDT–
Cytarabine (Ara-C)
Daunorubicin
Thioguanine, 6-TG

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19
Q

MOA for Daunorubicin

A

free radical producer
intercolater
topo II inhibitor

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20
Q

Cytarabine MOA

A

pyrimidine antimetabolite

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21
Q

Thioguanine MOA

A

purine antimetabolite

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22
Q

Daunorubicin class

A

anthracycline

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23
Q

Side effect of Daunorubicin

A

cardiac toxicity and arrhythmia

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24
Q

Side effects of AML induction regimine

A

all are myelosupressors–> opportunistic infection

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25
Q

Post remission therapy for AML

A

cytarabine and HSCT

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26
Q

APML

A

ATRA + Dunorubicin or Idarabine + cytarabine

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27
Q

class of atra

A

retinoid drug

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28
Q

retinoic acid syndrome

side effect of ATRA

A

fever, SOB, weight GAIN, pulmonary infiltrates, and pleural/pericardial effusions

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29
Q

other tx for PML-RARa fusion gene found in PML

A

Arsenic

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30
Q

Arsenic trioxide MOA

A

causes proteolysis of the PML-RARa fusion protein–> allows myelocytes to differentiate and not proliferate

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31
Q

Warnings with ARSENIC trioxide

A

BLACK BOX warning involving CV

-AV block, QT prolong, electrolyte imbalance

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32
Q

are CV effects seen with ATRA

A

NO

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33
Q

SIde effect seen wit Arsenic other than CV

A

differntiation syndrome

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34
Q

define differentiation syndrome

A

fever, SOB, weight GAIN, pulmonary infiltrates, pleural/pericardial effusions

AND leukocytosis

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35
Q

ALL tx regimine (general)

A

prednisone + vincristone + anthracycline + asparaginase

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36
Q

List the drugs aproved for tx of ALL

60-80% response in adults

A 
pegasperaginase
doxorubicin
prednisone
imatinib
vincristine
daunorubicin
methotrexate
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37
Q

how do you treat a BCR-ABL kinase tumor

A

imatinib always

response in 90% of adults

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38
Q

how to you accomplish CNS prophylaxis with ALL tx

A

IT methotrexate and systemic methotrxate

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39
Q

Consolidation therapy for ALL

A

methotrexate and mercaptopurine

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40
Q

ASPARAGINASE moa

A

enzyme that degrades asparagine–> cell cannot make proteins without this amino acid
–<starves protein synthesis

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41
Q

why pegylate

A

extends duration and increase activity in the body

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42
Q

whe to use imatinib

A

chronic phase of myeloid leukemia

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43
Q

first line tx of CML

A

imatinib

44
Q

CML drugs

A 
imatinib
nilotinibi
dasatinib
cytarabine
Interferon alfa-2a
45
Q

imatinib, nioltinib and dasatinib are all

A

tyrosine kinase inhibitors that bind to a highly conserved ATP binding site on the tk
*only consitent curatie tx for CML

46
Q

resitance mechanism to TKI

A

mutations in the thymine gate
T3151
T6701 etc

47
Q

Tx for CLL

A

Fludarabine
Cyclophosphamide
Rituximab

and diff combinations of these 3

48
Q

rituximab class

A

MAB that targets CD20 on B cells

*compliment dep and ADCC cell death

49
Q

fludarabine class

A

antimetabolite

50
Q

cyclophosphamide

A

alkylating agent

51
Q

Fludarabine comlication

A

worsens Autoimmune hemolytic anemia

(obv drug induced) tx is with corticosteroids

52
Q

hyperurcemia tx

A

allopurinol and hydration

53
Q

bendamustine

A

antimetabolite and an alkylating agent

result in DNA ds break, activate p53 and inhibits mitotic check point–> cells enter cycle wiht DNA damage and apoptosis happens

54
Q

Hairy cell leukemia

A

Cladribine

Pentostain–> both antimetabs and interferon alfa2a

55
Q

Hodgkin Lymphoma

A

ABVD

56
Q

ABVD therapy

A

doxorubicin, belomycin, vinblastine, dacarabazine

57
Q

CHOP

A

cyclophosphamide, doxorubicin, vincristine, prednisone +/- prednisone

58
Q

HL tx gernarlities

A

anthracylin, carbazine, alkylating agent, mitotic spindle inhibitor

59
Q

recurrence of HL

A

autologous stem cell transplant

*second chemo regimine not likley to work

60
Q

high or low cure rate with HL

A

high but refractory disase is usally lethal

61
Q

NHL tx

low stage disease

A

COMP

methotrxate + prednisone for 6 months

62
Q

High stage B cell NHL

DLBC and Burkitt’s

A

R-CHOP*

rituximab + doxorubicin, cyclophosphamide, vincristine and prednisone

63
Q

diff bw how we can trrat HL vs NHL

A

NHL will usualy epress CD20 therefore rituximab is an option

64
Q

recurrent NHL tx

A

high dose therapy and SCT

65
Q

Adverse effects of NHL tx

A

MDS and AML due to alkylating agents

sterility, secondary malignancy (brain lung, kidney), LV dysfunciton, MDS and AML

66
Q

MABs with radioactivity to CD 20

A

tositumomab (I131)
ibritumomab (Y90)

apoptosis, phagoctyosis, radionuclide damage
*no binding in lymphoid tissue

67
Q

side effects of radionuclide therapy

A

myelosupression (thrombocytopenia, neutropenia, anemia)

N/V, fever, chills

68
Q

Burkitt’s Tx CYLCLICAL

A

cyclophosphamide (alkylating agent)
vincristine + doxorubicin
cytarabine (ara-c)

69
Q

Burkitts has a close association with which virus

A

EBV

70
Q

Why intracethcal chemo is used in Tx. of Burkitt’s

A

to ensure CNS coverage

71
Q

ALL tx

A

prednisone, vincristine, asparaginase plus intracathecal methotrexate

72
Q

AML TX

A

CYTARABINE, IDRUBACIN OR DAUNORUBICIN

73
Q

BURKITT’S TX

A

cyclophosphamide and methotrexate, vincristine and doxorubicine, possible add cytarabine

74
Q

CML tx

A

imatinib, newer TKI’s interferon alfa2a

75
Q

CLL tx

A

fludarabine + cyclophosphamide and or rituximab

76
Q

Hairy Cell Leukemia tx

A

Cladaribine, Interferon, pentostatin

77
Q

Hodgkins tx

A

ABVD+ prednisone

anthracyclin, bleomycin, vincristin, dacarbazine

78
Q

NHL tx

A

CHOP or R-CHOP

cyclophosphamide, doxorubicin, vincristine and prednison + rituximab)

79
Q

APML

A

atra, arsenic, idarubicin

80
Q

Cytarabine MOA

A

bio-activated ARACTP inhibits DNA polymerase

81
Q

Dacarbazine moa

A

DNA methylator

82
Q

Arsenic and ATRA MOA

A

degrade PML-RARa

83
Q

ASPARAGINASE moa

A

denies asparagine availability for protein synthesis

84
Q

belomycin MOA

A

drug-ion complex oxidizes nucleotide deoxyribose

85
Q

Anthracyclins

A

DNA intercolators, topo II inhibitors, free radical generators

86
Q

Fludarabine MOA

A

bio activated in cell, produces DNA strand termination

87
Q

interferon MOA

A

direct antiproliferative effect + immunomodulator

88
Q

Imatinib moa

A

tki for BCR-ABL TK

89
Q

methotrexate MOA

A

DHFRi

90
Q

pentostatin moa

A

adenosine deaminase inhibitor that causes apoptosis

91
Q

prednisone moa

A

inhibition of lymphocyte prolif

92
Q

rituximab moa

A

CD20 mab that cuases adcc, cdc and direct apoptosis

93
Q

vincristine

A

inhibitis mitotic spindle

94
Q

arsenic toxicity

A

acute PML, differntiation syndrome + leukocytosis

95
Q

asparaginase toxicity

A

bleeding, glucose intolerane

96
Q

bleomycin toxicity

A

pulmonary fibrosis, alopecia pneumonitis

97
Q

cyclophosphamide toxicity

A

BM supression, hemorrhagic cystitis

98
Q

cytarabine toxicity

A

BM suppression and opp. infection

99
Q

dacarbazine toxicity

A

BM supression hepatotoxicity, 2ndary malig

100
Q

Vincristine toxicity

A

peripheral neuropathy paralytic illeus

101
Q

pentostatin toxicitiy

A

renal failure, seizure, pulmonary edema

102
Q

interferon toxicity

A

flue like symptoms ,myalgia, fever, neutropenia

103
Q

Anthracylins toxicity

A

cardiotoxicity

104
Q

only drug breast feeding might be ok

A

rituximab

*all other are no breast feeding

105
Q

only drug proven to cause birth defects

*(category X)

A

methotrexate

106
Q

Cat C drugs

A

asparaginase, dacarbazine, interferon, rituximab

*all others are Category D

107
Q

drugs associated with paternal teratogenicity

A 
cyslophosphamide
doxorubicin
epirubucin
inf alfa 2a
methotrexate

Haematology (7 decks)

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