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Flashcards in Hematology pt 1 Deck (130):
1

leukemia etiology

-unknown
-culmination of multiple processes resulting in genetic damage

2

things that can cause leukemia

-radiation
-carcinogens (benzene)
-chemotherapy

3

leukemia symptoms result from:

-bone marrow failure
-tissue infiltration
-circulating leukemia

4

labs that indicate bone marrow failure when low

WBC (leukopenia)
RBC (anemia)
platelets (thrombocytopenia)

5

technique to diagnose and stage leukemia

bone marrow aspiration and biopsy

6

AML

acute myelogenous leukemia

7

population AML is most common in

elderly

8

regular intense induction therapy for AML

7 + 3
-3 days of an anthracycline
-7 days of cytarabine

9

low intensity induction therapy for AML

azacitadine or decitabine

10

consolidation therapy for AML

-HiDAC (high dose cytarabine) for all cytogenetics
-AlloHSCT can be used for intermediate or high risk cytogenetics

11

salvage chemo for AML

-CLAG/CLAG-M (cladribine, cytarabine, GCSF +/- mitoxantrone)
-FLAG/FLAG-IDA (fludarabine + cytarabine + GCSF +/- idarubicin)
-MEC (mitoxantrone + etoposide + cytarabine)

12

APL

acute promyleocytic leukemia

13

APL etiology

fusion of chromosome 15 and 17 to form PML-RAR-alpha

14

effects of PML-RAR alpha in APL

-binds to DNA and blocks transcription
-prevents differentiation
-fusion to retinoic acid receptor (RAR)

15

APL induction treatment

-ATRA (all-trans retinoic acid)
aka tretinoin
given emergently
-ATRA + ATO (arsenic trioxide)
*curative*

16

APL has high risk of what complication and how does it work

hemorrhage
annexin II produced in APL cells bind plasminogen and tPA to increase plasmin activity

17

APL differentiation syndrome (retinoic acid syndrome) symptoms

-fever
-respiratory distress
-interstitial pulmonary infiltrates
-pleural or pericardial effusions
-weight gain
-hypotention

18

how does APL differentiation syndrome lead to death

pleural effusion -> pulmonary infiltration -> pulmonary hemorrhage

19

how to treat APL differentiation syndrome

dexamethasone
OR
prophylactic prednisone

20

arsenic trioxide MoA

-low concentrations = differentiation inducer
-high concentrations = direct apoptosis inducer

21

arsenic trioxide toxicities

-QT prolongation
-hepatotoxicity

22

ALL

acute lymphoblastic leukemia

23

where does ALL stem from

disorder of lymphoid progenitor cells

24

ALL is most common in which patients

children

25

ALL subtypes

B cell
T cell

26

ALL subtype with the better prognosis in adults

T cell

27

ALL prognosis in children

good, unless philadelphia chromosome is present

28

risk factors for ALL CNS relapse

-T cell ALL
-leukocytosis
-high risk cytogenetics
-presence of leukemic cells in CSF

29

Induction treatment for ALL

cortidosteroid
vincristine
anthracycline
+/- asparaginase
+/- BCR-ABL TKI

30

consolidation treatment for ALL

-continue chemo +/- TKI
-allogeneic stem cell transplant if age <65 and no comorbidities

31

L-asparaginase mechnism

catalyzes hydrolysis of asparagine to aspartic acid which depletes resources for RNA and DNA synthesis, leading to apotosis

32

L-asparaginase adverse effects

PE
pancreatitis
thrombosis
hepatotoxicity

33

drugs for relapsed/refractory ALL

blinatumomab
inotuzumab

34

blinatumomab MoA

bispecific T cell engager that binds both B and T cells at the same time

35

Inotuzumab MoA

binds to CD22 of B cells which allows for calicheamicin to induce double stranded breaks in the cell

36

CML

chronic myeloid leukemia

37

CML is most common in which patients

adult to elderly

38

CML is caused by what

bcr/abl philadelphia chromosome

39

phases of CML

chronic
accelerated
blast

40

chronic phase of CML features

-largely asymptomatic
-some splenomegaly and anemia
-lasts 3-5 years
-makes up 90% of new diagnoses

41

accelerated phase of CML features

-splenomegaly, anemia, bone/joint pain, fever
-lasts months
-cell maturation arrest

42

blast phase of CML features

-anemia, infections, bleeds
-duration is days to weeks
-presents as acute

43

treatment goal of CML

complete cytogenetic response in 1 year

44

treatment of CML

TKIs
imatinib first line

45

most TKIs are inhibitors and substrates for what CYP

3A4

46

TKI with a BBW for vascular occlusion

ponatinib

47

discontinuation of TKI

its a trick
-guidelines recommend indefinite continuation in pts. with responsive disease
-this is to reduce relapse

48

treatment of CML accelerated phase

-imatinib
-dasatinib
-nilotinib
-omacetaxine
-allogeneic HSCT

49

CLL

chronic lymphocytic leukemia

50

CLL pathophysiology

clonal proliferation and accumulation of CD5 B cells in blood, bone marrow, lymph, and spleen

51

key genetic marker in CLL that indicates poor chemo response

Del 17p, most of which have P53 mutation

52

first line treatments for CLL with no del 17p present in pts <65

-fludarabine, cyclophosphamide, rituximab
-bendamustine, rituximab

53

first line treatments for CLL with no del 17p present in pts >65 or comorbidities

-obinutuzumab + chlorambucil
-ibrutinib

54

ibrutinib MoA

-covalently binds bruton tyrosine kinase to inhibit proliferation and survival of B cells

55

ibrutinib common side effects

n/d
fatigue
cough

56

ibrutinib and bleeding risk

-do not administer with warfarin
-hold for 3-7 days before and after surgery

57

preferred treatment of relapsed CLL without del 17p present

ibrutinib
OR
idelalisib + rituximab

58

idelalisib MoA

-PI3K delta inhibitor
-inhibits B cell and CSCR 4/5 signaling which prevents trafficking and homing of B cells to lymph and marrow

59

idelalisib adverse effects

hepatotoxicity
diarrhea/colitis
pneumonitis
infection

60

first line treatment for CLL with del 17p

-ibrutinib
-HDMP + R
others

61

treatment for relapsed/refractory CLL with del 17p

ibrutinib
venetoclax
idelalisib + R
others

62

venetoclax MoA

targets BCL-2 in order to help restore the process of apoptosis

63

venetoclax indication

CLL relapsed/refractory with del 17p present

64

two types of bone marrow transplant

allogeneic
autologous

65

type of BMT that has problems with graft vs. host

allogeneic

66

complications seen after stem cell transplant

infection
GVHD
pulmonary complications

67

autologous stem cell source

the patient

68

phases of SCT

-conditioning/ preparative from day-7 to day-3
-transplatation day 0
-post transplant

69

engraftment

when transplanted cells start to grow

70

acute GVHD features

-occurs before day +100
-affects skin, GI tract, liver

71

chronic GVHD features

-occurs after day +100
-affects all organ systems

72

GVHD prophylaxis is given to who

all allogeneic recipients

73

GVHD prophylaxis drugs

immunosuppressants
-cyclosporine/tacro + methotrexate
-cyclosporine/tacro + mycophenolate
-sirolimus + tacrolimus

74

vaccines that are contraindicated in pts with SCT

MMR
varicella
*live ones*

75

structures in the lymphatic system

-bone marrow
-lymph nodes
-spleen
-thymus
-tonsils
-MALT

76

bone marrow lymphocytes are primarily what type

b cells

77

role of b cells

-produce antibodies
-mature into memory b cells

78

types of t cells

cytotoxic CD8
helper CD4

79

role of cytotoxic CD8 cells

recognize infected cell membranes and destroy them

80

role of helper t CD4 cells

release cytokines that attract other WBCs

81

role of Natural killer cells

recognize foreign or infected cells via MHC 1

82

what is lymphoma

blood cancer that begins in the lymph node

83

pathophysiology of hodgkins lymphomas

malignant Reed-Sternberg cells recruit more cells

84

Reed-Sternberg cell features

large
bi-nucleated
express CD30 and CD15

85

risk factors for hodgkin lymphoma

*not well defined*
-same sex siblings as HL pt. have greater risk
-many tumors have Epstein-Barr virus
-previous solid organ transplant
-HIV

86

signs and symptoms of hodgkin lymphoma

-painless rubbery mass, most often in neck
-fever
-drenching night sweats
-often times asymptomatic

87

lymphoma age distribution for hodgkins lymphoma

bimodial
peak in 20-30s then again over 50
-death more common in older patients

88

diagnosis and work up of HL

-biopsy
-chest Xray
-CT
-PET scan *most important*

89

staging of HL

-stage 1 = single node region or structure
-stage 2 = two or more nodes regions on same side of diaphragm
-stage 3 = lymph nodes regions on both sides of diaphragm
-stage 4 = diffuse or disseminated involvement

90

factors used in the International Prognostic Score for advanced stage HL

-albumin < 4
-hemoglobin <10.5
-male
-stage 4
-age >45
-WBC >15000
-lymphopenia <600

91

treatment modalities for HL

radiation
chemo
surgery
autologous SCT

92

HL cure rate

81%

93

chemo regimens for acute HL

MOPP
ABVD

94

MOPP regimen drugs

mechlorethamine
vincristine (oncovin)
procarbazine
prednisone
-28 day cycle

95

problem with MOPP

lots of secondary leukemias occur

96

ABVD regimen drugs

doxorubicin (adriamycin)
bleomycin
vinblastine
dacarbazine
-28 day cycle

97

acute toxicities of ABVD and MOPP

N/V
myelosuppression
anemia
mucositis/stomatitis

98

long term toxicities of ABVD and MOPP

-secondary malignancies (MOPP)
-pulmonary fibrosis - bleo
-CHF - doxorubicin
-gonadal dysfunction/sterility (MOPP)

99

treatment for favorable early stage HL

ABVD for 2-4 cycles + involved field RT

100

treatment for unfavorable early stage HL

ABVD for 4-6 cycles +/- RT

101

indicators of unfavorable early stage HL

b symptoms
bulky disease
extra nodal or >3 sites

102

treatment for advanced stage HL

ABVD for 6 cycles
escalated BEACOPP for unfavorable

103

escalated BEACOPP regimen

bleomycin
etoposide
doxorubicin (adriamycin)
cyclophosphamide
vincristine (oncovin)
procarbazine
prednisone
*21 day*

104

brentuximab vedotin MoA

-targets CD30
-carries MMAE which potentially disrupts microtubule polymerization

105

brentuximab side effects

peripheral neuropathy
neutropenia

106

risk factors for non hodgkins lymphoma

-older people
-Hx of lymphoma
-exposure to radiation, pesticides
-immuno-suppressants
-lupus, RA
-HIV
-epstein-barr
-hep C

107

clinical presentation of non hodgkins lymphoma

-lymphadenopathy
-B symptoms (fever, night sweats)

108

NHL diagnosis

-biopsy
-molecular tests
-cell surface markers
-cytogenetics (C. 14)

109

NHL staging

same as HL, but does not work as well because spread is not contiguous

110

prognostic index for NHL

-age >60
-serum LDH >normal
-performance status 2-4
-stage 3 or 4
-extranodal involvement

111

main indolent NHL example

follicular lymphoma

112

aggressive NHL type

diffuse large b-cell lymphoma

113

highly aggressive NHL type

burkitt lymphoma

114

indolent NHL definition

-survival of untreated disease is measured in years
-waxing and waning of lymph nodes is commonly seen

115

aggressive NHL definition

survival of untreated disease is measured in months

116

highly aggressive NHL definition

survival of untreated disease is measure din weeks

117

treatment for indolent NHL

-watch and wait b/c its slow growing
-single-agent chemo
o chlorambucil
o cyclophosphamide
o fludarabine
-immunotherapy - rituximab
-chemo-immuno combo - R-CHOP
-targeted - ibrutinib

118

treatment for aggressive NHL

R-CHOP
DA-R-EPOCH
-CODOX-M

119

R-CHOP drugs

Rituximab
Cyclophosphamide
Hydroxydaunorubicin (doxorubicin)
Oncovin (vincristine)
Prednisone

120

rituximab adverse reactions

fever
chills
rigors
*push through these because they really only show in the first cycle or two

121

rituximab requires what pre-medication

tylenol
diphenhydramine
ranitidine

122

rituximab MoA

causes apoptosis by:
-recruiting NK cells
-activating compliment cytotoxicity
-apoptosis via calcium influx

123

cyclophosphamide adverse effects

SIADH
-hemorrhagic cystitis
-pulmonary tox
-alopecia

124

cyclophosphamide MoA

alkylator
forms covalent bonds at N7 of quanine

125

doxorubicin MoA

topo II inhibitor

126

vincristine MoA

microtubule stabilization

127

NHL type with best chance for cure

aggressive

128

treatments for NHL relapse after autologous BMT

ICE
DHAP
GemOx
Yescarta

129

treatment for highly aggressive NHL

R-CODOX-M/IVAC
DA-R-EPOCH
*R-CHOP is not adequate*

130

which lymphoma is harder to cure

NHL