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PT3 Oncology > Hematology pt 1 > Flashcards

Hematology pt 1 Flashcards

1
Q

leukemia etiology

A
  • unknown

- culmination of multiple processes resulting in genetic damage

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2
Q

things that can cause leukemia

A
  • radiation
  • carcinogens (benzene)
  • chemotherapy
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3
Q

leukemia symptoms result from:

A
  • bone marrow failure
  • tissue infiltration
  • circulating leukemia
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4
Q

labs that indicate bone marrow failure when low

A

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

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5
Q

technique to diagnose and stage leukemia

A

bone marrow aspiration and biopsy

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6
Q

AML

A

acute myelogenous leukemia

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7
Q

population AML is most common in

A

elderly

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8
Q

regular intense induction therapy for AML

A

7 + 3

  • 3 days of an anthracycline
  • 7 days of cytarabine
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9
Q

low intensity induction therapy for AML

A

azacitadine or decitabine

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10
Q

consolidation therapy for AML

A
  • HiDAC (high dose cytarabine) for all cytogenetics

- AlloHSCT can be used for intermediate or high risk cytogenetics

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11
Q

salvage chemo for AML

A
  • CLAG/CLAG-M (cladribine, cytarabine, GCSF +/- mitoxantrone)
  • FLAG/FLAG-IDA (fludarabine + cytarabine + GCSF +/- idarubicin)
  • MEC (mitoxantrone + etoposide + cytarabine)
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12
Q

APL

A

acute promyleocytic leukemia

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13
Q

APL etiology

A

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

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14
Q

effects of PML-RAR alpha in APL

A
  • binds to DNA and blocks transcription
  • prevents differentiation
  • fusion to retinoic acid receptor (RAR)
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15
Q

APL induction treatment

A 
-ATRA (all-trans retinoic acid)
aka tretinoin
given emergently 
-ATRA + ATO  (arsenic trioxide)
*curative*
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16
Q

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

A

hemorrhage

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

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17
Q

APL differentiation syndrome (retinoic acid syndrome) symptoms

A
  • fever
  • respiratory distress
  • interstitial pulmonary infiltrates
  • pleural or pericardial effusions
  • weight gain
  • hypotention
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18
Q

how does APL differentiation syndrome lead to death

A

pleural effusion -> pulmonary infiltration -> pulmonary hemorrhage

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19
Q

how to treat APL differentiation syndrome

A

dexamethasone
OR
prophylactic prednisone

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20
Q

arsenic trioxide MoA

A
  • low concentrations = differentiation inducer

- high concentrations = direct apoptosis inducer

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21
Q

arsenic trioxide toxicities

A
  • QT prolongation

- hepatotoxicity

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22
Q

ALL

A

acute lymphoblastic leukemia

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23
Q

where does ALL stem from

A

disorder of lymphoid progenitor cells

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24
Q

ALL is most common in which patients

A

children

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25
Q

ALL subtypes

A

B cell

T cell

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26
Q

ALL subtype with the better prognosis in adults

A

T cell

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27
Q

ALL prognosis in children

A

good, unless philadelphia chromosome is present

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28
Q

risk factors for ALL CNS relapse

A
  • T cell ALL
  • leukocytosis
  • high risk cytogenetics
  • presence of leukemic cells in CSF
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29
Q

Induction treatment for ALL

A 
cortidosteroid
vincristine
anthracycline
\+/- asparaginase
\+/- BCR-ABL TKI
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30
Q

consolidation treatment for ALL

A
  • continue chemo +/- TKI

- allogeneic stem cell transplant if age <65 and no comorbidities

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31
Q

L-asparaginase mechnism

A

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

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32
Q

L-asparaginase adverse effects

A

PE
pancreatitis
thrombosis
hepatotoxicity

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33
Q

drugs for relapsed/refractory ALL

A

blinatumomab

inotuzumab

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34
Q

blinatumomab MoA

A

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

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35
Q

Inotuzumab MoA

A

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

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36
Q

CML

A

chronic myeloid leukemia

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37
Q

CML is most common in which patients

A

adult to elderly

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38
Q

CML is caused by what

A

bcr/abl philadelphia chromosome

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39
Q

phases of CML

A

chronic
accelerated
blast

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40
Q

chronic phase of CML features

A
  • largely asymptomatic
  • some splenomegaly and anemia
  • lasts 3-5 years
  • makes up 90% of new diagnoses
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41
Q

accelerated phase of CML features

A
  • splenomegaly, anemia, bone/joint pain, fever
  • lasts months
  • cell maturation arrest
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42
Q

blast phase of CML features

A
  • anemia, infections, bleeds
  • duration is days to weeks
  • presents as acute
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43
Q

treatment goal of CML

A

complete cytogenetic response in 1 year

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44
Q

treatment of CML

A

TKIs

imatinib first line

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45
Q

most TKIs are inhibitors and substrates for what CYP

A

3A4

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46
Q

TKI with a BBW for vascular occlusion

A

ponatinib

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47
Q

discontinuation of TKI

A

its a trick

  • guidelines recommend indefinite continuation in pts. with responsive disease
  • this is to reduce relapse
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48
Q

treatment of CML accelerated phase

A
  • imatinib
  • dasatinib
  • nilotinib
  • omacetaxine
  • allogeneic HSCT
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49
Q

CLL

A

chronic lymphocytic leukemia

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50
Q

CLL pathophysiology

A

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

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51
Q

key genetic marker in CLL that indicates poor chemo response

A

Del 17p, most of which have P53 mutation

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52
Q

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

A
  • fludarabine, cyclophosphamide, rituximab

- bendamustine, rituximab

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53
Q

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

A
  • obinutuzumab + chlorambucil

- ibrutinib

54
Q

ibrutinib MoA

A

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

55
Q

ibrutinib common side effects

A

n/d
fatigue
cough

56
Q

ibrutinib and bleeding risk

A
  • do not administer with warfarin

- hold for 3-7 days before and after surgery

57
Q

preferred treatment of relapsed CLL without del 17p present

A

ibrutinib
OR
idelalisib + rituximab

58
Q

idelalisib MoA

A
  • PI3K delta inhibitor

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

59
Q

idelalisib adverse effects

A

hepatotoxicity
diarrhea/colitis
pneumonitis
infection

60
Q

first line treatment for CLL with del 17p

A

-ibrutinib
-HDMP + R
others

61
Q

treatment for relapsed/refractory CLL with del 17p

A

ibrutinib
venetoclax
idelalisib + R
others

62
Q

venetoclax MoA

A

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

63
Q

venetoclax indication

A

CLL relapsed/refractory with del 17p present

64
Q

two types of bone marrow transplant

A

allogeneic

autologous

65
Q

type of BMT that has problems with graft vs. host

A

allogeneic

66
Q

complications seen after stem cell transplant

A

infection
GVHD
pulmonary complications

67
Q

autologous stem cell source

A

the patient

68
Q

phases of SCT

A
  • conditioning/ preparative from day-7 to day-3
  • transplatation day 0
  • post transplant
69
Q

engraftment

A

when transplanted cells start to grow

70
Q

acute GVHD features

A
  • occurs before day +100

- affects skin, GI tract, liver

71
Q

chronic GVHD features

A
  • occurs after day +100

- affects all organ systems

72
Q

GVHD prophylaxis is given to who

A

all allogeneic recipients

73
Q

GVHD prophylaxis drugs

A

immunosuppressants

  • cyclosporine/tacro + methotrexate
  • cyclosporine/tacro + mycophenolate
  • sirolimus + tacrolimus
74
Q

vaccines that are contraindicated in pts with SCT

A

MMR
varicella
live ones

75
Q

structures in the lymphatic system

A
  • bone marrow
  • lymph nodes
  • spleen
  • thymus
  • tonsils
  • MALT
76
Q

bone marrow lymphocytes are primarily what type

A

b cells

77
Q

role of b cells

A
  • produce antibodies

- mature into memory b cells

78
Q

types of t cells

A

cytotoxic CD8

helper CD4

79
Q

role of cytotoxic CD8 cells

A

recognize infected cell membranes and destroy them

80
Q

role of helper t CD4 cells

A

release cytokines that attract other WBCs

81
Q

role of Natural killer cells

A

recognize foreign or infected cells via MHC 1

82
Q

what is lymphoma

A

blood cancer that begins in the lymph node

83
Q

pathophysiology of hodgkins lymphomas

A

malignant Reed-Sternberg cells recruit more cells

84
Q

Reed-Sternberg cell features

A

large
bi-nucleated
express CD30 and CD15

85
Q

risk factors for hodgkin lymphoma

A
  • not well defined*
  • same sex siblings as HL pt. have greater risk
  • many tumors have Epstein-Barr virus
  • previous solid organ transplant
  • HIV
86
Q

signs and symptoms of hodgkin lymphoma

A
  • painless rubbery mass, most often in neck
  • fever
  • drenching night sweats
  • often times asymptomatic
87
Q

lymphoma age distribution for hodgkins lymphoma

A

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

88
Q

diagnosis and work up of HL

A
  • biopsy
  • chest Xray
  • CT
  • PET scan most important
89
Q

staging of HL

A
  • 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
Q

factors used in the International Prognostic Score for advanced stage HL

A
  • albumin < 4
  • hemoglobin <10.5
  • male
  • stage 4
  • age >45
  • WBC >15000
  • lymphopenia <600
91
Q

treatment modalities for HL

A

radiation
chemo
surgery
autologous SCT

92
Q

HL cure rate

A

81%

93
Q

chemo regimens for acute HL

A

MOPP

ABVD

94
Q

MOPP regimen drugs

A 
mechlorethamine
vincristine (oncovin)
procarbazine
prednisone
-28 day cycle
95
Q

problem with MOPP

A

lots of secondary leukemias occur

96
Q

ABVD regimen drugs

A 
doxorubicin (adriamycin)
bleomycin
vinblastine
dacarbazine
-28 day cycle
97
Q

acute toxicities of ABVD and MOPP

A

N/V
myelosuppression
anemia
mucositis/stomatitis

98
Q

long term toxicities of ABVD and MOPP

A
  • secondary malignancies (MOPP)
  • pulmonary fibrosis - bleo
  • CHF - doxorubicin
  • gonadal dysfunction/sterility (MOPP)
99
Q

treatment for favorable early stage HL

A

ABVD for 2-4 cycles + involved field RT

100
Q

treatment for unfavorable early stage HL

A

ABVD for 4-6 cycles +/- RT

101
Q

indicators of unfavorable early stage HL

A

b symptoms
bulky disease
extra nodal or >3 sites

102
Q

treatment for advanced stage HL

A

ABVD for 6 cycles

escalated BEACOPP for unfavorable

103
Q

escalated BEACOPP regimen

A 
bleomycin
etoposide
doxorubicin (adriamycin)
cyclophosphamide
vincristine (oncovin)
procarbazine
prednisone
*21 day*
104
Q

brentuximab vedotin MoA

A
  • targets CD30

- carries MMAE which potentially disrupts microtubule polymerization

105
Q

brentuximab side effects

A

peripheral neuropathy

neutropenia

106
Q

risk factors for non hodgkins lymphoma

A
  • older people
  • Hx of lymphoma
  • exposure to radiation, pesticides
  • immuno-suppressants
  • lupus, RA
  • HIV
  • epstein-barr
  • hep C
107
Q

clinical presentation of non hodgkins lymphoma

A
  • lymphadenopathy

- B symptoms (fever, night sweats)

108
Q

NHL diagnosis

A
  • biopsy
  • molecular tests
  • cell surface markers
  • cytogenetics (C. 14)
109
Q

NHL staging

A

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

110
Q

prognostic index for NHL

A
  • age >60
  • serum LDH >normal
  • performance status 2-4
  • stage 3 or 4
  • extranodal involvement
111
Q

main indolent NHL example

A

follicular lymphoma

112
Q

aggressive NHL type

A

diffuse large b-cell lymphoma

113
Q

highly aggressive NHL type

A

burkitt lymphoma

114
Q

indolent NHL definition

A
  • survival of untreated disease is measured in years

- waxing and waning of lymph nodes is commonly seen

115
Q

aggressive NHL definition

A

survival of untreated disease is measured in months

116
Q

highly aggressive NHL definition

A

survival of untreated disease is measure din weeks

117
Q

treatment for indolent NHL

A

-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
Q

treatment for aggressive NHL

A

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

119
Q

R-CHOP drugs

A 
Rituximab
Cyclophosphamide
Hydroxydaunorubicin (doxorubicin)
Oncovin (vincristine)
Prednisone
120
Q

rituximab adverse reactions

A

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

121
Q

rituximab requires what pre-medication

A

tylenol
diphenhydramine
ranitidine

122
Q

rituximab MoA

A

causes apoptosis by:

  • recruiting NK cells
  • activating compliment cytotoxicity
  • apoptosis via calcium influx
123
Q

cyclophosphamide adverse effects

A

SIADH

  • hemorrhagic cystitis
  • pulmonary tox
  • alopecia
124
Q

cyclophosphamide MoA

A

alkylator

forms covalent bonds at N7 of quanine

125
Q

doxorubicin MoA

A

topo II inhibitor

126
Q

vincristine MoA

A

microtubule stabilization

127
Q

NHL type with best chance for cure

A

aggressive

128
Q

treatments for NHL relapse after autologous BMT

A

ICE
DHAP
GemOx
Yescarta

129
Q

treatment for highly aggressive NHL

A

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

130
Q

which lymphoma is harder to cure

A

NHL

PT3 Oncology (9 decks)

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