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PHRM 864 > Exam 2: Hematologic Malignancies > Flashcards

Exam 2: Hematologic Malignancies Flashcards

1
Q

What cells are affected in lymphoma?

A
  • B and T lymphocytes
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2
Q

What are the two types of lymphomas?

A
  • Hodgkin Lymphona
  • Non-hodgkin lymphoma
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3
Q

What are the two subtypes of lymphomas?

A
  • Hodgkin lymphoma
  • Non-Hodgkin (NHL)
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4
Q

Hodgkin Pathology

A
  • Reed-Sternberg Cells
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5
Q

Where does Hodgkin originate?

A

B-lymphocytes

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6
Q

HL Risk Factors

A
  • impaired immune function
  • EBV
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7
Q

HL Presentation

A
  • painless, rubbery, enlarged lymph node
  • B symptoms
  • pruritius
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8
Q

B Symptoms

A
  • fever greater 38º
  • drenching sweats
  • unintentional weight loss greater than 10% in ≤ 6 months
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9
Q

HL Diagnosis

A

Excisional biopsy
bone marrow biopsy in advanced stage

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10
Q

Early-stage favorable HL

A

stage I-II without unfavorable factors

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11
Q

Early-stage unfavorable HL

A

stage I-II with unfavorable factors

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12
Q

Advanced stage HL

A

stage III-IV

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13
Q

Unfavorable factors

A
  • large mediastinal adenopathy
  • multiple involve nodal regions
  • B symptoms
  • extranodal involvement
  • ESR
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14
Q

International Prognostic Score (IPS) for HL

A
  • higher the number of factors, the worse progression free survival
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15
Q

HL Treatment Treatment options

A
  • Radiation
  • Autologous stem cell transplant

Combo Chemo
- ABVD
- Stanford V
- BEACOPP
- AAVD

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16
Q

Stage IA, IIA Favorable Treatment

A
  • ABVD + RT
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17
Q

Stage I-II Unfavorable

A
  • ABVD + RT
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18
Q

Stage III/IV

A
  • ABVD + RT
  • AAVD
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19
Q

ABVD

A
  • Doxorubicin (Adriamycin)
  • Bleomycin
  • Vinblastine
  • Dacarbazine
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20
Q

Toxicities of ABVD

A
  • cardio (doxorubicin)
  • Pulmonary (bleomycin)
  • Peripheral neuropathy (vinblastine)
  • Dacarbazine (myelosupression)
  • N/V
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21
Q

AAVD

A
  • Doxorubicin
  • Brentuximab vendotin
  • vinblastine
  • Dacarbazine
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22
Q

AAVD Toxicities

A
  • Cardiotoxicity (doxirubicin)
  • increased myelosuppression
  • increased peripheral neuropathy
  • N/V
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23
Q

ABVD Stage I or II HL

A

4 cycles

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24
Q

ABVD Stage III/IV HL

A

6 cycles

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25
Q

Relapsed HL Treatment

A

high dose chemo with autologous stem cell rescue ± maintenance brentuximab vendotin (if high risk disease post transplant)

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26
Q

NHL Patho

A

Malignant B or T lymphocytes and precursors (B cell more common)

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27
Q

NHL Risk Factors

A
  • EBV (Burtkitt -> TLS, AIDS)
  • Immunodeficiency
  • environmental/physical agents
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28
Q

NHL Presentation

A
  • B Cell: lymph nodes, spleen, bone marrow
  • T cell: extrandal sites (skin and lungs)
  • b symptoms in some patients
  • primary CNS lymphoma
  • NO ITCH
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29
Q

NHL Diagnosis

A

excisional biopsy
lumbar puncture in patients at high risk or symptoms as NHL can metastasize in the brain

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30
Q

Indolent B Cell lymphomas NHL

A

usually incurable

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31
Q

Aggressive B Cell lymphoma NHL

A
  • rapid growth
  • short survival
  • usually curable
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32
Q

Highly aggressive B cell NHL

A
  • doubling tine = 18 hours
  • usully curable
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33
Q

what type of cancer is DLBCL

A

NHL

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34
Q

NHL Treatment Approaches

A
  • RT
  • multi-agent chemo (backbone)
  • immuno
  • high dose chem with stem cell rescue
  • CAR-T
  • T-cell engagers
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35
Q

What type of cancer is Follicular Lymphoma

A

NHL (2nd most common type)

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36
Q

What can follicular lymphoma transform into

A
  • Richter’s transformation (aggressive nHL)
  • treat like DLBCL with rituzimab
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37
Q

DLBCL Genetic abnormalities

A
  • Double/triple hit (MYC+ BCL2 or BCL6 transformation or all three)
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38
Q

DLBCL Treatment Regimens

A
  • R-CHOP
  • DA-EPOCH + Rituximab
  • Pola + R + CHP
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39
Q

R-CHOP

A
  • rituximab
  • cyclophos
  • doxorubicin
  • vincristine
  • prednisone
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40
Q

DA-EPOCH + RituximB

A
  • Etop
  • Prednisone
  • Vincristine
  • Doxorubicin
  • cyclophose
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41
Q

Pola + R + CHP

A
  • polatuzumab vedotin
  • rituximab
  • cyclophose
  • doxorubicin
  • prednison

VERY Expensive

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42
Q

Stage I-II DLBCL treatment

A

3 cycles R-CHOP + RT
OR
6 cycles R-CHOP

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43
Q

Stage III-IV (+bulky stage 2)

A
  • 6 cycles R-CHOP
  • 6 cycles Pola + R + CHP
    IPI ≥ 2
44
Q

R-CHOP Toxicities

A
  • neutropenia
45
Q

NHL Rituximab and Hep B

A
  • test for HBsAg and HBcAb prior to anti-CD20 directed therapy
  • treat wit hentecavir 0.5 mg daily
46
Q

Anti-CD20 late neutropenia DLBCL treatment

A

G-CSF
IVIG for refractory

47
Q

Relapsed DLBCL/Aggressive NHL

A
  • salvage chemo followed by autologous stem cell rescue
  • better outcome if patient in complete remission going into transplant
  • Bendamustine + rituximab + polatuzumab (palliative)
  • BITE (epcoritamab, glofitamab)
48
Q

What is the target antigen for CAR T-cells

A

CD19

49
Q

BITE

A
  • third line option after 2 lines of systemic therapy
  • CD3 on t cell and CD20 on b cells
  • activation of t cells =b cell lysis
50
Q

CRS Treatment

A
  • tocilizumab (anti-IL 6)
  • steroids
  • supportive care
51
Q

ICANS (neurotoxicity syndrome)

A
  • tremors, AMS, seizures, cerebral edema, neurological assessments (hand writing)
  • steroids
52
Q

MM Pathology

A
  • plasma cells and MM cells produced from differentiated B cells
  • secrete immunoglboulins (IgG, IgA)
53
Q

Transformation to MM

A
  • precedued by MGUS ans smoldering (asymptomatic MM)
54
Q

MM CRAB

A
  • Calcium > 11.5 mg/dL
  • renal dysfunction SCr > 2 mg/dL or CrCL < 40 mL/min
  • ANemia <10 or 2 g/dL below normal
  • Bone: osteolytic lesions of patho fractures
55
Q

MM Treatment Overview

A
  • induction (chemo)
  • consolidation (autologus stem cell transplant)
  • maintenance
56
Q

MM is the patient a transplant candidate

A
  • No: 3 drug regimen
  • Yes: 3 drug regimen x3-4 then stem cell transplant
57
Q

MM Agents

A
  • steroids
  • thalidomide (-domide)
  • proteasome inhibitors (-zomib)
  • traditional chemo (cyclophos, doxorubicin)
  • Mabs (daratumumab)
  • Car T-cell therapy
  • Selinexor
  • BITE
58
Q

VRD MM

A

lenalidomide
dexamethasone
bortezomib
(more neuropathy, longer progressive free survival)

59
Q

CML Patho

A
  • unregulated myeloid proliferation –> excess mature neutrophil production
  • BCR-ABL
60
Q

CML Presentation

A
  • incidental finding durign routine exam
  • Leukostasis (1,000,000 cells/ mm3)
61
Q

CML Diagnosis

A
  • bone marrow biopsy required
  • FISH to assess philidelphia chromosome
  • PCR to assess bCR-aBL transcript baseline
62
Q

Chronic Phase CML

A

< 10% blasts

63
Q

CML Accelerated Phase

A
  • progressive
  • 10-19% blasts
  • increasing spleen size
  • bone marrow evidence of progresssion
64
Q

Blast Crisis CML

A
  • terminal stage
  • resembles acute leukemia
65
Q

CML

A
  • only cure is allogenic stem cell transplant
  • TKI for disease control
66
Q

CML Molecular response

A

Early: BCR-ABL ≤ 10% at 3 and 6 months

Major (MMR)≤0.1% or ≥ 3 log decrease

Deep: BCR-ABL ≤ 0.01%

67
Q

CML TKI

A
  • imatinib
  • dasatnib, nilotinib, bosutinib
  • all are approved in first line setting
68
Q

What should you avoid with dasatinib

A

acid reducers

69
Q

Which BRC-ABL TKI causes qtc prolongation and metabolic syndrome?

A

nilotinib

70
Q

Posatinib side effects

A
  • ischemic rxn
  • vascular occlusion
  • hypertension
71
Q

Aciminib

A
  • CML
  • can be used in T315I resistent CML
72
Q

2nd line treatment CML

A
  • dose escalation of imatinib
  • second generation TKI
  • 3rd generation TKI (pon, asciminib, omacetazine)
  • allogenic SCT
73
Q

CML TKI Discontinuation

A
  • no history of AP or BP
  • on TKI for 3 years
  • Deep molecular response
  • stable deep response for ≥ 2 years, seen 4 times with test at least 3 months apart
74
Q

Monitoring after TKI discontinuation

A
  • PCR q 3 months
75
Q

CLL Patho

A

monoclonal b lymphocyte transformation

76
Q

CLL Cytogenetics

A
  • Del (11q) associated with exgtensive lymphadenopathy, shorter median survival
  • Del (17p) worst outcomes
77
Q

Where does the CLL 17p deletion impact

A

G2 checkpont, causes the cell to keep dividing

78
Q

Favorable CLL prognosis

A

Del (13q) only abnormality
wild type Tp53

79
Q

CLL Treatment

A
  • stage II or IV
  • Clinical symptoms
  • end organ dysfunction
  • do not treat a number!
80
Q

No Del17q/p53 mutation CLL treatment

A
  • BTK inhibitor ± anti-CD20mAB
  • venetoclax + obinutuzumab
  • chemo immunotherappy
81
Q

No Del17q/p53 mutation CLL treatment

A

BTK + obinutuzumab
or venetoclax + obinutuzumab

82
Q

Ibrutinib vs Zanubrutinib vs Acalabrutinib

A
  • CLL BTK inhbitior
  • Zanubrutinib less toxicities, better response
  • acalabrutinib decreases atrial fibrilation
83
Q

-brutinib indication

A

indicated for relapse, disease refractory

84
Q

Venetoclax Interactions

A
  • PGP
  • CYP 3A4
85
Q

Lymphocytosis or Tumor flare in CLL

A
  • BTK inhibitors
86
Q

AML Patho

A

leukemic cells proliferate and crowd out normal cells

87
Q

Which treatments cause secondary AML

A
  • topo II
  • alkylating agent
88
Q

AML Presentation

A
  • pancytopenia
  • bone pain
  • gum hypertrophy
89
Q

AML Diagnosis

A
  • bone marrow biopsy
  • greater than >20% blast
90
Q

Poor AML

A

FLT3 mutation
- midostaurin
- quizartinib
- gilteritinib (2nd line)

91
Q

AML Treatment Overview

A
  • bone marrow for diagnosis
  • induction (remission
  • bone marrow to confirm remisison
  • consolidation (chemo or SCT)
92
Q

Intensive induction eligible

A

Cytarabine (7 days) and idarubicin or daunorubicin (3 days)

93
Q

Intensive induction inelegible (AML)

A
  • venetoclax + hypo-methylating agent
94
Q

AML consolidation

A
  • 3-4 cycles of high dose cytarabine
  • continue venetoclax + hypmethylating agent
  • allogenic stem cell transplatn
95
Q

AML APL

A
  • t(15;17) = PML:RARA
  • trans retinoic acid
  • arsenic trioxide
96
Q

ALL Patho

A

leukemic cell crowds out normal cells

97
Q

Risk factors for ALL

A

genetic
EBV
HIV
radiaiton

98
Q

ALL presentation

A
  • pancytopenia
  • bone pain
  • gum hypertrophy
  • lymphadenopathy
  • abdominal masses
  • painless testicular enlargement
99
Q

ALL Diagnosis

A

bone marrow biopsy with ≥ 20% blasts
mostly b cell

100
Q

ALL metastases

A
  • brain and testis
  • intrathecal chemo
101
Q

FAcotr in ALL

A

BRC-aBL or 9;22 mutation

102
Q

Ph Positive ALL

A

tKI + multiagent chemo
TKI + steroids
TKI + blinatumumab

maintenance: TKI+vincristine+ pred

103
Q

PH negative

A

multiagent chemo
maintenance MTX+6mp+vincristine

104
Q

ALL HyperCVAD

A
  • hyperfractionated cyclophos
  • vincristine
  • docorubicin
    -dexamethadose
    for 21 days

+

mtx, cytarabine, vincristine intrathecal
for 21 days

105
Q
A

PHRM 864 (10 decks)

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