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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
Relapsed HL Treatment
high dose chemo with autologous stem cell rescue ± maintenance brentuximab vendotin (if high risk disease post transplant)
26
NHL Patho
Malignant B or T lymphocytes and precursors (B cell more common)
27
NHL Risk Factors
- EBV (Burtkitt -> TLS, AIDS) - Immunodeficiency - environmental/physical agents
28
NHL Presentation
- B Cell: lymph nodes, spleen, bone marrow - T cell: extrandal sites (skin and lungs) - b symptoms in some patients - primary CNS lymphoma - NO ITCH
29
NHL Diagnosis
excisional biopsy lumbar puncture in patients at high risk or symptoms as NHL can metastasize in the brain
30
Indolent B Cell lymphomas NHL
usually incurable
31
Aggressive B Cell lymphoma NHL
- rapid growth - short survival - usually curable
32
Highly aggressive B cell NHL
- doubling tine = 18 hours - usully curable
33
what type of cancer is DLBCL
NHL
34
NHL Treatment Approaches
- RT - multi-agent chemo (backbone) - immuno - high dose chem with stem cell rescue - CAR-T - T-cell engagers
35
What type of cancer is Follicular Lymphoma
NHL (2nd most common type)
36
What can follicular lymphoma transform into
- Richter's transformation (aggressive nHL) - treat like DLBCL with rituzimab
37
DLBCL Genetic abnormalities
- Double/triple hit (MYC+ BCL2 or BCL6 transformation or all three)
38
DLBCL Treatment Regimens
- R-CHOP - DA-EPOCH + Rituximab - Pola + R + CHP
39
R-CHOP
- rituximab - cyclophos - doxorubicin - vincristine - prednisone
40
DA-EPOCH + RituximB
- Etop - Prednisone - Vincristine - Doxorubicin - cyclophose
41
Pola + R + CHP
- polatuzumab vedotin - rituximab - cyclophose - doxorubicin - prednison VERY Expensive
42
Stage I-II DLBCL treatment
3 cycles R-CHOP + RT OR 6 cycles R-CHOP
43
Stage III-IV (+bulky stage 2)
- 6 cycles R-CHOP - 6 cycles Pola + R + CHP IPI ≥ 2
44
R-CHOP Toxicities
- neutropenia
45
NHL Rituximab and Hep B
- test for HBsAg and HBcAb prior to anti-CD20 directed therapy - treat wit hentecavir 0.5 mg daily
46
Anti-CD20 late neutropenia DLBCL treatment
G-CSF IVIG for refractory
47
Relapsed DLBCL/Aggressive NHL
- 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
What is the target antigen for CAR T-cells
CD19
49
BITE
- 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
CRS Treatment
- tocilizumab (anti-IL 6) - steroids - supportive care
51
ICANS (neurotoxicity syndrome)
- tremors, AMS, seizures, cerebral edema, neurological assessments (hand writing) - steroids
52
MM Pathology
- plasma cells and MM cells produced from differentiated B cells - secrete immunoglboulins (IgG, IgA)
53
Transformation to MM
- precedued by MGUS ans smoldering (asymptomatic MM)
54
MM CRAB
- 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
MM Treatment Overview
- induction (chemo) - consolidation (autologus stem cell transplant) - maintenance
56
MM is the patient a transplant candidate
- No: 3 drug regimen - Yes: 3 drug regimen x3-4 then stem cell transplant
57
MM Agents
- steroids - thalidomide (-domide) - proteasome inhibitors (-zomib) - traditional chemo (cyclophos, doxorubicin) - Mabs (daratumumab) - Car T-cell therapy - Selinexor - BITE
58
VRD MM
lenalidomide dexamethasone bortezomib (more neuropathy, longer progressive free survival)
59
CML Patho
- unregulated myeloid proliferation --> excess mature neutrophil production - BCR-ABL
60
CML Presentation
- incidental finding durign routine exam - Leukostasis (1,000,000 cells/ mm3)
61
CML Diagnosis
- bone marrow biopsy required - FISH to assess philidelphia chromosome - PCR to assess bCR-aBL transcript baseline
62
Chronic Phase CML
< 10% blasts
63
CML Accelerated Phase
- progressive - 10-19% blasts - increasing spleen size - bone marrow evidence of progresssion
64
Blast Crisis CML
- terminal stage - resembles acute leukemia
65
CML
- only cure is allogenic stem cell transplant - TKI for disease control
66
CML Molecular response
Early: BCR-ABL ≤ 10% at 3 and 6 months Major (MMR)≤0.1% or ≥ 3 log decrease Deep: BCR-ABL ≤ 0.01%
67
CML TKI
- imatinib - dasatnib, nilotinib, bosutinib - all are approved in first line setting
68
What should you avoid with dasatinib
acid reducers
69
Which BRC-ABL TKI causes qtc prolongation and metabolic syndrome?
nilotinib
70
Posatinib side effects
- ischemic rxn - vascular occlusion - hypertension
71
Aciminib
- CML - can be used in T315I resistent CML
72
2nd line treatment CML
- dose escalation of imatinib - second generation TKI - 3rd generation TKI (pon, asciminib, omacetazine) - allogenic SCT
73
CML TKI Discontinuation
- 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
Monitoring after TKI discontinuation
- PCR q 3 months
75
CLL Patho
monoclonal b lymphocyte transformation
76
CLL Cytogenetics
- Del (11q) associated with exgtensive lymphadenopathy, shorter median survival - Del (17p) worst outcomes
77
Where does the CLL 17p deletion impact
G2 checkpont, causes the cell to keep dividing
78
Favorable CLL prognosis
Del (13q) only abnormality wild type Tp53
79
CLL Treatment
- stage II or IV - Clinical symptoms - end organ dysfunction - do not treat a number!
80
No Del17q/p53 mutation CLL treatment
- BTK inhibitor ± anti-CD20mAB - venetoclax + obinutuzumab - chemo immunotherappy
81
No Del17q/p53 mutation CLL treatment
BTK + obinutuzumab or venetoclax + obinutuzumab
82
Ibrutinib vs Zanubrutinib vs Acalabrutinib
- CLL BTK inhbitior - Zanubrutinib less toxicities, better response - acalabrutinib decreases atrial fibrilation
83
-brutinib indication
indicated for relapse, disease refractory
84
Venetoclax Interactions
- PGP - CYP 3A4
85
Lymphocytosis or Tumor flare in CLL
- BTK inhibitors
86
AML Patho
leukemic cells proliferate and crowd out normal cells
87
Which treatments cause secondary AML
- topo II - alkylating agent
88
AML Presentation
- pancytopenia - bone pain - gum hypertrophy
89
AML Diagnosis
- bone marrow biopsy - greater than >20% blast
90
Poor AML
FLT3 mutation - midostaurin - quizartinib - gilteritinib (2nd line)
91
AML Treatment Overview
- bone marrow for diagnosis - induction (remission - bone marrow to confirm remisison - consolidation (chemo or SCT)
92
Intensive induction eligible
Cytarabine (7 days) and idarubicin or daunorubicin (3 days)
93
Intensive induction inelegible (AML)
- venetoclax + hypo-methylating agent
94
AML consolidation
- 3-4 cycles of high dose cytarabine - continue venetoclax + hypmethylating agent - allogenic stem cell transplatn
95
AML APL
- t(15;17) = PML:RARA - trans retinoic acid - arsenic trioxide
96
ALL Patho
leukemic cell crowds out normal cells
97
Risk factors for ALL
genetic EBV HIV radiaiton
98
ALL presentation
- pancytopenia - bone pain - gum hypertrophy - lymphadenopathy - abdominal masses - painless testicular enlargement
99
ALL Diagnosis
bone marrow biopsy with ≥ 20% blasts mostly b cell
100
ALL metastases
- brain and testis - intrathecal chemo
101
FAcotr in ALL
BRC-aBL or 9;22 mutation
102
Ph Positive ALL
tKI + multiagent chemo TKI + steroids TKI + blinatumumab maintenance: TKI+vincristine+ pred
103
PH negative
multiagent chemo maintenance MTX+6mp+vincristine
104
ALL HyperCVAD
- hyperfractionated cyclophos - vincristine - docorubicin -dexamethadose for 21 days + mtx, cytarabine, vincristine intrathecal for 21 days
105

PHRM 864 (11 decks)

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