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PHM 703: Crit Care/Heme/Onc > Onco 2: Lymphohohohoma > Flashcards

Onco 2: Lymphohohohoma Flashcards

1
Q

risk factors for lympohma

A
  1. male
  2. older age (and younger agen in hodgkiins)
  3. immunosuppression
  4. enovironmental
  5. radiaiton
  6. infections (Epstein and HIV)

numbered for footnote, not in order

  • 3, 4, 5 esp in DLBCL
  • 6 esp in Hodgkin’s
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2
Q

B symptoms

A

seen in 30% of all B cell lympohomas
- fever
- wt loss (10% over 6 months)
- nigh sweats

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3
Q

Diffuse large B cell (DLBCL) relapse

A
  • even though it’s curable, it’s so aggressive, high chance of relapse
  • CAR-T
  • BsAb (bispecifc Ab)
  • autologous stem cell transplant
  • salvage chemo
    - R-ICE
    - GDP
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4
Q

R-ICE

A
  • Rituximab
  • Ifosfamide
  • Carboplatin
  • Etoposide
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5
Q

GDP

A
  • Gemcitabine
  • Dexamethasonne
  • carboPlatin

refractory - salvage chemo

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6
Q

DLBCL presentaiton

A
  • B symptoms
  • nodal mass
  • elevated lactate dehydrogease
  • bone marrow involvement
  • AMS
  • laboratory abnoralities: SCr, uric acid, LFTs, electolytes

ympoh nodes lysing (can lead to TLS) -> the dehydrogenase and alb abnormalities

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7
Q

DLBCL dx

A

lympoh node bioposy
- IHC panel to look for ccertain mutations: for non-Hodgkin’s, CD20 is important
- imaging (PET scan) to fiure out what to biopsy

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8
Q

DLBCL prognosis

A

use the IPI (international prognosis index)
- low score = high risk -> poorer outcomes

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9
Q

DLBCL treatment

standard treatment (does not include the ifs: EF, CNS, frail)

A
  • preferred: R-CHOP or pola-R-CHP
  • other: DA-R-EPOCH

  • no difference between pola-R-CHP and R-CHOP except that pola may be better for pts with subtype ABC
  • DA-R-EPOCH preferred in more aggressive lympohomas: CMAC, BCL2 and BCL6
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10
Q

DLBCL treatment in pts with EF < 40%

A

canNOT receive doxorubucin at regular dose/infusion/formulation
- DA-R-EPOCH: slower infusion -> less cardiotox
- R-CDOP: liposomal doxorubicin instead of regular
- R-CEOP

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11
Q

DLBCL treatment in frail pts or pts > 80

A
  • R-mini-CHOP
  • R-CDOP
  • R-CEOP
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12
Q

DLBCL treatment in pts with parenchymal presnetiaton

A

R-CHOP + high dose MTX

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13
Q

DLBCL treatment in pts iwth leptomenigeal presentaiton

A

intrathecal MTX/cytarabine

OR R-CHOP with high dose MTX

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14
Q

R-CHOP

A
  • Rituxima
  • Cyclophosphamide
  • Hdryoxydaunorubicin (doxorubicin)
  • Ocovin (vincristine)
  • Prednisone
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15
Q

Pola-R-CHP

A
  • Polatuzumab vedotin
  • Rituximab
  • Cyclophosphamide
  • Hdryoxydaunorubicin (doxorubicin)
  • Prednisone

NO vincrisitne dt severe neuropathy risk

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16
Q

DA-R-EPOCH

A
  • Dose Adjusted
  • Rrituximab
  • Etoposide
  • Cyclosphosphamide
  • Hdryoxydaunorubicin (doxorubicin)
  • Ocovin (vincristine)
  • Prednisone

give G-CSF ppx dt febrile neutorpenia risk

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17
Q

R-CDOP

A
  • Rituxima
  • Cyclophosphamide
  • Doxorubicin (liposomal)
  • Ocovin (vincristine)
  • Prednisone
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18
Q

R-CEOP

A
  • Rituxima
  • Cyclophosphamide
  • Etoposide
  • Ocovin (vincristine)
  • Prednisone
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19
Q

R-CEPP

A
  • Rituxima
  • Cyclophosphamide
  • Etoposide
  • Prednisone
  • Procarbazine
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20
Q

what makes DA-R-EPOCH “dose adjusted”

A

twice weekly labs
- ANC and plts too high icrease dose
- ANC and plts too low, decrease dose

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21
Q

why did R-CHOP become the mainstay isntad of CHOP

A

MiNT trial: rituxuimab improves surival vs CHOP wihtout increasing tox

22
Q

R-CHOP overall ADR

A
  • high emetic risk
  • moderate febrile neutropenia risk (consdier G-CSF)
  • infections
  • fattigue
  • anemia, neutropenia, thromboctyopenia
  • alopecia
23
Q

doxorubicin ADR

A

cardiotox -> max lifetime dose

24
Q

vincristine ADR

A
  • peripheral neuropathy: max dose 2mg
  • constipation
25
Q

cyclosphosphamdie ADR

A

hemorrhagic cystitis (though this is unlikely at CHOP dose)

26
Q

rituximab MOA

A

anti-CD20

27
Q

rituximab ADR

A
  • infusion relataed rxn -> premiedicae and give first dose over 6 hrs (if well tolerated can give susbequent doses in like 60-90min)
  • HepB reactivation
  • hypergammaglobinuemia (B cell depletion) - consider holdign for first cycle if lyphoma in GI tract dt perforation
  • progressive multifocal leukoencephalopathy
28
Q

when to give entavacir in pts receiving rituximab

A

if pt has chronic HepB
- HBsAg (+) and antiHBC (+)

29
Q

polatuzmab MOA

A

antiCD79B antibody-drug (vedotin) complex
- mab directly delivers drug to tumor

30
Q

polatuzumab ADR

A
  • constsipation
  • skeletomuscular pain
  • peripheral neuropathy
  • infusion reaction
  • anemia, neutropenia, thrombocytopenia
31
Q

CLL/SLL

A

accumulation of immunologically dysfunctional mature B lympohcytes
- up to 50% pts do NOT need treatment

32
Q

CLL/SLL sympotms

A

only 30% of pts symptomatic
- enlarged lympoh nodes
- enlarged spleen or liver
- B symptoms
- autoimmune cytopenia; hemolytic anemia or ITP
- hypergamaglobinemia -> frequent infeciotsn

33
Q

CLL/SLL prognosis factors

A

unfavorable outcomes if
- del(17p)
- Tp53 mutation

34
Q

who gets treatment in CLL/SLL

A
  • sympotomatic: B sympoms
  • end organ damage
  • progression of bulky disease: splenomegaly or lypohadenopathy
  • bone marrow failure: anemia, thrombocytopenia
  • disease outside of lymph ndes
35
Q

CLL/SLL treatment: of pts who are getting treatment, who gets fixed duration adn who gets indefinite and what’s the treatment

A
  • indefiite: elderly, poor performing, pt preference
    - (acalabrutinib +/- obinutuzumab) OR (zanubrutinib)
  • fixd duraiton: younger, good performing (no comorbidites, no renal impairment
    - venetoclax + obinutuzumab
36
Q

Obinutuzumab MOA

A

2nd gen antiCD-20 (lil more potent than rituximab)
- Ab dependent cellular cytotox
- complement dependent cytotox
- Ab dependent phagocytosis
- activation of lysosomes -> cell death

37
Q

Obinutuzumab ADR

A
  • infusion reaction -> titration schedule for first cucle and pre-medicate
  • Hep B reactivation - chekc panel prior to start
  • incrased risk of viral infectionN: acyclovir ppx
38
Q

BTKi MOA

A

bruton tyrosine kinase inhibitors
- bind to BTK enzyme -> prevent BCR sgnaling
- prevent proliferation and surivval of malignant nad normal cells

on initiation may have transient increase in lympohcyte count -> does NOT mean disease progression

39
Q

BTKi ADR

by agent

A
  • ibrutinib: neutropenia, afib, HTN, bleed, diarrhea
  • acalabrutinib: HA and musculosketela pain (self resolving, APAP and NSAIDs prn)
  • zanubrutinib: neutropenia (and least likely to cause afib)
40
Q

classical Hodgkin’s presentaiton

A

presence of mature B cells with 2 nuclei (Reed-Sternberg cells)
- B sympotoms
- lymphadenopathy - lympoh node biopsy (+) for CD30+
- gneralize malaise: cough, SOB, decreased appetite

41
Q

classical Hodgkin’s treatment

cHL

A

goal is cure
- stage I/II (whether or not favorable or bulky: ABVD
- stage III/IV: ABVD or BV+AVD

42
Q

ABVD

A
  • Adriamycin (doxorubicin)
  • Bleomycin
  • Vinblastine
  • Dacarbazine
43
Q

BV-AVD

A
  • Brentuximab Vedotin
  • Adriamycin (doxorubicin)
  • Vinblastine
  • Dacarbazine

no bleomycin dt pulm tox

44
Q

ABVD general ADR

A
  • high emetic risk -> high anti-emetic ppx
  • infection
  • fatigue
  • anemia, neutropenia, thrombocytopenia
  • alopecia
45
Q

bleomycin ADR

A

pulm tox
- avoid G-CSF despite some febrile neutropenia risk for ABVD; if pt at high risk for recurrence, can dc bleomycin and do G-CSF

can also dc bleomycin if pt doing well? we want to use lowest dose

46
Q

dacarbizine ADR

A

cytopenias

47
Q

brentuximab vedotin MOA

A

antiCD30 Ab-drug conjugate

48
Q

brentuximab vedotin ADR

A
  • peripheral neuroapthy
  • infusion rxn
  • anemia, neutropenia, thrombocytopenia
  • pulm tox
  • constipation

MUST give with G-CSF (febrile neutropenia risk?)

49
Q

non-Hodgkin’s relapse/refractory treatment

DLBCL

A

typically occurs within 3 yrs
- salvage chemo: R-ICE OR GVD
- autologous stem cell transplant
- immunotherapy (can add to salvage therapy): nivolumbab or pembrolizumab

50
Q

GVD

A
  • Gemcitabine
  • Vinorelbine
  • Doxorubicin (lipsomal)

PHM 703: Crit Care/Heme/Onc (16 decks)

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