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444-Oncology and Neurology > Lymphoma and MM > Flashcards

Lymphoma and MM Flashcards

1
Q

what is lymphoma

A

group of lymphoproliferative disorders originating in lymphocytes/ lymphatic tissue

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2
Q

what is the defining feature of hodgkin’s lymphoma

A

reed-sternbery cell

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3
Q

describe hodgkin’s lymphoma

A

B cell only, aggressive

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4
Q

3RF for hodgkin’s lymphoma

A

prolonged EBV infection, family Hx, (siblings of same sex), HIV

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5
Q

nonhodgkin’s lymphoma RFs

A

HIV, FHx (first degree), EBC, H pylori, MALD, burkitt, weakened immune sx, autoimmune disease

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6
Q

types of NHL

A

B (DLBCL), T, or NK/T cell
can be indolent or aggressive

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7
Q

diagnosis of B cell lymphoma rquires

A

Excisional lymph node biopsy of preferably largest regionally involved lymph node
For extranodal lymphomas = use sizable biopsy from organ of origin
Fine needle biopsy inadequate for initial diagnosis

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8
Q

when the excised lymph node is examined by the pathologist, what will they look for?

A

phenotyping- CD20 on B cells
gene rearrangements
EBV

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9
Q

what additional workup may be done for lymphomas besides lymph node examination

A

CT/PET
IPI score
lab chemistries
testing for comorbidities- pregnancy, HIV, EBV, hep B, pulmonary and ECHO/MUGA test if bleomycin or anthracyclines

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10
Q

stage of lymphoma if Single lymph node region (I) or one extralymphatic organ

A

1

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11
Q

stage of lymphoma if local extralymphatic extension plus lymph nodes, same side of diaphragm

A

2

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12
Q

stage of lymphoma if 2 or more lymph node regions, same side of diaphragm

A

2E

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13
Q

stage of lymphoma if local extra lymph extensions

A

3E

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14
Q

stage of lymphoma if lymph node regions on both sides of the diaphragm either alone

A

3

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15
Q

stage of lymphoma if Diffuse involvement of one or more extralymphatic organs or sites

A

4A (if no B sx)

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16
Q

stage of lymphoma if Diffuse involvement of one or more extralymphatic organs or sites with unexplained weight loss >10% from baseline within 6 mths of staging, unexpected fever >38C, or drenching night sweats

A

4B

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17
Q

list the 3 B sx

A

unexplained weight loss >10% from baseline in 6mths
unexpected fever >38C
drenching night sweats

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18
Q

what is treatment for DLBCL

A

RCHOP
rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone

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19
Q

rituximab 3 sus MOA

A

binds CD20 and cells die either by being recognized by effector cells, complement activation, or direct cell death

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20
Q

most common rituximab AE + what to do to prevent it

A

infusion reaction
premedicate with acetaminophen, diphenhydramine or loratidine, hydrocortisone, ranitidine or famotidine
hold ACEi/ARBs 24hrs pre

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21
Q

how should rituximab therapy be initiated

A

first dose should always be given IV, if no AEs, next dose can be given SQ
if first dose was not complete due to AEs, must have one full IV dose before SQ possible

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22
Q

what is the difference between IV and SQ rituximab

A

IV is dosed by 375mg/m2, SQ is a fixed flat dose of 1400mg

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23
Q

cyclophosphamide AEs

A

hemorrhagic cystisis
N/V- HEC with doxorubicin in RCHOP
myelosuppression, alopecia, fertility suppression

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24
Q

cyclophosphamide MOA

A

Alkylating agent- nitrogen mustard type: binds to DNA + cross links DNA and RNA = no protein synthesis

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25
Q

doxorubicin MOA

A

Anthracycline: inhib TP2 and prevents relegation of DNA during replication
Damages DNA and cell membranes by producing free radicals

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26
Q

doxorubicin AEs

A

cardiotoxicity
- late onset: reduced LVEF or CHF (more common)
- early onset: acute transient ECG changes to arrhythmia
myelosuupression
HEC with cyclophosphamide in RCHOP
alopecia
discoloration of urine

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27
Q

what must be done before initiating doxorubicin in RCHOP

A

ECHO or MUGA- LVEF must be =>50%

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28
Q

vincristine MOA

A

Vinca alkaloid - binds to tubulin (protein on spindle) and prevents mitosis
IV admin only (fatal if intrathecal)

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29
Q

vincristine AEs

A

Neurotoxicity
Peripheral neuropathy
Autonomic neuropathy- constipation (may require stool softeners and laxatives prophylactically)

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30
Q

what to monitor for prednisone in RCHOP

A

blood glucose- diabetics esp
mood changes
insomnia- may require zopiclone on prednisone days
GERD- take with food

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31
Q

what is included in supportive care for RCHOP

A

antinauseants
infection prevention (entecavir or tenofovir for HepB prophylxis)
prophylaxis for tumor lysis syndrome

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32
Q

factors reducing chances of cure in hodgkin’s lymphoma

A

Stage IV, ≥3 extranodal sites
Age ≥45yrs old
Male gender
Albumin <40
High WBC count (≥15)
Lymphocytopenia (lymphocytes <8% or <0.6%)
Hg <105

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33
Q

factors that reduce ability to tolerate intense chemo in hodgkin’s

A

≥60yrs old
ECOG >2
HIV +

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34
Q

2 treatments for hodgkin’s

A

Esc-BEACOOP
ABVD

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35
Q

what is Esc-BEACOOP for HL
(BLEHCOPP)

A

bleomycin
etoposide
doxorubicin
cyclophosphamide
vincristine
procarbazine
prednisone

36
Q

what is ABVD
(DBVD)

A

doxorubicin
bleomycin
vinblastine
dacarbazine

37
Q

the A in HL treatments stand for

A

doxorubicin

38
Q

bleomycin MOA

A

Causes DNA strand scission through formation of an intermediate metal complex

39
Q

bleomycin AEs

A

respiratory effects- pulmonary tests + CXR before and periodically
derm effects
mucositis and stomatitis
loss of appetite

40
Q

vinblastine MOA

A

vinca alkaloid that binsd to tubulin and prevents mitosis

41
Q

AEs of vinblastine

A

less neurotoxicity than vincristine
more myelosuppression

42
Q

which is more myelosuppressive
1. vincristine
2. vinblastine

A

2

43
Q

which is more neurotoxic
1. vincristine
2. vinblastaine

A

1

44
Q

dacarbazine MOA

A

Prodrug for MTIC -cytotoxicity thought to be due to methylcarbonum ions that attach nucleophilic groups in DNA

45
Q

dacarbazine N/V severity

A

HEC

46
Q

procarbazine MOA

A

Alkylating agent- MOA not clear, could be free radical damage

47
Q

what to watch out for with procarbazine

A

MAOi activity = avoid high tyramine content foods and alcohol- disulfaram reaction
avoid sympathomimetic drugs

48
Q

procarbazine AEs

A

infertility (ovarian failure, azoospermia), bone marrow suppression, secondary malignancies

49
Q

T or F: MM is curable with transplant

A

F- incurable

50
Q

what is CRAB in MM

A

calcium >2.75
renal function (Cr >176)
anemia
bone lesions or osteopenia with compression fractures

51
Q

what is a common symptom of MM

A

hypercalcemia

52
Q

hypercalcemia is an oncologic emergency when

A

it causes sig phys dysfxn like: dehydration, mental status changes, cardiac arrhythmias, renal insuff or failure

53
Q

what is a normal serum Ca level

A

2.2-2.6

54
Q

what is important to consider when reading a pt’s calcium level

A

most labs report Ca as total calcium both bound and unbound
those with hypoalbuminemia may have high unbound, but total still looks normal
use corrected calcium for estimation of phys active calcium

55
Q

corrected calcium equation

A

Corrected calcium (mmol/L) = measured calcium (mmol/L) + ([40-albumin (g/L)]x0.02)

56
Q

tx of hypercalcemia

A

hydration with NS
bisphosphonates (promotes Ca elimination + inhibits further Ca release from bone)
calcitonin (promotes excretion of Ca)

57
Q

malignant expansion of plasma cells usually in bone marrow, monoclonal protein (M-protein) in serum or urine.

A

multiple myeloma

58
Q

what is the marker in multiple myeloma

A

CD38 o nplasma cells

59
Q

is MM aggressive or indolent

A

aggressive

60
Q

what type of cell does MM affect

A

plasma cells

61
Q

what type of cells does lymphoma affect

A

lymphocytes

62
Q

what is the M protein

A

monoclonal protein secreted by malignant plasma cell- can be produced uncontrollably + not functional

63
Q

what is the problem in MM with having too many malignant plasma cells

A

crowding of bone marrow = pancytopenia
bone damage from bone marrow crowding- increased osteoclast function and decreased osteoblast function = bone weakening and hypercalcemia
no normal plasma cell functioning = inefctions

64
Q

what is the issue in MM with haaving too many monoclonal proteins

A

too many proteins in bloodstream = kidney damage = cast nephropathy, anemias
increased serum viscosity

65
Q

what is the diagnostic criteria for MM

A

M protein in serum and/ or urine
Clonal bone marrow plasma cells or plasmacytoma
Presence of myeloma sx

66
Q

what is the ß2M (Beta-2-microglobulin)

A

protein on membrane of nucleated cells that becomes elevated with high cell turnover. Elevated levels = poor prognostic factor in MM

67
Q

which of the following is not a goal of therapy with MM
1. cure
2. disease control
3. improve QoL
4. prolong survival

A

1

68
Q

treatment for MM typically include ________ for transplant eligible pts

A

induction, consolidation, autologous transplant, maintenance

69
Q

what is the treatment for MM if pt is not eligible for transplant

A

pharmacotherapy to reduce tumor burden

70
Q

4 drugs for transplant ineligible MM pts

A

bortezomib
dexamethasone
daratumumab
lenalidomide

71
Q

bortezomib MOA

A

reversible inhibitor of the 26S proteasome- inhibition alters regulatory proteins = cell cycle arrest + apoptosis
Can be given IV or SC, fatal if given intrathecally

72
Q

AEs of bortizomib

A

herpes zoster reactivation (all pts should be given HSV/VZV prophylaxis with acyclovir or valacyclovir), neuropathy, thrombocytopenia, constipation/ diarrhea

73
Q

bortezomib interacts with

A

green tea- lowered bortezomib’s antiproliferative effect of myeloma cells

74
Q

dexamthasone MOA in MM

A

cytotoxic to myeloma cells likely via apoptosis
Pulse dosing (ex 40 mg po once weekly)

75
Q

daratumumab MOA in MM

A

monoclonal abx that targets CD38

76
Q

daratumumab AEs and how to deal

A

infusion rxn in 50% = premedicate with antihistamines, acetaminophen, corticosteroids, H2 acid inhibitors

77
Q

lenalidomide MOA

A

thalidomide derivative = immunomodulatory, antiangiogenic, and antineoplastic characteristics via multiple mechs

78
Q

lenalidomide AEs

A

teratogenic, DVT/PT, edema, thrombocytopenia and neutropenia
Requires renal dosing adjustment if kidney fxn poor

79
Q

T or F: with the REVAID program, pharmacists must counsel with every rx, even a refill for thalidomide derivatives

A

T

80
Q

what do BPs do in MM

A

prevent hypercalcemia by enhancing Ca elimination and preventing further skeletal release of Ca
less vertebral fractures, skeletal related events, pain

81
Q

bisphosphonate AEs

A

osteonecrosis of jaw precipitated by dental work involving manipulation of mandibular and maxillary bones

82
Q

how to minimize risk of ONJ with BPs

A

Prior to initiating therapy with bisphosphonates, a comprehensive dental evaluation should be performed and all invasive dental procedures be completed.
Annual dentist visits and maximal preventive care.
Avoid dental extractions if possible.

83
Q

what to do if a pt on BPs with MM needs a dental extraction

A

hold BPs 1mth before procedure and resume after recovery

84
Q

all _______ pts should receive prophylaxis for shingles with acyclovir or valacyclovir

A

bortezomib

85
Q

what is used to mobilize stems cells into peripheral blood for an autologous stem cell transplant

A

filgrastim or chemo or both

444-Oncology and Neurology (22 decks)

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