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Oncology Exam 3 > Multiple Myeloma > Flashcards

Multiple Myeloma Flashcards

1
Q

Median age of diagnosis MM

A

70 years

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2
Q

T/F MM is more common in African Americans compared to Caucasians

A

True

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3
Q

MM occurs in which cells?

A

plasma cells –> Ig producing cells

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4
Q

MGUS (monoclonal gammopathy of unknown significance) is what?

A

pre-myeloma disease

1% per year progression to MM

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5
Q

What do MM cells secrete?

A

cytokines/chemokines

IL-6, VEGF, RANKL, etc

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6
Q

______ are activated and ______ are inactivated in MM causing -_________

A

osteoclasts
osteoblasts
severe bone disease

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7
Q

CRAB acronym is for what?

What does it stand for?
Incidence of each?

A 
MM
C = hypercalcemia (25%)
R = renal failure (50%)
A = anemia (70%)
B = bone lesions (80%)
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8
Q

Symptoms of MM

A

bone pain
fatigue
recurrent infection

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9
Q

T/F about 20% of MM lack light chain and secrete heavy chain

A

False

20% lack heavy chain
Secrete light chain

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10
Q

What is detected on SPEP in 80-90% of MM when coupled with immunofixation?

A

m protein

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11
Q

Diagnosis of MM requires

A

plasma cells in marrow or plasmacytoma
+
M protein in serum/urine

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12
Q

What all is used in diagnosis of MM?

A

lytic bone lesion

urine electrophoresis

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13
Q

Low risk smoltering MM treatment

A

Observation or

Lenalidomide + low dose dexamethasone

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14
Q

High risk smoltering MM treatment

A

Observation or

Lenalidomide + low dose dexamethasone

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15
Q

Ultra high risk smoltering MM treatment

A

Lenalidomide + low dose dexamethasone

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16
Q

Characteristics of high risk smoltering MM

A

free light chain ratio of at least 8 and cytogenetics

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17
Q

Anemia in MM

A

fatigue, weakness, SOB

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18
Q

Renal dysfunction in MM

A

rising SCr due to tubular obstruction with light chains, IgG and IgA

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19
Q

Hypercalcemia in MM

A

due to bone lesions

dehydration, CNS, etc

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20
Q

Bacterial infections in MM

A

decreased normal IgG and decreased lymphocyte function

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21
Q

Osteolytic lesions in MM

A

Local secretion of IL-6, IL-1, RANK-L leads to increase osteoclast activity and decreased osteoblast activity

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22
Q

Neurologic symptoms in MM

A

cord compression

hyeprviscosity syndrome

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23
Q

Partial response (PR) in MM

A 
>/= 50% decrease in M protein
>/= 90% decrease in 24 hour urine light chain
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24
Q

Very good partial response (VgPR) in MM

A

Negative SPEP

Serum and urine M protein detected on immunofixation

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25
Q

Complete remission (CR) in MM

A

negative SPEP and negative urine immunofixation
no soft tissue plasmacytomas
<5% plasma cell in bone marrow

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26
Q

Stringent CR (sCR) in MM

A

meets all criteria for CR and normal free light chain ratio (FLC)

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27
Q

Immunomodulatory drugs (IMiDs) in MM

A
  • Thalidomide
  • Lenalidomide
  • Pomalidomide
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28
Q

T/F Lenalidomide has a higher %CR in MM than thalidomide

A

true

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29
Q

T/F lenalidomide is not teratogenetic?

A

false!
none in rabbits
yes in monkeys

REMS program

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30
Q

ADE of thalidomide

A
  • REMS
  • VTE
  • sedation
  • neuropathy
  • toxic epidermal necrolysis
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31
Q

ADE of lenalidomide

A
  • REMS
  • VTE
  • myelosuppression
  • rash
  • fatigue
32
Q

ADE of pomalidomide

A

similar to lenalidomide

33
Q

T/F combination chemotherapy is still use to treat MM

A

False!

no longer used due to better tolerated and more active alternatives

34
Q

T/F high dose dexamethasone is NOT used in MM treatment anymore

A

True!
Not well tolerated in older patients
Less active than combinations

35
Q

T/F low doses of oral melphalan + prednisone is used to treat MM

A

true
But seldom used due to well tolerated more active newer agents

  • cheap, oral, well tolerated
36
Q

Which of the IMiDs has more data for use in relapsed/refractory patients?

A

Pomalidomide

37
Q

T/F thalidomide is an analog of lenalidomide

A

False!

Lenalidomide is an analog of thalidomide

38
Q

Which proteasome inhibitors are used in MM?

A

Bortezomib
Carfilzomib
Ixazomib

39
Q

What is the main treatment regimen for MM?

A

IMiDs + low dose dexamethasone

40
Q

ADE of bortezomib

A

Myelosuppression
Neuropathy
Immunosuppression

41
Q

ADE of carfilzomib

A 
myelosuppression
liver
cardiac
neuropathy
pulmonary
42
Q

ADE of ixazomib

A

myelosuppression

neuropathy

43
Q

What is the first oral proteasome inhibitor used in MM?

A

Ixazomib

44
Q

Induction therapy for MM

A

ASCT

45
Q

ASCT non-candidates

A

frail low risk patients - use 2 drug regimen (Rd)

frail high risk patients - use 3 drug regimen (VRD)

46
Q

How many cycles of induction do ASCT candidates use?

A

4 cycles
VRd
KRd

47
Q

MM chemotherapy IMiD combinations

A
  • Melphalan or CTX + IMiDs or proteasome inhibitors
  • Liposomal doxorubicin + bortezomib
  • Bendamustine + lenalidomide + bortezomib
48
Q

Novel agents in MM

A

Panobinostat
Elotuzumab
Daratumumab

49
Q

MOA of panobinostat

A

Pan histone deacetylase inhibitor

50
Q

MOA of elotuzumab

A

antibody which targets SLAM F7

51
Q

MOA of daratumumab

A

antibody which targets CD38

52
Q

When are the novel agents used in MM?

A

salvage therapy

53
Q

What is panobinostat used with?

A

carfilzomib and panobinostat + bortezomib + dexamethasone

54
Q

What is elotuzumab used with?

A

bortezomib + dexamethasone

55
Q

What is daratumumab used with?

A

bortezomib or lenalidomide + dexamethasone

56
Q

ADE of panobinostat

A

myelosuppression
diarrhea
neuropathy

57
Q

ADE of elotuzumab

A

myelosuppression

infusion reactions

58
Q

ADE of daratumumab

A

myelosuppression

infusion reactions

59
Q

T/F two AutoHSCT transplants (tandem) may be used in MM patients

A

true!

in patients who receive suboptimal response with first transplant

60
Q

t/f low dose melphalan is used to prepare patients for autoHSCt

A

false

High dose

61
Q

T/F autoHSCT cannot be used at the time of relapse

A

false

62
Q

Stem cell collection in MM for autoHSCT

A

collect sufficient cells to do multiple transplants BEFORE receiving HD melphalan

63
Q

Allogeneic transplant in MM

A

full intensity transplant –> high early mortality

reduced intensity transplant –> high relapse rates

64
Q

T/F allogeneic transplant is first line in MM

A

false!

no major role in treating MM

65
Q

Should triple therapy or double therapy be used in MM?

A

triple therapy has improved progression free survival

66
Q

Who would you use Melphalan + prednisone in MM?

A

older patients with symptoms

67
Q

How long is induction in MM before autoHSCT?

A

4 months!

68
Q

When would you consider someone relapsed/refractory MM?

A

if progression occurs > 6 months after end of primary induction

69
Q

T/F in relapsed/refractory MM you can repeat the same induction therapies

A

false!

switch to a different drug1

70
Q

T/F relapsed MM patients have a higher risk of VTE than newly diagnosed

A

false

other way around

71
Q

Which drug class doesn’t add to VTE risk in MM?

A

proteasome inhibitors

72
Q

VTE in MM is usually due to which drugs?

A

IMIDs or dexamethasone

73
Q

MM patient with underlying risk of VTE or high risk drug combo what do you give?

A

LMW heparin

74
Q

MM patient without underlying risks for VTE and receiving lenalidomide + low dose dexamethasone what do you give?

A

ASA

75
Q

Bone disease in MM treatment

A

Bisphosphonates

reassess in 2 years –> risk of ONJ and renal toxicity

Oncology Exam 3 (6 decks)

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