Multiple Myeloma Flashcards by Chelsea Luedtke

Median age of diagnosis MM

70 years

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

True

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MM occurs in which cells?

plasma cells –> Ig producing cells

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MGUS (monoclonal gammopathy of unknown significance) is what?

pre-myeloma disease

1% per year progression to MM

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What do MM cells secrete?

cytokines/chemokines

IL-6, VEGF, RANKL, etc

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

osteoclasts
osteoblasts
severe bone disease

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CRAB acronym is for what?

What does it stand for?
Incidence of each?

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

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Symptoms of MM

bone pain
fatigue
recurrent infection

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

False

20% lack heavy chain
Secrete light chain

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

m protein

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Diagnosis of MM requires

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

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What all is used in diagnosis of MM?

lytic bone lesion

urine electrophoresis

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Low risk smoltering MM treatment

Observation or

Lenalidomide + low dose dexamethasone

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High risk smoltering MM treatment

Observation or

Lenalidomide + low dose dexamethasone

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Ultra high risk smoltering MM treatment

Lenalidomide + low dose dexamethasone

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Characteristics of high risk smoltering MM

free light chain ratio of at least 8 and cytogenetics

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Anemia in MM

fatigue, weakness, SOB

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Renal dysfunction in MM

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

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Hypercalcemia in MM

due to bone lesions

dehydration, CNS, etc

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Bacterial infections in MM

decreased normal IgG and decreased lymphocyte function

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Osteolytic lesions in MM

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

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Neurologic symptoms in MM

cord compression

hyeprviscosity syndrome

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Partial response (PR) in MM

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

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Very good partial response (VgPR) in MM

Negative SPEP

Serum and urine M protein detected on immunofixation

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Complete remission (CR) in MM

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

Stringent CR (sCR) in MM

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

Immunomodulatory drugs (IMiDs) in MM

- Thalidomide - Lenalidomide - Pomalidomide

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

true

T/F lenalidomide is not teratogenetic?

false! none in rabbits yes in monkeys REMS program

ADE of thalidomide

- REMS - VTE - sedation - neuropathy - toxic epidermal necrolysis

ADE of lenalidomide

- REMS - VTE - myelosuppression - rash - fatigue

ADE of pomalidomide

similar to lenalidomide

T/F combination chemotherapy is still use to treat MM

False! | no longer used due to better tolerated and more active alternatives

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

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

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

true But seldom used due to well tolerated more active newer agents - cheap, oral, well tolerated

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

Pomalidomide

T/F thalidomide is an analog of lenalidomide

False! | Lenalidomide is an analog of thalidomide

Which proteasome inhibitors are used in MM?

Bortezomib Carfilzomib Ixazomib

What is the main treatment regimen for MM?

IMiDs + low dose dexamethasone

ADE of bortezomib

Myelosuppression Neuropathy Immunosuppression

ADE of carfilzomib

``` myelosuppression liver cardiac neuropathy pulmonary ```

ADE of ixazomib

myelosuppression | neuropathy

What is the first oral proteasome inhibitor used in MM?

Ixazomib

Induction therapy for MM

ASCT

ASCT non-candidates

frail low risk patients - use 2 drug regimen (Rd) | frail high risk patients - use 3 drug regimen (VRD)

How many cycles of induction do ASCT candidates use?

4 cycles VRd KRd

MM chemotherapy IMiD combinations

- Melphalan or CTX + IMiDs or proteasome inhibitors - Liposomal doxorubicin + bortezomib - Bendamustine + lenalidomide + bortezomib

Novel agents in MM

Panobinostat Elotuzumab Daratumumab

MOA of panobinostat

Pan histone deacetylase inhibitor

MOA of elotuzumab

antibody which targets SLAM F7

MOA of daratumumab

antibody which targets CD38

When are the novel agents used in MM?

salvage therapy

What is panobinostat used with?

carfilzomib and panobinostat + bortezomib + dexamethasone

What is elotuzumab used with?

bortezomib + dexamethasone

What is daratumumab used with?

bortezomib or lenalidomide + dexamethasone

ADE of panobinostat

myelosuppression diarrhea neuropathy

ADE of elotuzumab

myelosuppression | infusion reactions

ADE of daratumumab

myelosuppression | infusion reactions

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

true! | in patients who receive suboptimal response with first transplant

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

false | High dose

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

false

Stem cell collection in MM for autoHSCT

collect sufficient cells to do multiple transplants BEFORE receiving HD melphalan

Allogeneic transplant in MM

full intensity transplant --> high early mortality reduced intensity transplant --> high relapse rates

T/F allogeneic transplant is first line in MM

false! | no major role in treating MM

Should triple therapy or double therapy be used in MM?

triple therapy has improved progression free survival

Who would you use Melphalan + prednisone in MM?

older patients with symptoms

How long is induction in MM before autoHSCT?

4 months!

When would you consider someone relapsed/refractory MM?

if progression occurs > 6 months after end of primary induction

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

false! | switch to a different drug1

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

false | other way around

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

proteasome inhibitors

VTE in MM is usually due to which drugs?

IMIDs or dexamethasone

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

LMW heparin

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

ASA

Bone disease in MM treatment

Bisphosphonates | reassess in 2 years --> risk of ONJ and renal toxicity