Muyltiple Myeloma 3/23/13 Flashcards

1
Q

What is an M spike?

A

When doing gell electrophoresis on the serum of a MM patient, you will get an M spike because of the over production of monoclonal antibodies.

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2
Q

What is multiple myeloma?

A

A malignancy of late B cells that mature principally into neoplastic plasma cells that generally produce a complete and or partial light chain immunoglobulin antibody

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3
Q

What is an IFE?

A

Immunofixation test

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4
Q

What does the immunofixation test tell you?

A

It will tell you what type of monoclonal antibody it is is. (IgE kappa. IgG lambda etc…

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5
Q

Name the four components of CRAB

A

hyperCalcemia (leads to renal problems and mental impairment), Renal failure/insufficiency, Anemia, Bone destruction…..also can develop hypogammaglobulinemia which leads you susceptible to infection, amyloidosis, visouc blood.

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6
Q

What is MGUS?

A

Monoclonal gammopathy of uncertain significance. Not multiple Myeloma but it is a precursor. You have M protein in the serum and some bone marrow clonal plasma cells but no organ or tissue impairment.

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7
Q

What signals a transition from MGUS to myeloma?

A

Increased protein

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8
Q

What is SMoldering Myeloma?

A

Basically in between MGUS and Multiple Myeloma

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9
Q

Mechanism of bone destruction in MM

A

osteoblast differentiation is blocked by RANKL which stimulates osteoclast production. The DKK1 produced by myeloma cells is what stimulates RANKL production.

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10
Q

What are the two staging systems for MM?

A

Durie Salmon and ISS

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11
Q

Describe ISS staging

A

Only looks at Beta 2 Microglobulin and Albumin.
Stage 1- Normal B2M and normal Alb
Stage 2- in between
Stage 3- B2M over 5.5

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12
Q

Describe Durie Salmon staging

A

Stage 1- Hb above 10, Ca below 12, M protein below 5, Bence Jones below 4
Stage 2- in between
Stage 3- Hb below 8.5, Ca above 12, M pro above 7
Most everyone that presesnts is stage 3

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13
Q

Whats the worst prognostic indicator in MM

A

del 17p

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14
Q

What two classifications of new drugs have changed the way MM is treated?

A

IMiDs and Proteasome inhibitors

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15
Q

What the hell is an IMiD

A

An immune modulator (hence the IM) that works by activating NK cells to destroy tumor cells. Also alter the stromal structure that may stimulate myeloma cells.

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16
Q

What is the major proteasome inhibitor used against MM?

A

Bortezomib

17
Q

How does Bortezomib work>

A

Proteasomes degrade proteins. In some way, inhibiting this destroys the Myeloma cell. I have no idea….

18
Q

Why do you use an autologous transplant?

A

Its a way of giving high does chemo to the bone marrow alone. You take the marrow out, blast it, put it back in.

19
Q

When is autologous transplant used?

A

If you are under 70 and in decent health

20
Q

What is Waldenstrom’s macroglobulinemai

A

Excess IgM. Low grade lymphoma.

Most who present are over 40, fatigue wt. loss, abnormal bleeding Hyperviscosity syndrome

21
Q

WHy do they present with Hyperviscosiity syndrome more often than MM pts?

A

B/c IgM is a big ass molecule.

22
Q

What do you treat Waldenstrom’s macroglubulinemia with?

A

Rituximab- maybe, botezomib- maybe….mixing lymphoma and myeloma drugs

23
Q

Causes of Amyloidosis

A

Monoclona serum antibodies, transthyretin, Chronic osteomyelitis

24
Q

Who gets MM?

A

Old African Americans

25
Q

Morphology

A

Look for rouleax cells in blood.