Multiple Myeloma Flashcards

1
Q

What are risk factors for developing multiple myeloma

A

Race (Black)
Age > 65
Gender (male)
Radiation therapy
Obesity
Toxin exposure (pesticides, herbicides)
Genetics (hx of MGUS or first degree relative)
Immune system suppression (on SOT drugs, HIV/AIDS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is multiple myeloma? What is the most common Ig found?

A

A plasma cell disorder where B cells make non-functional antibodies
Most common = IgG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the 2 stages before ultimate progression to multiple myeloma?

A
  1. MGUS - M protein < 3. Bone plasma cells < 10%. No end organ damage.
  2. Smoldering MM - M protein > 3. Bence-Jones protein ≥ 500 mg/day. Bone plasma cells 10-59%. No end organ damage.
  3. MM - Bone marrow plasma cells ≥ 10%. Biopsy proven bony or extramedullary plasmacytoma. End organ damage.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the pneumonic for the pathophysiology of MM?

A

Sixty - ≥60% bone marrow plasma cells
Light chains - uninvolved light chain ratio is ≥ 100
MRI - >1 lesion on MRI ≥5mm
Calcium - SCa > 1 mg/dL above ULN OR >11 mg/dL
Renal - CrCl < 40 mL/min OR SCr > 2 mg/dL
Anemia - Hgb > 2 mg/dL below LLN OR < 10 mg/dL
Bone - ≥1 osteolytic lesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How does MM infiltration affect bone activity?

A

Increased osteoclast activity (increased RANK-L)
Increasing focal lesions (lytic lesions)
Anemia (invasion into bone marrow)
Hypercalcemia** (from bone resorption)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How does MM cause renal impairment?

A

Renal dysfunction is caused by:
- Hypercalcemia from bone invasion
- myeloma cast nephropathy
- concomitant nephrotoxic agents

Leads to decreased erythropoietin/adds to anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What kinds of diagnostic workups are required for MM?

A

Blood tests
24 hr urine test
Bone marrow biopsy
Whole body CT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the patient presentation of MM?

A

Bone pains (back, ribs, hips)
Fracture
Frequent infections
Anemia (SoB, fatigue, palor)
Rare: hyperviscosity and peripheral neuropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is a major supportive care measure for MM? What are some other possible supportive care measures?

A

Bisphosphinates!
(Or denosumab)
Must get dental clearance before initiating
Recommended use for 2 years

Erythropoietin/transfusions (Anemia)
IVIG (serious recurrent infection)
Acyclovir (for HSV reactivation)
Levofloxacin prophylaxis (newly dx MM)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the triplet and quadruplet regimens? (MM)

A

Gold standard - triplet regimen RVd
- Revlimid (lenalidomide), Velcade (bortezomib), dexamethasone

Some pts may benefit from quadruplet regimen Dar-RVd
- Daratumumab, Revlimid (lenalidomide), Velcade (bortezomib), dexamethasone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What kind of transplant is preferred after chemo in MM? How many cells should be collected? What are some considerations?

A

Preferred - autologous stem cell transplant (self-cells), allogenic has high toxicity
Collect enough cells for 2 transplants
Consider: age, renal/hepatic/cardica function, performance status, caregiver support

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are some premedication and post medication medications for DARATUMUMAB? (MM)

A

Premed:
Dexamethasone/MPS
APAP
Benadryl
Montelukast for first dose

Postmed:
MPS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are some side effects of Daratumumab? (MM)

A

Infusion rx
Herpes zoster reactivation
Hepatitis B reactivation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the MOA of Daratumumab? (MM)

A

Anti-CD38 kappa human mAb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the MOA of Bortezomib? (MM)

A

Proteasome inhibitor = causes major apoptosis!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What formulation of Bortezomib is preferred and why?

A

SQ
IV causes terrible peripheral neuropathy!

17
Q

What are some AEs of Bortezomib? (MM)

A

Herpes zoster reactivation
Thrombocytopenia
Peripheral neuropathy (IV bortezomib > SQ Bortezomib > ixazomib&raquo_space; carfilzomib)

18
Q

What is the MOA for Lenalidomide? (MM)

A

Immunomodulator drug (IMiD)
Anti-angiogenic (like VEGFi)
Upregulation of pro-apoptotic factors/enhanced recruitment of T-cells and NK-cells

19
Q

What is the route of admin for Lenalidomide and what is the admin schedule? (MM)

A

Oral!
Take days 1-21 of the 28 day schedule
OR
Days 1-14 of a 21 day schedule

20
Q

What are some AEs of Lenalidomide? (MM)

A

BIRTH DEFECTS [REMS program]
Hematologic toxicity
Thrombosis
Somnolence
Increased secondary malignancy
Rash + skin toxicity
Diarrhea
Peripheral neuropathy

21
Q

What is a special program Lenalidomide patients must be enrolled in? What do they have to do to qualify for the drug?

A

REMS program
Confidential surveys must be completed monthly for females who can get pregnant and males
OR
Every 6 months for females who cannot get pregnant

MUST USE highly effective birth control + barrier method

22
Q

How should we counsel couples who cannot get pregnant and want to use Lenalidomide?

A
  • Many different people could be exposed to the medications
    Wash hands/use gloves, store in original packaging, proper disposal
23
Q

What increases risk of thrombosis in MM patients? What can decrease the risk?

A

INCREASED risk:
Prior VTE
High dose steroids
Obesity
Catheters
Fractures
Lenalidomide use

DECREASED risk:
Asian/Pacific islander

24
Q

What anticoagulation prophylaxis should MM patients get if they are already on pre-existing anticoagulation?

A

Continue prescribed anticoagulation in most cases (Eliquis, enoxaparin, etc)
DO NOT decrease intensity!

25
Q

What anticoagulation prophylaxis should MM patients get if they are on lenalidomide after a partial response with no other risk factors?

A

Aspirin 81 mg

26
Q

What are side effects of dexamethasone? (MM)

A

• Insomnia
• Mood changes
• Increased appetite
• GI upset/reflux
• Hyperglycemia
• Edema
• Weight gain
• Hypertension

27
Q

MM patients can have varied chemo regimens based on what they have previously received. Elotuzumab is one of these; what is the MOA?

A

Humanized IgG antiAb
Directly activates NK cells

28
Q

MM patients can have varied chemo regimens based on what they have previously received. Elotuzumab is one of these; what are the medications used for premedication?

A

APAP
Benadryl
Famotidine
Dexamethasone (3-24 hrs before, then immediately before)

29
Q

MM patients can have varied chemo regimens based on what they have previously received. Elotuzumab is one of these; what are some AEs?

A

Infusion reactions
Thrombocytopenia
Herpes Zoster reactivation

30
Q

What are the Bispecific T-cell Engagers (BiTEs)? What is their MOA?

A

Talquetamab
Teclistamab
Elranatamab

MOA - Targets one tumor antigen and one immune-related molecule (or 2 tumor antigens/immune-related molecules)

31
Q

Patients on the BiTEs drugs in MM are required to enter a REMS program. What is required for these patients to receive their drug?

A

Verify prescribers have completed training, forms etc. and that patients are being counseled on the side effects

32
Q

What are two MAJOR side effects of all the BiTEs drugs (MM)?

A

Cytokine Release Syndrome
Immune Effector Cell-Associated Neurotoxicity

33
Q

Describe Cytokine Release Syndrome in BiTEs patients (MM). What is the presentation?

A

Increased cytokines due to T-cell activation which causes a systemic inflammatory response

Presentation: Fever, hypotension, hypoxia

34
Q

Describe Immune Effector Cell-Activated Neurotoxicity in BiTEs patients (MM). What is the presentation? What can it be treated with?

A

Disruption of the blood brain barrier and increased cytokines in the CSF.
Worst presentation: stupor/unarousable, prolonged, seizures, focal edema, motor weakness

Treatment: antiepileptics, steroids, supportive

35
Q

Talquetamab has significantly more AEs than the other BiTEs. What are they?

A

UNIQUE to drug:
Skin AE (eczema, fissures, hyperpigmentation, lesions/ulcers)
Nail AE (nail bed disorder, hypertrophy, ridging, onycholysis)
Rash AE (dermatitis, rash)
Oral AE (dry mouth and food tastes BAD)
Weight Loss

ALL BiTEs:
Cytopenia
Cytokine Rekease Syndrome/Immune Effector Cell-Associated Neurotoxicity
[many people d/c because of AEs]

36
Q

What are the AEs of BiTEs Elranatamab and Teclistamab? (MM)

A

Cytopenia
Cytokine Rekease Syndrome
Immune Effector Cell-Associated Neurotoxicity