Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Haematology > Myeloma > Flashcards

Myeloma Flashcards

1
Q

What is multiple myeloma and how can it be identified histologically?

A

Patchy disease of tumour of plasma cells in bone marrow

Large number of plasma cells with eccentric nuclei

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

What is the most common disease associated with multiple myeloma? What are the implications of this disease?

A

Bone disease
Causes pain and increase mortality and morbidity
Indicates treatment needs to commence

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

What acts a cancer marker for multiple myeloma? What causes the levels of this marker to increase or decrease?

A

M- protein (myeloma protein)

Increase= relapse
Decrease= treatment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How many types of intact Ig are produced in myeloma? What can be produced instead of intake Ig?

A

1 type= monoclonal Ig

Kappa and lambda light chains can be produced instead of paraprotein (intact protein)

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

What are the symptoms of active myeloma? When should you consider multiple myeloma with patients?

A 
C= hypercalcaemia 
R= renal impairment 
A= anaemia + fatigue 
B= Bone pain + destruction i.e. fracture and cord compression 
I= infection

When patient continually presenting with back pain along with other symptoms

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

What is the diagnostic criteria for multiple myeloma?

A

M-protein >30g/L
+/- bone marrow plasma cells >10% (Norm= 5%)
Symptoms of end organ damage (CRABI)

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

What is MGUS? How does it differ to multiple myeloma?

A

Monoclonal gammopathy of uncertain significance

Pre-malignant condition= no symptoms (no end organ damage)
Monoclonal protein <30g/L
Bone marrow damage <10%

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

Why does bone disease arise in multiple myeloma? What kind of lesions does it result in?

A

Altered metabolism in MM prevents new bone from forming

Lytic lesion
I.e. diagnostic and differentiates from other forms of bone cancer which produce sclerosis lesions

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

Why is renal failure associated with multiple myeloma?

A

MAIN= Light chain component from Ig precipitates into tubules
Leads to cast neuropathy= myeloma kidney

Addition reasons:

  • dehydration
  • infection
  • hypercalacaemia
  • uric acid
  • amyloid
  • acute tubular necrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Why is hyperviscosity associated with multiple myeloma? What are the symptoms associated with hyperviscosity?

A

High Ig concentration

Headaches 
Confusion
Visual disturbance 
Bleeding
Ischaemic event 
Angina
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What can cause amyloid sardoisis in multiple myeloma?

A

Light chains can be deposited as EC protein

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

What is plasmacytoma and how does it relate to multiple myeloma?

A

Localise deposition of plasma cells in bony or soft tissue

Risk factor for developing multiple myeloma

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

What are the main complications of raised Ig levels in multiple myeloma?

A

Renal failure

Hyperviscosity

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

How would you diagnose myeloma? What are other clinical signs to look out for?

A
  1. Blood test= excess of monoclonal Ig i.e. M-protein
    NOTE: need to check for light chains (present in 15% of cases)
  2. Protein electrophoresis i.e. separation of proteins with peak for Ig
  3. Bone marrow aspirate i.e. looking for plasma cells >5%
  4. Skeletal survey i.e. core whole body MRI
  5. FBC
  6. Blood chemistry i.e. looking for hypercalcaemia
  7. B2 microglobulin

Clinical signs:

  • anaemia
  • renal impairment
  • total protein raise
  • hypercalcaemia
  • immunoparesis (suppression of other Ig)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Why is it hard to treat multiple myeloma?

A

Disease evolves over time
Patients have heterogenous response to treatment
Non-curable
Can enter plateau phase after treatment which can last for years

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

What genetic change is associated with multiple myeloma?

A

Translocations into 14q32

17
Q

Why is the BM microenvironment important for myeloma progression?

A
  • Protects the myeloma and encourages drug resistance
  • Immunosuppressive molecules alter the stroma to promote growth
  • Stromal cells increase expression of OPGL (osteoprotegrin ligand) and down regulate OPG == increased osteoclast stimulation= increased bone resorption
18
Q

What are examples of supportive management in multiple myeloma?

A

Pain= individual to the patient

Anaemia= erythropoietin injections or blood transfusions

Infection= IV antibiotics

Bone pain= radiotherapy

Hypercalcaemia= IV fluids/ Pamidronate IB (bisphosphonate) i.e. switches off osteoclasts activity

Depression/anxiety= support groups

Bone disease= Analgesia/radiotherapy/chemo/orthopaedic surgery/ Bisphosponate

19
Q

What are the 2 medical emergencies which can arise with multiple myeloma? How are they managed?

A
  1. Renal failure
    - Aggressive hydration
    - Stop nephrotoxic drugs i.e. NSAIDs
    - Treat myeloma with dexamethosone
  2. Cord compression due to posterior movement damaged vertebrae
    - Surgery if unstable
    - Radiotherapy if stable
    - Treat myeloma
20
Q

What is anti-myeloma treatment and when is it indicated?

A

Drugs specifically targeting myeloma cells

Symptomatic patients i.e. those with end organ damage

21
Q

What are the anti-myeloma drugs available as part of intensive treatment? State the mechanisms and adverse effects.

A

Bortezomid (Velcade)
Blocks proteasome to cause cell death via build up of toxins
A.E= nausea/diarrhoea/fatigue/headaches/constipation/thrombocytopenia/ peripheral neuropathy/ neutropenia

Thalidomide
Stimulates increased NK and TC activity and modifies cytokines and acts as anti-angiogenic

Lenalidomide (Revilimid)

A.E.= myelosuppression and increased risk of thrombosis

22
Q

What are the current drug treatment regimens for multiple myeloma?

A

VTD (velcade-thalidomide-dexamethasone)
VCD (velcade- cyclophosphamide-dexamethasone)
CTD (cyclophospamide-thalidomide-dexamethason)

23
Q

What is the process of stem cell transplant for multiple myeloma?

A

Myeloma needs to be remission and controlled before transplantation

Stimulate stem cells to enter blood via GCSF and mild chemo
Collect on apheresis machine (centrifuge)

24
Q

How does autologous peripheral blood stem cell transplant differ from other stem cell transplant?
What are the associated risks?

A

Stronger dose of chemo required to save from BM failure

Risks due to lacking white cells for 2-3 weeks:

  • infection
  • mucousitis
  • fatigue
  • anorexia
25
Q

When is non-intensive treatment used for multiple myeloma?

What are the current regimens?

A

When patient not suitable for BM transplant i.e. majority of time

VMP (Velcade-melphalan-predniolone)
VCD (Velcade-cyclophosphamide-dexamethasone)

Or Alkylating agent-steroid-thalidomide
Eg MPT or CTD

26
Q

What is a common complication with myeloma therapy and how is it managed?

A

Thrombosis

Anticoagulents therapy
I.e. Full dose warfarin (INR 2-3) or Asparin + full dose LMWH

27
Q

How is Daratumumab used to treat myeloma?

A

Monoclonal Ab

Has better response in patients w/o previous hx of treatment (decreased risk of resistance)
Increased efficacy when in combo with other drugs

Haematology (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions