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Multiple Myeloma Flashcards

1
Q

What is multiple myeloma a disease of?

A

Plasma cells (proliferation)

  • fill up the bone marrow
  • produce aberrant antibodies (immunoglobulins)
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2
Q

It is the …. most common haematological malignancy

A

Second

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3
Q

What is the median age at presentation?

A

70

But 10-15% are less than 45

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4
Q

Who is it more common in?

A

Men

Black Africans

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5
Q

What causes myeloma?

A

Genetic mutations - occurs as B lymphocytes differentiate into mature plasma cells (HLA Cw5 or Cw2 May play role)
Defects that carry poor prognosis: chromosome 13 abnormalities, p53 deletions

Environmental- exposure to agricultural, food, petrochemical industries, long term hair dye exposure

Radiation

MGUS - approx 19% develop MM

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6
Q

A typical antibody is composed of…

A 
2 immunoglobulin (Ig) heavy chains 
2 immunoglobulin (Ig) light chains
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7
Q

What 5 heavy chain isotypes are there?

A

MAGED

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8
Q

What 2 light chain isotypes are there?

A

Kappa

Lambda

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9
Q

What are the abnormal antibodies produced in myeloma called?

A

Paraproteins (also called M protein/ M spike / monoclonal gammopathy)

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10
Q

What is the most common immunoglobulin abnormality in multiple myeloma?

A

IgGk (55%)

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11
Q

How is myeloma classified?

A

Based on Ig product
IgG in 2/3
IgA in approx 1/3
Few are IgM or IgD

Other Ig levels are low (increased infection susceptibility)

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12
Q

What is Bence Jones proteinuria?

A

Free Ig light chains of kappa or lambda filtered by kidneys into urine

Usually light chains synthesised in excess and cleared by kidney - normally less than 10mg/ day. In MM more than 10mg/ day

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13
Q

Is Bence Jones proteinuria detected by traditional urine dipstick?

A

No - only detects albumin proteins

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14
Q

What does serum electrophoresis of plasma proteins show in MM?

A

Increased gamma globulins = monoclonal spike (M spike)

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15
Q

What can immunoelectrophoresis tell you?

A

Which type of immunoglobulin is abundant

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16
Q

What type of immunity is affected?

A

Humoral immunity - so increased risk of infection by staphylococcus aureus, e-coli etc

NOT viruses

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17
Q

How does it present?

A

CRABBI

C - hypercalcaemia 
R - renal failure 
A - anaemia 
B - bleeding 
B - bone pain 
I - infection risk
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18
Q

Why does hypercalcaemia occur?

A

Increased osteoclast activity with no corresponding increase in osteoblast activity - causing LYTIC lesions

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19
Q

Myeloma cells stimulate the production of specific cytokines that stimulate osteoclast activity. What are they?

A

IL-6 and RANK ligand

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20
Q

Where do the lytic lesions typically occur?

A

Skull

Vertebrae

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21
Q

What symptoms are associated with hypercalcaemia?

A 
Weakness
Nausea 
Constipation 
Confusion 
Polyuria and polydipsia
22
Q

The bone destruction can lead to…

A

Pathological Fractures

Spinal cord compression

23
Q

What causes the renal impairment?

A 
Combination of factors: 
Obstruction due to Bence Jones proteins 
Direct toxicity of the light chains 
Hypercalcaemia
Hyperuricaemia 
Long term use of NSAIDS can cause damage to kidneys
24
Q

Renal failure occurs in what percentage of patients?

25
What symptoms /signs can renal failure cause?
``` Oedema SOB Nausea and vomiting Weight loss Lethargy ```
26
What type of anaemia occurs?
Normocytic and normochromic
27
How frequently is anaemia a symptom?
70% of patients
28
Why does anaemia occur?
The bone marrow is infiltrated by malignant cells | Also get neutropenia and thrombocytopenia
29
Where does bone pain most often occur?
Back due to vertebral lytic lesions
30
What imaging detects the lytic lesions?
X-ray (bone scan not effective as osteoblasts not stimulated)
31
Why do patients get recurrent bacterial infections?
Immunoparesis | Neutropenia from disease process and due to chemotherapy
32
What infections are most commonly seen?
Pneumonia | Pyelonephritis
33
Why can hyperviscosity occur?
Increased circulating immunoglobulins
34
What can hyperviscosity cause?
``` Spontaneous bleeding - gums, epistaxis, rectal Visual changes Vertigo Headaches Reduced cognition ```
35
How can hyperviscosity be treated?
Plasmapheresis to remove light chains
36
What blood tests should be requested?
FBC - normocytic normochromic anaemia, WCC and platelets normal or low U&E - raised urea and creatinine, hypercalcaemia CRP - raised ESR persistently raised LFTS especially for ALP - usually normal as osteoblasts not activated
37
Other than bloods, what other investigations should be done?
Serum or urine electrophoresis - raised concentration of monoclonal IgG/IgA present (in urine they are known as Bence Jones proteins) Immunoelectophoresis Bone marrow aspiration and trephine biopsy confirms diagnosis if number of plasma cells significantly raised
38
What tests are useful prognostic indicators?
LDH | Beta 2 microglobulin
39
What imaging is done?
Skeletal survey - plain X-ray showing “pepper pot” appearance MRI whole body to detect lesions not seen on X-ray
40
What does a blood film show?
Rouleaux formations = RBCs stacking together
41
What is the diagnostic criteria?
1) Monoclonal protein band in serum or urine electrophoresis 2) Increased plasma cells on marrow biopsy 3) Evidence of end organ damage - hypercalcaemia, renal damage, anaemia 4) bone lesions
42
Why is it important to accurately diagnose myeloma?
Treatment must begin immediately due to risk of complications occurring as a result of end organ damage
43
Is myeloma considered curable?
No , a chronic relapsing and remitting malignancy | Management aims to control symptoms, reduce complications and prolong survival
44
In younger, healthier patients, how is it managed?
Induction therapy: bortezomib (chemotherapy) plus dexamethasone Then autologous stem cell transplant
45
In those unsuitable for transplantation, induction therapy is typically continued for how long and what does it consist of?
12-18 months or until paraprotein level plateaued Consists of: thalidomide and alkylating agent plus dexamethasone
46
Do patients often relapse after initial therapy?
Yes, need 3 monthly monitoring - bloods, electrophoresis If occurs - Bortezomib monotherapy
47
How should bone pain be managed?
Analgaesia- not NSAIDS | Zolendronic acid to all patients - reduce fracture rates and bone pain
48
How can anaemia be managed?
Transfusion | EPO
49
How can renal failure be managed?
Rehydrate | Dialysis may be needed if acute
50
How should infections be managed?
Annual influenza vaccination Immunoglobulin replacement therapy Treat rapidly with broad spec antibiotics until culture results known

Haematology (16 decks)

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