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Haematology > Multiple Myeloma > Flashcards

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?

A

20-30%

25
Q

What symptoms /signs can renal failure cause?

A 
Oedema 
SOB 
Nausea and vomiting
Weight loss
Lethargy
26
Q

What type of anaemia occurs?

A

Normocytic and normochromic

27
Q

How frequently is anaemia a symptom?

A

70% of patients

28
Q

Why does anaemia occur?

A

The bone marrow is infiltrated by malignant cells

Also get neutropenia and thrombocytopenia

29
Q

Where does bone pain most often occur?

A

Back due to vertebral lytic lesions

30
Q

What imaging detects the lytic lesions?

A

X-ray (bone scan not effective as osteoblasts not stimulated)

31
Q

Why do patients get recurrent bacterial infections?

A

Immunoparesis

Neutropenia from disease process and due to chemotherapy

32
Q

What infections are most commonly seen?

A

Pneumonia

Pyelonephritis

33
Q

Why can hyperviscosity occur?

A

Increased circulating immunoglobulins

34
Q

What can hyperviscosity cause?

A 
Spontaneous bleeding - gums, epistaxis, rectal
Visual changes
Vertigo
Headaches
Reduced cognition
35
Q

How can hyperviscosity be treated?

A

Plasmapheresis to remove light chains

36
Q

What blood tests should be requested?

A

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
Q

Other than bloods, what other investigations should be done?

A

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
Q

What tests are useful prognostic indicators?

A

LDH

Beta 2 microglobulin

39
Q

What imaging is done?

A

Skeletal survey - plain X-ray showing “pepper pot” appearance
MRI whole body to detect lesions not seen on X-ray

40
Q

What does a blood film show?

A

Rouleaux formations = RBCs stacking together

41
Q

What is the diagnostic criteria?

A

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
Q

Why is it important to accurately diagnose myeloma?

A

Treatment must begin immediately due to risk of complications occurring as a result of end organ damage

43
Q

Is myeloma considered curable?

A

No , a chronic relapsing and remitting malignancy

Management aims to control symptoms, reduce complications and prolong survival

44
Q

In younger, healthier patients, how is it managed?

A

Induction therapy: bortezomib (chemotherapy) plus dexamethasone
Then autologous stem cell transplant

45
Q

In those unsuitable for transplantation, induction therapy is typically continued for how long and what does it consist of?

A

12-18 months or until paraprotein level plateaued

Consists of: thalidomide and alkylating agent plus dexamethasone

46
Q

Do patients often relapse after initial therapy?

A

Yes, need 3 monthly monitoring - bloods, electrophoresis

If occurs - Bortezomib monotherapy

47
Q

How should bone pain be managed?

A

Analgaesia- not NSAIDS

Zolendronic acid to all patients - reduce fracture rates and bone pain

48
Q

How can anaemia be managed?

A

Transfusion

EPO

49
Q

How can renal failure be managed?

A

Rehydrate

Dialysis may be needed if acute

50
Q

How should infections be managed?

A

Annual influenza vaccination
Immunoglobulin replacement therapy

Treat rapidly with broad spec antibiotics until culture results known

Haematology (16 decks)

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