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Haematology Week 3 > Plasma Cell Disorders > Flashcards

Plasma Cell Disorders Flashcards

1
Q

What is a plasma cell? What is its function?

A

A fully differentiated B cell / to pump out soluble antibodies

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2
Q

Antibodies are produced by what?

A

B cells and plasma cells

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3
Q

What are antibody proteins made up of?

A

2 heavy chains and 2 light chains

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4
Q

Name antibodies which are each of the following shapes: a) monomer? b) dimer? c) pentamer?

A

a) IgD, IgE, IgG b) IgA c) IgM

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5
Q

Normally, B cells and plasma cells will be polyclonal. What does this mean?

A

They will be diverse, with thousands of small clones all producing different antibodies

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6
Q

What is meant by a cell being monoclonal?

A

One clone develops and expands so there is overexpression of one particular clone of plasma cells - lots of similar antibodies will be produced

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7
Q

Monoclonal antibodies are derived from what?

A

Clonal expansion of a single B cell

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8
Q

A monoclonal antibody can also be known as what? What is the use of this?

A

Paraprotein / can be used as a marker of underlying clonal B cell disorders

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9
Q

What are the two stages of detecting immunoglobulins?

A

Serum electrophoresis detects abnormal protein bands / serum immunofixation is used to classify the abnormal protein band

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10
Q

A band on serum electrophoresis which shows up bright suggests the presence of what?

A

A monoclonal antibody

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11
Q

What are Bence-Jones proteins?

A

Immunoglobulin light chains detected by urine electrophoresis

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12
Q

When immunoglobulins are synthesised in plasma cells, more light chains than heavy chains are produced. What happens to the excess free light chains?

A

Secreted into the plasma, along with intact immunoglobulin

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13
Q

In Bence-Jones proteins, which type of free light chain will be seen as each of the following: a) monomers? b) dimers?

A

a) Kappa free light chains b) Lambda free light chains

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14
Q

Why do Bence-Jones proteins occur?

A

If there is an increase in the number of plasma cells then the amount of free light chains in the plasma increase and excess can leak into the urine

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15
Q

What is myeloma?

A

A plasma cell malignancy

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16
Q

What are the 3 stages of the development of myeloma?

A

MGUS, asymptomatic myeloma, myeloma

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17
Q

What are some direct tumour effects of myeloma?

A

Bone lesions/pain, hypercalcaemia, pancytopenia due to marrow failure

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18
Q

What are some paraprotein mediated effects of myeloma?

A

Renal failure, immunosuppression, hyperviscosity, amyloid

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19
Q

How does myeloma cause lytic bone disease?

A

Interacts with bone marrow stromal cells to produce IL-6 to suppress osteoblasts but activate osteoclasts causing a net loss of bone

20
Q

How can lytic bone disease of myeloma manifest?

A

As osteoporosis, or as focal lesions

21
Q

What are some features of hypercalcaemia which may be seen in myeloma?

A

Stones, bones, abdominal groans, psychiatric moans / dehydration, thirst, renal impairment

22
Q

What effects do light chains in myeloma have on the kidneys?

A

Tubular cell damage and cast nephropathy

23
Q

Are the renal effects of myeloma reversible? What are some treatment options?

A

Yes, if treated promptly / hydrate, stop nephrotoxic drugs, steroids and chemotherapy

24
Q

What is the median age at diagnosis of myeloma?

A

65

25
Q

What is the mainstay of treatment for myeloma?

A

Combination chemotherapy

26
Q

What other drug should always be given alongside chemotherapy for myeloma?

A

Corticosteroids (activity against plasma cells)

27
Q

In myeloma treatment, alkylating agents can be used. Give an example?

A

Cyclophosphamide

28
Q

In myeloma treatment, novel agents can be used. Give some examples?

A

bortezomib and lenalidomide

29
Q

What is a treatment option for myeloma which is only used in younger, fitter patients?

A

High dose chemotherapy and autologous stem cell transplant

30
Q

What is used to monitor response to myeloma treatment?

A

Paraprotein levels

31
Q

What are some treatments which can be used for symptom control in myeloma?

A

Opiate analgesics, local radiotherapy, bisphosphonates, vertebroplasty

32
Q

What are the survival outcomes of myeloma?

A

5-10 years for younger patients, though relapse is inevitable

33
Q

What happens every . time there is a remission of myeloma?

A

The period of remission becomes less

34
Q

In terms of paraproteins and plasma cells, what is seen in MGUS?

A

Paraproteins present at a level of < 30g/L and the bone marrow plasma cells are < 10%

35
Q

What are the clinical features of MGUS?

A

None

36
Q

Prevalence of MGUS increases with what? It is twice as common in who?

A

Age / Black people

37
Q

What is the risk of progression to myeloma from MGUS?

A

1% risk every year

38
Q

What is the mechanism behind AL amyloidosis?

A

Mutations in the light chains lead to altered structure. They then precipitate in tissues as an insoluble beta pleated sheet.

39
Q

What is the clinical presentation of AL amyloidosis?

A

Causes organ damage which is slowly progressive - often presents late with end organ failure

40
Q

How should AL amyloidosis be treated? What is its prognosis?

A

Chemotherapy to switch off the light chains / poor prognosis

41
Q

What is used to diagnose AL amyloidosis? What will this show under polarised light?

A

Organ biopsy with Congo red stain / apple green birefringence

42
Q

What is Waldenstrom’s macroglobulinaemia? What type of paraprotein is seen?

A

Clonal disorder of cell intermediates between a lymphocyte and plasma cell / IgM

43
Q

What are the tumour effects of Waldenstrom’s macroglobulinaemia?

A

Lymphadenopathy, splenomegaly, marrow failure

44
Q

What are the paraprotein effects of Waldenstrom’s macroglobulinaemia?

A

Hyperviscosity and neuropathy

45
Q

What are some ‘B symptoms’ of Waldenstrom’s macroglobulinopathy?

A

Night sweats and weight loss

46
Q

How is Waldenstrom’s macroglobulinaemia treated?

A

Plasmapheresis and possible chemotherapy

Haematology Week 3 (9 decks)

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